The primary outcome is the proportion of carers without depressive symptoms and the secondary outcomes include carer and care recipient physical function and activity, carer burden, health service usage, and care recipient falls. This is a well designed study investigating a potentially cost effective option to reduce carer depression and burden. PD98059 chemical structure Potential confounders may be if a large proportion of the carers recruited have high levels of depression on the Geriatric Depression Scale, they may

improve but not drop below the cut off score of 4; people with depression may find it difficult to engage in a home exercise program; and if the care recipient has moderate or severe dementia it may be difficult for them to undertake a structured exercise program. Despite these potential confounders, this is a significant

http://www.selleckchem.com/products/gsk1120212-jtp-74057.html study as it represents one of a handful of studies that addresses an urgent issue in the care and wellbeing of older people. “
“Summary of: Costa LCM, et al (2012) The prognosis of acute and persistent low-back pain: a meta-analysis. CMAJ 184. DOI:10.1503/maj.111271 [Prepared by Margreth Grotle and Kare Birger Hagen, CAP Editors.] Objective: To review the evidence of clinical course of pain and disability in patients with acute and persistent low-back pain, and to investigate whether pain and disability had similar courses. Data sources: MEDLINE, CINAHL and Embase databases were searched from 1950 to November, 2011. This search was supplemented by searching of reference

lists from eligible studies. Study selection: Inception cohort studies involving patients with acute (< 6 weeks) and persistent (≥ 6 weeks) low-back pain in which pain or disability outcomes were reported. Data extraction: Two reviewers extracted data and discrepancies 4-Aminobutyrate aminotransferase were resolved by consulting a third reviewer. Methodological quality was assessed using 5 criteria suggested by Altman (2001). A meta-analysis of pain and disability outcome data was conducted, in which pain and disability were modelled as a function of time. Data synthesis: Of 28 613 studies initially identified by the search, 43 studies (33 cohorts) with a total of 11 166 patients met the selection criteria. Data quality was insufficient in many of the studies; only 52% of the studies explicitly reported methods for assembling a representative sample, 73% had a follow-up of at least 80%, and 88% had a follow-up for at least one prognosis outcome at three months or longer. Based on the quantitative pooling of 24 cohorts and 4994 patients the variance-weighted mean pain score (0–100) was 52 (95% CI 48 to 57) at baseline, 23 (95% CI 21 to 25) at 6 weeks, 12 (95% CI 9 to 15) at 26 weeks, and 6 (95% CI 3 to 10) at 52 weeks after the onset of pain for cohorts with acute pain.

B01, KoKo.B02, KoKo.B05, KoKo.B06), three supernatants also recognized recombinant Hsp70 from MTb (KoKo.B03, KoKo.B04, KoKo.B08), 3 supernatants recognized bovine Hsc70 (KoKo.B04, KoKo.B07, KoKo.B08) and only one supernatant recognized recombinant Hsp70 from E. coli (KoKo.B03) ( Fig. 1B). Comparison of binding of the 8 MAP Hsp70 specific monoclonal antibodies in ELISA to the recombinant deletion Selleck Autophagy inhibitor mutant protein RBS70 (containing the N-terminal amino acids 1–359 of wild type MAP Hsp70) indicated that KoKo.B01, KoKo.B02 and KoKo.B06 recognize an epitope at the C-terminus

of Hsp70, which is not present in RBS70. The other five antibodies recognized epitopes in the N-terminal RBS70 mutant molecule ( Fig. 1C). All 8 antibodies reacting with recombinant MAP Hsp70 were tested for recognition of synthetic MAP Hsp70 peptides to identify linear epitopes. In a primary screening, three antibodies (KoKo.B01, KoKo.B02 and KoKo.B03) displayed reactivity to specific pools

of MAP Hsp70 peptides (data not shown). The other five monoclonal antibodies did not recognize linear peptide epitopes. Subsequent, fine mapping of the epitopes using the single peptides of the pools in a solid phase ELISA confirmed that KoKo.B01, KoKo.B02, KoKo.B03 recognized linear epitopes in MAP Hsp70. The antibodies KoKo.B01 (IgG1 isotype) and MEK inhibitor KoKo.B02 (IgG2b isotype) recognized the aminoacid sequence P595–603 (PDGAAAGGG) ( Fig. 2A and B), located in the C-terminal part of MAP Hsp70. The third antibody, KoKo.B03 (IgG2a isotype), recognized a conserved epitope in the N-terminus of the MAP Hsp70 protein with the apparent core region sequence P111–124 (ITDAVITVPAYFND) ( Fig. 2C). The specificity of the monoclonal antibodies KoKo.B01–03 in relation to homologous Hsp70 proteins was tested by Luminex multiplex immunoassay. The data indicated that Fossariinae KoKo.B01 (not shown) and KoKo.B02 recognize an epitope which is present and identical

