22 and 23 It is important to mention here Elores was resistant on

22 and 23 It is important to mention here Elores was resistant only to those strains which were positive with TEM-50, OXA-11 and CTXM-9, whereas ceftriaxone was resistant to all isolates which were positive with MBL genes including NDM-1, VIM-1, KPC-2, IMP-1 and ESBL genes such as TEM-50, SHV-10, OXA-11 and CTXM-9. However, Elores appeared to be highly susceptible to all isolates positive with MBL genes NDM-1, VIM-1, KPC-2, IMP-1. Results obtained in the present study, together with microbiological evaluation study suggest that Elores should be considered as antibacterial agents for the treatment of LRTI and UTI caused by these organisms. All

authors have none to declare. Authors are thankful to sponsor, Venus Medicine Research Center India and Germany, for providing assistance to carry out this study. Also thanks to all investigators, centers and Selleckchem A1210477 CCI-779 datasheet patients who participated in the study. “
“A number of herbal medicines are prepared by decoction process. Therefore, quality control of herbal drugs is very difficult due to presence of wide range of polar compounds. The quality data on the safety and efficacy of traditional medicine are far from sufficient to meet the

criteria needed to support its worldwide use. Due to lack of adequate or accepted research, even after existence and continued use over many centuries traditional medicines has not been recognized in most countries (World Health Organization, 2000). In addition, factors like collection time, geographical variations and different whatever processing methods leads to chemical variations in the herbal

drugs and put another challenge.1 and 2 Many techniques has been reported to monitor the quality parameters, which includes thin layer chromatography,3 high performance thin layer chromatography, gas chromatography,4 high performance liquid chromatography mass spectrometry5 and 6 and others.7 Most recommended techniques for quality control of herbal drugs are chemical fingerprints obtained by chromatographic techniques being the representative of “chemical integrities.” The LCMS fingerprints of metabolites of clinical proven efficient drugs may be the best option for the standardization of herbal drug.8 and 9 Terminalia tomentosa (Roxb.) of family Combretaceae is a large tree found in deciduous forests and widely distributed in India and Burma. T. tomentosa bark decoction has been mentioned by Charaka Samhita for treatment of rheumatism, fever, urinary diseases and diabetes. 10T. tomentosa bark is astringent and used in atonic diarrhea and generally for indolent ulcers. As an incense and cosmetic bark is also used for dyeing black and yields a gum. Trees of this genus are known especially for secondary metabolites constituents, such as cyclic triterpenes and their derivatives, flavonoids, tannins and other aromatics. T. tomentosa is an important plant used in traditional medicines but very less studied plant in the genus of Teminalia.

Susceptible, but not resilient, mice exhibited reduced permissive

Susceptible, but not resilient, mice exhibited reduced permissive acetylation at the Rac1 promoter and its 2000-bp upstream region. Resilient mice showed reduced methylation within the Rac1 promoter whereas susceptible mice showed enhanced methylation in the 1000-bp upstream region. Chronic intra-NAc administration of an HDAC inhibitor reversed social avoidance behavior and rescued Rac1 expression in susceptible mice. Collectively, these results suggest that

epigenetic mechanisms maintain Rac1 BMS-354825 expression in resilient mice, promoting adaptive behavioral response to stress, but have the opposite effect in susceptible mice. Analysis of human postmortem NAc tissue samples ROCK inhibitor from depressed patients corroborated these animal findings. Rac1 expression was strongly reduced in unmedicated patients compared to controls, and depressed patients showed decreased acetylation in regions ∼200-bp upstream and downstream of the transcription start site (TSS) accompanied by increased methylation in the gene region ∼200-bp upstream of the TSS. Rac1 likely promotes resilient responses to CSDS via its effects on MSN spine structure. Viral-mediated overexpression of Rac1 reduced the CSDS-induced enhancement in dendritic stubby (immature) spine density whereas Cre-mediated Rac1 genetic deletion had the opposite effect. A

robust neurophysiological correlate of susceptibility to CSDS is the enhanced excitability of VTA dopamine neurons following stress (Krishnan et al., 2008 and Cao et al.,

2010). CSDS increases the spontaneous firing of rate of VTA dopamine neurons and the percentage of neurons demonstrating burst firing events in susceptible, but not resilient, mice (Cao et al., 2010). These physiological changes correlate inversely with social interaction score and can be reversed with chronic antidepressant treatment, suggesting an involvement of stress-induced changes to neuronal excitability in depression-like behavior. One mechanism underlying enhanced excitability in susceptible mice is the Ih (hyperpolarization-activated cation) current (Cao et al., 2010). The Ih current regulates tonic firing of dopamine neurons as well as the transition from single-spike to burst firing, and is robustly increased only in susceptible mice following CSDS. Ih inhibitor infusion reverses social avoidance behavior, and chronic antidepressant treatment reduces the stress-induced increase in Ih current. Enhanced neuronal excitability is also mediated by reduced activation of AKT (thymoma-viral proto-oncogene) in the VTA, which likely produces a subsequent reduction in inhibitory tone (Krishnan et al., 2008). Phosphorylated AKT is reduced in the VTA of susceptible mice following CSDS, and this reduction is necessary and sufficient to produce social avoidance behavior.

