166
Convert 1101011110111100 (base 2) to base 9.
83674
Convert -214421a (base 11) to base 7.
-44013240
-12460322 (base 8) to base 16
-2a60d2
What is 10111110000011010 (base 2) in base 8?
276032
What is -43220300 (base 6) in base 13?
-3598bc
What is 105712 (base 8) in base 2?
1000101111001010
-1421373 (base 9) to base 3
-1110201102110
What is -2134324 (base 8) in base 16?
-8b8d4
-805e40 (base 15) to base 10
-6095085
-21011011202 (base 3) to base 7
-1124366
Convert 2922192 (base 10) to base 13.
7b4110
Convert 42014220 (base 5) to base 8.
1241547
Convert 19b12 (base 13) to base 2.
1100010000100000
Convert c4a (base 15) to base 11.
2099
What is -6b1c9 (base 14) in base 13?
-91a90
Convert -442420334 (base 5) to base 12.
-7871ba
What is -3287732 (base 9) in base 15?
-24e958
Convert -330030212 (base 4) to base 7.
-2044565
c2a2b (base 15) to base 3
1011022201212
Convert 22936 (base 14) to base 11.
58234
Convert 204515564 (base 7) to base 16.
b87540
-104de2 (base 15) to base 2
-10111101011101001100
-27008 (base 13) to base 12
-35b65
Convert 2342355 (base 6) to base 16.
1de1f
Convert 5020002 (base 7) to base 8.
2206231
-2333110233 (base 4) to base 15
-1072e3
1311122130 (base 4) to base 9
812630
What is 122ac (base 16) in base 7?
426642
-1110110010111010101101 (base 2) to base 12
-1370665
Convert -100222211 (base 4) to base 15.
-1535b
Convert -3b857 (base 14) to base 6.
-3052525
174c68 (base 13) to base 11
3683a2
Convert 1021020001222201 (base 3) to base 13.
39caa68
Convert 153827 (base 11) to base 9.
404158
What is -31502142 (base 6) in base 8?
-3420216
What is -996b64 (base 12) in base 14?
-47676c
What is -103032233 (base 4) in base 7?
-445433
Convert -153460 (base 8) to base 2.
-1101011100110000
2065204 (base 7) to base 13
8a63a
What is 2814717 (base 11) in base 9?
10115161
Convert -1212b59 (base 13) to base 9.
-11481561
Convert -120230142 (base 5) to base 15.
-ae6d2
Convert 1011203001 (base 4) to base 12.
118a29
What is 62b828 (base 15) in base 10?
4696463
12114 (base 9) to base 6
101321
2012234030 (base 5) to base 2
1111010110011111001001
Convert -321130123300 (base 4) to base 13.
-3173275
What is 4130142 (base 5) in base 6?
1240415
What is -112121110011 (base 3) in base 2?
-1000110001101000010
Convert 2a7b98 (base 12) to base 13.
1c224b
10011011010101111001 (base 2) to base 3
1012022210222
1c0ba40 (base 13) to base 5
4340330414
Convert 76875 (base 9) to base 13.
1a2b5
What is -373476 (base 8) in base 13?
-46840
451663 (base 7) to base 3
11001121211
Convert 247aa (base 15) to base 16.
1c705
What is -2220816 (base 11) in base 12?
-137a403
What is -dd9a9 (base 15) in base 16?
-abeb8
-1508783 (base 9) to base 13
-2322c3
Convert a1913 (base 12) to base 13.
749c7
Convert -2410385 (base 9) to base 7.
-14046314
1113013212 (base 4) to base 7
3014226
Convert 1fcfd (base 16) to base 12.
634a5
55163 (base 8) to base 4
11221303
What is -110130021 (base 4) in base 13?
-2c151
Convert -2010100210000 (base 3) to base 5.
-242112214
-520313 (base 9) to base 13
-aa622
Convert 194839 (base 10) to base 11.
123427
Convert 1011001110000000 (base 2) to base 16.
b380
4096 (base 15) to base 4
3111021
What is -155611400 (base 7) in base 15?
-ddd2e8
What is 430603 (base 14) in base 11?
1309857
Convert -607705 (base 11) to base 8.
-3563133
Convert -1ad17 (base 16) to base 12.
-5369b
What is 2547554 (base 9) in base 3?
2121121121211
Convert -19668b (base 12) to base 6.
-13324255
-3d878 (base 16) to base 15
-4ea19
What is -ba765 (base 16) in base 9?
-1383600
What is -540721 (base 8) in base 4?
-230013101
What is -7540 (base 15) in base 4?
-12003222
723da (base 14) to base 4
1003023230
-4b13bb (base 13) to base 14
-34cac9
Convert -1043032 (base 5) to base 15.
-5747
What is 15202000 (base 6) in base 10?
529200
What is 62eca (base 15) in base 11?
1a487a
Convert 27057222 (base 8) to base 13.
133c487
What is 302230441 (base 6) in base 9?
10621807
What is -111111110111110111111 (base 2) in base 3?
-10221100001012
What is 7a729 (base 13) in base 7?
1616324
What is 840531 (base 10) in base 15?
1190a6
Convert -104c1 (base 16) to base 7.
-365421
Convert 1410323203 (base 5) to base 9.
6703766
What is -587a117 (base 11) in base 7?
-153140542
Convert 113032112 (base 5) to base 9.
868233
1012350 (base 12) to base 2
1011011111000001101100
-355513 (base 7) to base 12
-31324
Convert 3451414 (base 6) to base 5.
21143142
What is 1165730 (base 10) in base 15?
180605
What is -150b1 (base 13) in base 11?
-27902
What is 335a8e (base 15) in base 2?
1001010101111101101011
Convert 8123 (base 9) to base 11.
4505
Convert -210645 (base 8) to base 4.
-101012211
Convert -18d392 (base 16) to base 9.
-3048766
Convert 2165a62 (base 12) to base 14.
bb6150
What is -185644 (base 10) in base 7?
-1402144
10110001222112 (base 3) to base 16
1bf41c
Convert -a06331 (base 11) to base 2.
-110001011001111001101
Convert 53704413 (base 8) to base 12.
3a2940b
What is -110405115 (base 6) in base 4?
-13212101213
Convert 354a53 (base 11) to base 10.
562950
Convert -7433897 (base 10) to base 2.
-11100010110111010101001
-52961 (base 10) to base 5
-3143321
Convert -506027 (base 11) to base 7.
-6625023
Convert -227956 (base 12) to base 16.
-86e92
315445 (base 12) to base 4
2331210311
101111001010110000111101 (base 2) to base 4
233022300331
Convert -4215244 (base 6) to base 9.
-341651
What is 2498c (base 13) in base 3?
10102122202
-1141123145 (base 6) to base 7
-214641524
What is -2022120101112 (base 3) in base 9?
-2276345
What is 4224442 (base 5) in base 12?
34a52
What is 1220110122 (base 4) in base 7?
3426513
Convert 57963 (base 11) to base 13.
2c11c
184120 (base 13) to base 11
386412
What is 661516 (base 7) in base 14?
3030d
-414654 (base 7) to base 8
-213246
-140150354 (base 6) to base 13
-77695c
-11101110010010110 (base 2) to base 3
-20012100202
What is 7c9d21 (base 16) in base 4?
133021310201
Convert -210112001002212 (base 3) to base 13.
-24a5749
What is -3975486 (base 11) in base 12?
-2375b1a
448056 (base 9) to base 7
2165166
Convert 672586 (base 9) to base 11.
255172
What is -122136 (base 11) in base 12?
-93943
What is -221012200021 (base 3) in base 14?
-ccb9b
Convert -102013120 (base 4) to base 14.
-1d080
Convert 51521036 (base 8) to base 10.
10920478
Convert 714a2 (base 14) to base 5.
32210312
7682b2 (base 13) to base 6
135433340
Convert -133303121303 (base 4) to base 13.
-195b957
111001001110111111001 (base 2) to base 13
508844
Convert -24266413 (base 9) to base 10.
-11853876
Convert 6236c3 (base 13) to base 10.
2292644
-72176 (base 9) to base 8
-134657
64a27 (base 14) to base 9
410868
Convert -32134 (base 7) to base 3.
-101220221
What is -3816d (base 14) in base 11?
-94334
Convert -829359 (base 12) to base 10.
-2048181
Convert -7c523 (base 13) to base 3.
-102112121112
-408c2c (base 13) to base 6
-52130422
What is -2dc62 (base 15) in base 16?
-241cd
Convert 333012213 (base 4) to base 13.
90855
6fba08 (base 16) to base 13
1694a20
Convert -14a2425 (base 15) to base 2.
-111000111111111101101100
What is -160057 (base 9) in base 2?
-11000000010100011
60680c (base 15) to base 10
4578312
What is -665239 (base 12) in base 13?
-44c373
Convert 10021403 (base 5) to base 3.
11001012021
-101000110101100111011 (base 2) to base 5
-320310141
What is 220102011012 (base 3) in base 15?
9759e
What is -84fd8 (base 16) in base 14?
-102732
What is -13441100 (base 5) in base 14?
-3910a
Convert 2232a (base 12) to base 2.
1011000101010010
10221012001112 (base 3) to base 15
2b443e
What is 146992 (base 11) in base 13?
801a4
256626 (base 12) to base 2
10010101100011111110
-133123110332 (base 4) to base 16
-7db53e
What is -1102302002 (base 4) in base 14?
-8b7d8
What is 1201021122 (base 3) in base 2?
1000001111001100
-5367284 (base 10) to base 6
-311012312
12502264 (base 7) to base 3
2011002212111
Convert 10826068 (base 9) to base 13.
1128092
Convert -97140 (base 10) to base 11.
-66a8a
50a9b5 (base 15) to base 7
44402255
21003424 (base 5) to base 15
3610e
Convert 11222321 (base 5) to base 7.
602112
357ba (base 15) to base 8
515004
115044 (base 6) to base 10
10180
-4b6259 (base 15) to base 6
-205252503
32324241 (base 5) to base 16
43955
Convert 152fbe (base 16) to base 6.
45432050
-1359612 (base 10) to base 5
-322001422
-33079 (base 11) to base 16
-bb