in Hsp70 from MAP and MAA, but absent in Hsp70 from MB, MTb, and E. coli and bovine Hsc70 ( Fig. 3A). Finally, the data regarding KoKo.B03 indicate that conserved mycobacterial homologues (MB, MTb) are equally well recognized, while recognition of the E. coli homologue is at approximately 50% of that of the MAP epitope, while recognition of the bovine homologue is near background levels ( Fig. 3B). In cattle, Hsp70 specific antibody responses were detected 3 weeks post vaccination [9] (data not shown). In goats, Hsp70 specific antibody responses were detected 4 weeks post vaccination, remained stable between 4 and 12 weeks post vaccination and were not influenced by exposure to MAP ( Fig. 4A). The MAP Hsp70 antibody responses in unvaccinated goats remained at background levels during 12 weeks irrespective of exposure to MAP. Similar kinetics were observed using the ELISA with the RBS70 molecule (data not shown).

Women classified as off treatment ranged from a few months to many years after treatment. Future observational studies repeating measures of physical function before, during, and after treatment are needed to more accurately determine the expected pattern of change in physical function throughout the cancer trajectory. Another source of variation between studies was the specific testing protocol used. Submaximal and maximal exercise tests may be performed on either a cycle ergometer or a treadmill XL184 in vitro and may use a ramp or incremental protocol with a number of possibilities in length of test stage and workload increment per stage.

Values for VO2peak have been shown to be higher using a treadmill than cycle ergometer protocol in women diagnosed with breast cancer.31 Values for upper and lower extremity strength, such as grip strength, maximal contraction for leg press, or knee flexion/extension, may be reported as average of three trials or maximum value obtained. There was also variation in the protocols used for assessing muscular endurance and the chair stand test, which prevented click here pooling of the results together. This highlights the importance of reporting full details of

the testing protocol in order to determine whether comparisons can be made between studies. Overall, 56 (66%) studies included some measure of aerobic capacity, indicating recognition of the importance of this component of health-related physical fitness. The most common method of measurement used was the gold-standard, maximal, cardiopulmonary exercise test, followed by a submaximal Calpain exercise test terminated at a specified percentage of age-predicted heart rate reserve or maximal heart rate. Although formal, large-scale assessment of the safety of the cardiopulmonary exercise testing procedure in individuals with cancer has not been performed, it does appear to be relatively safe with appropriate screening and monitoring during the test.32 Submaximal exercise testing is considered

to be a safer option, and may not require medical supervision, but is not as accurate for quantifying VO2peak.11 Finally, walking tests (6MWT and 12MWT) were commonly reported. Research is needed to determine if the 12MWT is a more appropriate test for capturing physical function in women with breast cancer than the 6MWT. It may be that women diagnosed with breast cancer have greater physical capacity than individuals in cardiac and pulmonary rehabilitation where the 6MWT is commonly used, and therefore may experience a ceiling effect with the 6MWT.12 Grip strength was the most commonly used measure of strength in this review and has been recommended as an assessment of muscle function for oncology rehabilitation.

In the appropriate clinical scenario, a local caregiver directly contacted the interventional cardiologist at the PCI-capable hospital with the use of the CHap. Using the application, the care team

briefly presented the case and showed the electrocardiogram to the interventional cardiologist on call. (Fig. 2) Based on this interaction, both parties would then decide on the best management approach, which could include the activation of the catheterization laboratory for possible primary PCI or an elective inter-hospital transfer for subsequent observation PLX3397 concentration or non-emergent PCI. When activation of the catheterization laboratory was considered appropriate, the on-call interventionalist activated the catheterization laboratory by contacting a central number where an expediter mobilized the entire team, and coordinated the transfer in the AZD2014 in vivo cases initiated at other institutions. After implementation of the CHap, all interactions using the system were recorded, and there were no exclusions. The interactions regarding a possible ACS were archived and subsequently matched to our institution’s ongoing

database of catheterization laboratory activations. Matching involved date of intervention, timing of call, referral site, interventionalist involved, and interventional outcome. In addition, the accuracy of the matching details was confirmed against hospital admission and referral databases as well as quality databases at MedStar Washington Hospital Center and the MedStar Health Research Institute. CHap-generated activations were compared to those utilizing standard channels of activation over the same time period. Of note, although the use of CHap was widely encouraged, previously established channels

