/*
 * Copyright DataStax, Inc.
 *
 * Licensed under the Apache License, Version 2.0 (the "License");
 * you may not use this file except in compliance with the License.
 * You may obtain a copy of the License at
 *
 * http://www.apache.org/licenses/LICENSE-2.0
 *
 * Unless required by applicable law or agreed to in writing, software
 * distributed under the License is distributed on an "AS IS" BASIS,
 * WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
 * See the License for the specific language governing permissions and
 * limitations under the License.
 */
package com.datastax.dse.driver.api.mapper.reactive;

import static org.mockito.Mockito.mock;

import com.datastax.oss.driver.api.core.CqlIdentifier;
import com.datastax.oss.driver.api.core.DefaultProtocolVersion;
import com.datastax.oss.driver.api.core.ProtocolVersion;
import com.datastax.oss.driver.api.core.cql.ColumnDefinitions;
import com.datastax.oss.driver.api.core.cql.Row;
import com.datastax.oss.driver.api.core.detach.AttachmentPoint;
import com.datastax.oss.driver.api.core.type.DataType;
import com.datastax.oss.driver.api.core.type.DataTypes;
import com.datastax.oss.driver.api.core.type.codec.registry.CodecRegistry;
import com.datastax.oss.driver.internal.core.cql.EmptyColumnDefinitions;
import edu.umd.cs.findbugs.annotations.NonNull;
import java.nio.ByteBuffer;
import java.util.Collections;
import java.util.List;

class MockRow implements Row {

  private int index;

  MockRow(int index) {
    this.index = index;
  }

  @Override
  public int size() {
    return 0;
  }

  @NonNull
  @Override
  public CodecRegistry codecRegistry() {
    return mock(CodecRegistry.class);
  }

  @NonNull
  @Override
  public ProtocolVersion protocolVersion() {
    return DefaultProtocolVersion.V4;
  }

  @NonNull
  @Override
  public ColumnDefinitions getColumnDefinitions() {
    return EmptyColumnDefinitions.INSTANCE;
  }

  @NonNull
  @Override
  public List<Integer> allIndicesOf(@NonNull String name) {
    return Collections.singletonList(0);
  }

  @Override
  public int firstIndexOf(@NonNull String name) {
    return 0;
  }

  @NonNull
  @Override
  public List<Integer> allIndicesOf(@NonNull CqlIdentifier id) {
    return Collections.singletonList(0);
  }

  @Override
  public int firstIndexOf(@NonNull CqlIdentifier id) {
    return 0;
  }

  @NonNull
  @Override
  public DataType getType(int i) {
    return DataTypes.INT;
  }

  @NonNull
  @Override
  public DataType getType(@NonNull String name) {
    return DataTypes.INT;
  }

  @NonNull
  @Override
  public DataType getType(@NonNull CqlIdentifier id) {
    return DataTypes.INT;
  }

  @Override
  public ByteBuffer getBytesUnsafe(int i) {
    return null;
  }

  @Override
  public boolean isDetached() {
    return false;
  }

  @Override
  public void attach(@NonNull AttachmentPoint attachmentPoint) {}

  // equals and hashCode required for TCK tests that check that two subscribers
  // receive the exact same set of items.

  @Override
  public boolean equals(Object o) {
    if (this == o) {
      return true;
    }
    if (!(o instanceof MockRow)) {
      return false;
    }
    MockRow mockRow = (MockRow) o;
    return index == mockRow.index;
  }

  @Override
  public int hashCode() {
    return index;
  }
}


Q:

MVC 5 Global User Account Object

I have a application with the following Layout. In the Shared Views Folder I have, _Layout.cshtml, _SideNav.cshtml and _CurrentUser.cshtml.
In the _Layout.cshtml I have:
@{ Html.RenderPartialIf("_SideNav", Request.IsAuthenticated); }

In the _SideNav.cshtml I have:
@{ Html.RenderPartial("_CurrentUser"); }

In the _CurrentUser.cshtml I have:

            @User.Identity.Name

We use FormsAuthentication to authenticate a user. We are not using the standard Identity authentication which ships with ASP.Net MVC 5 because we are using a LDAP Server.
FormsAuthentication.SetAuthCookie(username, isPersistent);
.....
HttpContext.Current.User = new GenericPrincipal(new GenericIdentity(username, "Forms"), roles);

We use the username in the cookie so that we can easily get information from the LDAP server.
Problem: @User.Identity.Name returns that username. But I need to display the full name of the user. I have access to the full name when we authenticate. but not sure how to use it.
How can I pass the FullName value from the AccountController to the _CurrentUser.cshtml partial view? Kind of like a Global Container like @User.Identity with more attributes that can be set.

A:

You can use something like this
FormsAuthenticationTicket ticket = new FormsAuthenticationTicket(1,
                                                                viewModel.Email,
                                                                YOUR_ISSUE_DATE,
                                                                YOUR_EXPIRE_DATE,
                                                                viewModel.RememberMe,
                                                                JsonConvert.SerializeObject(user),
                                                                FormsAuthentication.FormsCookiePath);

string hash = FormsAuthentication.Encrypt(ticket);
HttpCookie authcookie = new HttpCookie(FormsAuthentication.FormsCookieName, hash);

Response.Cookies.Add(authcookie);


package validate

import (
	"github.com/hashicorp/terraform-plugin-sdk/helper/validation"
)

// deprecated use validation.IsURLWithHTTPS instead
func URLIsHTTPS(i interface{}, k string) (_ []string, errors []error) {
	return validation.IsURLWithHTTPS(i, k)
}

// todo ad to sdk
// deprecated use validation.IsURLWithScheme instead
func URLIsHTTPOrHTTPS(i interface{}, k string) (_ []string, errors []error) {
	return validation.IsURLWithScheme([]string{"http", "https"})(i, k)
}


Isolation and characterization of Tula virus, a distinct serotype in the genus Hantavirus, family Bunyaviridae.
A Vero E6 cell culture isolate of Tula virus (TUL), a hantavirus first detected in European common voles (Microtus arvalis and M. rossiaemeridionalis) by RT-PCR was obtained after initial passaging of TUL-infected vole lung samples in laboratory-colonized M. arvalis. TUL was defined as a classical serotype by a cross-focus-reduction neutralization test (FRNT) and was also shown to be distinct from other hantaviruses by haemagglutination inhibition assay. The sequences of S, M and partial L genome segments of the isolate were determined: the S segment was 99.9% identical to the original rodent-derived sequence. Serological evidence for a previous TUL infection was obtained from the serum of a blood donor living near a TUL focus in Moravia, Czech Republic, showing at least a 16-fold higher FRNT titre to TUL as compared to Puumala or other hantaviruses.


Introduction {#s1}
============

Inappropriate prescribing of analgesics or self-administration through over the counter formulations results in regular often negative reporting within the media. Indeed, their abuse within elite through to recreational sport is not uncommon (Feucht and Patel, [@B21]; Warden, [@B74]; Tscholl and Dvorak, [@B69]; Brewer et al., [@B12]). For example, acetaminophen (ACT; commonly known as paracetamol) use is even prevalent in young sub-elite athletes, who consume ACT or other analgesics \[e.g., non-steroidal anti-inflammatory drugs (NSAIDs)\] to decrease pain from previous athletic exertion or prophylactically to reduce pain in subsequent training/competition (Garcin et al., [@B30]). Related recent headlines include a former FIFA Chief Medical Officer stating that "about half of players competing at the past three World Cups routinely took NSAIDs like ibuprofen" whilst former players report pressure to use such drugs "to get through games" (BBCSport, [@B6]). NSAIDs and ACT are the most commonly used antipyretic and analgesic drugs worldwide (Hinz and Brune, [@B33]). Given they are available over the counter, their use even with careful club/team physician oversight can be difficult to police within a professional sport environment. If team clinicians ban over the counter analgesia use, players can and do simply self-administer, increasing risk of drug interaction with clinician prescribed medications and/or over-dose risk (inadvertently or otherwise).

ACT has been used globally since 1955 and is considered a safe effective analgesic (Bunchorntavakul and Reddy, [@B13]). The analgesic properties of ACT are similar to NSAIDs, yet ACT does not share similar NSAID mediated anti-inflammatory actions (Graham et al., [@B31]). ACT carries fewer, if any, side-effects when used at appropriate dosages compared to NSAIDs (Towheed et al., [@B68]; Jones et al., [@B37]). NSAIDs side-effects can include gastrointestinal and arterial wall damage, gastrointestinal ulcers, arterial blood clotting, myocardial infarction, stroke and hemorrhage perforation, amongst others (Ong et al., [@B50]; Van Wijck et al., [@B70]). The well evidenced and publicized side-effect of ACT is liver necrosis in cases of acute overdose \[e.g., ACT at 250 mg.kg, \~15 g for a 60 kg human (Prescott et al., [@B55]; Prescott, [@B52]; Raffa et al., [@B56])\], evidently not seen under appropriate acute and/or regular use (Skoglund et al., [@B62]; Dippel et al., [@B18]). Although uncommon relative to ACT chronic use, liver necrosis has been reported when concomitant with other factors such as fasting/malnutrition, alcoholism and the use of cytochrome P450 enzyme inducing drugs (Vitols, [@B73]).

Novel research has seen ACT used outside of its typical clinical parameters, including exercise performance domains (Mauger et al., [@B47], [@B48]; Foster et al., [@B28]) and to induce mild hypothermia within afebrile humans (Foster et al., [@B27], [@B26]). ACT use whilst safe in many scenarios (Ong et al., [@B50]; Graham et al., [@B31]) does present risk in others (Hinz and Brune, [@B33]; Aminoshariae and Khan, [@B2]), across research and clinical agendas. This opinion piece will detail the variable acute dose and chronic dosages, and their pharmacological safety across established and emerging research fields. In particular, this article will present evidence to support the following opinions: ACT should not be advocated for use within a sporting context, given the present evidence is from tightly controlled laboratory studies which do not replicate the multifaceted physiological, biochemical, and environmental perturbations to homeostasis during sporting performance.ACT may provide a useful tool in determining fundamental biochemical thermoregulatory mechanisms *in vivo* in humans, when appropriate experimental controls and designs are employed.

Emerging acetaminophen use within physiology research {#s2}
=====================================================

Evidence presented/discussed herein focuses on orally administered ACT in adult populations (unless stated otherwise). An "acute" ACT dose constitutes one-time single administration, whilst a chronic ACT "dosage" describes multiple doses over a day(s). An adult therapeutic dose of ACT is a 1 g single dose or a dosage of 4 ^\*^ 1 g daily at 4--6 h intervals (Bunchorntavakul and Reddy, [@B13]). Children aged 2--12 years are normally given an individualized body weight derived therapeutic dose at 10--15 mg.kg (Jackson et al., [@B36]). ACT has been used beyond its primary functions as an analgesic and antipyretic in attempts to understand or augment athletic performance (Mauger et al., [@B47], [@B48]; Mauger and Hopker, [@B46]; Foster et al., [@B28]) and manipulate/characterize thermoregulation within temperate, cold and hot environments (Dippel et al., [@B19], [@B20]; Coombs et al., [@B17]; Taylor et al., [@B66]; Foster et al., [@B27], [@B26]). From these specific fields of research, no evidence of adverse reactions to ACT have been reported. The evidence informed safety of ACT from seminal work across a variety of populations will be discussed later in this article (see ACT dose and pharmacokinetics section).