This invention relates to an improved fence guard for restricting the growth of grass, weeds and the like directly adjacent to or beneath a fence line.
Past fence guards have utilized first and second elongated panels generally L-shaped in cross-section. The vertical leg of each panel abuts the opposed sides of the fence with the horizontal leg extending from the bottom of the vertical leg and along the ground. The vertical legs protect the lower portion of the fence while the horizontal legs preclude the growth of any grass, weeds, etc. adjacent the fence line.
Although such fence guards are assumably effective in their operation, a problem has arisen in that weeds grow in the channel presented between the first and second vertical legs. The removal of such weeds is difficult as it is hindered by the bottom of the fence protruding into the channel.
Various solutions have been suggested to address this problem including the use of various types of permanent barriers installed underneath the fence line to preclude the appearance of vegetation therealong. Other growth-impeding devices have included the use of specially designed panel members which present a barrier underneath the line upon intraengagement of the panel members.
As the bottom of preexisting fences normally contact the ground, past devices are not easily adaptable for installation to fences already in place. Also vegetation along preexisting fence lines further inhibits the installation of such devices therebelow. Thus, past devices have increased the costs and complexity of manufacture and/or installation.
In response thereto I have invented an improved fence guard which utilizes first and second L-shaped panel members having vertical and horizontal leg members therein. The vertical leg of each panel is positioned on opposed sides of the fence with the bottom edge of the fence being positioned in a channel presented therebetween. Prior to connection of the first panel to the second panel by means of nuts, bolts, clips etc., a strip of batt insulation is placed between the bottom edge of the fence and the vertical leg of one of the panel members. Upon connection of the panels, the insulation is compressed between the panel and the fences. This compression urges the insulation material through the open portions/interstices of the adjacent fence for contact with the interior face of the vertical leg of the opposed panel. The insulation material fills the resulting channel which precludes entry of moisture and/or sunlight on the ground beneath the fence line. Thus, the undesirable growth of vegetation between the panels and below the fence line is inhibited. The novel use of the compressible insulation material allows my fence guard to be easily installed on existing fence lines and eliminates the need to utilize relatively complex fence guards and the resulting labor costs.
Accordingly, it is an object of the present invention to provide an improved fence guard for restraining the growth of grass, weeds and the like directly underneath and adjacent a fence line.
Another object of this invention is to provide a fence guard, as aforesaid, which utilizes a compressible filler material to preclude the growth of vegetation along the fence line.
A still further object of this invention is to provide a fence guard with compressible material, as aforesaid, which fills the interstices of a chain link fence so as to preclude the growth of vegetation along the ground-adjacent fence line.
Another object of this invention is to provide a fence guard which can be inexpensively installed on existing or new fences.
Other objects and advantages of this invention will become apparent from the following description taken in connection with the accompanying drawings, wherein is set forth by way of illustration and example, an embodiment of this invention.


Chpts 15 - 18 lecture

HLTB03H3Y: Foundations in Health Department of Health Studies University of Toronto at Scarborough Winter 2011 Instructor: Anna Walsh. Term: Winter 2011: Wednesdays 9 a.m.-11 a.m. Lecture Room: Room HW 216 E-mail: [email protected] Office: BV506. Office Hours: Mondays: 2 p.m.-3 p.m. March 16 The Health of Children & Youth. Ch. 15 and 16. Family Law Act 31.(1) Every parent has an obligation to provide support for his or her unmarried child who is a minor or is enrolled in a full time program of education, to the extent that the parent is capable of doing so. (2) The obligation under subsection (1) does not extend to a child who is sixteen years of age or older and has withdrawn from parental control. R.S.O. 1990, c. F.3, s. 31 (2). Obligation of child to support parent 32. Every child who is not a minor has an obligation to provide support, in accordance with need, for his or her parent who has cared for or provided support for the child, to the extent that the child is capable of doing so. R.S.O. 1990, c. F.3, s. 32. Income and Poverty Inequalities of wealth and income produce unequal life chances. Poverty translates into homelessness, ill health, short life expectancy, malnutrition, amid hunger. A significant number of Canadians live in poverty. The number of poor people was nearly 5 million in 2003 and the poverty rate was nearly 16 percent. These income disparities produce an inequality of opportunities and life chances and create negative outcomes for individuals in low-income and poor families. Income and Health Those with high incomes, for instance, live longer, healthier and more disability -free lives on average than those who are poor. Similar patterns of disease, illness, and mortality prevail for children. Life Expectancy Number of years a person would be expected to live based on mortality statistics for a given observation period. Life expectancy is a measure of longevity and not quality of life. It is a widely used indicator of the health status of the population. 1 www.notesolution.com


/**********************************************************************
 * File:        tlog.h
 * Description: Variant of printf with logging level controllable by a
 *              commandline flag.
 * Author:      Ranjith Unnikrishnan
 * Created:     Wed Nov 20 2013
 *
 * (C) Copyright 2013, Google 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.
 *
 **********************************************************************/
#ifndef TESSERACT_TRAINING_TLOG_H_
#define TESSERACT_TRAINING_TLOG_H_

#include "commandlineflags.h"
#include "errcode.h"
#include "tprintf.h"

DECLARE_INT_PARAM_FLAG(tlog_level);

// Variant guarded by the numeric logging level parameter FLAGS_tlog_level
// (default 0).  Code using ParseCommandLineFlags() can control its value using
// the --tlog_level commandline argument. Otherwise it must be specified in a
// config file like other params.
#define tlog(level, ...) {                        \
  if (FLAGS_tlog_level >= level) {                \
    tprintf_internal(__VA_ARGS__);                \
  }                                               \
}

#define TLOG_IS_ON(level) (FLAGS_tlog_level >= level)

#endif  // TESSERACT_TRAINING_TLOG_H_


In one standard process for manufacturing printed circuit boards (PCBs), a master reticle is generated by a computerized system that exposes a one-to-one image of the desired PCB pattern on a film or other substrate. Subsequently, masks are created for contact printing of metallized PCB substrates that have a photoresist coating. When the resist is developed, the metal is etched to reveal the original interconnect pattern of the master reticle. The board will then be laminated together with the other boards representing the different levels of a finished PCB. Then the finished PCB is tested. If a design flaw, as opposed to a process flaw, is found, the entire process must be redone.
Creation of the master reticle is expensive. After the master reticle is completed, it must be transferred to a working film, which is also costly. With many flaws, this can be become extremely expensive, not to mention time consuming. There is a need for a method of manufacturing PCBs that does not involve repetitive manufacture of master reticles, or periodic replacement of working reticles.


Sure, but first, one of them has to beat the rest.

If national polls are to be believed (and that is always a dubious assumption), Perry is best positioned to win the GOP nomination. Which is why it was a curious - if not risky - strategy to come out swinging against Romney. Indeed, the Texas governor can't seem to pass up a fight; he attacked Paul, as well as a Republican who wasn't even on the stage: former Bush adviser Karl Rove.

And yet Perry played the martyr. "I kind of feel," he said, "like the piñata here at the party." With good reason. Romney, a former Massachusetts governor, started the fight with an early and subtle dig at Perry's long career in government. Romney's campaign quickly followed up with a press release calling Perry a "career politician." In case anybody missed the point, the press release included photos of Perry aging in office.

Perry praised Romney for creating jobs as a private businessman, but said he record as governor "did not match that."

Romney accused Perry of taking credit for creating jobs in Texas that were the result of conditions outside of Perry's control. To claim credit, Romney said, would be "like Al Gore saying he created the Internet."

Ouch. It's a low blow in GOP politics to compare a rival to Gore, especially when that rival is Perry - a former Democrat who once supported Gore.

Perry hit lower. "Mike Dukakis created jobs three times faster than you did, Mitt," he said.

"As a matter of fact," Romney replied, George W. Bush and his predecessors "created jobs faster than you did."

Same to you and more of it.

"It's nice to see everyone came prepared for tonight's debate," cracked NBC's Brian Williams, co-moderator of the debate.

Indeed, candidates not named Perry and Romney also had good nights. Huntsman stood out as a reasonable and moderate candidate who could go toe-to-toe with the first tier ("I have to say, Mitt, now is not the time ... to start a trade war."). Rep. Michele Bachmann took the steadiest aim at President Barack Obama, underscoring her impressive discipline and polish ("ObamaCare is killing jobs"). And Paul, after a slow start, finally got the attention he craves, even though it came with Perry questioning his loyalty to the GOP.

But it was the Texas cowboy and Massachusetts businessman who stole the show and stuck to their talking points. "Maybe it's time to have some provocative language in this country," Perry said, delivering all that and more.

He refused to back down from calling Social Security a Ponzi scheme, saying "it is a monstrous lie" to suggest to young Americans that Social Security will be available for them as it stands. Reminded that Rove has called such language "toxic," Perry snapped, "You know, Karl has been over the top for a long a time in some of his remarks. So I am not responsible for Karl anymore."

Nope, but Perry is responsible for every outside-the-mainstream policy he backed and every over-the-top statement he made in his eleven years as governor. Evolution. Texas succession. And more, much more, if Romney has his way.

Image credit: Mario Anzuoni/Reuters


-- ACME http-01 domain validation plugin for Haproxy 1.6+
-- copyright (C) 2015 Jan Broer
--
-- usage:
--
-- 1) copy acme-webroot.lua in your haproxy config dir
--
-- 2) Invoke the plugin by adding in the 'global' section of haproxy.cfg:
--
--    lua-load /etc/haproxy/acme-webroot.lua
--
-- 3) insert these two lines in every http frontend that is
--    serving domains for which you want to create certificates:
--
--    acl url_acme_http01 path_beg /.well-known/acme-challenge/
--    http-request use-service lua.acme-http01 if METH_GET url_acme_http01
--
-- 4) reload haproxy
--
-- 5) create a certificate:
--
-- ./letsencrypt-auto certonly --text --webroot --webroot-path /var/tmp -d blah.example.com --renew-by-default --agree-tos --email my@email.com
--

acme = {}
acme.version = "0.1.1"

--
-- Configuration
--
-- When HAProxy is *not* configured with the 'chroot' option you must set an absolute path here and pass
-- that as 'webroot-path' to the letsencrypt client

acme.conf = {
	["non_chroot_webroot"] = ""
}

--
-- Startup
--
acme.startup = function()
	core.Info("[acme] http-01 plugin v" .. acme.version);
end

--
-- ACME http-01 validation endpoint
--
acme.http01 = function(applet)
	local response = ""
	local reqPath = applet.path
	local src = applet.sf:src()
	local token = reqPath:match( ".+/(.*)$" )

	if token then
		token = sanitizeToken(token)
	end

	if (token == nil or token == '') then
		response = "bad request\n"
		applet:set_status(400)
		core.Warning("[acme] malformed request (client-ip: " .. tostring(src) .. ")")
	else
		auth = getKeyAuth(token)
		if (auth:len() >= 1) then
			response = auth .. "\n"
			applet:set_status(200)
			core.Info("[acme] served http-01 token: " .. token .. " (client-ip: " .. tostring(src) .. ")")
		else
			response = "resource not found\n"
			applet:set_status(404)
			core.Warning("[acme] http-01 token not found: " .. token .. " (client-ip: " .. tostring(src) .. ")")
		end
	end

	applet:add_header("Server", "haproxy/acme-http01-authenticator")
	applet:add_header("Content-Length", string.len(response))
	applet:add_header("Content-Type", "text/plain")
	applet:start_response()
	applet:send(response)
end

--
-- strip chars that are not in the URL-safe Base64 alphabet
-- see https://github.com/letsencrypt/acme-spec/blob/master/draft-barnes-acme.md
--
function sanitizeToken(token)
	_strip="[^%a%d%+%-%_=]"
	token = token:gsub(_strip,'')
	return token
end

--
-- get key auth from token file
--
function getKeyAuth(token)
        local keyAuth = ""
        local path = acme.conf.non_chroot_webroot .. "/.well-known/acme-challenge/" .. token
        local f = io.open(path, "rb")
        if f ~= nil then
                keyAuth = f:read("*all")
                f:close()
        end
        return keyAuth
end

core.register_init(acme.startup)
core.register_service("acme-http01", "http", acme.http01)


Crypto mining has become very common these days for hackers to earn a handsome income while putting a person’s devices at risk. Slowing computers, rising electricity bills, and other issues are caused because a hacker has infiltrated a computer through a malicious link or software. A new type of crypto mining malware was found recently that was posing as an Adobe Flash update. Once installed, it pushes a Monero cryptocurrency miner onto the computer, handing its owner an increased electricity bill while the hacker enjoys the riches.

