411 N.W.2d 875 (1987)
CENTRAL LAKES EDUCATION ASSOCIATION, et al., Respondents,
v.
INDEPENDENT SCHOOL DISTRICT NO. 743, SAUK CENTRE, Minnesota, Appellant.
No. C6-87-401.
Court of Appeals of Minnesota.
September 8, 1987.
Review Denied November 13, 1987.
*876 John M. Roszak, David S. Bartel, Ratwik, Roszak, Maloney & Bartel, Minneapolis, for appellant.
Donald W. Selzer, Jr., Ann M. Curme, Oppenheimer, Wolff & Donnelly, St. Paul, for respondents.
Heard, considered and decided by LESLIE, P.J., SEDGWICK and LANSING, JJ.

*877 OPINION
SEDGWICK, Judge.
This suit arises out of contract negotiations between respondent Central Lakes Education Association ("CLEA") and appellant Independent School District No. 743 ("District"). The CLEA sued the District, alleging its unilateral implementation of its last contract offer constituted unfair labor practices under the Public Employment Labor Relations Act, Minn.Stat. §§ 179A.01-.25 (1986) ("PELRA"). The District appeals from a temporary injunction restraining it from implementing its proposal and from refusing to continue negotiating. We reverse.

FACTS
The CLEA is the exclusive collective bargaining representative of schoolteachers in Sauk Centre. The CLEA and the District were parties to a collective bargaining agreement covering the 1981-82 and 1982-83 school years. In May 1983, they began negotiating for a new agreement covering 1983-85. Since 1985, the parties have been negotiating for an agreement covering 1985-87 as well. They have been participating in mediation since 1984.
The main areas of dispute are salary and workload. Under the old contract, the secondary teachers' daily workload was five classes per day and one supervisory period (e.g., study hall) per day for half the year. At an October 2, 1986, mediation session, the District offered a $6,400 total average salary increase if the workload was increased to include one supervisory period per day for the full year. The CLEA responded that it would accept the salary increase if it could allocate the raises and the workload remained at one supervisory period for half the year. The District rejected this proposal. The mediator told the parties there would be no more mediation sessions unless one of the parties indicated it was prepared to make a significant new proposal.
On December 8, 1986, the District approved a resolution stating that the parties are at an impasse and that to end the negotiations it was unilaterally implementing its last offer, effective December 10, 1986. In accordance with its resolution, the District issued retroactive paychecks to teachers and made new teaching assignments for the second semester of the 1986-87 school year. On December 11, 1986, the Sauk Centre teachers voted to reject the District's last offer and to seek further mediation.
A final mediation session was held on December 22, 1986. The CLEA proposed a salary increase of $7,064, which the District characterizes as an old proposal it had previously rejected.
The CLEA then brought this suit. It seeks a declaration that the District committed unfair labor practices under PELRA by adopting the December 8 resolution; an injunction restraining the District from implementing its last offer until the teachers file a notice of intent to strike and impasse in negotiations is reached; and damages.
On January 28, 1986, the trial court granted the CLEA a temporary injunction (1) enjoining the District from failing to comply with the 1981-83 bargaining agreement, and specifically its work-load provisions; (2) enjoining the District from failing to negotiate in good faith for agreements covering 1983-85 and 1985-87; and (3) ordering the back-pay paid by the District under its resolution to be placed in escrow.

ISSUES
1. Does the trial court's memorandum decision adequately set forth the basis of its ruling to permit meaningful appellate review?
2. Did the trial court abuse its discretion by granting the temporary injunction?

ANALYSIS

I.
The District first argues that we must remand because the trial court failed *878 to make findings on the five factors set forth for reviewing grants or denials of temporary injunctions in Dahlberg Brothers, Inc. v. Ford Motor Co., 272 Minn. 264, 274-75, 137 N.W.2d 314, 321-22 (1965). Minn.R.Civ.P. 52.01 states:
In all actions tried upon the facts without a jury * * *, the court shall find the facts specially and state separately its conclusions of law thereon * * *; and in granting * * * interlocutory injunctions the court shall similarly set forth the findings of fact and conclusions of law which constitute the grounds of its action.
The primary purpose of this requirement is "to aid the appellate court by affording it a clear understanding of the ground * * * of the decision." Asch v. Housing and Redevelopment Authority, 256 Minn. 146, 155, 97 N.W.2d 656, 664-65 (1959).
Here, meaningful appellate review is possible because the material facts are not in dispute, the trial court's memorandum contains findings of fact and conclusions of law (although not labeled as such), and it clearly sets forth the basis of its decision. This case is therefore distinguishable from others in which we have reversed for inadequate findings and conclusions. See BioLine, Inc. v. Burman, 404 N.W.2d 318 (Minn.Ct.App.1987) (no findings or analysis); Crowley Co. v. Metropolitan Airports Commission, 394 N.W.2d 542 (Minn. Ct.App.1986) (no findings, conclusion or explanation of basis of decision). While the trial court's memorandum decision should have addressed the Dahlberg factors and labeled its findings of fact and conclusions of law as such, in this context its failure to do so does not justify reversal.

II.

A.
A temporary injunction is an extraordinary equitable remedy that preserves the status quo pending a trial on the merits. Miller v. Foley, 317 N.W.2d 710, 712 (Minn.1982). The party seeking a temporary injunction must show it lacks an adequate remedy at law and that interim relief is needed to prevent "great and irreparable injury." Cherne Industrial, Inc. v. Grounds & Associates, 278 N.W.2d 81, 92 (Minn.1979). The threatened injury must be real and substantial, not imagined. AMF Pinspotters, Inc. v. Harkins Bowling, Inc., 260 Minn. 499, 504, 110 N.W.2d 348, 351 (1961).
The granting of a temporary injunction rests within the sound discretion of the trial court, and the sole issue on appeal is whether there was a clear abuse of that discretion by a disregard of either the facts or principles of equity. County of Wright v. Litfin, 386 N.W.2d 757, 758 (Minn.Ct. App.1986).
The trial court did not address the issue of great and irreparable injury. (Its decision rested entirely on the CLEA's likelihood of success on the merits.) We believe the CLEA has failed to meet this prerequisite for a temporary injunction.
The CLEA argues that if the District is able to avoid negotiating pending trial, this would irreparably harm the CLEA's ability to function effectively as a collective bargaining representative. The CLEA also cites decisions of the New Jersey Public Employees Relations Commission which hold that unilateral implementation of contract provisions create an irreparable chilling effect on negotiations. See, e.g., County of Morris v. Morris Council # 6, No. CO-87-169 (N.J. PERC Jan. 28, 1987).
We are unable to accept the contention that a temporary (assuming the CLEA wins at trial) end to bargaining and implementation of the District's last offer would substantially and irreparably injure the CLEA's ability to negotiate. This is not a case of a school district attempting to undermine the credibility of a teachers' bargaining representative by refusing to negotiate for a successor agreement  the parties have been negotiating for over three years and have met over 25 times.
*879 The CLEA also argues it would have suffered irreparable injury because some teachers would have been forced to work an additional supervisory period, resulting in less preparation time and lower morale. We do not believe this constitutes an injury sufficiently "real and substantial" to justify the extraordinary remedy of a temporary injunction.

B.
The central dispute between the parties is whether the District has the right to end negotiations and implement unilaterally its last offer under PELRA because collective bargaining has reached an impasse. The trial court's order was based on its conclusions that (1) no impasse had been reached, and (2) even if there was an impasse, PELRA requires that the last contract remain in effect so long as the teachers have not served a notice of intent to strike. Although we hold that the CLEA is not entitled to a temporary injunction because it has failed to show great and irreparable injury, we will address the merits of the legal issues decided by the trial court to ensure this case is not tried on erroneous rules of law.

Impasse
Under the National Labor Relations Act (the "NLRA"), an employer may unilaterally implement its last offer when goodfaith negotiations have reached an impasse. See, e.g., American Federation of Television and Radio Artists v. NLRB, 395 F.2d 622, 624 (D.C.Cir.1968), aff'g Taft Broadcasting Co., 163 N.L.R.B. 475, 64 L.R.R.M. (BNA) 1386 (1967); cf. Foley Education Association v. Independent School District No. 51, 353 N.W.2d 917, 921 (Minn.1984) (stating that unilateral change not unfair labor practice if employer shows there was not a bad faith refusal to bargain). The District argues this principle applies under PELRA. Since the CLEA does not dispute this, we will assume it applies for purposes of this appeal.
The trial court found that the parties had not reached "impasse" as defined by federal case law. The District argues it was error for the court to base its finding on case law because PELRA defines impasse in its section on interest arbitration, and this provision abrogates the commonlaw definition.
The relevant section provides, in part:
For all public employees except those specified in subdivision 2, the director shall certify a matter * * * for binding interest arbitration if:
(a) the director has determined that further mediation would serve no purpose and has certified an impasse, or impasse has occurred because the exclusive representative and the employer have participated in mediation for the period required in section 179A.18, subdivisions 1 and 2, and the collective bargaining agreement has expired * * *.
Minn.Stat. § 179A.16, subd. 1 (1986). There is no dispute "impasse" has occurred under this section: the parties have mediated for the "period required" under the statute and that the collective bargaining agreement has expired. The CLEA argues, however, that this definition is inapplicable. We agree.
Since PELRA does not provide for an employer's unilateral implementation of its last offer, it follows that the legislature did not intend § 179A.16 to define "impasse" for purposes of determining when an employer may do so. This is a common law doctrine under the NLRA, and the doctrine includes a definition of impasse. See, e.g., Electric Machinery Co. v. NLRB, 653 F.2d 958, 963 (5th Cir.1981). It does not make sense to apply the common law doctrine only in part, substituting for its definition of impasse the definition found in § 179A.16. Not only does that section define impasse specifically for determining when interest arbitration is available, but even in that context it does not purport to be an exclusive definition: the director may determine that an impasse has been reached without reference to whether the conditions relied on by the District have been fulfilled. § 179A.16, subd. 1(a); see *880 also id., subd. 2 (parties may request arbitration by "stating that an impasse has been reached").
The District argues the interest arbitration section's definition of impasse should apply because then impasse (and hence unilateral implementation) would occur when the teachers have the right to strike. Compare § 179A.16, subd. 1, with § 179A.18, subds. 2-3. It has been held, however, that the maturation of the right to strike does not necessarily mean the employer has the right to implement its last offer. NLRB v. J.H. Bonck Co., 424 F.2d 634 (5th Cir.1970) (affirming finding of no impasse despite strike).