of activation persisted concomitantly and were more frequently used, especially during Bumetanide the initial months after deployment. Primary source documents for all events were obtained and used to adjudicate STEMI cases. Adjudications were performed by physicians unaware of the activation system utilized during a particular case. Quality measures pertaining to STEMI management and system performance were adjudicated by a centralized dedicated team not involved in the study. The institutional review boards of MedStar Washington Hospital Center and the MedStar Health Research Institute (Washington, DC) approved this study. Experienced staff at a dedicated data-coordinating center performed all clinical data collection, entry, and analysis. Data regarding baseline clinical and procedural data, together with post-procedure inpatient events, were obtained from hospital chart review. Electrocardiographic criteria defining a STEMI included the presence of at least 1 mm of ST-segment elevation in at least two contiguous leads, or the occurrence of a new left bundle branch block.

The vaccine, Rotavin-M1, manufactured by POLYVAC-Vietnam, was developed from a G1P [8] strain recovered in 2003 from a child hospitalized for the treatment of acute gastroenteritis

in Nha Trang city (KH0118-2003) [6]. The master and working seeds PS-341 supplier of this vaccine were produced under GLP conditions using qualified Vero cells and reagents at the US Centers for Disease Control and Prevention (CDC). Pilot vaccine lot, passage 48, was produced by one passage in Vero cells from the working seed, which was provided by the Japanese Polio Research Institute and approved for vaccine production by WHO. These cells have been used for oral poliomyelitis vaccine production at POLYVAC. The master virus seed for Rotavin-M1 was tested for porcine circovirus using real-time RT-PCR at the US CDC and appeared to be free of porcine circovirus DNA. The test for porcine circovirus in pilot vaccine lot was not done. The trials were planned in two stages, the first – a Phase 1 trial

for safety in adult volunteers of a high titer preparation of the vaccine (106.3 FFU/dose). When results of this trial were evaluated by the Data Safety and Monitoring Committee and the vaccine was deemed to be safe for further study in infants, a Phase 1 and 2 adaptive trial was conducted. This trial assessed the safety and immunogenicity of two different preparations of vaccine, one of low titer (106.0 FFU/dose) and buy SB431542 the second with high titer (106.3 FFU/dose) that was administered in either a 2 vs. 3 dose schedules to infants 6–12 weeks of age. A comparison group was included GBA3 of infants who received the lyophilized Rotarix™ vaccine, an established rotavirus vaccine of GSK that was licensed to be used in Vietnam. The study was conducted according to Good Clinical Practice and in accordance with the Declaration of

Helsinki, as amended in Somerset West, Republic of South Africa, in October 1996. The protocol and consent form was reviewed and approved by the Ethical and Scientific Committees of the National Institute of Hygiene and Epidemiology (NIHE) and of the Ministry of Health, Government of Vietnam, prior to initiating the study. The Phase 1 study was conducted in a Career Training School, Thanh Son district, Phu Tho province with a total of 29 healthy adult volunteers 18–49 years of age. Following receipt of informed consent, each of the volunteers was screened by a physician to ensure they were healthy with no active medical problems and asked to provide a blood specimen to test for blood counts and levels of blood urea nitrogen (BUN) and transaminase. The volunteers then each received 2 doses of the high titer vaccine, 106.3 focus-forming units [FFU], at 1-month interval. After administration of each dose of the vaccine, the volunteers were followed daily for 10 days for adverse events and for fecal sample collection. During the next 20 days, the volunteers were followed by phone to ensure they had no sequelae (e.g. diarrhea, vomiting and intussusception).

We then used the unpaired t-test to estimate the between-group difference. The significance level was set at p < 0.05. Analysis was according to the principle of intention-to-treat. Eighty participants were recruited to the study. The baseline characteristics are presented in Table 1. Forty participants were allocated to the experimental group and 40 to the control group. Figure 1 outlines the flow of participants AT13387 nmr through the trial and the reasons for loss to follow-up. A qualified, registered physiotherapist and a medical doctor with four years of experience in exercise

programs, supervised all exercise sessions. In addition, the physiotherapist received further training in the specific exercise program for this study. The study was conducted at three hospitals specialising in antenatal care, which were located in different