That Flash Update? It’s Fake

Unit 42, the threat intelligence team at Palo Alto Networks, identified new malware that started appearing in August. It looks like a typical Flash update from the official Adobe installer and fools the users into believing that it is downloading a genuine update. Once done, the XMRig cryptocurrency miner, which is used to mine Monero, a privacy coin very commonly associated with the dark web, starts eating away the computer’s resources.

Advertisement

Interestingly, the malware also updates a victim’s Flash Player to the latest version, giving it a more authentic appeal. Victims are less likely to identify it as an unusual activity as the fake update works fine while the miner is running in the background. The researchers noted that a Windows computer would issue a warning to users before running the downloaded file for the update. Therefore, users must be proactive and remove the file immediately from their computer.

A Spurt in Illegal Crypto Mining

In a previous report, Unit 42 suggested that 5 percent of Monero in circulation has been mined through malicious activities. Another security firm, McAfee, noted that illegal crypto mining has increased by 629 percent in the first quarter of 2018 alone.

The researchers first noticed malicious activity when they found Windows executable files starting with the name adobeFlashPlayer that originated from non-Adobe destinations in cloud-based servers. A common text string helped the researchers find 113 samples of malware since March 2018, two-thirds of which were crypto miners. The remaining samples had at least some characteristics similar to crypto miners.

Palo Alto Networks said that organizations with “decent web filtering” have a lesser chance of infection. Thus, adopting proactive security measures is vital.

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Since her parents first taught her the practice of tikkun olam as a young girl growing up in Glasgow, Scotland, Carole Price has seen firsthand the unique benefits of giving back to her community. Tikkun olam is the Jewish idea of “repairing the world”, and ever since Carole’s life brought her across the Atlantic and all the way to Austin, she’s seen her tireless dedication to the idea make a big impact on more than just those she serves.

For the past twenty years, Carole Price has devoted herself to volunteering with Hospice Austin – from folding linens and making coffee to organizing huge fundraisers and managing strategic partnerships, she’s done a little bit of everything over thousands of volunteer hours. Primarily serving in Hospice Austin’s in-patient facility called Christopher House, Carole has shown a knack for offering one-to-one companionship to hospice patients and is one of a special group of skilled, compassionate volunteers trained by registered nurses to assist with patient bed baths. On a larger scale, Carole’s been responsible for marshalling major resources from the community – she secured a weekly flower donation from Whole Foods as well as food for Christmas lunch each year, she’s kept the Hospice Austin food pantry stocked by connecting to groups like Keep Austin Fed and St. Mark’s Episcopal Church resulting in thousands of patients being fed, and she’s even set up a trust with her husband Kerry to benefit Hospice Austin for years to come. “She will do whatever is needed,” says Rev. Nancy Chester McCranie, Director of Volunteer and Bereavement Services at Hospice Austin. “She has given so much to our community through her service to our organization, from her time and energy as a hands-on volunteer, to spearheading food drives for our food pantry, to helping raise money, to providing a delicious lunch every Christmas Day. She’s simply amazing.”

“Carole’s life mission is to help others,” adds Hospice Austin’s volunteer coordinator Phillip Sadler. “She is a tireless, devoted, big hearted, and generous supporter of Hospice Austin. Her value to the organization and our community cannot be overstated.”

So why does she do what she does? Carole believes she might be the only Scottish Jewish person in Texas, and that her unique position allows her to represent both her faith and her heritage with every interaction. But longtime friend Chaka Varley believes there’s more to it than that. “Her parents were actually hospice volunteers in Scotland,” she says. “She was greatly influenced by her parents and their desire to not only give back to the community but to make it part of life. That’s what I think sparked her interest – they were very happy and gratified as hospice volunteers. It’s been a big piece of her life the past 20 years.” Chaka laughs, then admits, “Even when Carole has birthday parties she has people bring canned good to donate to the pantry. She does good things!”

RecognizeGood: THE Foundation (commonly known as simply RecognizeGood) is a local nonprofit that provides a means for individuals, businesses and other nonprofits to illuminate selfless volunteers, charitable acts and community service throughout the greater Austin area. There are several active RecognizeGood programs that work toward this mission from different angles, but the common theme is simple – the illumination of GOOD in our community.


/*++

Copyright (c) 1995  Microsoft Corporation

Module Name:

    region.c

Abstract:

    This module implements a simple region buffer manager that is MP safe.

Author:

    David N. Cutler (davec) 25-Novy-1995

Revision History:

--*/

#include "exp.h"

VOID
ExInitializeRegion(
    IN PREGION_HEADER Region,
    IN ULONG BlockSize,
    IN PVOID Segment,
    IN ULONG SegmentSize
    )

/*++

Routine Description:

    This function initializes a region header.

Arguments:

    Region - Supplies the address of a region header to initialize.

    BlockSize - Supplies the block size of the allocatable units within
        the region. The size must be larger that the size of the initial
        segment, and must be 64-bit aligned.

    Segment - Supplies the address of a segment of storage.

    SegmentSize - Supplies the size in bytes of the segment.

Return Value:

    None.

--*/

{

    SINGLE_LIST_ENTRY FirstEntry;
    PSINGLE_LIST_ENTRY LastEntry;
    PSINGLE_LIST_ENTRY NextEntry;
    ULONG TotalSize;

    //
    // If the host system is a small system and the segment size is greater
    // than two pages, then bugcheck.
    //

    if ((MmQuerySystemSize() == MmSmallSystem) && (SegmentSize > (2 * PAGE_SIZE))) {
        KeBugCheckEx(NO_PAGES_AVAILABLE, 0x123, SegmentSize, 0, 0);
    }

    //
    // If the segment address is not quadword aligned, or the block size is
    // greater than the segment size minus size of the segment header, then
    // the region is not valid - bugcheck.
    //

    if ((((ULONG)Segment & 7) != 0) ||
        ((BlockSize & 7) != 0) ||
        (BlockSize > (SegmentSize - sizeof(REGION_SEGMENT_HEADER)))) {
        KeBugCheckEx(INVALID_REGION_OR_SEGMENT, (ULONG)Segment, SegmentSize, BlockSize, 0);
    }

    //
    // Initialize the region header.
    //

    ExInitializeSListHead(&Region->ListHead);
    Region->FirstSegment = (PREGION_SEGMENT_HEADER)Segment;
    Region->BlockSize = BlockSize;
    TotalSize = ((SegmentSize - sizeof(REGION_SEGMENT_HEADER)) / BlockSize) * BlockSize;
    Region->TotalSize = TotalSize;

    //
    // Initialize the segment free list.
    //

    FirstEntry.Next = NULL;
    NextEntry = (PSINGLE_LIST_ENTRY)((PCHAR)Segment + sizeof(REGION_SEGMENT_HEADER));
    LastEntry = (PSINGLE_LIST_ENTRY)((PCHAR)NextEntry + TotalSize);
    do {
       NextEntry->Next = FirstEntry.Next;
       FirstEntry.Next = NextEntry;
       NextEntry = (PSINGLE_LIST_ENTRY)((PCHAR)NextEntry + BlockSize);
    } while (NextEntry != LastEntry);
    Region->ListHead.Next.Next = FirstEntry.Next;
    return;
}

VOID
ExInterlockedExtendRegion(
    IN PREGION_HEADER Region,
    IN PVOID Segment,
    IN ULONG SegmentSize,
    IN PKSPIN_LOCK Lock
    )

/*++

Routine Description:

    This function extends a region by adding another segment's worth of
    blocks to the region.

Arguments:

    Region - Supplies the address of a region header.

    Segment - Supplies the address of a segment of storage.

    SegmentSize - Supplies the size in bytes of Segment.

    Lock - Supplies the address of a spinlock.

Return Value:

    None.

--*/

{

    ULONG BlockSize;
    SINGLE_LIST_ENTRY FirstEntry;
    KIRQL OldIrql;
    PSINGLE_LIST_ENTRY LastEntry;
    PSINGLE_LIST_ENTRY NextEntry;
    ULONG TotalSize;

    //
    // If the segment address is not quadword aligned, or the block size is
    // greater than the segment size minus size of the segment header, then
    // the region is not valid.
    //

    BlockSize = Region->BlockSize;
    if ((((ULONG)Segment & 7) != 0) ||
        ((BlockSize & 7) != 0) ||
        (BlockSize > (SegmentSize - sizeof(REGION_SEGMENT_HEADER)))) {
        KeBugCheckEx(INVALID_REGION_OR_SEGMENT, (ULONG)Segment, SegmentSize, BlockSize, 0);
    }

    //
    // Initialize the segment free list.
    //

    TotalSize = ((SegmentSize - sizeof(REGION_SEGMENT_HEADER)) / BlockSize) * BlockSize;
    FirstEntry.Next = NULL;
    NextEntry = (PSINGLE_LIST_ENTRY)((PCHAR)Segment + sizeof(REGION_SEGMENT_HEADER));
    LastEntry = (PSINGLE_LIST_ENTRY)((PCHAR)NextEntry + TotalSize);
    do {
       NextEntry->Next = FirstEntry.Next;
       FirstEntry.Next = NextEntry;
       NextEntry = (PSINGLE_LIST_ENTRY)((PCHAR)NextEntry + BlockSize);
    } while (NextEntry != LastEntry);

    //
    // Acquire the specified spinlock, insert the next segment in the segment
    // list, update the total segment size, and carefully merge the new segment
    // list with the current list.
    //
    // N.B. The merging of the free list is done very carefully such that
    //      manipulation of the free list can occur without using spinlocks.
    //

    ExAcquireSpinLock(Lock, &OldIrql);
    ((PREGION_SEGMENT_HEADER)Segment)->NextSegment = Region->FirstSegment;
    Region->FirstSegment = (PREGION_SEGMENT_HEADER)Segment;
    Region->TotalSize += TotalSize;
    NextEntry = (PSINGLE_LIST_ENTRY)((PCHAR)Segment + sizeof(REGION_SEGMENT_HEADER));
    LastEntry = (PSINGLE_LIST_ENTRY)((PCHAR)LastEntry - Region->BlockSize);
    do {

        //
        // The next entry in the region list head is a volatile entry and,
        // therefore, is read each time through the loop.
        //

        FirstEntry.Next = Region->ListHead.Next.Next;

        //
        // The last entry in the new segment list, i.e., the one with a link
        // of NULL, is merged with the current list by storing the captured
        // region next link in the free entry. A compare and exchange is then
        // done using the merged link address as the comparand and the head
        // of the new free list as the exchange value. This is safe since it
        // does not matter if the next link of the first region entry changes.
        //

        NextEntry->Next = FirstEntry.Next;
    } while (InterlockedCompareExchange((PVOID)&Region->ListHead.Next,
                                        LastEntry,
                                        FirstEntry.Next) != FirstEntry.Next);

    ExReleaseSpinLock(Lock, OldIrql);
    return;
}


In Western societies, obesity is a pervasive disease affecting both human and companion animal populations in similar magnitudes. In 2013--2014, a national survey of 5455 adults conducted in the USA found that nearly 40 % were obese^(^[@ref1]^)^. Several studies have also investigated the prevalence of obesity in populations of companion dogs, reporting like findings with 33·5--38·9 % of dogs classified as overweight^(^[@ref2]^--^[@ref4]^)^. In humans, vitamin D deficiency, which is generally defined as serum 25-hydroxyvitamin D (25 (OH)D) concentration of \<20 ng/ml, is also a worldwide health issue^(^[@ref5]^)^. In addition to vitamin D\'s established roles in Ca homeostasis and skeletal health, a vast body of evidence now describes many extraskeletal physiological effects of vitamin D status in people. Associations have been discovered between hypovitaminosis D and numerous immune-mediated, endocrine, cardiorespiratory, neoplastic and inflammatory diseases^(^[@ref6]^--^[@ref14]^)^. Additionally, though causality has not been elucidated, an association between vitamin D deficiency and human obesity has been documented for decades^(^[@ref15]^--^[@ref18]^)^.