Contract in effect
Even if it is determined at trial that an impasse has been reached, the District could be prevented from unilaterally implementing its last offer by PELRA's "contract in effect" provision. Minn.Stat. § 179A.20, subd. 6 (1986), provides:

Contract in effect. During the period after contract expiration and prior to the date when the right to strike matures, * * * the terms of an existing contract shall continue in effect and shall be enforceable upon both parties.
(Emphasis added.)
The parties dispute whether the teachers' right to strike has "matured." Their right to strike is governed by the following provisions:
Subd. 2. School district requirements. Except as otherwise provided by section 179A.17, subdivision 1, teachers employed by a local school district * * * may strike only under the following circumstances:
(1)(a) the collective bargaining agreement between their exclusive representative and their employer has expired or, if there is no agreement, impasse under section 179A.17, subdivision 1, has occurred; and
(b) the exclusive representative and the employer have participated in mediation over a period of at least 30 days * *; and
(c) neither party has requested interest arbitration or a request for binding interest arbitration has been rejected; or
(2) the employer violates section 179A.13, subdivision 2, clause (9).
Subd. 3. Notice. In addition to the other requirements of this section, no employee may strike unless written notification of intent to strike is served on the employer and the director by the exclusive representative at least ten days prior to the commencement of the strike.
Minn.Stat. § 179A.18, subds. 2-3 (1986) (emphasis added).
The CLEA argues, and the trial court concluded, that the right to strike does not "mature" for purposes of the "contract in effect" provision until the teachers serve a notice of intent to strike under § 179A.18, subd. 3. The District argues that the right to strike "matures" after the agreement expires and the parties have mediated for thirty days; the teachers then have the right to strike, and the notice of intent to strike is the means of exercising that right.
We agree with the District that the teacher's right to strike matures when they have the right to file a notice of intent to strike. This is indicated by a number of factors.
First, the structure of § 179A.18 reflects the distinction between having the right, or power, to strike, and exercising that right: subdivision 2 describes the "circumstances" under which teachers are authorized to strike, while subdivision 3 merely requires ten days notice that they intend to strike.
This distinction between having the right to strike and exercising that right (by serving notice) is also reflected in the legislative history of 1985 amendments to PELRA's right to strike provisions. Minutes of a meeting of the Advisory Council on Bargaining Impasse Resolution contain the following recommended change:
No Notice of Intent to Strike can be issued nor would the right to strike mature until:

*881 a) Contract has expired; and
b) Mediation Period has expired.
Minutes of Advisory Council on Bargaining Impasse Resolution 2 (Nov. 14, 1984) (emphasis added).
The Advisory Council's final report recommended:
Retain the existing right of teachers to strike but modify the procedures for exercising that right as follows:
* * * * * *
B. Allow teachers to initiate a single opportunity to strike by the filing of a written notice.
Advisory Council on Bargaining Impasse Resolution, Final Report 19 (Jan. 1985).
The CLEA moved this court to strike copies of this legislative history from the District's reply brief because it (a) is irrelevant; (b) is evidence outside the record of which we may not take judicial notice; and (c) is not in response to new matter in its brief. We deny the motion. The materials are relevant and responsive to assertions in the CLEA's brief about the 1985 amendments, and they are not "evidence" outside the record. Since it was proper to cite the materials, it was proper for the District to append copies to its reply brief.
Second, the contract in effect section provides that it applies until "the date when the right to strike matures." § 179A.20, subd. 6 (emphasis added). This suggests an intent that there be a date certain, after which the provision no longer applies. Under the District's interpretation, the provision no longer applies when the contract expires and the parties have participated in mediation for 30 days. Under the CLEA's interpretation, it is uncertain when, if ever, the provision no longer applies. The teachers could keep a contract in effect indefinitely merely by not filing a notice.
Third, since employees (other than teachers) can file a notice of intent to strike, then not strike, then file a notice, and so on, under the CLEA's interpretation the right to strike could mature and unmature. This would result in the contract alternating between being in effect and not being in effect. Although a court could avoid this absurd result by not allowing the right to strike to unmature, this implication of a straightforward application of the CLEA's interpretation suggests the District's interpretation is more tenable.
Both sides argue their interpretation maintains equality of bargaining power. The District correctly notes that the CLEA's position would result in employees having sole control over keeping the prior contract in effect.
The CLEA contends that employers would have no incentive to bargain under the District's interpretation, because they could wait for the 30-day mediation period to expire and then implement their last offer. This ignores the fact that (1) there must be an impasse before unilateral implementation, which requires good faith bargaining, see, e.g., Electric Machinery Co., 653 F.2d at 963, and (2) employees would still have the right to strike, which would give employers incentive to negotiate.
Finally, the District argues that the trial court lacked jurisdiction to grant the temporary injunction because it failed to comply with certain requirements of the anti-injunction provisions of the "Little Norris-LaGuardia Act." See Minn.Stat. §§ 185.07, -.13 (1986). Specifically, the District argues this statute was violated because there was (1) no testimony in open court and no opportunity for cross-examination; (2) no findings of fact; and (3) no finding of irreparable harm or inadequate remedy at law. The CLEA argues the statute does not apply. See Minn.Stat. § 179A.24.
In light of our holding that the temporary injunction should not have been granted because the CLEA failed to meet the common law requirement of showing great and irreparable harm, we need not decide whether the anti-injunction statute applies.

DECISION
The trial court's memorandum decision is adequate to permit meaningful appellate *882 review. The trial court erred in granting a temporary injunction because CLEA failed to show it would otherwise suffer great and irreparable harm. The trial court did not err in using the common law definition of impasse. The right to strike matures under Minn.Stat. § 179A.20 (1986) when the provisions of Minn.Stat. § 179A.18, subds. 1-2 (1986), are satisfied, not when a notification of intent to strike is served.
Reversed.


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Hi ladies, I just want to say that I am really, really blessed by knowing I'm not alone in my oversupply, forceful letdown issues. With baby #1, this forum was the ONLY thing that saved our BFing relationship -- and I am so thankful. This is baby #2, and as I feared, my body has begun going crazy again producing more milk than baby V could ever need! Dealing with it is painful, time-consuming, and frustrating -- I've even started feeling extreme guilt for how these things affect my little guy :(

I will be spending some time going through the recent posts, and expect to be on here quite a bit. I do have one immediate question...

For those of you that have oversupply issues (and who block feed / once breast per feeding), how do you deal with engorgement issue at night? I literally feed off *one* side all night...and wake up with one breast tremendously, painfully, HOT and ENGORGED.

August 13th, 2013, 06:45 PM

@llli*maddieb

Re: So glad... but still need help!

With my most recent edition, I had to wake her up and encourage her to nurse several times a night because even as a brand newborn she would sleep 6 or more hours sometimes and I would wake up with cannon balls. I put my phone with alarm set under my pillow and set it for every two hours or so until things started calming down. Usually she WOULD rouse enough to nurse, if not, I would hand express.

Are you nursing on one side all night in order to block feed? Because either that block is too long or you want to be hand expressing or nursing at least enough on the "non nursing" side to keep from getting so engorged.


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

Stress situations happen during real or perceived threat to homeostasis or well-being. Stressors include either interoceptive changes (e.g., blood volume or osmolality changes) or environmental threat that may be physical (e.g., hypoxia) or psychological (e.g., presence of a predator). During stress a spectrum of physiological responses are evoked to maintain the physiologic integrity of the organism [@pone.0083900-Joels1]. The physiological responses to stress are mainly characterized by autonomic nervous system alterations, increase in plasma catecholamine levels and activation of the hypothalamus-pituitary-adrenal (HPA) axis [@pone.0083900-Joels1], [@pone.0083900-Alves1]. Autonomic responses include increase on both blood pressure and heart rate (HR) [@pone.0083900-Dampney1], [@pone.0083900-Campeau1]. Furthermore, cardiovascular changes during stress are accompanied by a resetting of baroreflex toward higher arterial pressure values, thus allowing simultaneous blood pressure and HR increases [@pone.0083900-Crestani1]--[@pone.0083900-Schenberg1].

Several central nervous system areas, including the prefrontal cortex, were described to be part of the brain circuitry involved on cardiovascular adjustments during stress [@pone.0083900-Dampney1], [@pone.0083900-Campeau1], [@pone.0083900-Fornari1], [@pone.0083900-Resstel1]. In rats, two regions of the prefrontal cortex involved in control of cardiovascular function are the insular cortex (IC) and the medial prefrontal cortex (MPFC) [@pone.0083900-Krettek1], [@pone.0083900-Leonard1]. It has been described that the IC is involved in cardiovascular control [@pone.0083900-Verberne1]--[@pone.0083900-Nagai1] and baroreflex modulation [@pone.0083900-Alves3]--[@pone.0083900-Zhang1]. Furthermore, previous results from our group demonstrated that bilateral microinjection of the unspecific neurotransmitter blocker CoCl~2~ into the IC of rats reduced both cardiovascular and behavioral responses evoked by either conditioned (contextual fear conditioning) or unconditioned (acute restraint stress) aversive stimuli [@pone.0083900-Alves1], [@pone.0083900-Alves4]. These results provided the first evidence of a role of the IC in cardiovascular adjustments during stress. However, due to the nonselective blockade of local neurotransmission caused by CoCl~2~ [@pone.0083900-Kretz1], [@pone.0083900-Lomber1], the specific neurotransmitter involved in the IC modulation of cardiovascular responses to stress is yet unknown.

Central noradrenergic circuitry is shortly activated after a stressful event [@pone.0083900-Joels1]. Conversely, it has been identified an enhanced release of noradrenaline after stress in several limbic brain regions including the central (CeA) and medial (MeA) amygdaloid nuclei, bed nucleus of the stria terminalis (BNST), lateral septal area (LSA), hippocampus and prefrontal cortex [@pone.0083900-Joels1], [@pone.0083900-Cecchi1]--[@pone.0083900-Cecchi2]. Noradrenergic terminals in the prefrontal cortex originate mainly from the locus coeruleus and play an important role in the regulation of cortical function [@pone.0083900-Morrison1]--[@pone.0083900-Ungerstedt1]. We have previously reported that noradrenergic neurotransmission within the IC is involved in the modulation of baroreflex activity [@pone.0083900-Alves5]. Also, microinjection of noradrenaline into the IC causes elevation of blood pressure and bradycardia [@pone.0083900-Alves2]. Although above evidence, the involvement of IC noradrenergic neurotransmission in the control of cardiovascular function during stress situations has never been investigated.

Therefore, given the involvement of IC-noradrenergic neurotransmission in cardiovascular control, we hypothesized an involvement of IC α-adrenoceptors in cardiovascular responses elicited by acute restraint stress in rats. To test this hypothesis, we investigated the effect of bilateral microinjections into the IC of selective α-adrenoceptor antagonists in restraint-evoked pressor and tachycardiac responses.