An acute ≤ 1.5 g ACT dose has been used in athletic performance research to improve time trial, time to exhaustion and repeated sprint exercise performance (Mauger et al., [@B47], [@B48]; Mauger and Hopker, [@B46]; Foster et al., [@B28]). These effects were attributed to ACT-mediated reductions in exercise induced pain, resulting in maintenance of a higher power output and/or an increased time to exhaustion, despite no change in perceived pain or exertion compared to a placebo condition (Mauger et al., [@B47], [@B48]; Foster et al., [@B28]). Whilst tolerance of exercise induced pain can be crucial to athletic performance (Ayoub et al., [@B5]; Amann et al., [@B1]; Astokorki and Mauger, [@B4],[@B3]), it also serves to provide essential feedback on injury and/or fatigue \[i.e., a deterrent/modulator of an activity potentially causative of harm (Mauger, [@B45])\]. Indeed, complete inhibition of pain elicited adoption of an over-aggressive sub-optimal cycling pacing strategy resulting in greater peripheral fatigue and no improvement in athletic performance, without injury pesentation (Amann et al., [@B1]). This suggests that pain may provide valuable feedback to higher centers to maintain an "optimal" distribution of work rate (Ayoub et al., [@B5]; Astokorki and Mauger, [@B4],[@B3]; St Clair Gibson et al., [@B64]).

Disruption of thermoregulatory mechanisms by ACT have been linked to improved time to exhaustion during cycling exercise in the heat (Mauger et al., [@B48]). Attributed to core temperature (Tc), skin temperature, body temperature and thermal sensation being significantly reduced in the ACT compared to placebo condition (Mauger et al., [@B48]). This suggests ACT disrupted thermoregulatory mechanisms and reduced thermal strain during exercise (Mauger et al., [@B48]), as observed elsewhere (Burtscher et al., [@B14]; Veltmeijer et al., [@B72]). These specific thermoregulatory effects of ACT may, or may not, have been complemented by the analgesic effects discussed above (Mauger et al., [@B47]; Foster et al., [@B28]). It must be stated here that the above exercise performance discussions are not advocating the use of ACT within these domains. The clinician and athlete (elite or otherwise) together should deliberate the ethical and safety considerations of strategies that override homeostatic controls before implementing them to enhance exercise performance, or indeed for any other purpose (clinically or otherwise).

ACT can alter thermoregulation in clinical (Dippel et al., [@B19], [@B20]; Koennecke and Leistner, [@B41]; Kasner et al., [@B39]) and healthy populations (Foster et al., [@B27], [@B26]). Up to half of patients who suffer an acute stroke present with a febrile Tc (Dippel et al., [@B19]). ACT administration elicited dose dependent Tc reductions of 0.4°C \[6 ^\*^ 1 g/day for 5 days (Dippel et al., [@B19], [@B20])\] and 0.22°C \[3.9 g/day for 5 days (Kasner et al., [@B39])\] in these patients. ACT ingestion \[20 mg.kg lean body mass (LBM)\] induced mild hypothermia (range: 0.1--0.39°C drop in Tc) in afebrile participants housed in ambient conditions of 20°C 40% relative humidity \[RH (Foster et al., [@B27])\]. Such conditions are below the human thermoneutral zone (TNZ) where the body invokes mechanisms to maintain a stable Tc (Stocks et al., [@B65]). Within a similar design to Foster et al. ([@B27]), Foster et al. ([@B26]) demonstrated within cold (10°C 40% RH) compared to thermoneutral conditions (25°C 40% RH), ACT ingestion (20 mg.kg LBM) elicited Tc instability (Foster et al., [@B26]). Specifically, Tc decreased in the cold condition (10°C 40% RH) with ACT ingestion (range: 0.16--0.57°C) and remained stable within the cold placebo condition whilst Tc stability was maintained in both placebo and ACT thermoneutral conditions (25°C 40% RH). This *in vivo* human data suggest ACT has inhibitory actions on heat producing mechanisms in certain febrile (Dippel et al., [@B19], [@B20]; Koennecke and Leistner, [@B41]; Kasner et al., [@B39]) and afebrile states (Foster et al., [@B27], [@B26]). Within afebrile states the limited data suggests hypothermic effects present only below the human TNZ (Foster et al., [@B27], [@B26]).

Mechanistically it appears ACT has an ability to disrupt "normal" thermoregulatory mechanisms in humans beneath the TNZ (Foster et al., [@B27], [@B26]). This is outside ACT\'s typical use as an analgesic and febrile antipyretic. Indeed, whilst explicitly described within rodents (Langenbach et al., [@B42]; Ayoub et al., [@B5]), the cyclooxygenase (COX)-prostaglandin E2 (PGE2) thermogenesis pathway (detailed below) has not been robustly determined *in vivo* within humans. COX1 knockout mice produced 99% less PGE2 than their wild type counterparts (Langenbach et al., [@B42]). No compensatory COX2 production to maintain PGE2 levels occurred when inflammation was not present (Langenbach et al., [@B42]). Such data indicate that PGE2 production, and thus thermogenesis, is somewhat dependent upon COX1 in the absence of a febrile and/or inflammatory state. Confirming the thermogenic influence of this COX1-PGE2 pathway in afebrile and non-inflammatory mammal\'s, housed beneath their TNZ, is a robust dose dependent drop in Tc within wild type mice \[i.e., not COX1 knockout mice (Ayoub et al., [@B5]; Fukushima et al., [@B29])\]. ACT administration in the largest doses (300 mg.kg) produced the greatest Tc decreases \[2 and 4°C (Ayoub et al., [@B5]; Fukushima et al., [@B29])\], and a 96% reduction in PGE2 concentrations (Ayoub et al., [@B5]). There is uncertainty within the literature on the function of a third COX isoform within mammals, a splice variant of COX1, COX3. This data suggests that COX3 could be the primary target of ACT (Botting, [@B11]; Chandrasekharan et al., [@B15]; Botting and Ayoub, [@B10]). These COX1-3 (Chandrasekharan et al., [@B15]; Botting and Ayoub, [@B10]) and/or PGE2 (Langenbach et al., [@B42]; Ayoub et al., [@B5]) results were generalized to humans without specific evidence (Kis et al., [@B40]) given the analgesic and antipyretic functions of ACT are closely related to COX2 inhibition (Graham and Scott, [@B32]; Graham et al., [@B31]). The human specific general consensus within the literature, is that the inhibition of COX isoforms, COX1 (maintains homeostasis) and COX2 \[combats pathophysiological states including inflammation, pain and fever (Fitzpatrick, [@B22]; Hinz et al., [@B34]; Rouzer and Marnett, [@B58]; Hinz and Brune, [@B33]; Graham et al., [@B31]; Józwiak-Bebenista and Nowak, [@B38])\] alter "normal" thermoregulatory physiological responses/controls. Yet this consensus is derived from rodents, albeit robustly (Langenbach et al., [@B42]; Ayoub et al., [@B5]), and not substantiated *in vivo* in humans. Research to confirm such consensus in humans is paramount given the wide variance of responses to ACT observed between and even within species (different strains) of laboratory animals (Bessems and Vermeulen, [@B8]). In light of the evidence from Foster et al. ([@B27]), Foster et al. ([@B26]) and related hypotheses (Foster et al., [@B25]) future well-controlled experimental trials, *in vivo* in humans, utilizing ACT to inhibit COX could characterize COX1-3 and PGE2 concentrations and their mechanistic relationship with thermogenesis.

Given the increasing prevalence of research conducted using ACT outside of its typical functions (Mauger et al., [@B47], [@B48]; Mauger and Hopker, [@B46]; Foster et al., [@B28], [@B27], [@B26]; Coombs et al., [@B17]) the matter of pharmacological safety is current, relevant and important. A plethora of evidence is available highlighting the safety of ACT, including doses/dosages beyond (e.g., 20 mg.kg, 20 mg.kg LBM, up to 2 g) the typical therapeutic range described earlier. Despite this, ACT often receives seemingly unwarranted negative exposure. This is likely due to a high incident rate of acute liver failure in cases of overdose, which accounts for 50% of all acute liver failure cases in the United States (Bunchorntavakul and Reddy, [@B13]; Yoon et al., [@B76]). In these ACT acute liver failure cases, treatment with ACT antidote N-acetyl cysteine produces low estimated mortality rates of 0.4% (Bunchorntavakul and Reddy, [@B13]; Yoon et al., [@B76]). Without rapid treatment of an overdose the risk of acute liver failure and death rises significantly (Blieden et al., [@B9]). The minimum acute ACT dose observed to induce acute liver failure is 125 mg.kg body mass (Prescott, [@B53]). However, incidents are more commonly observed when doses exceed 250 mg.kg body mass \[equivalent to 15 g for a 60 kg human (Prescott, [@B53])\], far greater than that utilized in recent novel applied research \[20 mg.kg LBM up to 1.5 g (Mauger et al., [@B47], [@B48]; Mauger and Hopker, [@B46]; Foster et al., [@B28], [@B27], [@B26]; Coombs et al., [@B17]; Taylor et al., [@B66])\]. From chronic use of ACT however, there are several incidents of hepatotoxicity from chronic therapeutic doses but these cases are concomitant with other drug use, periods of starvation, other illnesses and apparent allergic reactions (Vitols, [@B73]). When proposed for use within a research context and the dose exceeds what is typically considered therapeutic (1 g), ACT is often treated with non-evidence-informed scrutiny by ethical review boards. The next section of this article seeks to summarize existing literature and provide evidence of safe ACT doses/dosages, their pharmacokinetics and highlight the minimal risk ACT poses to health within research, when evidence informed dose/dosages are utilized.