Following trends in human medicine, there too is interest in the extraskeletal effects of vitamin D, and the vitamin\'s role in health and disease in companion dogs. While vitamin D is an increasingly active area of veterinary medical research, vitamin D sufficiency, the serum 25(OH)D concentration considered adequate for skeletal and general health for the majority of the population, remains undefined in dogs. One group has suggested serum 25(OH)D of 100--120 ng/ml as sufficient^(^[@ref19]^)^. Variable and wide ranges in serum 25(OH)D concentration have been reported in healthy dogs. Additionally, as compared with healthy or unaffected control dogs, low 25(OH)D concentrations have been found in dogs affected with such common canine diseases as protein-losing enteropathy, International Renal Interest Society stages 3 and 4 chronic kidney disease, and congestive heart failure^(^[@ref20]^--^[@ref23]^)^. Several studies have also reported on vitamin D status in dogs with neoplasia as compared with healthy control dogs. Specifically, lower serum 25(OH)D concentrations have been reported in dogs with splenic haemangiosarcoma, cutaneous mast cell tumours, neoplastic spirocercosis and lymphoma^(^[@ref19]^,^[@ref24]^--^[@ref26]^)^.

Despite the prevalence of canine obesity and research demonstrating the occurrence of systemic inflammation in obese dogs, to our knowledge, the relationship between vitamin D status and obesity in dogs has not been investigated^(^[@ref27]^--^[@ref29]^)^. In a recently published study evaluating plasma 25(OH)D concentrations in sixty-nine dogs with cancer and twenty-three healthy control dogs, a significant relationship between body condition score (BCS) and vitamin D status was not found^(^[@ref30]^)^. The majority of dogs in the study were in ideal body condition or overweight, and the number of obese subjects was not described^(^[@ref30]^)^. One goal of the present study was to assess the relationship between adiposity and vitamin D status (as indicated by serum 25-hydroxyvitamin D~3~ (25(OH)D~3~) and 24,25-dihydroxyvitamin D~3~ (24,25(OH)~2~D~3~) concentrations) in otherwise healthy adult dogs in ideal, overweight or obese body condition. A second goal was to evaluate the effect of body fat (BF) loss on vitamin D status in a cohort of overweight adult dogs during therapeutic weight reduction. We hypothesised that vitamin D status and adiposity would be negatively correlated in adult dogs, and that serum 25(OH)D concentrations would increase as overweight dogs lost body fat mass (BFM).

Materials and methods {#sec1}
=====================

Animals {#sec1-1}
-------

Lean dogs with an ideal BCS of 4--5/9 and overweight dogs with a BCS of 6--9/9 were recruited for participation in the study. Fifteen adult dogs, aged 1--12 years (median 5 years), privately owned by staff, faculty, and students at the university were volunteered. Three of the overweight dogs were recruited during their participation in a pet weight-loss programme run by veterinary students at the university. The study population was comprised of ten male neutered and five female spayed mixed breed and purebred dogs with body weights (BW) from 4·1 to 43·0 kg (median 18·4 kg) ([Table 1](#tab01){ref-type="table"}). Each dog was deemed clinically healthy at the time of enrolment based on evaluation of findings of physical examination by the same investigator (T. J. H.), complete blood cell count, serum biochemistry profile and urinalysis. Initial BCS and muscle condition scores were assessed by the same investigator (T. J. H.)^(^[@ref31]^,^[@ref32]^)^. Dogs with a BCS of less than 4/9, that were not amenable to handling, that were clinically ill, or that weighed less than 4·0 kg were excluded from the study. The owners of participating dogs completed a questionnaire detailing each dog\'s diet history, activity level and home environment. The owners consented to dietary modification with the study diet and agreed to follow the provided feeding instructions for the duration of the study. The study protocol was reviewed and approved by the University of Missouri Institutional Animal Care and Use Committee. The owners of participating dogs were required to sign an informed consent form prior to inclusion in the study. Table 1.Demographics of dogs in the control and treatment groups(Medians and ranges)GroupControl (*n* 7)Treatment (*n* 8)MedianRangeMedianRangeBody weight (kg)18·44·1--30·220·77·0--43·0Age (years)51--125·53--10Body condition score (nine-point scale)54--586--8SexFemale spayed (*n*)32Male neutered (*n*)46BreedBrittany spaniel (*n* 1), German shepherd (*n* 1), miniature pinscher (*n* 1), Pomeranian (*n* 1), mixed breed (*n* 3)Australian shepherd (*n* 1), beagle (*n* 1), Cairn terrier (*n* 1), golden retriever (*n* 1), rough coated collie (*n* 1), mixed breed (*n* 3)

Experimental design {#sec1-2}
-------------------

Prior to transition to the study diet and following overnight food withholding, blood (5 ml) was collected from all dogs by venepuncture from a peripherally accessible vein, and serum of the blood extracted. Serum was stored (−20°C) for analysis of vitamin D metabolites by HPLC at a later date. Aliquots of the same serum samples were later used to determine initial body composition using a ^2^H-labelled water dilution method. Subsequently, all dogs were gradually transitioned to the study diet over a period of approximately 7 d. Seven lean dogs with ideal BCS of 4--5/9 were assigned to the control group for which weight maintenance was the goal. Owners of dogs in the control group were instructed to maintain their dogs' historical daily metabolisable energy (ME) intake on the study diet, and were provided with written feeding orders for achieving this. Eight overweight or obese (BCS of 6--9/9) dogs were assigned to the treatment group for which weight loss was the goal. Owners of dogs in the treatment group were instructed to reduce their dogs' daily energy intake to achieve weight loss at the desired rate of 1--2 % of BW weekly^(^[@ref33]^)^ and were provided with written feeding orders. To aid in owner compliance, all dogs were provided a maximum allowance of 10 % of total daily energy intake from food items other than the study diet. Following transition to the study diet, each dog was weighed in 2- to 4-week intervals to determine the need for adjustment in energy intake based on the goal of weight maintenance or loss. Body and muscle condition scores were reassessed by the same investigator (T. J. H.) at weigh-ins, or as deemed appropriate. Approximately 8 weeks after transition to the study diet and after overnight food withholding, venous blood (5 ml) was collected for repeated analysis of serum vitamin D metabolite concentrations. For the aforementioned three dogs in the treatment group only, this was the initial blood collection. Dogs in the control group were intended to remain on the study diet for approximately 6 months. Overweight dogs were committed to remain on the study diet for approximately 6 months, or until a BCS of 4--5/9 was attained. At the end of the study and after overnight food withholding, venous blood (5 ml) was collected from dogs of both control and treatment groups for a final determination of serum vitamin D metabolite concentrations and repeated body composition analysis using the same methods.

Diet {#sec1-3}
----

The study diet was a commercially available therapeutic, canine weight-loss, dry-type diet that had undergone animal feeding tests using Association of American Feed Control Officials (AAFCO) procedures to demonstrate nutritional adequacy for the maintenance of adult dogs (Purina® Pro Plan® Veterinary Diets OM Overweight Management™ Canine Formula; Nestlé Purina). The diet was characteristic for use in weight loss in that compared with diets typically available to consumers for maintenance of dogs, it was lower in energy density and fat, and higher in protein and fibre. Manufacturer-reported nutrient profiles of the study diet are provided in [Table 2](#tab02){ref-type="table"}. The study diet was believed to be sourced from multiple batches based on differing lot numbers displayed on the product packaging. To determine batch variability in vitamin D content, four samples collected from different batches of the study diet were analysed for cholecalciferol (vitamin D~3~) and ergocalciferol (vitamin D~2~) contents at an external laboratory (Eurofins Nutrition Analysis Center, Des Moines, IA, USA). Table 2.Nutrient profile of the study diet and formula of the study diet briefly consumed by one dog in the treatment group (diet B) as provided by the manufacturerStudy diet: ME = 10980 kJ/kg (2624 kcal/kg)Diet B: ME = 11340 kJ/kg (2710 kcal/kg)Per 418 kJ (100 kcal) ME (g)As fed (%)DM (%)Per 418 kJ (100 kcal) ME (g)As fed (%)DM (%)Protein10·2927·0029·649·9627·0029·70Fat2·486·527·162·236·036·63Carbohydrate15·7041·1945·2215·4241·8045·98Crude fibre3·8510·1111·103·499·4610·41Total dietary fibre8·3822·0024·158·1222·0024·20Soluble fibre0·531·401·540·922·502·75Insoluble fibre7·8520·6022·627·2019·5021·45Ca0·431·121·230·371·001·10P0·320·850·930·310·840·92K0·280·740·820·441·191·31Na0·070·200·220·100·270·30Cl0·120·310·340·160·440·48Mg0·060·150·160·070·200·22Cu0·66 mg17·4 mg/kg19·1 mg/kg0·69 mg18·6 mg/kg20·4 mg/kgZn10·10 mg265 mg/kg291 mg/kg9·70 mg263 mg/kg289 mg/kgVitamin A1305 IU34 250 IU/kg37 604 IU/kg1040 IU28 184 IU/kg31 000 IU/kgVitamin E20·01 IU525 IU/kg576 IU/kg16·27 IU441 IU/kg485 IU/kgCholecalciferol55·8 IU1607 IU/kg41·6 IU1317 IU/kgEPA + DHA0·000·000·000·0040·010·01[^2]

Serum 25-hydroxyvitamin D metabolites {#sec1-4}
-------------------------------------