Experimental procedure {#s2}
======================

Ethical approval and animals {#s2a}
----------------------------

Experimental procedures were carried out following protocols approved by the Ethical Review Committee of the School of Medicine of Ribeirão Preto, (process number: 167/2007), which complies with the guiding principles for research involving animals and human beings of the National Institutes of Health. Fifty-seven male Wistar rats weighing approximately 250 g were used in the present experiment. Rats were housed in plastic cages in a temperature-controlled room (25°C) at the Animal Care Unit of the Department of Pharmacology, School of Medicine of Ribeirão Preto. Rats were kept under a 12 h :12 h light--dark cycle (lights on between 06:00 am and 6:00 pm) and had free access to water and standard laboratory food, except during the experimental period.

Surgical preparation {#s2b}
--------------------

Five days before the experiment, the rats were anesthetized with tribromoethanol (250 mg/kg, i.p.). After local anesthesia with 2% lidocaine, the skull was surgically exposed and stainless steel guide cannulas (26 G) were implanted bilaterally in the IC, using a stereotaxic apparatus (Stoelting, Wood Dale, Illinois, USA). Stereotaxic coordinates for cannula implantation in the IC were selected from the rat brain atlas of Paxinos and Watson (1997) and were: antero-posterior = +11.7 mm from interaural, lateral = 4.0 mm from the medial suture and dorso-ventral = −4.5 mm from the skull. Cannulas were fixed to the skull with dental cement and one metal screw. After surgery, the animals were treated with a polyantibiotic preparation of streptomycins and penicillins (i.m., 0.27 mg/kg, Pentabiotico, Fort Dodge®, Campinas, SP, Brazil) to prevent infection, and with the non-steroidal anti-inflammatory flunixine meglumine (2.5 mg/kg, i.m.; Banamine®, Schering Plough, Cotia, SP, Brazil) for post-operative analgesia.

One day before the experiment, rats were anesthetized with tribromoethanol (250 mg/kg, i.p.) and a catheter (a 4 cm segment of PE-10 heat-bound to a 13 cm segment of PE-50, Clay Adams, Parsippany, NJ, USA) was inserted into the abdominal aorta through the femoral artery, and later on used for arterial pressure and HR recording. The catheters were tunneled under the skin and exteriorized on the animal\'s dorsum. After surgery, the animals were treated with the non-steroidal anti-inflammatory flunixine meglumine (2.5 mg/kg, i.m.) for post-operative analgesia.

Measurement of Cardiovascular Responses {#s2c}
---------------------------------------

On the day of the experiment, the arterial cannula was connected to a pressure transducer and pulsatile arterial pressure was recorded using an HP-7754A amplifier (Hewlett Packard, Palo Alto, CA, USA) and an acquisition board (Biopac M-100, Goleta, CA, USA) connected to a personal computer. Mean arterial pressure (MAP) and HR values were derived from pulsatile arterial pressure recordings and were processed online.

Drugs and solutions {#s2d}
-------------------

WB4101 (Tocris, Westwoods Business Park Ellisville, MO, USA) and RX821002 (Tocris) were dissolved in artificial cerebrospinal fluid (ACSF) (ACSF composition: 100 mM NaCl; 2 mM Na~3~PO~4~; 2.5 mM KCl; 1 mM MgCl~2~; 27 mM NaHCO~3~; 2.5 mM CaCl~2~; pH = 7.4). Urethane (Sigma, St. Louis, MO, USA) and tribromoethanol (Sigma) were dissolved in saline (0.9% NaCl). Flunixine meglumine (Banamine®, Schering Plough, Brazil) and poly-antibiotic preparation of streptomycins and penicillins (Pentabiotico®, Fort Dodge, Brazil) were used as provided.

Drug injection into the insular cortex {#s2e}
--------------------------------------

The needles (33 G, Small Parts, Miami Lakes, FL, USA) used for microinjection into the IC were 1 mm longer than the guide cannulas and were connected to a hand-driven 2 µl syringe (7002-KH, Hamilton Co., Reno, NV, USA) through a PE-10 tubing. Needles were carefully inserted into the guide cannulas without restraint the animals. After a 30 s period, the needle was removed and inserted into the second guide cannula for microinjection into the contralateral IC. Drugs were injected in a final volume of 100 nl [@pone.0083900-Alves1], [@pone.0083900-Alves4].

Experimental procedure: acute restraint stress {#s2f}
----------------------------------------------

On the trial day, animals were brought to the experimental room in their home cages. Animals were allowed one hour to adapt to the conditions of the experimental room, such as sound and illumination, before starting cardiovascular recordings. The experimental room was temperature controlled (25°C) and the room was acoustically isolated from the other rooms. Constant background noise was generated by an air extractor to minimize sound interference within the experimental room. Baseline values of MAP and HR were recorded for at least 30 min. In the sequence, independent groups of animals received bilateral microinjection into the IC of vehicle (ACSF, 100 nl) or different doses of either the selective α~1~-adrenoceptor antagonist WB4101 (0.3, 5, 10 or 15 nmol/100 nl) or the selective α~2~-adrenoceptor antagonist RX821002 (0.3, 5, 10 or 15 nmol/100 nl) [@pone.0083900-Alves2], [@pone.0083900-Alves5], [@pone.0083900-Crestani2]. Ten minutes later, rats were submitted to acute restraint stress by placing them into a plastic cylindrical restraint tube (diameter  = 6.5 cm, length  = 15 cm), which were ventilated by holes (1 cm of diameter) that comprised approximately 20% of the tube surface. The restraint session lasted 60 min, after which the rats were returned to their home cages [@pone.0083900-Alves4], [@pone.0083900-Crestani3]. Each rat was submitted to one session of restraint in order to avoid habituation. Experiments were performed during the morning period in order to minimize possible circadian rhythm interferences.

Histological determination of the microinjection sites {#s2g}
------------------------------------------------------

At the end of experiments, animals were anesthetized with urethane (1.25 g/kg, i.p.) and 100 nL of 1% Evan\'s blue dye was injected into the IC as a marker of the injection site. They were then submitted to intracardiac perfusion with 0.9% NaCl followed by 10% formalin. Brains were removed and post fixed for 48 h at 4°C and serial 40 µm-thick sections were cut using a cryostat (CM1900, Leica, Wetzlar, Germany). Sections were stained with 1% neutral red for light microscopy analysis. The placement of the microinjection needles was determined analyzing serial sections and identified according to the rat brain atlas of Paxinos and Watson (1997).

Statistical Analysis {#s2h}
--------------------

Statistical analysis was performed using Prism software (GraphPad, SanDiego, CA, USA). The results are presented as mean±S.E.M. The Student\'s t-test was used to compare basal values of MAP and HR before and after pharmacological treatments. Time-course curves of MAP and HR changes were compared using two-way ANOVA for repeated measurements (treatment vs time) with repeated measures on the second factor. When interactions between the factors were observed, one-way ANOVA followed by Bonferroni\'s post-hoc test was used to compare the effect of the treatments. Nonlinear regression analysis was performed to investigate the dose--effect relationship of treatment with crescents doses of WB4101 and RX821002 on cardiovascular responses to restraint stress.

Results {#s3}
=======

A representative photomicrograph of a coronal brain section depicting bilateral microinjection sites in the IC of one representative rat is presented in [Figure 1](#pone-0083900-g001){ref-type="fig"}. A diagrammatic representation showing microinjection sites of vehicle, WB4101 and RX821002 into the IC and WB4101 and RX821002 into structures surrounding the IC is also presented in [Figure 1](#pone-0083900-g001){ref-type="fig"}.

![A photomicrograph of a coronal brain section, from one representative rat, which shows bilateral injection sites in the insular cortex.\
Diagrammatic representation based on the rat brain atlas of Paxinos and Watson (1997) indicating the microinjection sites of vehicle (white circles), WB4101 (black circles) and RX821002 (black squares) into the IC as well as WB4101 (gray circles) and RX821002 (gray squares) into structures surrounding the IC. Cg1 -- cingulate cortex, area; PrL -- prelimbic cortex, M1 -- primary motor cortex; insular cortex -- insular cortex, cc -- corpus callosum, forceps minor of the corpus callosum (fmi).](pone.0083900.g001){#pone-0083900-g001}

Effect of IC pretreatment with different doses of the selective α~1~-adrenoceptor antagonist WB4101 on cardiovascular changes evoked by acute restraint stress {#s3a}
--------------------------------------------------------------------------------------------------------------------------------------------------------------

Bilateral microinjection of different doses (0.3, 5, 10 and 15 nmol/100 nL, n = 5/group) of the selective α~1~-adrenoceptor antagonist WB4101 into the IC did not affect either MAP or HR baseline values ([Table 1](#pone-0083900-t001){ref-type="table"}). Representative experimental recordings showing effects of local microinjection of WB4101 into the IC on cardiovascular responses elicited by acute restraint stress are presented in [Figure 2](#pone-0083900-g002){ref-type="fig"}. Time-course analysis of restraint-evoked cardiovascular responses indicated that IC treatment with WB4101 (at doses of 5, 10 and 15 nmol/100 nl for MAP response and at dose of 15 nmol/100 nl for HR response) reduced both MAP (F~(4,660)~ = 336, P\<0.0001) and HR (F~(4,660)~ = 50, P\<0.0001) responses, when compared with ACSF-treated animals (n = 7) ([Figure 3](#pone-0083900-g003){ref-type="fig"}). There was also a significant effect over time for MAP (F~(29,660)~ = 70, P\<0.0001) and HR (F~(29,660)~ = 27, P\<0.0001) responses, as well as a treatment x time interaction for the pressor response (MAP: F~(116,660)~ = 6, P\<0.0001; HR: F~(116,660)~ = 1, P\>0.05). Nonlinear regression analysis revealed that WB4101 effects on restraint-evoked cardiovascular responses were dose-dependent, showing a significant association between drug dose and MAP (df = 18, r^2^ = 0.85, P\<0.05) and HR (df = 13, r^2^ = 0.60, P\<0.05) increases ([Figure 3](#pone-0083900-g003){ref-type="fig"}). The injection of WB4101 (n = 2) into structures surrounding the IC did not affect both MAP (F~(1,60)~ = 2,9, P\>0.05) and HR (F~(1,60)~ = 0,2, P\>0.05) responses to restraint stress.