Acetaminophen dose and pharmacokinetics {#s3}
=======================================

High rates of overdose incidents are likely due to the ease of access to ACT over the counter, (Bunchorntavakul and Reddy, [@B13]; Yoon et al., [@B76]). Taken orally ACT is rapidly metabolized in the gastrointestinal tract and then primarily by the liver into toxic and non-toxic compounds (Hodgman and Garrard, [@B35]). Absorption through the gastric mucosa is negligible but rapid from the small intestine and thus the rate of absorption is determined by the rate of gastric emptying (Prescott, [@B52]). Whilst gastric emptying can be slowed by food intake the total amount of ACT absorbed over time would not be affected (Prescott, [@B52]). The volume of distribution once in general circulation, in healthy adults, is circa 50 l (Forrest et al., [@B24]). Seminal and emerging research provides substantial evidence that ACT, even administered above the therapeutic dose (1 g), is safe. Within healthy, and some clinical populations, doses/dosages up to 2 g acutely and 2 g 4 ^\*^ daily over multiple days have been used within research (Forrest et al., [@B23]; Benson, [@B7]; Skoglund and Pettersen, [@B61]; Skoglund et al., [@B62]; Dippel et al., [@B19], [@B20]). The plasma half-life of acute therapeutic (1 g) and larger doses of ACT (20 mg.kg up to 1.5 g) ranges between 1.5 and 4 h in humans, with 95% of the dose excreted via urination 24 h post ingestion as unchanged ACT or conjugated with glucuronic acid, sulphuric acid, mercapturic acid and cysteine (Prescott et al., [@B55]; Forrest et al., [@B23], [@B24]; Prescott, [@B52]). Only in those with clinical liver damage is ACT plasma half-life prolonged up to and in excess of 4 h (Prescott et al., [@B55]; Forrest et al., [@B23]). Typically within clinical trials the zenith in plasma concentrations reach 10--25 μg/ml 1--2 h post ingestion (Slattery et al., [@B63]; Singla et al., [@B60]). A well-controlled pharmacokinetic study in healthy individuals saw peak plasma concentrations of 8--19 μg/ml from an individualized dose (20 mg.kg LBM) up to \~1.5 g (range: 1.019--1.42 g), reached within 120 min of oral ingestion (Foster et al., [@B27]). If peak plasma concentrations exceed 300 μg/ml liver damage is likely (Prescott, [@B53]). If plasma concentrations of 200 μg/ml 4 h post ingestion are seen the risk of developing hepatotoxicity significantly increases (Bunchorntavakul and Reddy, [@B13]). To contextualize, acute therapeutic doses (1 g) or those slightly larger (20 mg.kg up to 1.5 g) produce plasma concentrations of 8--25 μg/ml (Rawlins et al., [@B57]; Slattery et al., [@B63]; Singer et al., [@B59]; Foster et al., [@B27]). This is some 175 μg/ml lower than that typically associated with a risk of hepatotoxicity (Bunchorntavakul and Reddy, [@B13]) and 275 μg/ml lower than the established thresholds for liver damage (Prescott, [@B53]). Liver damage in response to therapeutic ACT doses have only been seen in very specific populations---those who are alcohol dependent, patients receiving enzyme-inducing drugs and those with specific infectious diseases such as measles and infectious mononucleosis (Collins and Starmer, [@B16]; Zimmerman and Maddrey, [@B77]; Prescott, [@B54]; Aminoshariae and Khan, [@B2]). Indeed, doses in the range of 1--1.5 g (when a 20 mg.kg LBM dose is employed) in exercise performance research (Mauger et al., [@B47], [@B48]; Mauger and Hopker, [@B46]; Foster et al., [@B28]) and 20 mg.kg LBM (up to a maximum of 1.5 g) in thermophysiology literature (Foster et al., [@B27], [@B26]) have been used, without reported side-effects; not unexpected given the previous comments regarding plasma ACT concentrations and liver damage. Indeed, 2 g acute doses (even when repeated within-day) have been tolerated without liver-related or any other side-effects (Skoglund and Pettersen, [@B61]). Despite this, ACT receives negative reactions when proposed for use within a research context regarding acute doses outside a range that is typically considered therapeutic (1 g). Even with evidence suggesting these are entirely safe (e.g., 20 mg.kg, 20 mg.kg LBM, or 1.5 g) provided they are not administered to the clinical populations outlined above and the fact that such doses have already been utilized regularly elsewhere (Skoglund et al., [@B62]; Dippel et al., [@B19], [@B20]; Mauger et al., [@B47], [@B48]; Foster et al., [@B28], [@B27], [@B26]).

Whilst no side-effects were reported from acute 2 g (Skoglund and Pettersen, [@B61]) and 20 mg.kg LBM (up to 1.5 g maximum) ACT administration (Foster et al., [@B28], [@B27]; Mauger et al., [@B48]; Coombs et al., [@B17]), gastrointestinal damage or liver necrosis were not quantitatively assessed. However, Benson ([@B7]), Dippel et al. ([@B19]), Dippel et al. ([@B20]) and Forrest et al. ([@B23]) who implemented a range of liver function tests (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and total bilirubin levels) demonstrated no liver-related side-effects using similar doses. Chronic dosages exceeding the therapeutic dose (6 ^\*^ 1 g/day) over five days in acute ischemic stroke patients (Dippel et al., [@B19], [@B20]) saw six adverse liver events in the ACT and ibuprofen condition and three in the placebo condition (Dippel et al., [@B20]). Overall adverse events (gastrointestinal damage, pneumonia, progressive stroke) were seen equally across ACT, ibuprofen and placebo condition (Dippel et al., [@B19], [@B20]) and therefore could not be fully attributed to the treatment with ACT. Furthermore, it must be emphasized that this data (Dippel et al., [@B19], [@B20]) is from a population presenting with pathophysiology (i.e., acute ischemic stroke) that increases the biomarkers typically associated with the diagnosis of liver related "adverse events." For example, an increase in direct bilirubin is correlated with the severity of stroke (Pineda et al., [@B51]; Luo et al., [@B43]; Muscari et al., [@B49]). Indeed, even within patients with stable, mild and severe chronic liver disease, ACT administration (1.5 g acute, 4 ^\*^ 1 g/day for 5 and 14 days) has not been shown to exacerbate liver damage (Forrest et al., [@B23]; Benson, [@B7]). Rather prolongation of the ACT half-life is seen (Forrest et al., [@B23]; Benson, [@B7]), which if not accounted for could lead to accumulative plasma concentrations of ACT beyond thresholds typically considered "safe" \[(e.g., 200 μg/ml (Bunchorntavakul and Reddy, [@B13])\] resulting in inadvertent overdose and thus further liver damage.

From the evidence presented here the standard therapeutic dose of ACT (1 g single dose up to 4 g daily every 4--6 h) has not been reported to induce liver damage (Benson, [@B7]). Acute doses up to 1.5 g and dosages up to 6 g/day have been shown to be safe within clinical (Forrest et al., [@B23]; Dippel et al., [@B19], [@B20]) and healthy athletic populations (Foster et al., [@B28], [@B27], [@B26]). Evidently with such an excellent safety record these dose/dosages should not be considered a significant risk in research studies. However, various control/safety measures have been employed or could be recommended to provide further reassurance of these albeit small risks for research participants. These could include: (1) utilization of alcohol use disorder identification test (AUDIT; as part of participant inclusion criteria for enrolment onto a research project); (2) breathalyzer use (prior to ACT ingestion); (3) the satisfactory completion of an ACT risk assessment questionnaire (Foster et al., [@B27], [@B26]). Following these processes if the researcher or participant are unsure of their suitability then medical clearance can be sought. These recommendations could act to reduce the already minimal risk of ACT-mediated side-effects in apparently healthy populations. Their adoption within germane ACT centric research designs should appease any ethically orientated and/or participant safety concerns. Indeed, such measures have seen use elsewhere already (Foster et al., [@B27], [@B26]).

Summary and conclusions {#s4}
=======================

From the evidence presented here ACT does not pose a major threat to health, particularly compared to the adverse events seen with NSAID use, unless taken in inappropriate dose/dosages and/or by certain clinical populations. Experimental controls have been suggested to reduce the already low side-effect risk from ACT administration within relevant human experimental designs. While there is evidence of ACT being beneficial during exercise, this is within a well-controlled research setting where interactions with other medication and supplements (NSAIDs, caffeine, etc.), other common conditions (redistribution of blood flow, hydration status, diet, etc.) and the intensity of exercise are explicitly controlled to ensure the safety of participants. ACT use during exercise where such robust controls are not in place must not be advocated, the risk of interaction with any of the stated factors is not known and may increase the danger of injury/damage to an individual. ACT may be a useful tool to explore and validate bio-chemical thermophysiological mechanisms within afebrile human populations. ACT may alter heat producing mechanisms via inhibition of COX and subsequently PGE2, which requires evidence *in vivo* from humans in lieu of rodent evidence discussed above. Drugs that have COX inhibiting mechanisms, are associated with potentially severe adverse side-effects (Ong et al., [@B50]) although, ACT has been shown to have a favorable risk profile compared to other common COX inhibiting drugs such as NSAIDs, particularly relative to gut damage (Towheed et al., [@B68]; Jones et al., [@B37]). Given the propensity of exercise stress to induce endotoxemia, intestinal hypoperfusion, and intestinal cellular injury/damage (van Wijck et al., [@B71]; ter Steege et al., [@B67]; March et al., [@B44]), a result of redistribution of blood flow during exercise compromising the intestinal mucosa wall (Van Wijck et al., [@B70]; Yeh et al., [@B75]), such damage could be incurred if ACT was to be used during uncontrolled exercise (i.e., outside of research) within any environment (although most likely a hot environment). However, no reports of any adverse effects have occurred thus far in the literature (Mauger et al., [@B48]; Coombs et al., [@B17]). Therefore, the potential for ACT to cause any intestinal injury must be established within experimental designs that explore ACT mechanisms during exercise and/or challenging thermal environments. The evidence discussed above rationalizes the following two opinions: ACT should not be advocated for use within a sporting context, given the present evidence is from tightly controlled laboratory studies which do not replicate the multifaceted physiological, biochemical and environmental perturbations to homeostasis during sporting performance.ACT may provide a useful tool in determining fundamental biochemical thermoregulatory mechanisms *in vivo* in humans, when appropriate experimental controls and designs are employed.

Author contributions {#s5}
====================

All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication.

Conflict of interest statement
------------------------------

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

[^1]: Edited by: Gary Iwamoto, University of Illinois at Urbana--Champaign, United States

[^2]: Reviewed by: Peter Michael Lalley, University of Wisconsin Health, United States; Jyoti Watters, University of Wisconsin-Madison, United States

[^3]: This article was submitted to Exercise Physiology, a section of the journal Frontiers in Physiology


Two structures placed back-to-back appear to be one house in sunny Venice, California.

Details: The Vernon House, a passive solar house in Venice, California, is home for two related families. While appearing to be a single building, the two structures are placed back-to-back, allowing for separate garden entries at the ground level.

A transparent sculptural stair activates each end of the facade leading up to a large communal roof deck that also serves as a bridge between the two households. dimsterarchitecture.com


Poor compliance early in filling in the neuropathic bladder.
A total of 30 patients with known neuropathy, mostly spina bifida, developed poor bladder compliance early in filling demonstrated urodynamically; 20 had bilateral hydronephrosis at the time of presentation and 5 also had severely impaired renal function. After appropriate treatment all of those with normal upper tracts or with bilateral hydronephrosis but normal renal function stabilised or improved. However, all 5 with severely impaired renal function progressed to end-stage renal failure. Poor compliance early in filling is an absolute indication for surgical intervention.