Serum 25(OH)D~3~ and 24,25(OH)~2~D~3~ concentrations were determined in our laboratory using modifications of previously described extraction and HPLC methods^(^[@ref34]^)^. Thawed serum samples (0·5 ml) were spiked with 25 ng of internal standards, 25(OH)D~2~ and 3-epi-24,25(OH)~2~D~3~ (Isosciences), vortex-mixed and incubated for 15 min at room temperature. Acetonitrile (0·5 ml) was added to each sample followed by centrifugation (20°C; 2000 ***g***; 10 min). The supernatant was removed and added to tubes containing doubly distilled water (0·5 ml). The tube contents were vortex-mixed, and loaded on cartridges containing 500 mg of C18 silica gel (Bond Elut; Agilent Technologies) after sequential conditioning with hexane, isopropanol, methanol, and water (2 ml each). The cartridges were washed with water (5 ml), methanol--water (70:30, v/v; 5 ml), and air-dried (10 min). Following air-drying, the 25(OH)D on cartridges was eluted with hexanes--methylene chloride (90:10, v/v; 5 ml) and the 24,25(OH)D eluted with hexanes--isopropanol (95:5, v/v; 5 ml). The eluents were combined and reduced to dryness by centrifugal evaporation at 35°C (Savant SPD 111 V; Thermo Electron). Residues were dissolved in HPLC mobile phase (hexanes--isopropanol, 88:12, v/v) and injected (0·2 ml) on a column (Zorbax Sil, 4·6 × 250 mm, 5 µm; Agilent Technologies) equilibrated with the mobile phase flowing at 2 ml/min. Eluting normal-phase fractions containing 25(OH)D and 24,25(OH)~2~D extracted from serum were collected and dried by centrifugal evaporation. After reconstitution in 0·15 ml methanol--water (67:33, v/v), the metabolites were quantified by the reverse-phase HPLC method described by Lensmeyer *et al.*^(^[@ref35]^)^. For this, 0·1 ml of reconstitute was injected into the mobile phase of methanol--water (67:33 v/v for 25(OH)D; 62:38 v/v for 24,25(OH)~2~D~3~) flowing at 1·2 ml/min through a cyanopropyl column (Zobax SB-CN, 4·6 × 250 mm, 5 µm; Agilent Technologies) heated to 50°C. AUC absorbances at 265 nm of eluting analyte and internal standard peaks were proportional to the amount of vitamin D metabolite injected. The lower limit of metabolite quantification was determined to be the amount equivalent to 5 ng/ml of the metabolite in serum.

Body composition {#sec1-5}
----------------

To quantify BFM and body lean mass (BLM), we used a modification of a previously validated ^2^H-labelled water dilution method^(^[@ref36]^)^. After overnight food withholding but with water provided to the dogs for *ad libitum* consumption, BW were determined and ^2^H-labelled water (99·8 %; Acros Organics) as a sterile saline solution (0·9 % NaCl) was administered to each dog subcutaneously at 0·4 g/kg BW. At 3 h later, peripheral venous blood was collected for extraction of serum, which was in turn stored at −20°C until later analyses. Upon thawing, water was distilled from aliquots of sampled serum^(^[@ref37]^)^ and its ^2^H-labelled water enrichment determined using infrared spectroscopy^(^[@ref38]^)^. Mass of body water was determined by dividing the amount (g) of subcutaneously administered ^2^H-labelled water by the ^2^H-labelled water enrichment in serum water (g/kg)^(^[@ref39]^)^. Lean mass of dogs was estimated as the mass of body water divided by the fractional moisture content of BLM, which across species is conventionally assumed to be 0·732^(^[@ref40]^)^. Fat mass of dogs was taken to be BW minus the estimated lean mass. The timing of equilibration of subcutaneously injected ^2^H-labelled water was determined in a prior trial. In this trial, injected ^2^H-labelled water was salinated and given at the same dosage as that described in the present study to a cohort of university-owned 4-year-old mixed-breed dogs, five of which were male (ranging from 7·1 to 11·2 kg), and five of which were female (ranging from 5·4 to 7·7 kg) . The ^2^H-labelled water enrichment in water extracted from sampled saliva was determined immediately before ^2^H-labelled water administration and hourly for 6 h afterward. Enrichment of ^2^H-labelled water in salivary water among the dogs was found to plateau beginning 3 h after the ^2^H-labelled water administration (R. C. B., unpublished results, 2015).

Statistical analysis {#sec1-6}
--------------------

Commercially available statistical software was used for analyses of effects of experimental group and sampling time on variable observations (SAS^®^ 9.4; SAS Institute Inc.). Evaluated variables were serum concentrations of 25(OH)D~3~ and 24,25(OH)~2~D~3~, BCS, BW, and amounts BLM, BFM and percentage BW as fat (BF%). Deviations from normality in statistically evaluated observations were determined using Shapiro--Wilk testing. Among variable observations significantly deviating from normality were BCS, final BFM and serum 24,25(OH)~2~D~3~ concentration. Wilcoxon two-sample testing was used to determine the significance of experiment group differences involving non-normal observations. Sign tests were used for determination of significance of change in the observations with time. For normally distributed variable observations, significances of differences between the experiment groups and changes with time were determined with two-sample *t* testing and paired *t* testing, respectively, or repeated-measures ANOVA. Linear regression analysis was used to test the significance of correlation between variable observations and serum 25(OH)D~3~ concentration and change in the concentration during the study. Significance of correlation between BF% and BCS was determined using Pearson analysis. Significance of statistical testing outcomes was concluded when analyses indicated a probability of a type I error as less than 5 %. The number of dogs initially recruited for inclusion in the control and treatment groups was based on results of a prior power analysis in which variance in serum concentrations of 25(OH)D~3~ of dogs was determined^(^[@ref41]^)^. A treatment effect resulting in a mean difference of 25 % in serum 25(OH)D~3~ concentration between groups was expected detectable as significant with α = 0·05, β = 0·80, and six to seven dogs in experimental groups.

Results {#sec2}
=======

Fifteen dogs were enrolled in the study, with seven assigned to the control group, and eight assigned to the treatment group ([Fig. 1](#fig01){ref-type="fig"}). Due to owner scheduling conflicts, three dogs in the control group completed the study early after collection of the second serum sample; thus, their second serum samples, collected approximately 8 weeks post-diet transition, were considered their final sampling. For the remaining four dogs in the control group, the median study end was 23 (range 16--28) weeks after diet transition. One dog from the treatment group received food other than that expected for a sustained period after collection of the second serum sample; therefore, only initial body composition observations and initial and 8-week vitamin D metabolite observations for this dog were included in analyses. For the remaining seven dogs in the treatment group, the median study end was 27 (range 15--46) weeks after diet transition. Fig. 1.Experimental design and flow of participants through the study period.

For a short but undefined period following transition to the study diet, one dog from the treatment group was unintentionally fed a different formula of the study diet (referred to in [Table 2](#tab02){ref-type="table"} as Diet B; Purina® Pro Plan® Veterinary Diets OM Select Blend Overweight Management™ Canine Formula; Nestlé Purina). On recognition of this error, the dog was changed to the correct study diet for the remainder of the study.

Analysis of vitamin D content in study diet {#sec2-1}
-------------------------------------------

The study diet samples analysed contained less than 40 IU of ergocalciferol per kg DM. The cholecalciferol content of three study diet samples ranged from 1580 to 1910 IU per kg DM. These values closely agreed with the manufacturer-reported cholecalciferol content of 1607 IU per kg DM. A sample of diet B contained 944 IU of cholecalciferol per kg DM; the manufacturer reported cholecalciferol content of this formula to be 1317 IU per kg DM.

Body condition score, body weight and body composition analyses {#sec2-2}
---------------------------------------------------------------

Median initial BCS of dogs assigned to the treatment group was consistent with the dogs being overweight in condition; it was greater (*P* \< 0·001) than that of the control group, which was in agreement with the control dogs being of ideal body condition. Between initial and final observations, BCS of the dogs in the control group did not significantly change, and BCS of the dogs in the treatment group decreased (*P* \< 0·01). Final BCS of dogs of the treatment group remained significantly greater (*P* \< 0·05) than dogs of the control group.

Initial BW of treatment and control group dogs were not significantly different ([Table 3](#tab03){ref-type="table"}). BW of dogs of the control group did not significantly change between initial and final observations. Final BW of dogs of the treatment group were significantly less than the initial BW (*P* \< 0·01). Table 3.Body condition score, body weight, and body composition observations for control and treatment group dogs(Medians and ranges)InitialFinalControl (*n* 7)Treatment (*n* 7[\*](#tfn3_1){ref-type="table-fn"})Control (*n* 7)Treatment (*n* 7)MedianRangeMedianRangeMedianRangeMedianRangeBody condition score (nine-point scale)54--58[†](#tfn3_2){ref-type="table-fn"}6--844--55[†](#tfn3_2){ref-type="table-fn"}[‡](#tfn3_3){ref-type="table-fn"}4--7Body weight (kg)18·44·1--30·218·37·0--43·017·44·0--30·915·5[^‡^](#tfn3_3){ref-type="table-fn"}5·8--36·0Lean body mass (kg)13·03·3--22·212·54·0--26·813·13·3--23·110·9[^‡^](#tfn3_3){ref-type="table-fn"}3·6--26·6Fat body mass (kg)5·30·8--8·06·93·0--20·54·30·7--7·84·6[^‡^](#tfn3_3){ref-type="table-fn"}1·8--14·5Percentage body fat (%)26·118·6--29·239·6[^†^](#tfn3_2){ref-type="table-fn"}31·4--48·125·117·2--33·829·5[†](#tfn3_2){ref-type="table-fn"}[‡](#tfn3_3){ref-type="table-fn"}23·6--40·4[^3][^4][^5]

Body composition data were collected at the time of study enrolment and again at the end of the study of each dog. Between groups of dogs, there was no significant difference in BLM or BFM at the initial observation ([Table 3](#tab03){ref-type="table"}). The BLM decreased in the treatment group over time (*P* \< 0·01). The BFM of the treatment group decreased (*P* = 0·01), whereas the BFM of the control group did not significantly change. The treatment group had a median initial BF% of 39·6 %, which was higher than that of the control group (median of 26·1 %) (*P* \< 0·001). By the end of the study, BF% was decreased in dogs of the treatment group (*P* \< 0·001), among which final median BF% was 29·5 %. For all dogs, initial BCS was correlated with initial BF% estimates (ρ = 0·891; *P* \< 0·001).

Serum 25-hydroxyvitamin D~3~ and 24,25-dihydroxyvitamin D~3~ {#sec2-3}
------------------------------------------------------------

At the time of study enrolment prior to dietary transition, serum vitamin D metabolite concentrations were determined in twelve dogs. At the initial observation, all dogs were consuming commercially available canine diets. Most of the dogs were maintained on a commercial dog food other than the study diet, with the exception of the three additional dogs later assigned to the treatment group which were already consuming the study diet. For these three dogs only, initial blood sampling for analyses of serum vitamin D metabolite concentrations occurred after approximately 7 weeks of exclusive consumption of the study diet, and these initial observations were excluded from analysis of effects of dietary transition. For the other twelve dogs, serum vitamin D metabolite concentrations were re-evaluated approximately 8 weeks after dietary transition; this 8-week point was considered the study end for three control dogs that were withdrawn early, and one treatment dog that was excluded for non-compliance thereafter. Finally, serum vitamin D metabolites were again measured in four dogs in the control group and all remaining seven dogs in the treatment group at study end. The median initial serum concentrations of 24,25(OH)~2~D~3~ were not significantly different between the control (57 ng/ml) and treatment (75 ng/ml) groups. For both groups, serum 24,25(OH)~2~D~3~ concentrations did not change between initial and final observations. The median initial serum 25(OH)D~3~ concentration was 74 (range 46--110) ng/ml for the control group, and 79 (range 53--129) ng/ml for the treatment group; these were not statistically different. As compared with the corresponding initial group observations, final median serum 25(OH)D~3~ concentrations of dogs in both the control and treatment groups, which were 86 (range 64--187) and 115 (range 89--163) ng/ml, respectively, were significantly (*P* = 0·02) increased ([Fig. 2](#fig02){ref-type="fig"}). Fig. 2.Serum 25-hydroxyvitamin D (25(OH)D) concentrations of dogs in the control and treatment groups, including initial observations (prior to transition to study diet) and final observations at study end. Each plot represents observations\' median (centre line), first quartile (lower box line), third quartile (upper box line), minimum (lower whisker) and maximum (upper whisker). \* Observations significantly different from corresponding initial group observations (*P*\<0.05).