![Representative recordings of mean arterial pressure (MAP), pulsatile arterial pressure (PAP) and heart rate (HR) of representative rats submitted to acute restraint stress.\
**A)** Recordings of MAP, PAP and HR of one representative rat treated with vehicle (ACSF) into the insular cortex and submitted to acute restraint stress. The onset of restraint is at t = 0. **B)** Recordings of MAP, PAP and HR of one representative rat treated with the selective α~1~-adrenoceptor antagonist WB4101 into the insular cortex and submitted to acute restraint stress. The onset of restraint is at t = 0. Note the decrease in the MAP, PAP and HR responses to restraint stress in animals treated with WB4101 into the insular cortex. C) Recordings of MAP, PAP and HR of one representative rat treated with the selective α~2~-adrenoceptor antagonist RX821002 into the insular cortex and submitted to acute restraint stress. The onset of restraint is at t = 0. Note the decrease in the MAP and PAP responses to restraint stress in animals treated with RX821002 into the insular cortex.](pone.0083900.g002){#pone-0083900-g002}

![Changes in mean arterial pressure (ΔMAP) and heart rate (ΔHR) evoked by acute restraint stress in animals treated with different doses of the selective α~1~-adrenoceptor antagonist WB4101 into the insular cortex.\
**(Left)** Time-course of ΔMAP and ΔHR during acute restraint stress in rats treated with vehicle (ACSF, 100 nl, n = 7) or different doses (0.3, 5, 10 and 15 nmol/100 nl, n = 5/group) of WB4101 into the insular cortex. The onset of exercise was at t = 0. Circles represent the mean and bars the S.E.M. \# P\<0.05, indicates a significant difference over the whole restraint stress period compared to vehicle treated animals; ANOVA followed by Bonferroni\'s post test. **(Right)** ΔMAP and ΔHR during acute restraint stress in rats treated with increasing doses of WB4101 (0.3, 5, 10 and 15 nmol/100 nl). V: vehicle (ACSF, 100 nl). Dose--effect curves were generated by nonlinear regression analysis. Data shown represent the means±S.E.M. of the variation of MAP and HR during the 60 min of restraint. \# P\<0.05, significantly different from vehicle group; one-way ANOVA followed by Bonferroni\'s post test.](pone.0083900.g003){#pone-0083900-g003}

10.1371/journal.pone.0083900.t001

###### Effect of bilateral microinjections into the IC of crescent doses (0.3, 5, 10 and 15 nmol/100 nl) of the selective α~1~-adrenoceptor antagonist WB4101 on mean arterial pressure (MAP) and heart rate (HR) baseline.

![](pone.0083900.t001){#pone-0083900-t001-1}

  Treatment                WB4101 0.3 nmol         WB4101 5 nmol          WB4101 10 nmol         WB4101 15 nmol
  --------------------- ---------------------- ---------------------- ---------------------- ----------------------
  N                               5                      5                      5                      5
  MAP--Before treat.            102±3                   98±3                   96±3                  103±3
  MAP--After treat.             100±4                  100±4                  104±3                   98±6
  Statistic              *t* = 0.4, *P*\>0.05   *t* = 0.3, *P*\>0.05   *t* = 2.6, *P*\>0.05   *t* = 1.8, *P*\>0.05
  HR -- Before treat.           368±12                 364±10                 356±9                  356±7
  HR -- After treat.            356±13                 382±9                  377±12                 367±10
  Statistic              *t* = 0.4, *P*\>0.05    *t* = 1, *P*\>0.05    *t* = 2.5, *P*\>0.05   *t* = 1.8, *P*\>0.05

Student\'s *t*-test.

Effect of IC pretreatment with different doses of the selective α~2~-adrenoceptor antagonist RX821002 on cardiovascular changes evoked by acute restraint stress {#s3b}
----------------------------------------------------------------------------------------------------------------------------------------------------------------

Bilateral microinjection of different doses (0.3, 5, 10 and 15 nmol/100 nL, n = 5/group) of the selective α~2~-adrenoceptor antagonist RX821002 into the IC did not affect either MAP or HR baseline values ([Table 2](#pone-0083900-t002){ref-type="table"}). Representative experimental recordings showing effects of RX821002 microinjection into the IC on cardiovascular responses induced by acute restraint stress are presented in [Figure 2](#pone-0083900-g002){ref-type="fig"}. Time-course analysis of restraint-evoked cardiovascular responses indicated that IC treatment with RX821002 at doses of 5, 10 and 15 nmol/100 nl reduced MAP response (F~(4,630)~ = 216, P\<0.0001) without affecting restraint-evoked tachycardia (F~(4,630)~ = 2, P\>0.05), when compared with ACSF-treated animals (n = 6) ([Figure 4](#pone-0083900-g004){ref-type="fig"}). There was also a significant effect over time for MAP (F~(29,630)~ = 54, P\<0.0001) and HR (F~(29,630)~ = 42, P\<0.0001) responses, as well as a treatment x time interaction for the pressor response (MAP: F~(116,630)~ = 3, P\<0.0001; HR: F~(116,630)~ = 0.6, P\>0.05). Nonlinear regression analysis revealed that RX821002 effect on restraint-evoked pressor response was dose-dependent, showing a significant association between drug doses and MAP increase (df = 18, r^2^ = 0.65, P\<0.05) ([Figure 4](#pone-0083900-g004){ref-type="fig"}). The injection of RX821102 into structures surrounding the IC did not affect both MAP (F~(1,60)~ = 1,4, P\>0.05) and HR (F~(1,60)~ = 0,005, P\>0.05) responses to restraint stress.

![Changes in mean arterial pressure (ΔMAP) and heart rate (ΔHR) evoked by acute restraint stress in animals treated with different doses of the selective α~2~-adrenoceptor antagonist RX821002 into the insular cortex.\
(Left) Time-course of ΔMAP and ΔHR during acute restraint stress in rats treated with vehicle (ACSF, 100 nl, n = 6) or different doses (0.3, 5, 10 and 15 nmol/100 nl, n = 5/group) of the selective α~2~-adrenoceptor antagonist RX821002 into the insular cortex. The onset of exercise was at t = 0. Circles represent the mean and bars the S.E.M. \# P\<0.05, indicates a significant difference over the whole restraint stress period compared to vehicle treated animals; ANOVA followed by Bonferroni\'s post test. (Right) ΔMAP and ΔHR during restraint stress in rats treated with increasing doses of RX821002 (0.3, 5, 10 and 15 nmol/100 nl). V: vehicle (ACSF, 100 nl). Dose--effect curves were generated by nonlinear regression analysis. Data shown represent the means±S.E.M. of the variation of MAP and HR during the 60 min of restraint. \# P\<0.05, significantly different from vehicle group; one-way ANOVA followed by Bonferroni\'s post test.](pone.0083900.g004){#pone-0083900-g004}

10.1371/journal.pone.0083900.t002

###### Effect of bilateral microinjections into the IC of crescent doses (0.3, 5, 10 and 15 nmol/100 nl) of the selective α~2~-adrenoceptor antagonist RX821002 on mean arterial pressure (MAP) and heart rate (HR) baseline.

![](pone.0083900.t002){#pone-0083900-t002-2}

  Treatment               RX821002 0.3 nmol       RX821002 5 nmol        RX821002 10 nmol       RX821002 15 nmol
  --------------------- ---------------------- ---------------------- ---------------------- ----------------------
  N                               5                      5                      5                      5
  MAP--Before treat.             96±3                   99±3                  103±4                   95±2
  MAP--After treat.             106±4                  101±2                  102±5                  101±2
  Statistic              *t* = 2.6, *P*\>0.05   *t* = 0.5, *P*\>0.05   *t* = 0.3, *P*\>0.05   *t* = 1.3, *P*\>0.05
  HR -- Before treat.           356±9                  353±10                 356±7                  384±12
  HR -- After treat.            380±16                 362±14                 358±12                 362±11
  Statistic              *t* = 1.5, *P*\>0.05   *t* = 0.8 *P*\>0.05    *t* = 0.1, *P*\>0.05    *t* = 1, *P*\>0.05

Student\'s *t*-test.

Discussion {#s4}
==========

The results of the present work provide the first direct evidence for the involvement of IC adrenoceptors in cardiovascular responses observed during aversive threats. We have shown that bilateral microinjection of the selective α~1~-adrenoceptor antagonist WB4101 into the IC reduced restraint-evoked pressor and tachycardiac responses in a dose-dependent manner. Moreover, IC treatment with the selective α~2~-adrenoceptor antagonist RX821002 dose-dependently reduced MAP increase observed during restraint stress without affecting tachycardiac response.

Restraint stress is well accepted in the literature as an unconditioned and unavoidable aversive stimulus that elicits neuroendocrine and cardiovascular responses, the latter being characterized by sustained elevation of blood pressure, HR and the sympathetic activity that last through the restraint period [@pone.0083900-Barron1]--[@pone.0083900-McDougall1]. The IC receives an organized representation of visceral information and is also highly interconnected with subcortical limbic and autonomic-related regions. Based on this combination of sensory input and limbic connectivity it has been descript as an important cortical center for the integration of autonomic and behavioral responses during aversive threats [@pone.0083900-Verberne1]. Conversely, we have demonstrated that CoCl~2~-induced acute bilateral inhibition of IC neurotransmission greatly attenuated both pressor and tachycardiac responses evoked by acute restraint stress [@pone.0083900-Alves4]. However, due to the nonselective blockade of local neurotransmission caused by CoCl~2~ [@pone.0083900-Kretz1], [@pone.0083900-Lomber1], the possible neurotransmitter involved was not identified.

It has been showed that diverse array of physical (e.g., immune challenge, hypoglycemia, hypotension, and cold exposure) and emotional (e.g., immobilization, electric shock, loud noise, and restraint stress) stressors activate brain noradrenergic mechanisms [@pone.0083900-Joels1], [@pone.0083900-Cecchi1], [@pone.0083900-Cecchi2], [@pone.0083900-Abercrombie1]--[@pone.0083900-Valentino1]. Noradrenergic neural terminals have been identified in the IC [@pone.0083900-Ungerstedt1]. This IC innervation is mainly originated from noradrenergic cells grouped in the locus coeruleus (noradrenergic cell group A6) [@pone.0083900-Morrison1], [@pone.0083900-Morrison2], [@pone.0083900-Ungerstedt1]. The present work has demonstrated that blockade of local α~1~-adrenoceptor by bilateral microinjection of WB4101 into the IC was able to reduce both pressor and tachycardiac responses evoked by restraint stress. These results corroborate with effects observed previously following CoCl~2~-induced acute bilateral inhibition of IC neurotransmission [@pone.0083900-Alves4], thus suggesting that local α~1~-adrenoceptors mediates, at least in part, the IC influence on cardiovascular responses to restraint stress. Interestingly, blockade of local α~2~-adrenoceptors caused by microinjection of RX821002 into the IC also reduced restraint-evoked pressor response, but without affecting tachycardiac response. Therefore, present data suggest that control of cardiac function during restraint stress by IC noradrenergic neurotransmission is due a selective activation of local α~1~-adrenoceptors, whereas control of blood pressure during seems to be mediated by coactivation of local α~1~- and α~2~-adrenoceptors.