'use strict'

const models = require('../../models')
const logger = require('../../logger')
const config = require('../../config')
const errors = require('../../errors')

const noteUtil = require('./util')
const noteActions = require('./actions')

exports.publishNoteActions = function (req, res, next) {
  noteUtil.findNote(req, res, function (note) {
    const action = req.params.action
    switch (action) {
      case 'download':
        exports.downloadMarkdown(req, res, note)
        break
      case 'edit':
        res.redirect(config.serverURL + '/' + (note.alias ? note.alias : models.Note.encodeNoteId(note.id)) + '?both')
        break
      default:
        res.redirect(config.serverURL + '/s/' + note.shortid)
        break
    }
  })
}

exports.showPublishNote = function (req, res, next) {
  const include = [{
    model: models.User,
    as: 'owner'
  }, {
    model: models.User,
    as: 'lastchangeuser'
  }]
  noteUtil.findNote(req, res, function (note) {
    // force to use short id
    const shortid = req.params.shortid
    if ((note.alias && shortid !== note.alias) || (!note.alias && shortid !== note.shortid)) {
      return res.redirect(config.serverURL + '/s/' + (note.alias || note.shortid))
    }
    note.increment('viewcount').then(function (note) {
      if (!note) {
        return errors.errorNotFound(res)
      }
      noteUtil.getPublishData(req, res, note, (data) => {
        res.set({
          'Cache-Control': 'private' // only cache by client
        })
        return res.render('pretty.ejs', data)
      })
    }).catch(function (err) {
      logger.error(err)
      return errors.errorInternalError(res)
    })
  }, include)
}

exports.showNote = function (req, res, next) {
  noteUtil.findNote(req, res, function (note) {
    // force to use note id
    const noteId = req.params.noteId
    const id = models.Note.encodeNoteId(note.id)
    if ((note.alias && noteId !== note.alias) || (!note.alias && noteId !== id)) {
      return res.redirect(config.serverURL + '/' + (note.alias || id))
    }
    const body = note.content
    const extracted = models.Note.extractMeta(body)
    const meta = models.Note.parseMeta(extracted.meta)
    let title = models.Note.decodeTitle(note.title)
    title = models.Note.generateWebTitle(meta.title || title)
    const opengraph = models.Note.parseOpengraph(meta, title)
    res.set({
      'Cache-Control': 'private', // only cache by client
      'X-Robots-Tag': 'noindex, nofollow' // prevent crawling
    })
    return res.render('codimd.ejs', {
      title: title,
      opengraph: opengraph
    })
  })
}

exports.createFromPOST = function (req, res, next) {
  let body = ''
  if (req.body && req.body.length > config.documentMaxLength) {
    return errors.errorTooLong(res)
  } else if (req.body) {
    body = req.body
  }
  body = body.replace(/[\r]/g, '')
  return noteUtil.newNote(req, res, body)
}

exports.doAction = function (req, res, next) {
  const noteId = req.params.noteId
  noteUtil.findNote(req, res, function (note) {
    const action = req.params.action
    switch (action) {
      case 'publish':
      case 'pretty': // pretty deprecated
        res.redirect(config.serverURL + '/s/' + (note.alias || note.shortid))
        break
      case 'slide':
        res.redirect(config.serverURL + '/p/' + (note.alias || note.shortid))
        break
      case 'download':
        exports.downloadMarkdown(req, res, note)
        break
      case 'info':
        noteActions.getInfo(req, res, note)
        break
      case 'pdf':
        if (config.allowPDFExport) {
          noteActions.createPDF(req, res, note)
        } else {
          logger.error('PDF export failed: Disabled by config. Set "allowPDFExport: true" to enable. Check the documentation for details')
          errors.errorForbidden(res)
        }
        break
      case 'gist':
        noteActions.createGist(req, res, note)
        break
      case 'revision':
        noteActions.getRevision(req, res, note)
        break
      default:
        return res.redirect(config.serverURL + '/' + noteId)
    }
  })
}

exports.downloadMarkdown = function (req, res, note) {
  const body = note.content
  let filename = models.Note.decodeTitle(note.title)
  filename = encodeURIComponent(filename)
  res.set({
    'Access-Control-Allow-Origin': '*', // allow CORS as API
    'Access-Control-Allow-Headers': 'Range',
    'Access-Control-Expose-Headers': 'Cache-Control, Content-Encoding, Content-Range',
    'Content-Type': 'text/markdown; charset=UTF-8',
    'Cache-Control': 'private',
    'Content-disposition': 'attachment; filename=' + filename + '.md',
    'X-Robots-Tag': 'noindex, nofollow' // prevent crawling
  })
  res.send(body)
}


1. The scene takes place in
2. The scene takes place in
3. The singer is speaking about
4. Ellis Island is a place where the immigrants were
5. For the immigrants America is
6. When they arrived the immigrants were
7. In Ellis island they haven't time to
8. Strange paradise means that
9. they are all sad because
10. the condition of travel were

End of the free exercise to learn English: ComprehensionA free English exercise to learn English.Other English exercises : | All our lessons and exercises


Serial measurements of cardiac troponin I in heart failure secondary to canine mitral valve disease.
Serial measurements of cardiac troponin I (cTnI) levels are considered to be better predictors of cardiac death than single-time-point analyses in human medicine. We hypothesised that cTnI levels could reflect the severity of myxomatous mitral valve disease (MMVD), and that serial changes in the cTnI level had a prognostic value in dogs with congestive heart failure (CHF) secondary to MMVD. Seventy-six dogs were initially enrolled and classified by the American College of Veterinary Internal Medicine (ACVIM) staging system. The single-timepoint cTnI concentration in these dogs significantly increased with the ACVIM stage. Twenty-seven dogs with CHF subsequently underwent serial measurement of cTnI levels, and the results showed that those who demonstrated a decrease in cTnI levels from the first to the third visit exhibited a higher risk of cardiac death than did those without such changes (P=0.012). We suspect that the downward trend in cTnI levels may be affected by medical treatment for CHF. In conclusion, although cTnI levels could reflect the severity of MMVD to a certain extent, the serial changes may be affected by medical treatment. Therefore, caution should be exercised when cTnI is used for assessment of the prognosis of CHF secondary to MMVD in dogs.


Search

"Be the person your dog thinks you are." ~Unknown.We welcome comments. Supportive feedback is what we enjoy most, but tips for improvement are valued too. It’s not required that you agree with us, only that you express your opinion civilly. Comments are moderated and will be posted following review. Read more.

April 07, 2016

Mixed breed: removing the labels and focusing on the individual dog

Editor's note: This is our second blog this week about breed labels. If you missed the first, find it here.

The majority of the pets in the care of the Richmond SPCA are ones we have transferred to our humane center from city- or county-operated shelters and a much smaller percentage are those relinquished to us by their owners. Although some dogs will be identified by their owners with certainty as belonging to a particular breed because he or she was purchased from a pet store or breeder, it is much more common that our staff has little more than an animal’s appearance to go on in designating one or two “breeds” to identify the dog, as is usually required by software. However, mixed breed dogs usually are not the offspring of two purebred parents; in fact, it’s likely that neither of their parents was purebred.

And while there is little reliability to breed labels assigned to mixed breed dogs, there is much weight given to those labels because people assume so much about traits and behavior characteristics. Manager of Admissions Laura Palin says she and the admissions counselors she supervises are keenly aware of the burden a breed label can place on a particular dog. A label like shepherd, Chow, pit bull or Rottweiler can cause people to eliminate that dog from consideration as a companion, not based on any behavior or history of that individual animal but because of stigmas associated with the “breed,” even when that breed designation is nothing more than a guess.

Palin said that the weighty decisions over breed label occasionally lead to internal disputes. “Each of us would have pictures from online, the breed books and would even dig up old DNA results to argue our breed reasoning, and in the end it was very rare that you would change anyone’s opinion,” she said. Palin went on to explain her enthusiasm for the Richmond SPCA’s decision not to place such labels on dogs of unknown breed. “A pet’s potential future could be decided by these opinions that not everyone can agree upon anyway.”

Many of the counselors can recall specific dogs whose “breed” identity has been a complex mystery, which they felt pressured to force into two neat boxes. One dog that Amberlyn Pryor and Alicia Kurz transferred from Petersburg Animal Control had been found as a stray, and the Petersburg shelter called her a Shiba Inu mix, possibly indicated by her thick coat and curved tail, but they also saw the build and long nose of a Labrador retriever. And, let’s face it highly exotic breeds are possible but not very likely.

“Admittedly we were only guessing,” said Pryor. “Writing ‘mixed breed’ is better than random guessing based on head shape or coat length because in the end the dog’s DNA could be a mixture of four or five breeds, many of which we never would have guessed.”

Another counselor, Natalie Ogden, adopted a dog who had been the subject of much discussion and debate. She had transferred Halligan from Dinwiddie Animal Control, where there was no history provided for the distinctive looking dog with one blue eye and one brown eye, distinctive spots, semi-erect ears and a stocky stance.

“After much speculation and discussion, I believe the breed mix we settled on was Dalmatian and Catahoula mix,” Ogden said. “Of course, 6 months later, I did a DNA test for him and the results came back saying he is a purebred American Staffordshire Terrier.”

It is part of human nature to want to categorize things, including animals. We have a much more evidence-based system of categories in Meet Your Match. Through this adoption program that has been used at the Richmond SPCA since 2008, we assign each dog a Canine-ality after an assessment of the dog’s behavior, energy level, focus and previous training. The fun labels that result – such as Go Getter, Couch Potato, Goofball and more – give much more insight than a guess about breed, and we share all the assessment notes with potential adopters, who learn whether their new companions are likely to settle quickly in a crate, how they like to greet visitors, and if they prefer tennis balls to squeaky plush toys, among other characteristics.

We recognize that our views on dogs as individuals are not yet universal, and particularly aren’t typically shared by landlords and insurance companies. When a dog has visual characteristics that are likely to be covered by breed-based exclusions, we will continue to counsel adopters about the restrictions and discrimination that they may face. For those who are looking for some certainty on a dog’s genetic makeup, our Lora Robins Gift Shop offers the Wisdom Panel DNA testing kit. With a simple cheek swab, you can send a sample of your dog’s saliva and receive results by email that will serve to satisfy curiosity or provide documentation.

Tabitha Treloar is the director of communications for the Richmond SPCA. Before posting a comment, please review our comment guidelines. Please note that our comment policy requires both your first and last name to be used as your screen name.