When the initial observations from dogs of control and treatment groups were pooled, BF% and serum 25(OH)D~3~ concentration were not significantly correlated (*r* 0·11; *P* = 0·69). Furthermore, when diet was controlled, that is when only the study diet was fed in amounts required for safe weight loss, fractional loss of BFM and decrease in BF% in dogs of the treatment group (*n* 7) did not significantly correlate with a change in serum 25(OH)D~3~ concentration (*r* 0·15, *P* = 0·74 and *r* 0·56, *P* = 0·19, respectively).

Effect of daily cholecalciferol intake on serum 25-hydroxyvitamin D~3~ {#sec2-4}
----------------------------------------------------------------------

For four dogs in the control group and seven dogs in the treatment group that remained in the study for greater than 8 weeks post-diet transition, daily cholecalciferol intake at the 8-week post-diet transition point was compared with daily cholecalciferol intake at the study end. While changes were observed, there was not a significant correlation between the fractional change in daily cholecalciferol intake and the change in serum 25(OH)D~3~ concentrations (*r* 0·032; *P* = 0·90). Three of the four dogs in the control group had no change in their daily cholecalciferol intake. One dog of the control group required a 33 % increase in energy intake to maintain ideal BW; thus, this dog\'s cholecalciferol intake increased by 33 %. Of the seven dogs remaining in the treatment group, one of these dogs had no change in its cholecalciferol intake. Another one of these dogs required an energy increase of 52 % to halt weight loss and stabilise BW; thus, this dog\'s cholecalciferol intake increased by 52 %. The remaining five dogs of the treatment group were consuming a median of 32 (range 1--49) % less cholecalciferol at the end of the study as compared with the time of 8 weeks post-diet transition.

Discussion {#sec3}
==========

The results of our study do not support degree of adiposity as influencing the vitamin D status of apparently healthy adult dogs. In dogs and other species, the concentration of the vitamin D metabolite 25(OH)D~3~ in peripheral venous serum is conventionally used as an indicator of vitamin D status^(^[@ref42]^)^. Across all the dogs presently studied, initial serum 25(OH)D~3~ concentrations were not significantly correlated with BF%. Also, loss of adiposity in study dogs as a result of energy restriction for therapeutic weight loss did not significantly affect serum 25(OH)D~3~ concentration.

The causality of the inverse relationship between vitamin D status and adiposity that occurs in humans remains unknown^(^[@ref15]^--^[@ref18]^)^. Vitamin D is fat-soluble and stored in adipose tissue. One predominant hypothesis in the human literature is that vitamin D is sequestered in the greater BFM of obese individuals as compared with lean cohorts, and that this leads to reduced bioavailability and circulating serum concentrations of 25(OH)D^(^[@ref43]^)^. Previous studies have measured vitamin D concentrations in fat deposits of people and rats, which are supportive of adipose tissue as a storage site for the vitamin^(^[@ref44]^,^[@ref45]^)^; however, the author is not aware of such studies in dogs. Though seemingly unlikely, it is possible that the distribution of vitamin D stores in the canine is unique for this species. More recently, in contrast to the theory of vitamin D sequestration, another group proposed that volumetric dilution is responsible for lower serum 25(OH)D levels in obese humans, and that cholecalciferol is simply distributed in the total BFM, which is greater in such individuals^(^[@ref46]^)^. It has also been suggested that obesity may be a consequence of hypovitaminosis D and that the vitamin plays complex regulatory roles in adipose, though some studies have demonstrated conflicting results and are inconclusive^(^[@ref47]^)^.

The present study population was comprised of a variety of dog breeds. A previous study of golden retriever and German shepherd dogs found that the latter had a 26 % higher median serum 25(OH)D concentration^(^[@ref48]^)^. In this prior study, however, diet was not controlled and vitamin D intake of individual dogs was unknown. Additionally, Sharp *et al.*^(^[@ref48]^)^ found that a sexually intact status affected the dogs' serum 25(OH)D concentration, a variable which was not controlled in their study. Differences in serum 25(OH)D concentration have been described in growing great Danes and miniature poodles; however, growth stage of the dogs studied also differed^(^[@ref49]^)^. Therefore, while it is conceivable that breed may affect vitamin D metabolism in dogs, this remains unknown. Age was not controlled in our study dogs, and ranged from young adult (1 year) to senior (12 years). Advancing age is a risk factor for vitamin D deficiency in people for reasons other than reduced sun exposure^(^[@ref50]^)^. A significant correlation between age and serum 25(OH)D has not been definitively demonstrated in dogs. Weidner *et al.*^(^[@ref30]^)^ did not observe a correlation between serum 25(OH)D concentration and age in a population of predominantly older dogs (≥6 years), but described a trend toward significance between the two variables. In another study of 320 dogs aged 0·4--14·5 years, a significant association between age and serum 25(OH)D concentration was not identified^(^[@ref48]^)^. Studying thirty-nine dogs aged 6 months to 11·3 years, Titmarsh *et al*.^(^[@ref51]^)^ also did not find age to be a predictor of serum 25(OH)D. Future studies are needed to determine if age and breed affect vitamin D metabolism of dogs.

A state of chronic inflammation has been observed in obese humans. In veterinary medicine, research has demonstrated inflammatory biomarkers in obese dogs, suggesting that low-grade inflammation may be a component of the condition in this species, too^(^[@ref27]^--^[@ref29]^)^. Furthermore, these reports provide evidence for a reduction in systemic inflammation following weight loss in obese dogs^(^[@ref27]^,^[@ref28]^)^. Vitamin D is considered an immunomodulatory negative acute-phase reactant^(^[@ref42]^,^[@ref52]^)^. Human studies have demonstrated the association of hypovitaminosis D and increased inflammatory biomarkers in obese individuals^(^[@ref53]^)^. The relationship between vitamin D status and systemic inflammation in dogs is less clear. In a group of twelve sled-racing dogs, increased serum C-reactive protein concentrations were associated with increased serum 25(OH)D concentrations during strenuous exercise^(^[@ref54]^)^. One study examining dogs with chronic enteropathy found a negative correlation between serum 25(OH)D concentrations and both leucocyte counts and IL-2 and IL-6 concentrations^(^[@ref51]^)^. Another group reported decreasing C-reactive protein concentrations in dogs as serum 25(OH)D concentrations reached the level they considered sufficient^(^[@ref19]^)^. Clearly, additional work is needed to understand the relationship between systemic inflammation and vitamin D status in dogs. While we did not measure such inflammatory biomarkers in the present study, previous work supports the assumption that these would be present in our population of obese dogs. With the opinion that fat loss would reduce systemic inflammation, we hypothesised in the present study that serum 25(OH)D concentrations would increase as overweight dogs lost BF mass. All dogs in our treatment group that completed the study lost weight and 71 % of these dogs reached an ideal BCS by the study end. However, when diet was removed as a variable, the change in serum 25(OHD) concentration did not reach significance for either group. The dogs in our treatment group underwent 27 weeks (median) of therapeutic weight loss. Over this timespan, the median BF% in the treatment group decreased from 39·6 % to 29·5 %, a reduction of 10·1 % BF. In a study of forty-seven adult humans undergoing weight loss through 15 % dietary energy restriction for 4 weeks, Ibero-Baraibar *et al.*^(^[@ref55]^)^ reported a BF% reduction of 3·38 % (as measured by dual-energy X-ray absorptiometry), associated with significant increases in the 25(OH)D concentrations of the subjects. Based on these results, we might consider the duration of our study and BF% lost to be adequate. While we did not measure BF mass of the dogs after 4 weeks of weight loss, the results of Ibero-Baraibar *et al.*^(^[@ref55]^)^ suggest more rapid BF loss than we probably achieved in the present study. Results of other human studies have suggested that significant increases in vitamin D status do occur with slower fat loss^(^[@ref56]^,^[@ref57]^)^. To our knowledge, whether the rate of fat loss affects change in vitamin D status is unknown.

The distribution of BF stores in overweight dogs may vary among individuals, and may differ from that of obese humans. It is possible that such differences could affect vitamin D status in an obese condition and during fat loss. Subcutaneous and visceral adipose tissue secrete different profiles of inflammatory markers in dogs^(^[@ref58]^)^. A previous study evaluated the distribution of adipose in three adult dogs of different breeds using computed tomography (CT) at 1 year old (at the time of castration) and again 1 year later^(^[@ref59]^)^. BF% increased in the dogs, with the rate of increase of subcutaneous BF significantly higher than thoracic or abdominal adipose, though the study population was limited in age and size^(^[@ref59]^)^. On CT scans of seventeen overweight and obese dogs of different breeds, Thengchaisri *et al.*^(^[@ref60]^)^ found greater amounts of subcutaneous fat as compared with intra-abdominal fat. Conversely, others reported that visceral fat accumulated more quickly than subcutaneous fat in a small group of beagles^(^[@ref61]^)^. Recently, Gangloff *et al.*^(^[@ref62]^)^ found that compared with loss of subcutaneous fat, loss of visceral adiposity had the greatest positive effect on 25(OH)D concentration in 103 adult men. Based on this information, it is conceivable that the distribution of adiposity in our subjects may have influenced the findings of the present study.

Consumption of the study diet appeared to lead to a significant increase in serum 25(OH)D concentration across both groups in our study. Dogs rely almost entirely on dietary intake of vitamin D and lack substantial cutaneous synthesis of the hormone in response to sunlight; this is believed to be a result of high activity of the enzyme 7-dehydrocholesterol Δ^7^-reductase^(^[@ref63]^,^[@ref64]^)^. Over the study period, the majority (64 %) of dogs required a change in energy intake to achieve weight loss or maintenance; some such changes were substantial. However, the fractional changes in energy (and thus, vitamin D~3~) intake were not correlated with the change in serum 25(OH)D~3~ concentration, meaning that increasing serum 25(OH)D concentrations cannot simply be attributed to increased cholecalciferol consumption over time. Our results agree with previous findings that diet has an effect on serum 25(OH)D concentration in dogs^(^[@ref48]^)^. The vitamin D content of the test diet is not extraordinary; it exceeds the National Research Council\'s recommended allowance (NRC RA) for dietary vitamin D for maintenance of adult dogs, but is well below the safe upper limit^(^[@ref65]^)^. Furthermore, when cholecalciferol intake was compared with the NRC RA for each dog (on a metabolic BW basis), intake ranged from 1·5--4·4 times the NRC RA (8 weeks after dietary transition) to 1·3--4·4 times the NRC RA (at study end). A recent study found that cholecalciferol supplementation of dogs at 5·1 times the NRC RA (which is just below the safe upper limit) affected a modest 12 % increase in vitamin D status in a cohort of dogs^(^[@ref41]^)^. While it is possible that fat loss does not make an impact on vitamin D status in dogs, another possibility is that the effect of the diet on increasing vitamin D status in the study population may have masked a smaller weight-loss effect. Interestingly, though it has been proposed that serum 24,25(OH)~2~D~3~ concentrations, which are positively correlated with 25(OH)D concentrations, may be a useful marker of vitamin D status in people^(^[@ref66]^)^, our results did not indicate a significant corresponding increase in concentrations of 24,25(OH)~2~D~3~ in dogs. This finding was surprising, as 24,25(OH)~2~D~3~ is expected to occur in direct proportion to 25(OH)D~3~ concentration. Investigation of 24,25(OH)~2~D~3~ functionality in dogs is warranted.