The presence of specific noradrenergic mechanisms within the IC controlling restraint-evoked pressor and tachycardiac responses indicates that different neuronal pathways originating in the IC are involved in control of vascular and cardiac functions during stress. The existence of specific central nervous system circuitries controlling autonomic activity to different organs provides the structural substrate for specific local IC noradrenergic neurotransmission mechanisms modulating cardiovascular adjustments during restraint [@pone.0083900-Morrison3]. Conversely, it has been demonstrated that several brain regions selectively modulate stress-evoked blood pressure and HR responses [@pone.0083900-Mayorov1]--[@pone.0083900-Tavares1]. The presence of specific noradrenergic mechanisms in the central nervous system modulating vascular and cardiac responses to stress has also been reported [@pone.0083900-Crestani3], [@pone.0083900-Daubert1]. Therefore, our results corroborate with previous evidence of selective neural substrates controlling vascular and cardiac function during aversive threats.

Noradrenaline is released in several central nervous system regions, including the prefrontal cortex [@pone.0083900-Cecchi1], [@pone.0083900-Cecchi2], shortly after the onset of a stressful situation [@pone.0083900-Joels1]. Since noradrenaline act through G protein-coupled receptors, which rapidly transfer their activation to downstream effectors, the rapid rise in their level is quickly translated into behavioral and physiological responses. This profile of fast release and action can explain why effects of local IC treatment with adrenoceptor antagonists are already observed during the early phase of restraint stress. However, it has been proposed that sustained and adaptive components of the stress responses (e.g., consolidation of the memory associated with the stressor) are mediated by mechanisms in the brain that affect gene expression and cell function [@pone.0083900-Joels1]. A main mediator of these latter effects is corticosteroids acting through glucocorticoid receptors [@pone.0083900-Joels1]. Since previous studies have demonstrated a role of the IC in the memory formation for aversive threat and hypothalamus-pituitary-adrenal axis control [@pone.0083900-Alves1], [@pone.0083900-Campeau1], [@pone.0083900-Fornari1], further studies are necessary to investigate a possible role of IC in latter consequences of restraint stress.

Tachycardiac and pressor responses during stress are sympathetically mediated since they are abolished after the blockade of β- and α-adrenoceptors, respectively [@pone.0083900-Crestani1], [@pone.0083900-Carrive1], [@pone.0083900-Carrive2]. Moreover, treatment with parasympathetic blocker increases the tachycardiac response evoked by psychological stress [@pone.0083900-Crestani3], [@pone.0083900-Baudrie1], [@pone.0083900-Iwata1], thus suggesting the simultaneous activation of cardiac parasympathetic and sympathetic activity during psychological stress. It has been reported that the IC modulate the sympathetic nervous activity through a mandatory synapse in the ventrolateral medulla [@pone.0083900-Butcher1], [@pone.0083900-Cechetto1]. An IC control of cardiac parasympathetic activity has also been shown [@pone.0083900-Alves5], [@pone.0083900-Oppenheimer1]. Therefore, activation of IC α~1~-adrenoceptors could facilitate restraint-evoked tachycardiac response by stimulating facilitatory inputs to sympathetic medullary neurons and/or by stimulating inhibitory inputs to vagal neurons. Connections from the IC to sympathetic medullary neurons could also be the neural substrate for the facilitatory influence of IC α~1~- and α~2~-adrenoceptors on the pressor response to stress.

Baroreflex stimulus--response curve resets toward higher blood pressure values during aversive threat [@pone.0083900-Crestani1], [@pone.0083900-Hatton1]. It has been proposed that such changes on baroreflex activity play a facilitatory role in stress-evoked cardiovascular responses [@pone.0083900-Dampney1], [@pone.0083900-Nosaka1]. We have previously demonstrated that IC noradrenergic neurotransmission acting through activation of α~1~-adrenoceptor modulates the baroreflex activity in a similar manner to that observed during stress [@pone.0083900-Alves5]. Therefore, activation of IC α~1~-adrenoceptors could facilitate cardiovascular responses to restraint stress through its modulation of baroreflex activity. However, once IC treatment with selective α~2~-adrenoceptors does not affect baroreflex activity [@pone.0083900-Alves5], it is possible that IC control of restraint-evoked pressor response through this adrenoceptor occurs by mechanisms independent of the baroreflex.

An antero-posterior organization of IC control of cardiovascular function has been proposed. Predominantly depressor responses have been reported following stimulation of rostral regions of the IC [@pone.0083900-Verberne1]. However, stimulation of the posterior IC elicits either pressor response associated with tachycardia (rostral sites within the posterior IC) or depressor response followed by bradycardia (caudal sites within the posterior IC) [@pone.0083900-Verberne1]. Although these pieces of evidence, a possible regionalization in the IC control of cardiovascular adjustments to stress has never been reported. The injection sites within the IC in studies investigating the role of this cortical region in the cardiovascular control during stress (including the present study) have centered within rostral regions of the IC [@pone.0083900-Alves1], [@pone.0083900-Alves4]. Therefore, further studies are necessary in order to investigate a possible rostro-caudal organization of the IC control of cardiovascular function during aversive threat.

IC treatment with adrenoceptor antagonists did not affect either MAP or HR baseline values. Therefore, although the present study supports the hypothesis that IC noradrenergic neurotransmission plays an important role in modulating the cardiovascular responses to restraint stress, this neurotransmission is not involved in the tonic maintenance of cardiovascular function. These results corroborate with our previous data demonstrating no changes in cardiovascular parameters after blockade of either glutamatergic receptors or adrenoceptors into the IC [@pone.0083900-Alves3], [@pone.0083900-Alves5]. However, present results contrast with data of other groups that observed increased arterial pressure and HR following microinjection of the neuronal blocker lidocaine into the IC of unanesthetized rats [@pone.0083900-Butcher1]. Lidocaine blocks both local synapses and passage fibers [@pone.0083900-Sandkuhler1]. Therefore, since local IC pharmacological treatment with agents that selectively inhibits synapses without affecting passage fibers (e.g., CoCl~2~) does not affect cardiovascular basal parameters [@pone.0083900-Alves4], it is possible that effects observed previously after local lidocaine treatment is due the inhibition of fibers passing through the IC and targeting other brain regions. Furthermore, it is important to mention that other studies did not identify effects of local lidocaine microinjection or IC lesion on cardiovascular baseline parameters [@pone.0083900-Saad1], [@pone.0083900-Saleh1], thus supporting our results of absence of IC role in the tonic maintenance of cardiovascular function.

In conclusion, the present results show that noradrenergic neurotransmission in the IC modulates cardiovascular adjustments during restraint stress in a complex way. Our data provide evidence that IC noradrenergic neurotransmission acting through activation of both α~1~- and α~2~-adrenoceptors has a facilitatory influence on pressor response during acute restraint stress. Moreover, IC α~1~-adrenoceptors also play a facilitatory role on restraint-evoked tachycardiac response.

The authors wish to thank I.A.C. Fortunato and S.S. Guilhaume for technical help.

[^1]: **Competing Interests:**The authors have declared that no competing interests exist.

[^2]: Conceived and designed the experiments: FHFA CCC LBMR FMAC. Performed the experiments: FHFA CCC. Analyzed the data: FHFA CCC. Contributed reagents/materials/analysis tools: FHFA CCC LBMR FMAC. Wrote the paper: FHFA CCC. LBMR FMAC.


Q:

click on div element inside an  tag

I have a set of div elements inside <a> tag with it's href.
The question is that there is a div inside of it with its own click event and I want that in case the div element trigger the click event, the <a> tag should not be triggered.
The function that manage the div click event try to stop propagation with no success.
if (!e) var e = window.event;
e.cancelBubble = true;
if (e.stopPropagation) e.stopPropagation();

What's wrong?

A:

If you're using jQuery to attach to the event, then do
e.preventDefault();

JQuery normalizes the event object so this method is available on all browsers (otherwise older IE's don't have it).
Here's the documentation for preventDefault().
If that doesn't help, then try attaching a click handler on the <a> itself and call preventDefault() from that.


Vascular endothelial growth factor in chronic subdural haematomas.
To elucidate molecular aspects of the mechanisms of expansion of chronic subdural haematomas (CSH), we examined the expression of two representative angiogenic factors, vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in CSH. We quantified VEGF and bFGF in haematoma fluid and serum of 20 patients with CSH using an enzyme-linked immunosorbent assay. Mean concentrations of VEGF in the haematoma fluid (10277 pg/ml) and in serum, (355 pg/ml) were much greater than those of bFGF (haematoma, 3.04 pg/ml; serum, 4.74 pg/ml). Surgical specimens, including dura and the outer membrane of the CSH were analysed by in situ hybridisation to detect VEGF mRNA. Macrophages and vascular endothelial cells in the outer membrane over expressed VEGF mRNA. Enhanced production of VEGF by macrophages and vascular endothelial cells in the outer membrane is thought to be pathogenetically important in CSH.


Ready for tighter sulphur regulations

Every year, thousands of deaths are caused by maritime sulphur emissions. In order to combat this environmental threat, the International Maritime Organization (IMO) will drop fuel oil sulphur limits in Emission Control Areas (ECAs) to 0.1 per cent on 1 January 2015. Erik Nyheim, WWL Chief Commercial Officer, discusses the ramifications of the new regulations and how WWL will address this issue going forward.

What are some of the main challenges facing the shipping industry when it comes to these new regulations?

The introduction of stricter sulphur regulations will have a huge impact on the shipping industry. To comply with the new regulations we have to change the fuel that our vessels run on, which is a challenge technically and carries a big cost. Switching from bunker to Marine Gas Oil (MGO) is the only readily available solution, and that is 50 per cent more expensive than bunker fuel. Already today, bunker fuel makes up 45 per cent of operating costs for a vessel, so the cost impact on operations in ECA zones will be very noticeable.

But responsible shipping companies face another big risk due to the current lack of enforcement of regulations. Given the huge financial incentives, there is a temptation for less scrupulous operators to cut corners which can seriously distort competition.

That’s why we started the Trident Alliance: to reduce business risk for us and our customers. The main focus is on communication to raise awareness of the issue, supported by member companies’ transparency on compliance, as well as on initiatives to foster innovation in enforcement technology.