regions of Cali, Colombia (Hospital Cañaveralejo, Centro de Salud Siloe, and Centro de Salud Melendez), with a combined throughput of 1200 pregnant women per year. Three participants in the experimental group and three in the control learn more group withdrew from the study before the 3-month assessment. In all cases the withdrawals were due to reasons unrelated to the intervention. Experimental participants received on average 28.9 out of 36 (SD 3.2) sessions over the 3 months. No adverse events occurred during or after the exercise in any participant. Group data are presented in Table 2 and individual data in Table 3 (see eAddenda for Table 3). At 3 months, the supervised aerobic exercise program reduced depressive symptoms significantly more in the experimental group than the control group. The between-group difference in improvement Sodium butyrate was 4 points (95% CI 1 to 7) on the 20-point CES-D score. A recent systematic review of the effect of exercise on antenatal depression found a small number of observational studies linking regular physical activity to improved selfesteem and reduced symptoms of anxiety and depression during pregnancy (Shivakumar et al 2011). However, no randomised controlled trials were

identified by this review. Therefore, we believe this is the first randomised trial to assess the effect of a supervised aerobic exercise program on depressive symptoms in nulliparous pregnant women. Our study showed that three months of aerobic exercise reduces symptoms of depression in pregnant women. In our clinical experience, we consider that a reduction of 4 points on the CES-D resulting from this intervention is clinically important. However, no threshold has been established empirically for the amount of improvement in the CES-D score that pregnant women typically feel makes aerobic training worthwhile. Our estimate of the average effect of the training had some uncertainty, with a 95% CI ranging from 1 to 7 points.

PBMC were plated in duplicate wells at 0.4 million

per well on MultiScreen 96-well HPVDF filtration plates (MAIPS4510, Millipore) after coating overnight at 4 °C with 10 μg/mL of anti-IFNγ (1-D1K, Mabtech) and blocking with the supplemented medium described above. Cells were incubated (37 °C, 5% CO2) for 18–20 h with positive (phytohaemagglutinin 10 μg/mL, Sigma) or negative (supplemented medium) controls or peptide pools consisting of up to 32 peptides (each 20mers overlapping by 10, final concentration 10 μg/mL/peptide). Plates were developed using biotin–streptavidin–ALP (Mabtech) with the addition of a chromogenic substrate (BioRad). Spots were counted using an ELISPOT reader and associated software (both Autoimmun Diagnostika). Final counts were expressed as sfu/million selleck inhibitor PBMC after averaging duplicate well counts and subtracting background. For larger proteins, responses from multiple peptide pools were summed to give the response against the whole protein. Data analysis

was carried out using Microsoft Excel®, GraphPad Prism® and STATACorp STATA® with Kaplan-Meier analysis in SPSS®. A total of 34 volunteers passed screening and were enrolled into study groups 1–7 between April and November 2006. Volunteer demographics are shown in Table 1. Fifteen volunteers received learn more one vaccination each in the dose-escalation groups 1–5 (n = 3 per group). Nineteen volunteers

were enrolled into the prime-boost vaccination groups 6 (or ‘FFM’ receiving the vaccine sequence FP9-PP/FP9-PP/MVA-PP, n = 9) and 7 (‘MMF’, n = 10). Mephenoxalone Three volunteers subsequently withdrew (one from the FFM group due to a pre-existing condition not revealed at screening and two from the MMF group due to unforeseen changes to work and travel plans). All available data has been included in the analysis for these volunteers. Fifteen of the 16 volunteers completing the prime-boost vaccination study subsequently volunteered to enter the separate but linked challenge study. They were joined by six newly-recruited unvaccinated malaria-naïve challenge control volunteers. No serious adverse events (SAEs) occurred during the study. Of 717 adverse events (AEs) recorded during the entire vaccination phase, 577 (81%) were judged probably or definitely related to vaccination (termed ‘vaccine-related’ from here on). Of these, 562 (97%) were AEs anticipated from previous studies of these vaccine vectors about which volunteers were specifically asked at each visit (solicited AEs, Fig. 1). The majority of all AEs reported during the vaccination phase were mild, with only 1 (0.1%) graded severe and 8% moderate in severity. The severe AE was local swelling at the vaccine site.