BCS was correlated with BF%, consistent with previous findings^(^[@ref31]^,^[@ref67]^)^. In the present study, a single individual (T. J. H.) assessed BCS, and the assigned scores slightly underestimated the BF% of dogs in both groups. Agreement of BCS and objectively measured BF may have been improved by having multiple investigators assess BCS of the subjects. While it is also plausible that body composition analyses using ^2^H-labelled water dilution were inaccurate due to the assumptions that are inherent to this method, previous work has demonstrated agreement between objective measures of BF (such as ^2^H-labelled water dilution and dual-energy X-ray absorptiometry) and the semi-quantitative BCS system for dogs^(^[@ref67]^)^. We considered the reduced procedural cost and lack of required general anaesthesia for the ^2^H-labelled water dilution method to be advantageous. However, in future studies, use of the conventional standard method of body composition analysis, dual-energy X-ray absorptiometry, may be considered.

The present study has several limitations. Dogs were considered clinically healthy based on physical examination findings and clinicopathological data. In the absence of an exhaustive medical workup, it is possible that some subjects had subclinical diseases that may have affected vitamin D metabolism. In addition, given the use of client-owned pet dogs in this study, the owners were relied upon to accurately quantify and dispense food according to the provided instructions. It is possible that the energy intake of the dogs (and thus vitamin D intake) was higher or lower than our calculations. Additionally, dogs may have consumed food items containing vitamin D that owners were not aware of, or those that went unreported. Three dogs consumed consistent quantities of dietary fish oil supplements for the duration of the study, which may have contained cholecalciferol, a known nutrient contained in fatty fish^(^[@ref68]^)^. One such dog, assigned to the treatment group, was given 2000 mg of anchovy and sardine oil per d. Prior to dietary transition, the dog\'s serum 25(OH)D concentration was 78 ng/ml. As the median initial serum 25(OH)D concentration of both the pooled groups and the treatment group was found to be 79 ng/ml, the supplement is not suspected to have contained a substantial amount of cholecalciferol. The other two dogs, which shared a household and were both assigned to the control group, consumed a product with fish oil of unknown origin. One of these dogs consumed 4000 mg of fish oil daily; the dog\'s initial serum 25(OH)D concentration was 52 ng/ml. The other dog was consuming 2000 mg of fish oil per d; the dog\'s initial serum 25(OH)D concentration was 98 ng/ml. None of the fish oil supplements was tested for cholecalciferol or 25(OH)D content, and this information may have been useful. Four dogs consumed joint health supplements for the duration of the trial. On review of the ingredients of the supplements, there were no obvious sources of vitamin D disclosed by the manufacturers; however, the possibility of a proprietary ingredient cannot be excluded. None of these dogs supplemented with joint health supplements had unexpectedly high serum 25(OH)D levels as compared with cohorts. A previous study did not find significant differences between median serum 25(OH)D levels in dogs receiving fish oil supplements or fortified dog biscuits as compared with those that were not. However, in the same study, dogs consuming salmon oil supplements had significantly higher serum 25(OH)D levels than dogs not consuming dietary supplements^(^[@ref48]^)^. Finally, while we determined the study to be sufficiently powered to detect significance of a modest treatment effect, our sample size was small, and this is a limitation to extrapolating our findings of a null effect of adiposity on vitamin D status of dogs in general.

In conclusion, the correlation we found between canine BCS and BF% is consistent with previously described work. Our study supports that diet has an effect on serum 25(OH)D concentration in dogs, as has been demonstrated by others. Our data did not support our hypotheses that an inverse relationship exists between body adiposity and vitamin D status in dogs, and that loss of BF would lead to increasing serum 25(OH)D concentrations in overweight dogs undergoing weight loss. Additional studies investigating larger sample sizes in which diet, age and breed are controlled, and inflammatory markers are measured, are warranted to further our understanding of whether relationships between obesity, inflammation and vitamin D status occur in companion dogs.

The authors wish to thank the owners of the dogs for their participation, and Dr Dan Su and Dr Lauren Young for their technical assistance.

The present study was supported by the Nestlé Purina Endowed Program in Small Animal Nutrition, College of Veterinary Medicine, University of Missouri, Columbia, MO 65211, USA. The funders did not have a role in study design, data analysis, or writing of this paper.

T. J. H. was the principal investigator of the study, and contributed to designing and carrying out the study, analysing the data, and writing the manuscript. R. C. B. and A. M. W. were the co-investigators of the study, and contributed to designing and carrying out the study, analysing the data and writing the manuscript.

There are no conflicts of interest.

[^1]: Present address: Royal Canin Canada Company, Puslinch, ON N0B 2J0, Canada

[^2]: ME, metabolisable energy.

[^3]: Observations for one treatment group dog for which only initial body composition analyses were available have been excluded.

[^4]: Observations significantly different from control observations at the same time (*P* \< 0·05).

[^5]: Observations significantly different from corresponding initial group observations (*P* \< 0·05).


There is no better time to be creative with your footwear than during winter. If you love looking chic during winter, here are some creative ways to pair your boots with winter outfits and accessories that will make you look hot, gorgeous and adorable.

Rock jeans. Jeans are golden throughout all seasons. But what makes them stand out when paired with boots is how you wear them. A lot of things matter, but there are two major ways to wear your jean with Stuart Weitzman boots and achieve a heads turning look. One is to tuck the jean into the boots like you would your leggings, but the second way is to let your jean lay flat over the boots.

If you go with the jean hanging over the boots look, make sure your jeans are 1 inch from the ground; else your jean will carry grime and get dirty. But if you chose to tuck them in, use a thin or tight jean as loose ones look bulky in the boots when tucked in.

Go for vibrant colors.

In the cold, colors shine brighter. White will make you look clean and classy while colors like grey and matt brown just make you stand out.

If you get caught up in the snow somewhere and end up with some drops of it on your coat, instead of looking wet or soaked, if your jacket is matt brown it sips up the wetness and gives your coat an even chocolaty color. Remember not to over color yourself but master the art of matching colors evenly. Stuart Weitzman sale are some excellent color matches you could consider. White long dress coat, black suede boots with a bright blue scarf Embellished boots flat boots with a cozy cream sweater dress and a classy golden watch to accessorize the look. You could also consider black tights paired with slouchy cream stacked boots with a finish of a long maroon cardigan.

Skirts are a must.

Skirts are another great way to rock boots during the winter. There are so many things you can do with skirts. If the cold is not stingy, you can go for a boot-skirt look that will reveal a bit of skin. A midi skirt paired with heeled or flat midi boots would do the trick. This look leaves the skin between the thighs and ankles peeping. You can also wear a super mini skirt and match it with cute ankle boots. A long pencil skirt with a slit that goes way up to the thigh is perfectly paired with both short boots and long ones.

Play around with scarfs.

Scarf’s are a must have accessory during the winter. Scarfs don’t only keep your neck warm; they help to match your boots and overall look. If you’re going to wear white boots, you may match them with a black scarf or another color you think will match the black. You could go like this; a purple knotted jersey scarf + purple boots + blue jeans + silky blouse and silver accessories.

More tips

If you’re looking for a high-end look, Leather coats pull off a more luxurious look.

Don’t add too many accessories when wearing boats that have embellishments; You might end up looking stuffed

Not all colors match any skin. If you don’t know what colors go well with your skin, do a simple Google search for ideas

Be careful when going for big clothes, unless you are trying to pull off some known look. Otherwise, you don’t want to dare the unknown.

Stuart Weitzman shoes www.stuartweitzman-online.com


Autophagy mediated by JNK1 resists apoptosis through TRAF3 degradation in osteoclastogenesis.
RANKL induces osteoclastogenesis via JNK1 signal that exerts an anti-apoptotic effect during osteoclastogenesis. However, the classic downstream c-Jun/AP-1 pathway is not included in anti-apoptosis of JNK1. Thus, the detail mechanism underlying JNK1-resisted apoptosis remains unknown during RANKL-induced osteoclastogenesis. RANKL-induced autophagy results in the degradation of the osteoclastogenesis-inhibitor TRAF3, and TRAF3 is thought as a regulator of apoptosis. Given the key effect of JNK1 in mediating autophagy, our study aims to investigate the significance of TRAF3 in bridging JNK1-mediated autophagy and apoptotic resistance during osteoclastogenesis. In this study, by using Bone Marrow-derived macrophages (BMMs) as osteoclast precursors (OCPs), we found that RANKL-induced TRAF3 degradation was significantly suppressed by JNK inhibitor (SP600125), which was restored by overexpression of Beclin1 (key autophagic protein). Nevertheless, TRAF3 silencing partially reversed the reduced osteoclastogenesis under SP600125 intervention. Besides, OCP apoptosis was positively regulated by TRAF3 overexpression, regardless of the application of autophagy inhibitor or SP600125. Remarkably, the enhanced apoptosis caused by the pharmacological inhibition of Beclin1 was reversed by TRAF3 silencing. Together, these results suggest that JNK1-mediated autophagy could promote RANKL-induced osteoclastogenesis via enhancing TRAF3 degradation. Importantly, JNK1 could prevent OCP apoptosis through autophagy-TRAF3 signaling, which provides more potential targets for clinical treatment of pathological bone loss.


The stars of Pash-Mara

K'rizz

Capital of the Thiefling empire that made deals with Demons of the ice hell plane that they bound into their service. The contract that the Binders had with the ice demons changed them in the first Jadi thiefling. This Capital was destroyed by Taus Malek through his cleric’s in the form of Sharen-rea. This form of Taus-Malek sealed the ice demons in the challice. The city is a frozen ruin at this moment. It lays in a valley on the west side of Mount Pamir. And the demons bound in the Cup are still calling the dissatisfied, grieved and powerhungy to make the Pact of the demon chalice with. Major locations


package v02.integration

import v02.model.Direction

abstract class RobotBaseScript extends Script {
  void move(Direction dir) {
    this.binding.robot.move dir
  }
}


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Port Pirie lead abatement Program, 1992.
The Port Pirie Lead Decontamination Program commenced in 1984 with a ten year mandate. The abatement programme involves identification of children with elevated blood lead levels, house decontamination, soil treatment, general City greening, family education and support and community education. Since 1984 the smelter has also implemented substantial new environmental controls.Blood lead and air monitoring programmes as well as some investigations of recontamination are in place. The blood lead monitoring programme has shown a significant decrease in the mean blood lead levels of the children, with the magnitude of the reduction being greatest in areas remote from the smelter.The results of the air monitoring programme suggest that there has been little change in the general air lead levels in the City over the period of the abatement programme. Analysis of the data suggests that re-entrainment of lead from the contaminated areas within the City is only a small contributor to air-borne lead levels compared with that from the smelter and its environs.Sources and pathways of lead for absorption by the children in Port Pirie are discussed.