At WWL, we are determined to find the most sustainable solution for the customers, our vessels and the environment. Over time we envisage using a combination of solutions depending on vessel, routes and market developments. We don’t have the answers yet, therefore we are working on a broad scale, taking a four stream approach to examining potential solutions.

Can you elaborate on this four-stream approach?

The first stream is to use MGO now. The second is to work for a reliable supply of ultra-low sulphur bunker oil, a fuel that until recently did not exist. We have made good progress here. In recent sea trials, oil and gas giant ExxonMobil asked us to be their partner to test what has become the first fully approved Ultra Low Sulphur Fuel Oil. The third stream involves exhaust gas cleaning systems, or scrubbers, which we are testing on one of our vessels. These remove the sulphur from the vessels’ exhaust fumes and make it possible to keep running on normal bunker oil. And the fourth involves the use of alternative fuels, which, in the long term, include a wide range of options. Liquid natural gas, biofuels, fuel cells and a variety of other options are all being explored. But it will take time to get scale and efficiency at usable levels.

Share this article on the links below and follow us for news, tips and behind the scenes stories on the upcoming new ECA regulations and more.

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Source: Xinhua| 2017-05-30 01:08:25|Editor: Zhang Dongmiao

Photo taken on May 10, 2017 shows the Emali station on Kenya's Mombasa-Nairobi Standard Gauge Railway (SGR). (Xinhua/Chen Cheng)

NAIROBI, May 29 (Xinhua) -- The 480 km railway linking Kenya's largest port city Mombasa to capital Nairobi, slated to be officially launched on May 31, will be a key infrastructure project that will push forward the East Africa nation's modernization drive, a senior company executive said Monday.

"The launch of the standard gauge railway (SGR) will undoubtedly contribute to Kenya's economic and social development as well as improve people's livelihoods and lead the country to prosperity," said Chen Yun, Vice President of China Communications Construction Company, parent company of the China Road and Bridge Corporation which built the mega-project.

In an interview with Xinhua on the sidelines of a ceremony held here in Nairobi for the release of the company's social responsibility report regarding the SGR project, Chen said that the company has endeavored to build the Kenya SGR project into a quality project that will endure the test of time.

"The Mombasa-Nairobi railway is also a way of cooperation, mutual benefits and prosperity," Chen said.

According to the report, the SGR project has created more than 46,000 jobs for the locals and the number of local workers who received training hit 45,000, gaining the much-needed skills and technical knowhow to help them grow. The SGR project is also estimated to be adding 1.5 percentage points to Kenya's GDP growth, a figure the Kenyan government reckons with.

As Africa strives for integration, Chen believed that Africa will continue to see the birth of many more railway projects on the continent.

He revealed that during a recent talk between him and Kenyan President Uhuru Kenyatta, the president said he would promote SGRs in the east Africa region so that the region can upgrade and renovate existing railways and enhance transport capacity.

Chen added that the Belt and Road Initiative proposed by China, which aims to build a trade and infrastructure network connecting Asia with Europe and Africa along and beyond the ancient Silk Road trade routes, will also provide immense opportunities for African countries, and companies involved.


Q:

What is the exponential trick to include laplacian term in Rayleigh-Bernard simulation

I have come across a Rayleigh-Bernard simulation code which doesn't have the laplacian term but an integrating factor (in the exponential form) containing viscosity and diffusivity. I found out that it is an exponential trick. I couldn't find any literature on it except that. I would like to know more. Can someone point me to a reference.

A:

I found what I was looking for, so I will share:
Check out: "Time integration and treatment of viscous/diffusive
terms" on page 5.
K. B. Winters, J. McKinnon, and B. Mills. A spectral model for process studies
of density stratified flows. J. of Atmos. Ocean. Techn. (submitted), 2003.
https://journals.ametsoc.org/doi/pdf/10.1175/1520-0426%282004%29021%3C0069%3AASMFPS%3E2.0.CO%3B2
The above article uses an exponential integrating factor while integrating and the laplacian term of the N-S equation and other scalar equations is treated through the integrating factor.
Similar was the case in the R-B simulation code, which I didn't understood at the time.


Monger, who lost both his legs after an Formula 4 accident at Donington Park in April, is linking up with the latest project launched by quadruple amputee and Le Mans racer Frederic Sausset.

The plan is for Monger, 18, to be on the driving roster for the planned Le Mans debut of Sausset's academy in 2020.

The first venture of the new La Filiere Frederic Sausset will be an appearance at the Estoril round of the VdeV Endurance Proto Series on November 4/5.

Monger and Sausset will share the Group CN Ligier-Honda JS53 Evo 2, in which Sausset began racing in 2015, with Le Mans veteran Christophe Tinseau.

Monger told Motorsport.com: "It was unbelievable that Fred reached out to me after my accident and asked me to be involved in his plan to get disabled people involved in motorsport at the top level.

"I definitely want to be out racing again. My priority is to get track time in a car and continue my physical work to return to full fitness."

Sausset, who raced an LMP2 Morgan i the 'Garage 56' slot for an innovative design at Le Mans last year, explained that he had contacted Monger straight after his accident two months ago.

"I wanted to show my support and then I invited him to be part of the project," he said.

"I want Billy to move forward and go to Le Mans: if everything works out, he will have a seat in 2020."

Sausset is inviting disabled people with motorsport ambitions to apply to his academy.

"I want to use my experience over the past couple of years to help people of all disabilities from around the world to race cars at all levels," he explained.

"We need to help disabled people access motorsport, and I have the support of Jean Todt and Pierre Fillon [respectively presidents of the FIA and the Le Mans organiser the Automobile Club de l'Ouest] for my ideas."

"I want a sustainable academy of excellence that is not just a one-shot."

The academy will hold its first trials on the Le Mans-Bugatti circuit in November.

Sausset is aiming to have one car racing in VdeV next year, ahead of an expansion into the European Le Mans Series in 2019 before the Le Mans assault the following year

He explained that it had yet to be decided in which class the outfit will race in next year and in the future.

Sausset revealed he is talking to manufacturers about a link-up that would involve racing a GT3 car next year and then a GTE car in 2019-2020, but said that LMP2 remained an option for the graduation to the ELMS and Le Mans.

He will not be part of the driver line-up at Le Mans in 2020, but said that he still had aspirations to return to the 24 Hours as a driver beyond that.


Expansion Tank fails repeatedly

I have a setup for radiant floor and DHW running on a Munchkin boiler. It all works great, with one exception. In five years I've gone through 3 expansion tanks! Each time, the tank fails by rusting through from the inside. I cannot believe I would get 3 defective tanks (they were bought at different times, from different vendors, but all same manufacturer).

I've tried to include some photos to show the setup.

Here is my theory: the tank that fails is at a low spot in the system (not the lowest spot, but close). The boiler and DHW are connected with black pipe, and the radiant zone pumps with copper. There are proper dielectric unions between them. Perhaps the iron pipe is corroding slightly, and the sediment is falling into the expansion tank, somehow causing excessive corrosion inside the tank? Does this make sense?

So, do I replace all the black pipe with copper? I am afraid there may be damage to the boiler that I cannot see, because that is truly the low point in the system. Would a trap or filter solve the problem?

By the way, there are 2 expansion tanks on the system, one up high near the inlet and one near the radiant manifold. It is only the one near the radiant that fails.

Comments

For example, Uponor make HePEX Plus, and AquaPEX. HePEX is OK with mild steel components, but AquaPEX is not...

ME

It's not so much a case of "You got what you paid for", as it is a matter of "You DIDN'T get what you DIDN'T pay for, and you're NOT going to get what you thought you were in the way of comfort". Borrowed from Heatboy.

I do not know who made the tubing, but it was described as "POLY PXC" tubing (7/8"). I can tell you that it is NOT an oxygen barrier tubing. That may have been a mistake, but it is too late now. I would welcome any suggestions to minimize the deterioration.

Fortunately, any components that would fail are accessible, i.e. the expansion tank and any steel piping in the near boiler piping configuration.

You could maintain the pH above 8.0 and it would slow any oxygen degradation. As for the tank replace it with a potable water expansion tank, which is rated for oxygen. Adjust the diaphragm pressure to around 12 to 15 PSI, assuming no more than a 2 story building.

The next components to start showing sign would be any steel pipe, then cast iron pump.

ME

It's not so much a case of "You got what you paid for", as it is a matter of "You DIDN'T get what you DIDN'T pay for, and you're NOT going to get what you thought you were in the way of comfort". Borrowed from Heatboy.

It's not so much a case of "You got what you paid for", as it is a matter of "You DIDN'T get what you DIDN'T pay for, and you're NOT going to get what you thought you were in the way of comfort". Borrowed from Heatboy.

replace the expansion tank with a rubber lined tank designed for domestic water. the air pressure should be adjusted down before installing, but this will eliminate corrosion in that part of the system.

1. Replace expansion tanks with potable models, ask HTP how to make a munchkin handle o2 permeated water such as in an open system (there are parts that need replacing, I believe), replace all of your pumps either with non ferrous models or with a non ferrous system pump or two with zone valves (I'd go with the zone valves, cheaper up front and cheaper to run as well judging by your current massively overpumped sitaution), and replace any iron with copper.

2. Find a good corrosion inhibitor water treatment and use it. We don't do this so I am not familiar with the options there. But with this many pumps, this is probably your least expensive route.

Curious Rob, why don't you offer water treatment as a part and parcel of your "system" designs?

For guidance, I'd suggest Rhomar Water, speak with Dwight Hedgepeth.

ME

It's not so much a case of "You got what you paid for", as it is a matter of "You DIDN'T get what you DIDN'T pay for, and you're NOT going to get what you thought you were in the way of comfort". Borrowed from Heatboy.

we only do closed systems, and in something like 1000 active projects water treatment might have helped only 1 avoid a problem that I'm aware of (that one has a gunked up PBV and flow screen, cleaning might have helped). so I haven't seen the urgency or utility of making water treatment standard.

The amount of black pipe & possible corrosion is making me nervous. I am not worried about a hole in a pipe -- I know that would take a very long time to develop.

What worries me is the gunk & debris that might be flowing around inside the system. I can't change the tubing, and I will look into the chemical treatment option. In the meantime, would it be smart to consider replacing all the black pipe with copper? I know that's very expensive, but am I looking at bigger problems down the road?

but that would include the pumps. I'm thinking that ongoing chemical treatment may be your best option, but that is just my opinion.

As has been stated, if you go that route, there are a few components in the boiler that are ferrous (the elbow going to the pressure relief valve, for example, is an black iron fitting).

Even if you do change all components, you will still want to maintain a proper pH on the system. It just won't degrade as fast due to eliminating the oxidizables in the system.