Anal. calcd. for C21H20N2O4S: C 63.62, H 5.08, N 7.07. Found: C 63.56, H 5.03, N 6.98. 5-(4-Hydroxybenzylidene)-N-[2-(4-methoxyphenyl)-2-oxoethyl]-1,3-thiazolidine-2,4-dione (3f): Pale yellow solid, IR (KBr, cm−1): 3031, 1734, 1632, 1463, 1408, 1183, 633. 1H NMR (300 MHz,

DMSO-d6, δ ppm): 9.3 (s, 1H, OH), 7.7–8.2 (m, 8H, Ar), 8.1 (s, 1H, CH), 5.05 (s, 2H, CH2), 3.78 (s, 3H, OCH3). Anal. calcd. for C19H15NO5S: C 61.78, H 4.09, N 3.79. Found: C 61.88, H 3.97, N 3.66. 5-(4-Hydroxy-3-methoxybenzylidene)-N-[2-(4-methoxyphenyl) -2-oxoethyl]-1,3-thiazolidine-2,4-dione (3g): Pale yellow solid, IR (KBr, cm−1): 3012, 1732, 1638, 1465, 1408, 1194, 1189, 634. 1H NMR (300 MHz, DMSO-d6, δ ppm): 9.4 (s, 1H, OH), 7.5–8.1 Selleck NU7441 (m, 8H, Ar), 7.9 (s, 1H, CH), 4.9 (s, 2H, CH2), 3.54 (s, 6H, OCH3). Anal. calcd. for C20H17NO6S: C 60.14, H 4.29, N 3.51.

Found: C 60.02, H 4.17, N 3.44. 5-(3,4-Dimethoxybenzylidene)-N-[2-(4-methoxyphenyl)-2-oxoethyl]-1,3-thiazolidine-2,4-dione (3h): Pale yellow crystals, IR (KBr, cm−1): 3031, 1775, 1656, 1451, 1202, 1156, 645. 1H NMR (300 MHz, DMSO-d6, δ ppm): 7.65–8.2 SNS-032 nmr (m, 8H, Ar), 7.8 (s, 1H, CH), 5.3 (s, 2H, CH2), 3.72 (s, 9H, OCH3). Anal. calcd. for C21H19NO6S: C 61.01, H 4.63, N 3.39. Found: C 60.87, H 4.44, N 3.19. 5-(Benzylidene)-N-(4-nitrobenzyl)-1,3-thiazolidine-2,4-dione (4a): Beige colour solid, IR (KBr, cm−1):

3113, 1737, 1660, 1524, 1417, 692. 1H NMR (300 MHz, DMSO-d6, δ ppm): 7.2–8.1 (m, 9H, Ar), 8.04 (s, 1H, CH), 5.1 (s, 2H, CH2). Anal. calcd. for C17H12N2O4S: C 59.99, H 3.55, N 8.23. Found: C 59.78, H 3.46, N 8.11. 5-(4-Chlorobenzylidene)-N-(4-nitrobenzyl)-1,3-thiazolidine-2,4-dione (4b): Pale yellow crystals, IR (KBr, cm−1): 3034, 1735, 1680, 1545, 1282, 1401, 756, 697. 1H NMR (300 MHz, DMSO-d6, δ ppm): 7.5–8.3 (m, 8H, Ar), 7.98 (s, 1H, CH), 4.95 (s, 2H, CH2). MS (ESI, tuclazepam m/z):374 (M+). Anal. calcd. for C17H11ClN2O4S: C 54.48, H 2.96, N 7.47, O 17.08. Found: C 54.23, H 2.65, N 7.22, O 17.01. N-(4-Nitrobenzyl)-5-(4-nitrobenzylidene)-1,3-thiazolidine-2,4-dione (4c): Half-white crystals, IR (KBr, cm−1): 3028, 1698, 1632, 1538, 1505, 1431, 638. 1H NMR (300 MHz, DMSO-d6, δ ppm): 7.1–8.1 (m, 8H, Ar), 7.8 (s, 1H, CH), 4.85 (s, 2H, CH2). Anal. calcd. for C17H11N3O6S: C 52.99, H 2.88, N 10.9. Found: C 52.79, H 2.75, N 10.76. 5-(4-Methoxybenzylidene)-N-(4-nitrobenzyl)-1,3-thiazolidine-2,4-dione (4d): Half-white solid, IR (KBr, cm−1): 2841, 1737, 1683, 1506, 1407, 1184, 702.