Wow I love this ad. Morning Joe released part of a video from Ted Cruz showing Hillary Clinton destroy a server in a spoof from a classic scene in the great movie, “Office Space.”

Take a look:

Just on a personal note, I really love the wit and humor of this ad. The panel on Morning Joe, who all hate Ted Cruz, of course were flabbergasted that he would do such a thing as transgress against Hillary, their Mother Gaia of liberalism. Well screw them, I think it’s hilarious.

BUT – will South Carolinians like it? If Cruz did it specifically to target my age demographic, then it’s brilliant. If it’s meant to be a general ad, then it might miss the mark among older Americans. Now I’m gonna watch it again and laugh, BRB!

We’ll post the whole ad once it’s available, keep checking back.

UPDATE: The full youtube version of the ad has been released. We’ve updated accordingly.


Subtypes of mild cognitive impairment in Parkinson's disease: progression to dementia.
The aim of this study was to establish the rate of progression from mild cognitive impairment (MCI) to dementia in patients with Parkinson's disease (PD). PD patients without dementia were recruited in 1997 from an ongoing prospective epidemiological study. The assessment included neurological and psychiatric examinations, a clinical interview based on the Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition (DSM-III-R) criteria for dementia, and a battery of neuropsychological tests. PD was diagnosed according to established criteria, dementia was diagnosed according to the DSM-III-R criteria, and subtypes of MCI were classified according to modified Petersen's criteria. Seventy-two nondemented PD patients were included. A total of 34 were cognitively intact, whereas 38 were diagnosed with MCI (amnestic, n = 6; single nonmemory domain, n = 17; multiple domains slightly impaired, n = 15). Fifty-nine patients (82%) completed follow-up examination 4 years later, and 18 (62%) of the patients with MCI and 6 (20%) of the cognitively intact PD patients were demented (P = 0.001). Single domain nonmemory MCI and multiple domains slightly impaired MCI were associated with later development of dementia (P = 0.003; P = 0.04), whereas amnestic MCI subtype was not (P = 0.76). We conclude that patients with PD and MCI had a higher risk of developing dementia than cognitively intact PD patients, suggesting that MCI in PD is an early manifestation of dementia. However, these findings should be interpreted with caution due to the relatively small number of subjects included in this study.


Department of Coastal Defense

Let’s Bring in the Military’s Expertise to Help with the Gulf Oil Disaster

The National Guard has a long record of supporting first responders when there is a problem on U.S. soil. It has recently been deployed to respond to domestic emergencies such as tornados in the Midwest, last summer’s forest fires in California, and security at the Southwest border. And all of this occurred while the military was fighting two wars in faraway lands. The National Guard’s next big mission—along with other branches of the military—ought to be taking charge of cleaning up the BP oil disaster.

The tragic BP disaster is unfolding in slow motion unlike the aforementioned catastrophes and many others that arrive suddenly and without warning. Since April 22, oil has flowed from the bottom of the ocean at the rate of 1.6 million to 4 million gallons per day. (The Exxon Valdez oil spill, in contrast, was 11 million gallons total.) After efforts to contain the oil flood failed over this past weekend, it appears likely that this horrendous oil cascade could continue until August when the relief wells BP is digging are finished. This could mean 400 million barrels of oil released into the Gulf of Mexico by August, with a large portion fouling marshes, poisoning spawning areas, blackening beaches, and destroying other fragile coastal areas from Texas to Florida.

In short, it is crystal clear that this disaster is much too big for BP to handle on its own.

The National Guard has already been mobilized to help clean up BP’s mess. The Obama administration has authorized 17,500 National Guard troops from the Gulf Coast states to respond to the disaster. Louisiana’s National Guard in particular has sprung into action and contributed the vast majority of troops and technical cleanup assistance to date. For instance, Louisiana’s “769th Engineer Battalion and the State Aviation Command completed sandbag drop operations filling a 115-foot area in the vicinity of Trinity Island on May 27.” In Alabama, too, video footage shows the National Guard is working on “putting up barriers protecting the shore from oil.”

According to Sgt. Carmen Gibson, the National Guard is preparing for the worst in Florida and the coastal Gulf states near Louisiana where much oil damage is predicted:

As of May 18, six Florida Army National Guard Soldiers were supporting the incident response by serving as liaisons in incident command centers in Florida, Alabama and Louisiana. Also, members of the Florida Air National Guard’s 601st Air Operations Group were supporting 1st Air Force response efforts in Louisiana.

In the event that this disaster proves catastrophic, up to 2,500 Florida National Guard Soldiers and Airmen have been approved by the federal government and may be activated to provide additional aid and clean-up support around the state. The Florida National Guard stands ready to support any state emergency at the direction of the governor and the State Emergency Response Team.

Although Florida’s coastline has had minimal impact from the oil spill disaster, division representatives continue planning and preparing for the worst.

Former Secretary of State and Chair of the Joint Chiefs of Staff Colin Powell also suggested that the military could play a unique and valuable role in minimizing damage from the BP oil disaster above and beyond what the National Guard has already done. Powell noted that:

The military brings organization, it brings control. It brings assets…Whether it’s Army, Coast Guard, local forces, it is time for a comprehensive, total attack on this problem to protect the shoreline, to protect the livestock, to protect the wetlands, but most of all to give the people in that part of our country a sense of hope that this is going to be solved.

Gen. Powell is right to suggest that the U.S. Armed Forces play a leadership role in the cleanup. A first step would be fully mobilizing the National Guard immediately in the most vulnerable Gulf states—Alabama, Florida, Louisiana, Mississippi, and Texas. This would provide guard units time to get organized and prepare for a truly calamitous event such as a tropical storm or hurricane in the gulf that could carry oil from the middle of the sea onto land. These troops could also lead efforts to minimize the destruction of vital coastal wetlands from oil contamination.

The U.S. Coast Guard—which is already leading efforts to contain oil still in the gulf—should also assist other federal, state, and community agencies in containing the oil flow’s impact before it hits land and destroys beaches, estuaries, and other fragile ecosystems. They could deploy their ships to place booms and skimmers that collect oil before it flows ashore. And they could expand the areas where controlled burns occur, which are designed to combust oil before it blackens beaches.

The Coast Guard should also lead a federal task force to respond to the BP oil disaster. The task force could form a “blue team” to lead training exercises for a government response to a severe storm or other extreme event linked to the oil disaster. As pointed out earlier, a severe tropical storm in the gulf could carry oil from the sea to the land, contaminating homes, businesses, farms, and even drinking water. Preparations for such a drastic event must begin now so that every step to safeguard people and their communities can be undertaken. This includes preparing for food or water contamination, disrupted commerce or agriculture, and other impacts of gallons of oil raining from the sky. This effort must not wait until a tropical storm is days away from landfall because it will be too late.

Sen. Bill Nelson (D-FL) is quite concerned about BP oil washing ashore in Florida. He wrote to President Barack Obama on June 1 to reiterate his suggestion that the military take charge of the cleanup mission:

It is my belief that the broader assets and command and control capability of the Department of Defense could better translate your directives into prompt, effective action.

Americans have relied on their military forces to accomplish tough missions—whether it’s pursuing terrorists in Afghanistan, helping tidal wave victims in Indonesia, or aiding Floridians recovering from a hurricane. Responding to the BP oil disaster undoubtedly falls in the tough mission category: Assistant to the President Carol Browner notes that the BP oil disaster is “probably the biggest environmental disaster we’ve ever faced in this country.” It’s time to put America’s skillful and dedicated forces in command of responding to this horrific oil catastrophe.


National News

Toronto's Rob Ford Finds Vulgar New Low, Apologizes

(NEWSER) – The Rob Ford chronicles reached a new low today, prompting yet another apology from the Toronto mayor. "I used unforgivable language and again I apologize," he said at a news conference, reports CTV News. The mea culpa comes after a give-and-take with the media that the National Post says left reporters gasping. In the course of denying allegations that he regularly used cocaine and visited prostitutes, Ford also denied that he once told a staffer, "I want to eat your p----." And that's when the mayor of the fifth-largest city in North America added, “I’m happily married, I have more than enough to eat at home."


Q:

database structure for unconstant items

I have a database which own events as following :
event(id, name, type, startDate, endDate)

The type is another custom object (Type(id, name, icon)) which is linked as one-to-many.
I want to add another custom object named EventDetail containing details, but the fields would be different with the type of the event.
For instance, if my event is a travel type, fields could be a weblink to the wikipedia of destination, a photo, but if event is an internship for work they would evidently be different.
What kind of structure could handle this type of situation ?
If it is important, I'm using java for android, with an ORM library named SugarORM
Final answer
I finally headed to ORM libraries for managing my database. Using a one-to-one relation between Type and EventDetail and one-to-many between Type and Event, it works really well for now.

A:

You can go a few different ways with this...
One would be to create a catch-all table for EventDetail that has every field would need for every type and use the type to determine which fields you read from in that table.
Another way, if you do not have a lot of different types, would be to create a table for each type that would be structured to the needs of that type, in your queries, you would need to join to each of the tables based on the type (probably with using UNION [ALL], one query per type - or create views).
A third, and probably more ideal depending on the situation and use, would be to remove that level of complexity from the database. Store your "Event Details" as a CLOB or BLOB or XMLTYPE, etc... and use the type to deserialize the data to an object on the client side.


Primary hyperparathyroidism predicts hypertension: Results from the National Inpatient Sample.
Primary hyperparathyroidism (pHPT), most commonly caused by solitary parathyroid adenomas, leads to mobilization of calcium and is known to result in nephrolithiasis and osteoporosis. To date, studies of pHPT and cardiovascular risk factors and events have produced discrepant findings, likely due to small sample sizes and enrolling populations with varying disease severity. We utilized a national registry, hypothesizing an association between pHPT and cardiovascular risk factors and events. Patients >18years with a diagnosis of pHPT were identified in the Nationwide Inpatient Sample 2009-2010 database using the Ninth Revision of International Classification of Diseases code 252.01. Demographics, risk factors, and cardiovascular event rates were collected and compared to general population data. pHPT was present in 0.1% (n=37,922) of hospital admissions. There was a significant increase in the prevalence of most cardiac risk factors including hypertension (HTN), diabetes mellitus, hyperlipidemia, obesity, and chronic kidney disease. The rates of heart failure (HF) and coronary artery disease (CAD) were higher in the pHPT population. However, after performing multivariate regression for age and cardiac risk factors, pHPT did not independently predict HF or CAD. The risk of HTN, however, was independently predicted by pHPT (OR 1.3; p<0.001). Primary hyperparathyroidism independently predicted the risk of hypertension in a patient population from a large national database. Despite significant differences in univariate analysis of cardiac risk factors and events, pHPT did not independently predict risk of HF or CAD after multivariate regression analysis. Future studies should explore potential mechanisms relating hypertension to pHPT.