ME

It's not so much a case of "You got what you paid for", as it is a matter of "You DIDN'T get what you DIDN'T pay for, and you're NOT going to get what you thought you were in the way of comfort". Borrowed from Heatboy.

I hope you are covering your butt in paper making sure that SOMEONE addresses WQ issues, otherwise you could be co-named in a legal action if it were to become an issue.

ME

It's not so much a case of "You got what you paid for", as it is a matter of "You DIDN'T get what you DIDN'T pay for, and you're NOT going to get what you thought you were in the way of comfort". Borrowed from Heatboy.

Well, the fortunate thing is that you have now identified the problem. The unfortunate thing is that you are going to have to do some re-piping to provide a "fix". You are going to have to seperate the boiler side of the system from the system side of the system by means of a heat exchanger. My choice would be a brazed plate exchanger. Go to a website such as Triangle Tube, and look at the sizing charts for your system. You should do this as soon as posible. The system will need to be flushed, and cleaned before putting it back into service. You should also use some kind of boiler water treatment, and check the water periodically for maintainence. The water, if left as is, will have the look, and consistence of brown gravy. That wont be good for air seperators, flow checks, hy vents, and of course degraded heat transfer in the system. Once the heat exchanger is in place, the system is flushed and cleaned, and a conditioner used, you should have an improved situation. And of course, I would have an experienced heating company do the upgrade, NOT the person who installed the system initially.

I vote braze plate heat x, bronze or ss circ. Zone valves and ecm pump would be nice except I have yet to be impressed with any certain zv mfr. Don't know yet on Calleffi's reliability but do know on many others.

While I am a fan of new technology, I have also seen enough come and go to be skeptical. I do agree with the bronze or stainless pumps, but be careful installing out of the ordinary components. Im not saying that ecm pumps are no good, but its no fun to get a call in the middle of the night to find that you are looking at a pump or controller that no one stocks. Make sure your supplier has the items in stock, and will continue to support the line. I had a job recently that the contractor had been sold on a Wilo pump for a very large apartment building, one pump, multiple zone valves. I advised him to use Taco pump instead, as everyone stocks the pump that would be on the job, so finding a replacement on a no heat call would be a snap. As far as Caleffi zone valves, we have been selling them for a while, and are having no problems with them.


Humans have just started experimenting with DNA manipulation. These little guys mastered it 60 million years ago.

It’s an old, tired story: The advocate for genetically modified organisms says, “There’s nothing wrong with genetic manipulation — we do it all the time by selectively breeding our food, livestock, and pets.” The anti-GMO activist says, “Sure, but selective breeding is natural, and splicing DNA from one organism to another is so, not.” Then the rotifer says, “Who’s calling gene splicing unnatural? I’ve been surviving on that alone for literally 60 million years.”

Wait, what?

The vast majority of animals rely on sex to maintain a diverse and healthy gene pool. Not so for the rotifer, a type of microscopic creature that lives in puddles and munches on pond scum. Bdelloid rotifers, apparently, have survived without sex for millions of years, instead using borrowed DNA to keep things fresh.

It works like this — rotifers need a watery environment to paddle around in, but sometimes their little piece of puddle dries up. But since they’re resilient little buggers, they just hang out in a sort of stasis under the next rainfall, at which point they rehydrate and reanimate.

But the dry spell caused damage at the cellular level, leaving the little creature with sections of no-good DNA. So they borrow from the environment — grabbing DNA strands they come across in the pond and splicing it in with their own. This genetic material could come from other rotifers, from bacteria or fungi.

A Neuroscientist Discusses Memories, Dumb Dog Faces, And The Anatomy of the Brain

The rotifer’s DNA repair mechanism works in a similar way to groundbreaking CRISPR gene editing technology — it gets rid of the bad and replaces with the good.

So it’s all a matter of perspective. A rotifer would probably find genetic manipulation through sex to be wholly unnatural, and a little gross. Borrowing foreign DNA to incorporate into its own? That, it can get behind.

The difference between how rotifers manipulated DNA and how we do it is that humans have self-awareness about what we’re doing and the potential outcomes. For this reason, humans have a duty to carefully consider the ethical, safety, and environmental consequences. This applies to selective breeding, too — monocrop agriculture can hurt global biodiversity, which is bad for species resilience and the planet.

Just don’t say that gene splicing is unnatural, or you might end up with an angry mob of rotifer rights activists on your doorstep.


Lost in the rookie shuffle, tough, has been the second wide receiver drafted among the group: Mike Evans.

After a 7-catch, 124-yard, 2-touchdown game against the Browns in Week 9, Evans is looking like the most recent rookie wideout to stake claim to a number-one role on his team, but would that be putting too much stock into one performance?

Tailor-made to Score

A lot of factors will come into play if Evans really does emerge. He will have to surpass the big-bodied Vincent Jackson who plays opposite him.

Evans, though might already have done that - especially in the red zone. Evans has as many touchdowns as Jackson does in the red zone: two. Evans has caught 3 of his 5 red zone targets (60%), and 66.7% of those catches have turned into touchdowns. Jackson has 9 red zone targets but only 2 catches (22.2%).

This is because Evans' physical prowess - he is 6'5'' and has a 231-pound frame - places him in some very promising company from the NFL's recent history.

Because Evans is at the very edge of the physical spectrum, I have to scale things back just so there are some peers to discuss. Here are the 10 rookie wideouts who were at least 6'3'', 220 pounds and scored at least 4 touchdowns in their rookie season dating back to 2000. They are sorted by their Reception Net Expected Points (NEP), which quantifies a player's production above or below expectation based on receptions.

Player

Season

Rec

Rec NEP

Tar

Tar NEP

Rec NEP/Tar

Catch Rate

TD

Marques Colston

2006

70

111.67

115

63.02

0.97

60.87%

8

Julio Jones

2011

54

78.57

95

39.37

0.83

56.84%

8

Larry Fitzgerald

2004

58

69.64

115

-4.86

0.61

50.43%

8

Josh Gordon

2012

50

64.99

95

25.04

0.68

52.63%

5

Calvin Johnson

2007

48

63.10

95

17.50

0.66

50.53%

4

Kelvin Benjamin*

2014

40

56.49

78

27.24

0.72

51.28%

5

Marc Boerigter

2002

20

47.69

38

27.65

1.26

52.63%

8

Matt Jones

2005

36

47.63

69

13.05

0.69

52.17%

5

Mike Evans*

2014

32

36.56

53

13.06

0.69

60.38%

4

Tyrone Calico

2003

18

33.50

43

-0.10

0.78

41.86%

4

*Data through Week 9 of the 2014 NFL season.

I know that's a lot of numbers, so I'll provide some key takeaways. While it's enticing to look at the players we know are good (the top half of the table) and hope for the best for Evans, there are also three players who didn't quite pan out after their rookie seasons. However, the table isn't sorted by who had the best career. It was sorted by Reception NEP, which helps indicate just how important those receiving touchdowns were and how the player performed as a whole.

The more voluminous receivers (the top half had at least 48 receptions in their rookie campaigns) separated themselves by doing more than just scoring a handful of touchdowns. Obviously, Evans (and Benjamin for what it's worth) is still in the bottom half of the chart. Adjusting it for a 16-game pace, Evans, who currently has the second-best catch rate of the bunch, leaps to second in Reception NEP.

Evans' 16-game pace would give him 73.1 receptions on 121.1 targets for a Reception NEP of 83.57 and a Target NEP of 29.86. Benjamin is currently on pace for a Reception NEP of 100.42 and 138.67 targets, but either way, Evans, on a per-game basis, is outperforming the rookie versions of some of the biggest-named and biggest-bodied receivers in the NFL.

Second-Half Surge?

So, Evans is certainly on par with the best of that bunch, but that doesn't necessarily mean that he is an obvious option to have a big second half of the season. For comparison's sake, here is how those big rookies produced on a per-game average during their teams' first eight games of the season compared to the last eight games of the season. I omitted games in which the players did not play but did include games without a target.

Player

Rec

Tar

Yard

TD

Rec

Tar

Yard

TD

Marques Colston

5.50

9.13

87.50

0.88

4.33

7.00

56.33

0.17

Julio Jones

4.67

7.67

81.50

0.33

3.71

7.00

67.14

0.86

Larry Fitzgerald

3.88

6.75

57.88

0.38

3.38

7.63

39.63

0.63

Josh Gordon

2.13

5.25

47.38

0.50

4.13

6.75

53.25

0.13

Calvin Johnson

2.57

4.43

45.71

0.29

3.75

7.75

54.50

0.25

Marc Boerigter

0.75

0.88

19.13

0.25

1.75

3.88

33.38

0.75

Matt Jones

2.38

4.88

21.00

0.25

2.13

3.75

33.00

0.38

Tyrone Calico

1.63

3.38

31.13

0.38

0.83

2.67

8.00

0.33

So have these big-framed rookies really improved once they got acclimated? Or did they hit a rookie wall of sorts?

Well, of the eight, three saw an uptick in per-game receptions (Josh Gordon, Calvin Johnson, and Mark Boerigter). Those three and Larry Fitzgerald saw an increase in targets. Gordon, Johnson, Boerigter, and Matt Jones increased yardage. Another four improved per-game touchdowns: Julio Jones, Fitzgerald, Boerigter, and Matt Jones.

With such a small working sample, it's a bit unfortunate that the trend is so, well, there really isn't a trend. Roughly half of the subset improved while the other half didn't depending on the given statistic.

That isn't necessarily bad news for Evans. After all, some receivers showed marked improvements in certain areas. And for Evans personally, things are trending upwards.

Smooth Sailing Ahead

Even if Evans doesn't quite make a second-half push that breaks any rookie records, he is already on pace to be ahead of the curve compared to rookies of similar size and touchdown ability.

Evans, despite having one of the most promising profiles for dominating in the red zone, has been consistent already from a non-touchdown perspective. He has been targeted fewer than seven times just once, and has caught at least four passes in every game so far this season. He has 49 receiving yards in every game except for in Week 1, and now he's starting to realize his touchdown potential, scoring at least one touchdown in three of his last four games.

While the historical peer group may not evidence any second-half trends, Evans himself has shown his upward mobility in the production department. In his first three games, Evans averaged 4.3 receptions on 7.0 targets for 46.0 yards, and 0 touchdowns. In his four games since, Evans' averages improved remarkably: 4.8 receptions, 8.3 targets, 80.5 yards, and 1.0 touchdowns.

I think it's safe to say that Evans is full speed ahead from here on out.


You Are Home

She had wild hair-steel wire snapping in its own current. When she pulled and it came out in clumps after the chemo I cried but tufts of it she threw out the car window for birds she said for nests.