Q:

Parsing json element

I am using Scrapy and a Regex to parse some none standard web source code. I then wish to parse the first element of the dictionary returned:
from scrapy.contrib.spiders import CrawlSpider, Rule
from scrapy.contrib.linkextractors.sgml import SgmlLinkExtractor
from scrapy.selector import Selector
from scrapy.item import Item
from scrapy.spider import BaseSpider
from scrapy import log
from scrapy.cmdline import execute
from scrapy.utils.markup import remove_tags
import time
import re
import json
import requests

class ExampleSpider(CrawlSpider):
    name = "goal2"
    allowed_domains = ["whoscored.com"]
    start_urls = ["http://www.whoscored.com"]
    download_delay = 5

    rules = [Rule(SgmlLinkExtractor(allow=('\Teams'),deny=(),), follow=False, callback='parse_item')]

    def parse_item(self, response):

        sel = Selector(response)
        titles = sel.xpath("normalize-space(//title)")
        print '-' * 170
        myheader = titles.extract()[0]
        print '********** Page Title:', myheader.encode('utf-8'), '**********'
        print '-' * 170

        match1 = re.search(re.escape("DataStore.prime('stage-player-stat', defaultTeamPlayerStatsConfigParams.defaultParams , ") \
                     + '(\[.*\])' + re.escape(");"), response.body)

        if match1 is not None:
            playerdata1 = match1.group(1)

            teamid = json.loads(playerdata1[0])
            print teamid

The key for the first element of 'playerdata1' is called 'TeamId'. I assumed the above method would work, however I am getting the following error:
    teamid = json.loads(playerdata1[0])
  File "C:\Python27\lib\json\__init__.py", line 338, in loads
    return _default_decoder.decode(s)
  File "C:\Python27\lib\json\decoder.py", line 366, in decode
    obj, end = self.raw_decode(s, idx=_w(s, 0).end())
  File "C:\Python27\lib\json\decoder.py", line 382, in raw_decode
    obj, end = self.scan_once(s, idx)
exceptions.ValueError: Expecting object: line 1 column 1 (char 0)

Can anyone see what the issue is here?

A:

match1.group(1) returns one string. You then index that string:
teamid = json.loads(playerdata1[0])

Here, [0] will give you the just the first character of that string. Remove the indexing expression there to use the whole string:
teamid = json.loads(playerdata1)

Now teamid is a list with player objects:
>>> len(teamid)
22
>>> teamid[0].keys()
[u'FirstName', u'LastName', u'KnownName', u'Field', u'GameStarted', u'AerialWon', u'TeamRegionCode', u'SecondYellow', u'ShotsBlocked', u'TotalShots', u'Assists', u'Red', u'Name', u'PositionText', u'Ranking', u'PositionLong', u'PlayerId', u'SubOff', u'Dispossesed', u'TeamId', u'TotalTackles', u'TotalLongBalls', u'Goals', u'SubOn', u'WasDribbled', u'AerialLost', u'Turnovers', u'ShotsOnTarget', u'WSName', u'Fouls', u'ManOfTheMatch', u'Height', u'TeamName', u'RegionCode', u'TotalPasses', u'TotalThroughBalls', u'Dribbles', u'DateOfBirth', u'OwnGoals', u'WasFouled', u'TotalClearances', u'Rating', u'PlayedPositionsRaw', u'Weight', u'AccurateLongBalls', u'OffsidesWon', u'AccuratePasses', u'Yellow', u'KeyPasses', u'TotalCrosses', u'AccurateCrosses', u'IsCurrentPlayer', u'Age', u'PositionShort', u'AccurateThroughBalls', u'Interceptions', u'Offsides']


package com.example.demo.base;

public enum Status {
    SUCCESS(200, "OK"),
    ETH_ERROR(1000, "以太坊错误");

    private int code;
    private String message;

    Status(int code, String message) {
        this.code = code;
        this.message = message;
    }

    public int getCode() {
        return code;
    }

    public void setCode(int code) {
        this.code = code;
    }

    public String getMessage() {
        return message;
    }

    public void setMessage(String message) {
        this.message = message;
    }
}


Spinel-type structured Li4+xTi5O12 (0 6 x 6 3 ) is actually one of the most promising anode materials for Li ion batteries. In its nanostructured form it is already used in some commercially available Li ion batteries. As ...


CIBC Wealth Management

CIBC Wealth Management is the brokerage division of the Canadian Imperial Bank of Commerce (CIBC). The CIBC prefers to use phrases like "wealth-building" and "wealth management" to describe its investment services. Like most banks, their financial products include stocks, bonds, mutual funds, managed portfolios, guaranteed investments, and credit. And like most retail businesses, they give free advice to their customers on what to buy.

In 2003, this division managed $193 billion in client assets and made $205 million of profit.

Wealth Management was headed by Gerald T. McCaughey, Chairman and Chief Executive Officer, CIBC World Markets and Vice Chair for Wealth Management. On July 31, 2014, CIBC announced the appointment of Victor Dodig as President and CEO which took effect on September 15, 2014.

This division was once called Wood Gundy and was once the biggest performing unit for CIBC.

References

CIBC annual report 2003

Category:Canadian Imperial Bank of Commerce


DLD-067                                                         NOT PRECEDENTIAL

                       UNITED STATES COURT OF APPEALS
                            FOR THE THIRD CIRCUIT
                                 ___________

                                      No. 10-3277
                                      ___________

                               ASSEM A. ABULKHAIR,
                                           Appellant

                                            v.

                   LIBERTY MUTUAL INSURANCE COMPANY;
                  ADA PRIDDY, Adjuster; KAREN KUEBLER, Esq.;
                  THE LAW OFFICES OF LINDA BAUMAN, ESQ.
                     ____________________________________

                     On Appeal from the United States District Court
                              for the District of New Jersey
                              (D.C. Civil No. 10-cv-00146)
                        District Judge: Honorable Jose L. Linares
                      ____________________________________

                       Submitted for Possible Summary Action
                  Pursuant to Third Circuit LAR 27.4 and I.O.P. 10.6
                                  December 16, 2010
             Before: BARRY, FISHER AND STAPLETON, Circuit Judges

                            (Opinion filed: January 12, 2011)
                                       _________

                                       OPINION
                                       _________

PER CURIAM.

       Assem A. Abulkhair, proceeding pro se, appeals two orders of the District Court.

The first order denied Abulkhair‟s motion for additional time to appeal the order that
dismissed his complaint, and the second order imposed restrictions upon Abulkhair‟s

right to file future complaints in the district court. For the reasons set forth below, we

will take summary action, see 3d Cir. LAR 27.4 and I.O.P. 10.6, and we will affirm in

part, vacate in part, and remand for further proceedings.

                                              I.

       Abulkhair commenced this suit in January 2010 by filing a pro se complaint under

42 U.S.C. § 1983 and state law against Liberty Mutual Insurance Company and other

defendants. The claims asserted stem from a dispute over insurance coverage for a 1998

car accident that Abulkhair was involved in with an uninsured motorist. By order entered

February 11, 2010, the District Court granted Abulkhair leave to proceed in forma

pauperis (“IFP”) and dismissed his complaint sua sponte for lack of subject-matter

jurisdiction. The District Court determined that the claims asserted were substantially

similar to claims that the Court had dismissed for lack of subject-matter jurisdiction in a

prior suit by Abulkhair. Although Abulkhair named a new defendant and added state law

claims in the present suit, the District Court concluded that it remained without subject-

matter jurisdiction, and it dismissed the complaint with prejudice. Furthermore, because

Abulkhair had commenced eight suits in the preceding six months related to the same car

accident, and a total of fifteen suits in the District of New Jersey since 2002, the District

Court ordered Abulkhair to show cause why he should not be required to obtain court

approval before filing any future complaint related to this car accident.

                                              2
       On March 31, 2010, Abulkhair filed a notice of appeal from the February 11 order.

The notice of appeal was untimely filed more than thirty days after entry of the February

11 order, see Fed. R. App. P. 4(a)(1)(A), and this Court dismissed the appeal for lack of

appellate jurisdiction. See C.A. No. 10-1949.

       Meanwhile, on April 12, 2010, Abulkhair filed a motion for an extension of time

to appeal the February 11 order or to reopen the appeal period. See Fed. Rules of App. P.

4(a)(5) and (a)(6). He submitted an Affidavit dated March 29, 2010, in which he averred

that the February 11 order “has never been served upon the Plaintiff by neither the Clerk,

nor [opposing] counsel.” Docket #9 at 1. Abulkhair claimed that he first received notice

of the order on March 29 when it was handed to him by the court clerk. Id. Defendants

opposed the motion, arguing that Abulkhair is a “serial litigator” who had failed to

monitor his case, and he should not be allowed “to convert the 30-day deadline for filing

notices of appeal into a 60-day deadline[.]” Docket #12 at 3-4. Abulkhair filed a reply in

which he noted that defendants did not dispute his claim that he failed to receive timely

notice of the February 11 order. Docket #13.

       In his March 29 Affidavit, Abulkhair also expressed opposition to entry of the

proposed injunction, arguing that he has “never filed a single frivolous suit against

anyone,” and that his conduct does not support a restriction upon future filings. Docket

#9 at 5-6. Abulkhair had argued earlier, in his reply to defendants‟ opposition to his IFP

motion, that his prior suits involved different claims and defendants, and that he believes

                                             3
there is a basis for exercising federal subject-matter jurisdiction. See Docket #6 at 1-2.

       By order entered July 23, 2010, the District Court denied Abulkhair‟s motion for

additional time to appeal. Addressing the motion solely as a request for an extension

time to appeal under Rule 4(a)(5), the District Court held that Abulkhair failed to show

excusable neglect. Among other things, the District Court explained that “an excuse that

Plaintiff did not receive a copy of the Order in time, without additional factual support or

information, is an excuse that is easily manufactured,” and that Abulkhair “has not

demonstrated that he made any efforts to monitor the docket in this matter.”

       By separate order entered July 22, 2010, the District Court entered an injunction

requiring Abulkhair to obtain court approval before filing future complaints related to the

same car accident. The District Court did not address Abulkhair‟s objections to the

injunction because it found that “Plaintiff did not respond to the Order to Show Cause.”

       Abulkhair timely filed a notice of appeal from the July 22 and July 23 orders.

                                             II.

       We have appellate jurisdiction because the orders appealed are “final decisions”

under 28 U.S.C. § 1291. We review for abuse of discretion a decision to deny a motion

for an extension of time to appeal, Ramseur v. Beyer, 921 F.2d 504, 506 n.2 (3d Cir.

1990), and a motion to reopen the appeal period, United States v. Rinaldi, 447 F.3d 192,

195 (3d Cir. 2006), while our review is plenary over the district court‟s application and

interpretation of the governing rules, Pedereaux v. Doe, 767 F.2d 50, 51 (3d Cir. 1985).

                                             4
We review for abuse of discretion a decision to impose restrictions upon a litigant‟s right

to file future litigation. Abdul-Akbar v. Watson, 901 F.2d 329, 331 (3d Cir. 1990).

                                             III.