The participating ABT-737 supplier centres were required to offer routine antenatal care and have facilities

to allow the conduct of a supervised exercise class. Participants in the experimental group were invited to participate in three 60-min exercise classes per week, starting between week 16 and 20 of gestation and continuing for 3 months. All subjects wore a heart-rate monitor during the training sessions to ensure that exercise intensity was moderate to vigorous (Ramírez-Vélez et al 2009, Ramírez-Vélez et al 2011b). Sessions consisted of walking (10 min), aerobic exercise (30 min), stretching (10 min), and relaxation (10 min). Aerobic activities were prescribed at moderate to vigorous intensity, aiming for 55–75% of maximal heart rate and adjusted according to ratings on the Borg scale (Borg, 1982). Adherence to the exercise program was encouraged by the physiotherapist

who supervised the exercise sessions. In order to maximise adherence to the training program, all sessions were: supervised by a physiotherapist and a physician, conducted in groups of three to five women, accompanied by music, Selleck MI-773 and performed in a spacious, airconditioned room. The control group received no exercise intervention, did not attend the exercise classes, and did not take part in a home exercise program. Both groups continued with their normal prenatal care (1 session per week for 3 months) and physical activity. One day before beginning the exercise program and immediately after the 3-month exercise period finished, all women were assessed for symptoms of depression using the Center

for Epidemiological Studies-Depression Scale (CES-D). The 20-item scale has adequate test-retest reliability, internal consistency, and concurrent validity (Wells et al ever 1987). Test-retest reliability over a one-month period on this sample was 0.79, suggesting some shortterm stability of depressive symptoms. A score of 16 on the CESD is considered the cut-point for depression (Radloff and Rae, 1979). We sought to detect a between-group difference in the change in the CES-D score of 4 points as we considered this a clinically important improvement in depressive symptoms. Assuming that the standard deviation in this score would be 6, similar to that observed in a similar sample of women during pregnancy (Carter et al 2000), a total sample size of 74 would provide 80% power to detect a difference of 4 points as statistically significant. We recruited additional participants to allow for withdrawals. Data were entered in an electronic database by investigators at the time of assessment. Random checks of data entry were performed and corrections made where possible by phoning participants for confirmation.

Finally, there are a substantial number of studies examining epigenetic mechanisms underlying resilience to

social stress but these are covered elsewhere in this issue and excellent recent reviews have been published (Wu et al., 2013, Griffiths and Hunter, 2014 and Nestler, 2014). Therefore, the impetus for this review is to highlight how mechanisms linked to either a passive or active coping strategy in the face of chronic psychosocial stress may underlie the pathogenesis of stress vulnerability and resiliency. The resident-intruder paradigm is an ethologically AP24534 order relevant animal model of social stress (Miczek, 1979) that has proven useful for identifying mechanisms mediating resilience or vulnerability to stress-related consequences (Wood et al., 2010, Wood et al., 2013a, Koolhaas et al., 2007, Krishnan et al., 2007 and Berube et al., 2013). This model is commonly employed using rodents (rats, mice, hamsters) or tree shrews and involves subjecting a

male “intruder” to aggressive threats from a larger, unfamiliar male “resident” by placing it in the resident’s home cage for a period consisting of anywhere from 5 to 60 min (Krishnan et al., 2007, Bhatnagar and Vining, 2003, Wood et al., 2010, Miczek, 1979, Sgoifo et al., 1996 and Buwalda et al., 1999). The acute response to social defeat (minutes to hours) results in robust sympathetic activation eliciting selleck screening library 30 times the number of arrhythmias as compared to other non-social experimental stressors such as foot shock or restraint (Sgoifo et al., 1999). Social stress also produces vagal withdrawal, increased blood pressure, elevated plasma catecholamines, hyperthermia, and increased activation of the hypothalamic–pituitary–adrenal axis (Wood et al., 2010, Sgoifo et al., 1999, Tornatzky and Miczek, 1994, Tornatzky and Miczek, 1993 and Bhatnagar isothipendyl et al., 2006). These acute physiologic stress responses are comparable to those reported in response to an experimental model

of psychosocial stress in humans. For example, the Trier Social Stress Test is designed to exploit the reactivity of the stress response to socially challenging situations in humans and produces robust activation of the HPA axis and the sympathetic nervous system (Hellhammer and Schubert, 2012 and Kirschbaum et al., 1993). In both humans and animals, these acute responses are adaptive in helping the individual cope with the stressor. However, if these stress responses are unabated in the face of chronic stress as may occur under conditions of inefficient stress coping, this can lead to pathological changes promoting psychiatric disorders such as depression, generalized anxiety and post-traumatic stress disorder. It is generally considered that two coping response patterns are distinguishable in response to social stress (Koolhaas et al., 1999). One is considered the active (or proactive) response and is characterized by territorial aggression and control, as was originally described by Walter Cannon (Cannon, 1915).