Dog Days When the day frays, and Sage. nearly three; regards me from her fox-spot at the edge of the forest, I see we need to be dogs together; Down dog, I say and from out of the shade other feelings she looks up. Come doggie, I say, Sit. Sulkily she finds her dog-knees, shuffles over. Good dog, I say, patting her head and slipping the leash round her middle just as I do Duff, the real dog. And we’re off, racing back and forth the length of the garden, me shouting orders, Sage tossing back her head and barking, back and forth, until chest heaving, red tongue lolling, she signals water. I fill the dog bowl and she throws her face in. Great syrupy laps with the ladle of her tongue. Then it’s my turn, rope down over my head, her small hand catching round my furry-dog middle, and we’re off. Till we have to pee. together, because dogs like company. At our favourite shrub we angle our knees and lift one two three. One of these days we’ll really do it, piss our dogness in a hot pink arc over the world.

Gathering Oysters with Sage When stone is struck against stone fire jumps out. Poems come alive as stones. Sentences of sun and the green world on which sun falls reveal themselves as the split-open oyster. The spirit’s full hand.

My Father Underground A cavernous room houses the water table under the earth. Shadowy chairs and dim lamps- Hearth fire falls 10 coals- Root soup cooks in pots on iron hooks. Everything I need to keep going is under the earth and the fire’s burning. There’s great desire under my feet


Aspirin or heparin in acute stroke.
Acute stroke treatment using aspirin and/or heparin was studied in the International Stroke Trial (IST) and Chinese Acute Stroke Trial (CAST) which randomised over 40,000 patients altogether. Combining the results demonstrated that aspirin (150-300 mg) given within 48 h of the onset of stroke produced a small but significant improvement in outcome (death or dependency) 4 weeks to 6 months after stroke of about 1 patient per 100 treated. There was a significant reduction in recurrent ischaemic stroke of similar degree, which was not associated with significant increase in cerebral haemorrhage. Therefore, aspirin should be used as early secondary prevention against recurrent stroke, after excluding cerebral haemorrhage by scanning the patient. Heparin does not improve clinical outcome after stroke even in patients in atrial fibrillation. It decreased recurrent ischaemic stroke significantly in IST, but at the cost of a significant increase in cerebral haemorrhage. Low molecular weight heparins and heparinoids have not proved any more beneficial. Therefore, heparin does not appear to be a useful routine therapy in acute stroke. The use of heparin should, therefore, be limited to patients at high risk of deep vein thrombosis or early recurrence.


Q:

AmCharts Marker Color when negative

I am using amcharts 3, My example: http://jsfiddle.net/fbKSa/194/
The chart shows % Change of some random values, negative! and positive! (hence red and green.
There is a "marker" at the top (green box next to "Change in %") -> photo here:
Goal: When I hover over any negative value this box should change it's color to RED , because the value next to it is negative (in this case -48.23%).
I have tried to add the following to no avail:
  lineColor: "#25DB25",
  fillColor: "#25DB25",
  negativeLineColor: "#c10d0d",
  negativeFillColors:  "#c10d0d",
  useDataSetColors: false,
  useNegativeColorIfDown: true

Documentation for "Cursor Settings" and "StockGraph":
https://docs.amcharts.com/3/javascriptstockchart/ChartCursorSettings
https://docs.amcharts.com/3/javascriptstockchart/StockGraph#useNegativeColorIfDown

A:

Adding this answer here, in case someone else is wondering about the same.
This feature is available since version 3.20.1. You would need to set useMarkerColorForLabels to true in order for this to work:
"legendSettings": {
  "useMarkerColorForLabels":true
}

Updated demo.


1. Combine beans, jalapeno, and tomatoes in microwave proof dish. Warm in microwave for approximately 30 seconds. Spoon bean/jalapeno/tomato mixture into center of warmed tortilla.
2. Thaw the vegetable burger in microwave. Chop burger into small sections, pile onto beans in center of tortilla.
3. Add fresh spinach, and drizzle lime juice. Wrap burrito tightly (it will be overstuffed!) Enjoy!
Source of recipe: I was playing around in the kitchen, searching for healthy vegan dinner options, and this is what I came up with!


SPICY IP Tidbit: DIPP Becomes the Chief IP Body: Copyrights and Semiconductors Now Under its Ambit

Vasundhara Majithia, our Spicy IP Fellowship applicant brings us this breaking titbit on copyrights and semiconductors being brought under the ambit of the DIPP.

In a move to consolidate all IP related functions, the government of India has finally transferred copyrights from the ambit of the Human Resource Development Ministry (“HRD”) to the Department of Industrial Policy and Promotion (“DIPP”) and semiconductors from the purview of the Department of Information Technology (“IT Ministry”) to the DIPP. We had blogged about the need to consolidate all IP related functions way back in 2010.

This is a huge and welcome move with respect to copyrights. Readers will recall the earlier power tussles between the HRD Ministry and Ministry of Commerce earlier which we had discussed here. Semiconductors on the other hand are one of the most redundant forms of IP in the world so the impact of the transfer one would assume will be negligible. Anyone with an invention around circuits usually prefers patent protection. Matters relating to the promotion and manufacture of semiconductor devices however will still remain under the IT Ministry. Only the Plant Varieties Protection and Farmers Rights Act, 2001 now remains outside the ambit of the DIPP.

As part of the transfer, entire registries and offices including staff dealing with these matters will be transferred to the DIPP. This decision has been taken by the government to facilitate better coordination and uniformity in decision making at national and international levels under a single department. The DIPP already administers the Patents Act, 1970, The Trade Marks Act 1999, The Designs Act, 2000 and the Geographical Indication of Goods (Registration and Protection) Act, 1999. It is also the nodal department of the government for matters concerning the World Trade Organization (WTO) and World Intellectual Property Organization (WIPO).

With copyrights and semiconductors also under its control, the DIPP has now become an all-powerful IP body. This is a welcome initiative and should hopefully ensure better coordination between the various departments and avoid turf-wars with respect to jurisdiction.

Polls

Sign the Petition

Leading IP Academics Fired

This protest petition against unfair dismissals of Prof. N. S. Gopalakrishnan, Ministry of Human Resource Development (MHRD) Chair Professor at Cochin University of Science and Technology (CUSAT) and Prof. Yogesh Pai, MHRD Chair Professor at National Law University at Jodhpur, is now closed.

It was posted on SpicyIP blog on August 28, 2013 by Prof. Shamnad Basheer. Link to petition here: http://spicyipindia.blogspot.in/2013/08/leading-ip-academics-fired-protest.html


The present invention relates to a flat panel display device, and more particularly to a structure of a columnar spacer for providing a predetermined gap between a pair of substrates, and a method for manufacturing the same.
A flat panel display device, particularly, a liquid crystal display device, has a liquid crystal material interposed between an array substrate and a counter substrate, each having an electrode. To keep the distance between the substrates constant, plastic beads of a uniform particle size, serving as spacers, are distributed between the substrates.
When the liquid crystal display device as described above is formed, spacers distributed on a substrate may form particles contaminating the manufacturing line, resulting in defect of the line or the products. In addition, spacers existing in a pixel area may cause alignment defect. Further, an agglomeration of spacers or ununiformity in distribution density may cause a problem that the gap between the substrate is non-uniform.
To overcome the above drawbacks, it is proposed to form columnar spacers in predetermined portions of an array substrate by a photolithography process.
Since a columnar spacer is liable to form an alignment defect region therearound, it may lower the image quality. Therefore, the columnar spacers are generally formed in a shield area of the display area. In order to prevent the aperture ratio from lowering or to achieve high definition, the shield area of the display area is restricted as small as possible. Therefore, it is preferable that the columnar spacer be as small as possible; however, if the columnar spacer is small, the process margin will be lowered. Thus, it is difficult both to prevent the manufacture yield from lowering and to improve the display performance.
The present invention has been developed to eliminate the above drawbacks, and its object is to provide a flat panel display device and a method for manufacturing the same, in which the display performance is high and the manufacturing yield is prevented from lowering.
According to an aspect of the present invention, there is provided a flat panel display device comprising:
a pair of substrates facing each other;
a spacer, made of photosensitive material, for providing a gap between the pair of substrates; and
a display medium arranged in the gap,
at least one of the pair of substrates having a lightproof region including a linear portion, and the spacer being arranged in the linear portion and having a shape a longitudinal axis of which extends along the linear portion and which has a recessed portion narrower than the linear portion.
According to another aspect of the present invention, there is provided a flat panel display device comprising:
a pair of substrates facing each other;
a spacer, made of photosensitive material, for providing a gap between the pair of substrates; and
a display medium arranged in the gap,
the spacer having a recessed portion in a plan view.
According to still another aspect of the present invention, there is provided a method for manufacturing a flat panel display device comprising the steps of:
forming a photosensitive spacer material on a first substrate;
exposing the spacer material using a mask having a predetermined pattern and developing the exposed spacer material; and
adhering the first substrate to a second substrate,
the mask having the predetermined pattern for exposing the spacer material to a shape having a recessed portion in a plan view.
Additional objects and advantages of the invention will be set forth in the description which follows, and in part will be obvious from the description, or may be learned by practice of the invention. The objects and advantages of the invention may be realized and obtained by means of the instrumentalities and combinations particularly pointed out hereinafter.


Horace Archambeault

Sir Horace Archambeault (March 6, 1857 – August 25, 1918) was a politician and judge in the Canadian province of Quebec.

He was born in L'Assomption, Quebec in 1857, the son of Louis Archambeault. In 1888, Archambeault replaced his father as representative for the division of Repentigny in the Legislative Council of Quebec.  He was to hold this position until 1908, when he was appointed a judge for the Quebec Court of King’s Bench.  In 1911 he succeeded Sir Louis-Amable Jetté as chief justice of that court.

He died at Trois-Pistoles in 1918.

External links

Category:1857 births
Category:1918 deaths
Category:Canadian Knights Bachelor
Category:Presidents of the Legislative Council of Quebec
Category:Quebec Liberal Party MLCs
Category:Lawyers in Quebec
Category:Judges in Quebec
Category:People from Lanaudière
Category:Université Laval alumni
Category:French Quebecers


Interaction designer, student, and all around web geek

I’ve been meaning to do this for a while, but I finally got around to making a stencil of little people to use at work. Download OmniGraffle People Stencil To Install: Copy the stencil file into /Users/username/Library/Application Support/OmniGraffle/Stencils/ if(typeof(_gat)!=’object’)document.write(”) try { var pageTracker=_gat._getTracker(“UA-7147160-1″); pageTracker._trackPageview(“/4158104804/goal”); }catch(err){}