       (i)    Order denying the motion to extend or reopen time to appeal

       Abulkhair moved to extend the time to appeal under Rule 4(a)(5) and to reopen the

time to appeal under Rule 4(a)(6) based on an allegation that he did not receive notice of

the February 11 order until March 29, 2010. The District Court addressed the motion

solely under Rule 4(a)(5) and denied relief. After a review of the record, we conclude

that the District Court did not abuse its discretion in holding that Abulkhair failed to

establish excusable neglect to support extending the appeal period under Rule 4(a)(5).1

  1
    “This court interprets Rule 4(a)(5) to require a finding of excusable neglect in those
  instances where the court, after weighing the relevant considerations is satisfied that
  counsel has exhibited substantial diligence, professional competence and has acted in
  good faith to conform his or her conduct in accordance with the rule, but as the result
  of some minor neglect, compliance was not achieved.” Consol. Freightways Corp. v.
  Larson, 827 F.2d 916, 920 (3d Cir. 1987). The District Court cited Abulkhair‟s
  extensive litigation history, his awareness of the governing rules, and the absence of a
  showing that he had made any effort to monitor the docket in this case. This record
  adequately supports the refusal to find excusable neglect. See, e.g., United States ex
  rel. McAllan v. City of New York, 248 F.3d 48, 53 (2d Cir. 2001) (“[A]ppellant‟s
  failure to file a timely notice of appeal is not excused by what he characterizes as the
  „serious administrative errors‟ and docketing irregularities of the … clerk‟s office,
  because parties have an obligation to monitor the docket sheet to inform themselves of
  the entry of orders they wish to appeal.”); see also Vianello v. Pacifico, 905 F.2d 699,
  701 (3d Cir. 1990) (explaining that a “district court may take into account, as one
  factor in making its decision [under Rule 4(a)(5)], the Clerk‟s failure to give notice of
  entry of judgment, but that the district court is not required to extend the time for filing
  a notice of appeal merely because of the Clerk‟s failure”).

                                              5
Accordingly, we will affirm the July 23 order insofar as the District Court denied Rule

4(a)(5) relief.

       As noted, however, the basis for Abulkhair‟s motion was an assertion that he was

not served with notice of a court order -- an assertion that directly implicates Rule

4(a)(6). “Fed. R. App. P. 4(a)(6) provides a mechanism for granting an extension of time

when a party would be unfairly deprived of an appeal because of the failure of a court

clerk.” Marcangelo v. Boardwalk Regency, 47 F.3d 88, 90 (3d Cir. 1995). The District

Court erred in failing to address Abulkhair‟s request for Rule 4(a)(6) relief.

       Under Rule 4(a)(6), a district court may reopen the appeal period for fourteen days

if it finds that the party did not receive notice under Federal Rule of Civil Procedure

77(d) of a judgment or order within twenty-one days after its entry, and that no party

would be prejudiced. Fed. R. App. P. 4(a)(6)(A), (C).2 The motion to reopen must be

filed by the earlier of 180 days following entry of the judgment or order or fourteen days

after the party receives notice of its entry. Fed. R. App. P. 4(a)(6)(B).

       The present record does not clearly foreclose Abulkhair from meeting the three

requirements for Rule 4(a)(6) relief, and, moreover, it is unclear whether relief would be

appropriate as a matter of discretion even if he meets the Rule‟s requirements. See Arai

  2
    Rule 77(d) provides that, “[i]mmediately after entering an order or judgment, the
  clerk must serve notice of the entry, as provided in Rule 5(b), on each party who is not
  in default for failing to appear. The clerk must record the service on the docket. A
  party also may serve notice of the entry as provided in Rule 5(b).” Fed. R. Civ. P.
  77(d)(1).
                                              6
v. Am. Bryce Ranches, Inc., 316 F.3d 1066, 1069 (9th Cir. 2003) (holding that a “district

court has the discretion to deny a Rule 4(a)(6) motion even when the rule‟s requirements

are met”). Accordingly, we will remand for the District Court to rule on Abulkhair‟s

Rule 4(a)(6) motion in the first instance.3

       In denying relief under Rule 4(a)(5), the District Court observed that “an excuse

that Plaintiff did not receive a copy of the Order in time, without additional factual

support or information, is an excuse that is easily manufactured.” Insofar as the District

Court might rely upon this same analysis for purposes of Rule 4(a)(6), we note that

Abulkhair supports his motion to reopen the appeal period with an Affidavit, submitted

under penalty of perjury, stating that he did not receive notice of the February 11 order

until March 29. Nothing in the present record shows that Abulkhair has “manufactured”

this contention, and defendants did not oppose the motion to reopen on that basis. If the

District Court concludes on remand that findings are warranted on whether Abulkhair has

fabricated the factual support for his motion, the District Court can conduct appropriate

proceedings to resolve the issue. At present, the record reveals no notation on either the

docket sheet or the February 11 order itself reflecting that the clerk served the order at the

time it was entered, and Abulkhair asserts that he did not receive notice from defendants.

  3
    On the issue of timeliness, Abulkhair‟s Rule 4(a)(6) motion could be considered
  timely filed on April 12, 2010, which was fourteen days after March 29, assuming the
  District Court determines that Abulkhair did not receive notice of the February 11
  order at an earlier time.
                                              7
In addition, Abulkhair seems to assert that he is not a registered electronic filer,

suggesting that the clerk had to serve him by another means specified under Rule 5(b)(2).

       The District Court also cited Abulkhair‟s failure to monitor the docket as a basis

for denying Rule 4(a)(5) relief. For purposes of Rule 4(a)(6), some courts have held that,

while a district court ultimately exercises its discretion in ruling on a motion to reopen

the appeal period, “where non-receipt [of an order] has been proven and no other party

would be prejudiced, the denial of relief cannot rest on a party‟s failure to learn

independently of the entry of judgment during the thirty-day period for filing notices of

appeal.” Nunley v. City of Los Angeles, 52 F.3d 792, 798 (9th Cir. 1995); see Avolio v.

County of Suffolk, 29 F.3d 50, 54 (2d Cir. 1994) (holding that denial of Rule 4(a)(6)

relief “may not be based on a concept of inexcusable neglect for not having learned of the

entry of judgment”); but cf. Kuhn v. Sulzer Orthopedics, Inc., 498 F.3d 365, 371 (6th Cir.

2007) (declining to follow Nunley and Avolio because “[b]oth cases were decided long

before electronic dockets became widely available”). This Court has not previously

addressed the issue, and we need not do so at this time. Because we will remand this

matter, the District Court should have the first opportunity to consider the particular

circumstances at issue here and to determine whether or the extent to which Abulkhair‟s

failure to monitor his case properly bears on the decision to afford him relief under Rule

4(a)(6).

                                              8
       In sum, we will affirm the denial of Abulkhair‟s Rule 4(a)(5) motion, and we will

remand for the District Court to consider Abulkhair‟s Rule 4(a)(6) motion.

       (ii)   Order restricting the filing of future complaints

       Abulkhair also challenges the District Court‟s order limiting his right to file future

complaints related to the underlying car accident at issue. The District Court entered its

injunction without addressing Abulkhair‟s objections because it found that Abulkhair

failed to respond to its February 11 order to show cause. As discussed above, however,

Abulkhair asserts that he did not receive notice of the February 11 order until March 29.

If the District Court were to accept that assertion on remand, then Abulkhair‟s failure to

respond to the show cause order within the twenty days specified by the District Court

may be excusable. Furthermore, Abulkhair filed his Affidavit raising objections to the

proposed injunction on March 31, which was two days after he purports to have first

received notice of the February 11 order.

       We have recognized that “a pattern of groundless and vexatious litigation will

justify an order prohibiting further filings without permission of the court.” Chipps v.

U.S. Dist. Ct., 882 F.2d 72, 73 (3d Cir. 1989); see In re Oliver, 682 F.2d 443, 445 (3d

Cir. 1982) (“It is well within the broad scope of the All Writs Act for a district court to

issue an order restricting the filing of meritless cases by a litigant whose manifold

complaints raise claims identical or similar to those that already have been adjudicated.”).

At the same time, “[a]ccess to the courts is a fundamental tenet of our judicial system,”

                                              9
and “legitimate claims should receive a full and fair hearing no matter how litigious the

plaintiff may be.” In re Oliver, 682 F.2d at 446. It is settled that an injunction against

filing “should not be imposed by a court without prior notice and some occasion to

respond.” Gagliardi v. McWilliams, 834 F.2d 81, 83 (3d Cir. 1987).

       Because the District Court entered its injunction without addressing the objections

raised in Abulkhair‟s Affidavit, and without considering whether Abulkhair‟s ability to

respond in a timely manner was prejudiced by his alleged failure to receive timely notice

of the February 11 order, we will vacate the July 22 order and remand. Restricting a

litigant‟s right to file suit is an “extreme remedy” that warrants meaningful consideration

of the litigant‟s objections prior to imposition of the injunction. Abdul-Akbar, 901 F.2d

at 332. The District Court should weigh Abulkhair‟s objections on remand against the

evidence of record and the need to curtail abusive litigation. We express no view on

whether an injunction is warranted here; we leave that determination to the District

Court‟s sound exercise of its discretion.

                                             IV.

       For the foregoing reasons, we will affirm the July 23 order insofar as the District

Court denied Rule 4(a)(5) relief, but we will otherwise vacate the order and remand for

the District Court to address Abulkhair‟s Rule 4(a)(6) motion. We will also vacate the

July 22 injunction order and remand for further proceedings consistent with this Opinion.

                                             10


1958 Women's British Open Squash Championship

The 1958 Ladies Open Championships was held at the Lansdowne Club in London from 17–23 February 1958. Janet Morgan won her ninth consecutive title defeating Sheila Macintosh (née Speight) for the third successive year in the final.

Seeds

Draw and results

First round

denotes seed *

Second round

Third round

Quarter-finals

Semi-finals

Final

References

Category:Women's British Open Squash Championships
Women's British Open Squash Championships
Women's British Open Squash Championships
Category:Squash competitions in London
Category:1958 in squash
Category:1958 in women's squash


Q:

powershell cannot ping a web address

I run powershell as Admin in Windows 10 64Bit. When I ping www.powershellgallery.com I get error:
PS C:\WINDOWS\system32> ping www.powershellgallery.com

Pinging psg-prod-eastus.cloudapp.net [40.87.85.101] with 32 bytes of data:
Request timed out.

Ping statistics for 40.87.85.101:
    Packets: Sent = 1, Received = 0, Lost = 1 (100% loss),

But when I ping other web addresses, google.com for example, everything is fine.
PS C:\WINDOWS\system32> ping www.google.com

Pinging www.google.com [216.58.213.68] with 32 bytes of data:
Reply from 216.58.213.68: bytes=32 time=15ms TTL=56
Reply from 216.58.213.68: bytes=32 time=14ms TTL=56
Reply from 216.58.213.68: bytes=32 time=13ms TTL=56
Reply from 216.58.213.68: bytes=32 time=13ms TTL=56

Ping statistics for 216.58.213.68:
    Packets: Sent = 4, Received = 4, Lost = 0 (0% loss),
Approximate round trip times in milli-seconds:
    Minimum = 13ms, Maximum = 15ms, Average = 13ms

Any ideas what is happening?

A:

This really is not a powershell issue. Matter of fact this isnt a issue at all. Ping is using ICMP. Its basically an echo message. Companies can block and not allow ICMP.
So just because there is no ping doesnt mean that something is not working.