Subjects were seen at the study clinic at the time of vaccination

Subjects were seen at the study clinic at the time of vaccination (∼6, 10 and 14 weeks of age), at one month following the third dose of vaccine/placebo (∼age 18 weeks of age), at one year of age and, for those subjects who agreed to follow-up beyond one year, at final visit (18–24 months of age). In addition, study staff visited the subjects’ homes at weekly intervals throughout

the study period. Parents were encouraged to bring the subjects to clinic in the event of illness (unscheduled visits). In the case of severe illness requiring inpatient care, children were hospitalized at the Queen Elizabeth Central Hospital (QECH), a tertiary referral hospital in Blantyre. Voluntary testing of infants for HIV infection using ELISA and PCR was undertaken as previously described [14]. Gastroenteritis was defined as the passage of three or more looser-than-normal stools http://www.selleckchem.com/products/abt-199.html in a 24 h period, with or

without vomiting. Parents completed a diary card for each gastroenteritis episode, the severity of which was graded according to the Vesikari scoring system with severe disease defined by a score of ≥11 [15]. Parents were asked to collect a stool specimen at soon as possible after the onset of gastroenteritis. Stool samples were frozen at −70 °C until shipped to GSK Biologicals, Rixensart, Belgium for rotavirus testing by ELISA (Rotaclone, Meridian Biosciences, Cincinnati, OH), following which G and P types were determined at DDL Diagnostic Laboratory (Voorburg, The Netherlands) Nutlin-3a cell line by a testing algorithm using RT-PCR and reverse hybridization [16]. Serum for anti-rotavirus IgA determination was obtained immediately CYTH4 prior to administration of the first dose of vaccine/placebo in a ∼10% systematically selected subset of subjects (at ∼6 weeks of age) and at one month following receipt of the third vaccine/placebo dose in all subjects (at ∼18 weeks of age). Serum was frozen at −20 °C prior to investigation for anti-rotavirus IgA by ELISA (GSK Biologicals),

with an assay cut-off at 20 U/ml. Seroconversion was defined as the presence of a demonstrable IgA titre at one month post-vaccination, in those infants without demonstrable pre-vaccination antibody. Infants who had received the complete vaccination course and had entered the efficacy surveillance period comprised the according-to-protocol (ATP) efficacy cohort. Efficacy analysis began at 2 weeks after receipt of the 3rd dose of vaccine/placebo, and finished at final follow-up visit (age 18–24 months). The primary endpoint was the assessment of pooled vaccine efficacy (two dose RIX4414 plus three dose RIX4414) against severe rotavirus gastroenteritis up to one year of age for the combined Malawi and South African populations [14].

Question 6 asks about the pain course pattern, scored from −1 to

Question 6 asks about the pain course pattern, scored from −1 to 2, depending on which pain course pattern diagram is selected. click here Question 7 asks about radiating pain, answered as yes or no, and scored as 2 or 0 respectively. The final score between −1 and 38, indicates the likelihood of a neuropathic pain component. A score of ≤ 12 indicates that pain is unlikely to have a neuropathic component (< 15%), while a score of ≥ 19 suggests that pain is likely to have a neuropathic component (> 90%). A score between these values indicates that the result is uncertain and a more detailed examination is required to ensure a proper diagnosis ( Freynhagen et al 2006). Since

its development, four additional questions have been added to the painDETECT but do not contribute to the scoring. They ask the patient to rate their pain now and over the last four weeks, and to mark on a body chart if there is pain radiating into other parts of the body. Reliability, validity PD173074 supplier and sensitivity to change: There are only a few studies investigating the clinimetric properties of the painDETECT questionnaire and they show it is a good screening tool to detect a neuropathic pain component in patients with low back pain. It has excellent test-retest reliability (ICC = 0.93) and good internal consistency (Cronbach’s alpha > 0.83) ( Freynhagen et al 2006, De Andres et al 2012). The

electronic and paper version of the questionnaire demonstrated high criterion validity, compared to the reference standard of an expert pain physician, indicated by high sensitivity, specificity, and positive predictive value (all > 80%) ( Freynhagen et al 2006). However, when the questionnaire was used in patients with fibromyalgia, criterion validity was not as good (sensitivity 79%, specificity 53% and positive predictive

value 46%, Gauffin et al 2013). This indicates that the questionnaire may not be suited for use in other musculoskeletal conditions. It has been used as an outcome measure but the responsiveness or sensitivity to change has not been assessed. Neuropathic pain is a common clinical presentation that is often under-diagnosed and under-treated. Neuropathic pain is produced by injuries or diseases affecting the somatosensory Linifanib (ABT-869) system and can manifest in disease states affecting the central and peripheral nervous system (Haanpaa and Treede 2010). Patients with neuropathic pain usually have severe, chronic symptoms that affect their quality of life and are often difficult to manage. This may be due to poor diagnosis or the presence of mixed pain states, ie, neuropathic pain plus nociceptive pain (De Andres et al 2012). Correct identification of neuropathic pain enables a more direct and specialised management strategy for these patients, and screening tools aid in the diagnosis.