Increased attentional demands impair contralesional space awareness following stroke.
Rate and severity of contralesional loss of awareness following stroke is highly variable across patients and assessment methods. We studied whether the degree of impairment for contralesional space awareness depends on the quantity of attentional resources that are available for task performance. A new computer-based paradigm was used to assess visual extinction and single-target detection rate in four right hemisphere stroke patients. In the single-task condition, they had to report only the position of the target(s) ("right", "left", or "both" sides). In the dual-task conditions, patients also performed a second task, visual or auditory, that recruited additional attentional resources. The same tasks were also performed by healthy controls and by a left hemisphere stroke patient. Patients' performance was apparently unimpaired in the single-task condition. In contrast, dramatic failures to report the left-sided target emerged in the dual-task conditions. The performance of control participants was unaffected by the dual-task manipulation, whereas the left stroke patient showed the opposite pattern (i.e., unawareness of right-sided targets). Severe contralesional space unawareness under dual-task conditions reveals that visuospatial deficits can dramatically emerge when attentional resources are consumed by a concurrent task. Apparently spared contralesional awareness may simply reflect the availability of resources that are just sufficient to perform a single-task. This finding has important implications for the assessment of contralesional space awareness following stroke, because everyday life activities are often more demanding than most of the tests adopted for diagnosing space awareness disorders.


The Psychoactive Surveillance Consortium and Analysis Network (PSCAN): the first year.
The Psychoactive Surveillance Consortium and Analysis Network (PSCAN) is a national network of academic emergency departments (ED), analytical toxicologists and pharmacologists that collects clinical data paired with biological samples to identify and improve treatments of medical conditions arising from use of new psychoactive substances (NPS). The aim of this study was to gather clinical data with paired drug identification from NPS users who presented to EDs within PSCAN during its first year (2016-17). Observational study involving patient records and biological samples. Seven academic emergency medical centers across the United States. ED patients (n = 127) > 8 years of age with possible NPS use who were identified and enrolled in PSCAN by clinical providers or research personnel. Clinical signs, symptoms and treatments were abstracted from the patients' health records. Biological samples were collected from leftover urine, serum and whole blood. Biological and drug samples, when available, were tested for drugs and drug metabolites via liquid chromatography-quadrupole time-of-flight mass spectrometry (LC-QTOF/MS). Patients in whom synthetic opioids were detected (n = 9) showed higher rates of intubation (four of nine), impaired mental status (four of nine) and respiratory acidosis (five of nine) compared with the rest of the cohort (nine of 118, P-value < 0.05). Patients in whom synthetic cannabinoid (SC) were found (n = 27) had lower median diastolic blood pressures (70.5 versus 77 mmHg, P = 0.046) compared with the rest of the cohort. In 64 cases of single drug ingestion, benzodiazepines were administered in 25 cases and considered effective by the treating physician in 21 (84%) cases. During its first year of operation, the Psychoactive Surveillance Consortium and Analysis Network captured clinical data on new classes of drugs paired with biological samples over a large geographical area in the United States. Synthetic cannabinoids were the most common new psychoactive drug identified. Synthetic opioids were associated with a high rate of intubation and respiratory acidosis.


apiVersion: apiextensions.k8s.io/v1beta1
kind: CustomResourceDefinition
metadata:
  creationTimestamp: null
  labels:
    controller-tools.k8s.io: "1.0"
  name: clusterdeprovisions.hive.openshift.io
spec:
  additionalPrinterColumns:
  - JSONPath: .spec.infraID
    name: InfraID
    type: string
  - JSONPath: .spec.clusterID
    name: ClusterID
    type: string
  - JSONPath: .status.completed
    name: Completed
    type: boolean
  - JSONPath: .metadata.creationTimestamp
    name: Age
    type: date
  group: hive.openshift.io
  names:
    kind: ClusterDeprovision
    plural: clusterdeprovisions
    shortNames:
    - cdr
  scope: Namespaced
  subresources:
    status: {}
  validation:
    openAPIV3Schema:
      properties:
        apiVersion:
          description: 'APIVersion defines the versioned schema of this representation
            of an object. Servers should convert recognized schemas to the latest
            internal value, and may reject unrecognized values. More info: https://git.k8s.io/community/contributors/devel/api-conventions.md#resources'
          type: string
        kind:
          description: 'Kind is a string value representing the REST resource this
            object represents. Servers may infer this from the endpoint the client
            submits requests to. Cannot be updated. In CamelCase. More info: https://git.k8s.io/community/contributors/devel/api-conventions.md#types-kinds'
          type: string
        metadata:
          type: object
        spec:
          properties:
            clusterID:
              description: ClusterID is a globally unique identifier for the cluster
                to deprovision. It will be used if specified.
              type: string
            infraID:
              description: InfraID is the identifier generated during installation
                for a cluster. It is used for tagging/naming resources in cloud providers.
              type: string
            platform:
              description: Platform contains platform-specific configuration for a
                ClusterDeprovision
              properties:
                aws:
                  description: AWS contains AWS-specific deprovision settings
                  properties:
                    credentialsSecretRef:
                      description: CredentialsSecretRef is the AWS account credentials
                        to use for deprovisioning the cluster
                      type: object
                    region:
                      description: Region is the AWS region for this deprovisioning
                      type: string
                  type: object
                azure:
                  description: Azure contains Azure-specific deprovision settings
                  properties:
                    credentialsSecretRef:
                      description: CredentialsSecretRef is the Azure account credentials
                        to use for deprovisioning the cluster
                      type: object
                  type: object
                gcp:
                  description: GCP contains GCP-specific deprovision settings
                  properties:
                    credentialsSecretRef:
                      description: CredentialsSecretRef is the GCP account credentials
                        to use for deprovisioning the cluster
                      type: object
                    region:
                      description: Region is the GCP region for this deprovision
                      type: string
                  type: object
                openstack:
                  description: OpenStack contains OpenStack-specific deprovision settings
                  properties:
                    cloud:
                      description: Cloud is the secion in the clouds.yaml secret below
                        to use for auth/connectivity.
                      type: string
                    credentialsSecretRef:
                      description: CredentialsSecretRef is the OpenStack account credentials
                        to use for deprovisioning the cluster
                      type: object
                  type: object
              type: object
          type: object
        status:
          properties:
            completed:
              description: Completed is true when the uninstall has completed successfully
              type: boolean
          type: object
  version: v1
status:
  acceptedNames:
    kind: ""
    plural: ""
  conditions: []
  storedVersions: []


"===============================================================================
" Plugin source
"===============================================================================
"'SirVer/ultisnips'

"===============================================================================
" Plugin Configurations
"===============================================================================
let g:UltiSnipsSnippetDirectories=["UltiSnips", "custom-snips"]
let g:UltiSnipsJumpForwardTrigger="9<Tab>"
let g:UltiSnipsEditSplit="vertical"

"===============================================================================
" Plugin Keymappings
"===============================================================================
nnoremap 9ue :UltiSnipsEdit<CR>

function! UltiSnipsCallUnite()
  Unite -start-insert -winheight=100 -immediately -no-empty ultisnips
  return ''
endfunction

inoremap 9<Tab> <C-R>=(pumvisible()? "\<LT>C-E>":"")<CR><C-R>=UltiSnipsCallUnite()<CR>
nnoremap 9<Tab> a<C-R>=(pumvisible()? "\<LT>C-E>":"")<CR><C-R>=UltiSnipsCallUnite()<CR>

"===============================================================================
" Unite Keymap Menu Item(s)
"===============================================================================
let g:unite_source_menu_menus.CustomKeyMaps.command_candidates += [['➤ Edit UltiSnips snippet file                                   9ue', 'normal 9ue']]
let g:unite_source_menu_menus.CustomKeyMaps.command_candidates += [['➤ Display snippet list                                          9<Tab>', 'echo "Use 9<Tab> to display available snippets"']]
let g:unite_source_menu_menus.CustomKeyMaps.command_candidates += [['➤ Jump to next UltiSnip edit point                              9<Tab>', 'echo "Use 9<Tab> to jump to the next editable snippet segment"']]


synthetic organic chemistry at Bryn Mawr

IDO inhibitor project

During their development tumors acquire the capability to escape immune control. Immune escape is a fundamental trait of cancer, but until recently there was little understanding of how it develops. IDO is an enzyme that we and others have found to drive immune escape in tumors, where IDO is often inappropriately switched on.

In the present project, we are moving forward to develop our discovery that drug-like small molecule inhibitors of the IDO enzyme stimulate the immune system to attack tumors in an animal in a manner that synergistically leverages the responses that can be achieved with chemotherapy or radiotherapy. The combination of a traditional chemotherapeutic agent, cytoxan (CTX), and 1-methyl-tryptophan (1-MT), a known IDO inhibitor, have demonstrated considerable therapeutic potential (see Combo in Figure 1; tumor is imaged with bioluminiscence).

We are currently exploring a new structural class that is based on the reported mechanism of IDO’s catalytic reaction (Figure 5 and Syun-Ru Yeh et al. PNAS 2009, 106, 17371-17376).

Figure 5: Reported IDO mechanism

Mimics of the reported indole-peroxy intermediate shown in the red box are being generated and tested for selective and more potent IDO inhibition (Figure 6).

Figure 6: Current inhibitor design with X and Y being oxygen mimics.

We gratefully acknowledge support of this work from the National Institutes of Health (National Cancer Institute, R01 CA109542-04A2) as a collaborative project with biologists at Lankenau Institute of Medical Research.


The Midshipmaid

The Midshipmaid is a 1932 British comedy film directed by Albert de Courville and starring Jessie Matthews, Frederick Kerr, Basil Sydney and Nigel Bruce. The film is based on a play by Ian Hay and Stephen King-Hall. it was released in the U.S. as Midshipmaid Gob. John Mills makes his film debut in a supporting role. It was shot at the Lime Grove Studios, with sets designed by the art director Alfred Junge.

Plot
In this comedy with musical interludes, pompous economy expert Sir Percy Newbiggin (Fred Kerr) visits the Naval Fleet in Malta to see what cuts can be made in their expenditure. The officers all fall over themselves to woo his beautiful daughter Celia (Jessie Matthews), who accompanies him: she becomes engaged to the son of the First Sea Lord and her father decides to leave economics to the Navy.

Cast
Jessie Matthews as  Celia Newbiggin
Frederick Kerr as Sir Percy Newbiggin
Basil Sydney as Commander Fosberry
Nigel Bruce as Major Spink
A.W. Baskcomb as AB Pook
Claud Allister as Chinley
Anthony Bushell as Lieutenant Valentine
Edwin Lawrence as Tappett
Archie Glen as Bunduy
Albert Rebla as Robbins
John Mills as Golightly
Anthony Holles as Lieutenant Kingsford
George Zucco as Lord Dore
Joyce Kirby as Dora
Steve Condos as Horse
Nick Condos as Horse
Hay Plumb as Sailor
John Turnbull as Officer
Wilma Vanne as Cora

References

External links

Category:1932 films
Category:1930s comedy films
Category:British films
Category:British comedy films
Category:English-language films
Category:Films based on works by Ian Hay
Category:Films directed by Albert de Courville
Category:Military humor in film
Category:British films based on plays
Category:Seafaring films
Category:Films set in England
Category:Films set in Malta
Category:Gainsborough Pictures films
Category:Films scored by Jack Beaver

Category:British black-and-white films


Q:

What is a flat rated engine?

I've heard that a "Flat Rated Engine" is an engine where the power is reduced to keep the internal temperature within certain limits when the ambient temperature is above a certain point. Is that correct? How does it work?

A:

Yes, a flat rated engine (my familiarity is with gas turbines, but the concept may apply to other engine types), is an engine for which the control system is designed to achieve the same level of thrust (hence the "flat" term), up to a certain OAT, then for higher ambient temperatures, the level of thrust decreases as a function of OAT, normally in a pretty linear fashion. This control system operation gives identical performance over the flat portion of the OAT range even while the engine degrades (until it degrades to the point it hits the EGT limit), making the plane performance predictable. But for higher OATs, it stops the EGT continuing to increase. The temperature at which the thrust starts to decrease is typically 25 or 30 deg C, and can be found in the EASA or FAA engine type certificates (e.g. see section 6 of this EASA one for the CFM56-5). See the graph from this CFM56 document below. So, your understanding was correct.


WASHINGTON (Reuters) - U.S. President Donald Trump will order the Treasury on Friday to find and reduce tax burdens and review post-financial crisis reforms that banks and insurance companies have said hinder their ability to do business.

Slideshow ( 4 images )

A White House official said on Thursday that Trump will issue an executive order directing the Treasury on the tax issues. He will also issue two memoranda asking for reviews of two parts of the 2010 Dodd-Frank Wall Street reform law - the Orderly Liquidation Authority that sets out how big banks can wind down during a crisis and the Financial Stability Oversight Council (FSOC), which is made up of the country’s top regulators.

The orders, which Trump will sign at the Treasury Department, next door to the White House, comes as the president works toward making good on a major campaign promise to lower taxes.

Treasury Secretary Steven Mnuchin will review significant tax regulations issued in 2016 to determine if any impose an undue financial burden on American taxpayers, add undue complexity or exceed statutory authority, the official’s statement said.

Mnuchin said earlier on Thursday that Treasury is working on tax reform “day and night” and will soon create a sweeping overhaul.

Congress recently failed in efforts to make good another Trump campaign promise to reform healthcare.

House of Representatives Speaker Paul Ryan said this week that the country’s first tax overhaul in decades may not be done until well into 2017. The review that Trump is ordering gives the administration a way to approach the issue independent of Congress.

The liquidation authority and the FSOC were both created as part of the Dodd-Frank law intended to prevent a repeat of the 2007-09 financial crisis, when the U.S. government injected billions of dollars in aid into failing banks to keep them from destroying the country’s economy.

In February Trump ordered a review of the law, saying he wanted to cut out much of it, and Mnuchin has said he would like to look into how the council, which he chairs, works.

House Republicans are also working to loosen Dodd-Frank regulations. Banks say the regulations have hurt their liquidity and created burdensome processes.

Trump will order an assessment of how the FSOC designates a financial institution as “systemically important,” which triggers requirements to hold more capital in case it comes into crisis.

Republican lawmakers say the FSOC uses a flawed process lacking transparency to designate non-bank institutions. Only two insurers, American International Group Inc and Prudential Financial Inc, currently carry the label, and a judge last year struck down the council’s designation of MetLife Inc.

Mnuchin will have 180 days to report to Trump on the liquidation authority, a tool for federal banking regulators to use if they need to step in during a financial emergency and help a failing bank unwind. The report will offer views on using bankruptcy as an alternative, the impact of failing companies on financial stability, and whether the authority could drive up taxpayer costs or encourage excessive risk-taking.


Q:

.hide doesn't work

I am making a jeopardy game. When I click a div I want to do some effect on it. However, I can't even get a simple .hide to work. Any ideas?
<!DOCTYPE html>

        <title>Jeopardy</title>
        <meta name="viewport" content="width=device-width, initial-scale=1.0">
        <link href="css/bootstrap-responsive.css" rel="stylesheet">
        <link href="css/bootstrap.css" rel="stylesheet">
        <link href="css/customStyles.css" rel="stylesheet">

100

100

100

100

100

100

javascript
$(function() {
    $('#span2').click(function() {
        $(this).hide(400);
        /*$('#span2').hide(400);  <--tried this also */
    });
});

I've used jquery to animate navigation on a site before. Am i missing something obvious?

A:

Your
$('#span2') // id selector

Should be
$('.span2') // class selector

Since it's a class

A:

Your problem is that you are using the hash # which is the id selector instead of the class selector which is a dot ..
Try
$(function() {
    $('.span2').click(function() {
        $(this).hide(400);
     });
 });

You might want to read up more on the different jQuery Selectors on the official documentation


Gaussian beam interaction with an air-gap Fizeau interferential wedge.
We describe a plane-wave-expansion approach for calculation of the fringe pattern in transmission and reflection for a Gaussian monochromatic beam. Both positive and negative incidence, at which the incident light beam undergoes multiple reflections within the wedge in direction of increasing or decreasing wedge thickness respectively, are analyzed. It is shown that the two opposite incidences of the light beam are described by the same mathematical expressions; i.e., the transmitted/reflected fringe pattern at positive incidence is a continuation of the pattern at negative incidence at some distance from the wedge. Numerical simulations are made for a high-reflectivity-coating air-gap Fizeau interferential wedge with apex angle of 5-100 microrad and thickness of 5-500 microm as a useful optical element in laser resonator design. Experimental verification is also provided.


Q:

Number of Commits between two Commitishes

How can I find the number of commits between two commitishes in git?
Additionally, is there some way that I could do the same with any project on GitHub (using the UI, not the API)?

A:

Before I give you an answer, consider this commit graph:
        o -----------
       /             \
... - A - o - o - o - B
       \         /
        o ----- o

Each o represents a commit, as do A and B (they're just letters to let us talk about specific commits).  How many commits are there between commits A and B?
That said, in more linear cases, just use git rev-list --count A..B and then decide what you mean by "between" (does it include B and exclude A? that's how git rev-list --count will behave).  In branchy cases like this, you'll get all the commits down all the branches; add --first-parent, for instance, to follow just the "main line".
(You also mentioned "commitish", suggesting that we might have annotated tags.  That won't affect the output from git rev-list, which only counts specific commits.)

Edit: Since git rev-list --count A..B includes commit B (while omitting commit A), and you want to exclude both end-points, you need to subtract one.  In modern shells you can do this with shell arithmetic:
count=$(($(git rev-list --count A..B) - 1))

For instance:
$ x=$(($(git rev-list --count HEAD~3..HEAD) - 1))
$ echo $x
2

(this particular repo has a very linear graph structure, so there are no branches here and there are two commits "between" the tip and three-behind-the-tip).  Note, however, that this will produce -1 if A and B identify the same commit:
$ x=$(($(git rev-list --count HEAD..HEAD) - 1))
$ echo $x
-1

so you might want to check that first:
count=$(git rev-list --count $start..$end)
if [ $count -eq 0 ]; then
    ... possible error: start and end are the same commit ...
else
    count=$((count - 1))
fi

A:

$ git log 375a1..58b20 --pretty=oneline | wc -l

Specify your start commit followed by your end commit, and then count the lines.  That should be the count of commits between those two commit ranges.  Use the --pretty=online formatting so that each commit takes up a single line.
As for the GUI in GitHub, I don't know of a way to accomplish this same task.  But that should be trivial, as the above is the possible way to do it directly in Git Bash.


This is going to be a tough column to write – it is because in my heart I know. Indeed barring the unforeseen, in the weeks or months to come; one of my favorite Los Angeles Dodgers ever will no longer be a part of the spectacle. And what a spectacle he has been: every tongue-wagging, daring, unpredictable, do something to make you shake your head moment.

These are the last days of Yasiel Puig, if you’re reading between the lines or even if you aren’t; the Dodgers are going to move on from The Wild Horse and are actively trying to do so.

According to a source, the Dodgers are actively trying to trade Yasiel Puig and/or Matt Kemp. — Mark Feinsand (@Feinsand) December 12, 2018

Moreover, maybe it’s okay. Of course, it’s not okay with me; but it never would be. In the world I live in, I would want Puig to play until he’s 45 years of age. Long after he’s providing positive value to a ball club – to my ball club – I would want him in right field. When he no longer crashed into sidewalls with reckless abandon or gunned down runners or missed cut off men fiercely, I would still want to call him mine.

And I would make a terrible general manager. It’s fair to say that with the rare player – I love too hard. Yasiel Puig has earned his place in my heart to be one of those guys.

Furthermore, one of my favorite pieces I’ve written on this site was on why Dodgers fans love Puig. This is what I said when I ended that column.

In a number of other big league cities, mountains would be moved for a fan base to have a player who entertains on a nightly basis like Puig. Nevertheless, I’m not sure that there is a city more perfectly suited to showcase him than The City of Angels. Something about Puig rounding the bases with reckless abandon – late in the night after all other games have gone final – seems like the correct synthesis within the baseball world.

It’s been special watching this guy grow up – and growing up along with him. I talk a lot about players who can make you feel. Puig is more than that. Rarely do those players who make you feel also serve to entertain with such ease. Yasiel Puig does both and you get the feeling it’s without being a try hard.

Something about my life attached to baseball won’t be right anymore when I can’t turn on the television after midnight to see Puig taking that extra base. Picking the pocket of the opposition, putting pressure on the other team without design. Doing something that should get a base coach fired. This player will never outrun the mark within him – but that mark all in the same is what makes him a little bit special.

I took the Dodgers to task the other day for supposedly involving Cody Bellinger in trade talks. Overwhelmingly, I feel that would be a mistake. In this case, I’m not so sure.

Sometimes, it’s just time for two parties to move on for one reason or another. Like a struggling couple hanging on only for reasons of time spent and complacency – it might be just time. While I want to keep the Wild Horse captive at Chavez for a while longer, people smarter than me have deemed that not doing so can lift the team to new heights.

If this is the end – I have done this right. I’ve defended the guy, savored him, loved him, and really soaked in every moment. When I call someone a ‘ballplayer’, it’s the ultimate sign of respect I can pay to a player. Puig is not only that, but a true warrior. He wears his heart on his sleeve, and he’s grown to love playing in Los Angeles. He plays with flavor and pride that some will never be able to. And that’s why we love him back. He’s that bad puppy dog that goes to the bathroom on your favorite throw rug. You’ll be a little upset for a minute, then you’ll want to hug him and scratch his belly an hour later.

My favorite Puig moment? It actually wasn’t on the field of play. It was heading into game six of the 2017 World Series against the Houston Astros. The team was wavering after the game five no one could forget. The loss of a lifetime. And what did Puig do? Something only Yasiel Puig could do. Something no one else would do at that moment.

He told Justin Verlander – unhittable to that point – that the Dodgers were coming for him in game six. That Verlander was going to be in for the ride of his life at the hands of the Dodgers. Puig guaranteed a game seven – and he made me believe. It was a shot in the arm that the team needed, and they delivered just as Puig said.

I will miss you Yasiel, and I love you. Thank you. There will be no expiration date on the memories you’ve left in my mind and heart.

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