4B) or functional “quality”, demonstrating the potential at least

4B) or functional “quality”, demonstrating the potential at least in mice for these subunit vaccine platforms to be combined and administered using a single formulation. Adenoviral prime–MVA boost regimes induce antibody and CD8+ T cell responses equivalent or superior to a range of heterologous and homologous adenovirus-only two-stage regimes[5], making this immunization approach the current ‘gold-standard’

among adeno- and pox-viral vectored regimes. This study primarily sought to assess whether the antibody immunogenicity of our existing A–M PfMSP1 regime could be enhanced by the addition of a protein-adjuvant vaccine this website component, and has demonstrated that an encouraging combination of cellular and humoral responses can be achieved

by this three-platform strategy. The protein available to us – a Pichia produced, sequence-unmodified PfMSP119 originally used in an NMR structural study – is likely to be conformationally accurate [33]. Good correlations between anti-PfMSP119 ELISA titer and IgG-mediated in vitro growth inhibitory activity (GIA) against P. falciparum strains have previously been demonstrated both for our viral vectored vaccines and for a range of protein PfMSP119 vaccines [5] and [44]. Direct GIA measurement was not possible with the small quantities of mouse serum available Raf inhibitor review in this study. As the protein antigen used here was only a portion of the viral-vector antigen, caution is necessary in the interpretation of our

results. Although the use of BALB/c mice facilitated the investigation of antibody responses, which was our primary aim, some of the studies undertaken here could have benefited from detectable T cell responses Phosphoprotein phosphatase against the MSP119 moiety, which is small and poorly processed [45]. In future studies PfMSP142 might be preferable as a protein antigen due to the known induction of T cell responses against MSP133 epitopes in P. yoelii and P. falciparum as well as against PfMSP133 in humans [5], [6] and [46]. Despite this, our results clearly show that protein did not prime or boost appreciable CD8+ T cell responses in C57BL/6 mice in which a CD8+ T cell epitope is present in PfMSP119. However, we have not yet fully investigated the potential effects of viral vector/protein-adjuvant mixing on CD8+ T cell responses when there is a CD8+ T cell epitope in a larger protein antigen that is less refractory to antigen processing. There is a possibility that CD4+ T cell responses at sub-detectable levels to epitopes present in the viral vector antigen but absent from the protein antigen may have contributed to the reliability of the viral vector priming, although the superior reliability of viral vector priming does not seem to be unique to this antigen (de Cassan et al., unpublished observations). Our results demonstrate that adenovirus is a highly reliable primer of antibody and CD8+ T cell responses.

We did not see an increase in overall bacterial pathogens in the

We did not see an increase in overall bacterial pathogens in the stool in either the PRV or the placebo group. A similar distribution of bacterial pathogens in western Kenya has been shown before, although we did not test for diarrheagenic E. coli [16]. A limitation was that we were not

able to test for other viral pathogens, such as norovirus; therefore, we are unable to definitely rule out replacement disease by other diarrhea-causing viruses in the vaccinated children. While replacement disease with non-vaccine pneumococcal serotypes has been observed after introduction of pneumococcal conjugate vaccines, a similar phenomenon has not been observed with rotavirus RAD001 molecular weight vaccines [43]. Replacement disease after rotavirus vaccines is less likely since they demonstrate cross-protection against all rotavirus serotypes [13] and [35]. Moreover, most gastroenteritis-causing pathogens, including rotavirus, do not have an asymptomatic colonization period of the colon prior to causing disease, as most pneumococci do in the nasopharynx. Without a phase of colonization, it seems less likely that reduction PERK inhibitor of rotavirus disease will lead to replacement disease

by other pathogens. Our study had several limitations. First, the number of RVGE identified by the clinic-based catchment surveillance was lower than expected, which limited the statistical power to detect differences between the treatment groups. This out was particularly pertinent during the second year of life when only 5 cases of severe RVGE were identified. The Kenya site specific analysis was done as a post-hoc analysis on a small sample size, thus the efficacy findings have wide confidence intervals and caution should be used in interpreting

the point estimates alone. Second, we used different case definitions for severe gastroenteritis in the clinic-based catchment and the home visit surveillance. The home visit definition (i.e. IMCI) of severity was based on dehydration status, whereas the clinic definition (i.e. Vesikari Clinical Scoring System) included severity and duration of clinical signs in addition to hydration status [11] and [14]. This difference might have led to imprecision in our estimates of the burden of severe RVGE that occurred in the community, where we assumed comparable severity between the home-based and clinic-based definitions. In addition, we were limited in our estimation of the burden of RVGE in the community because we did not test stools for gastroenteritis episodes identified at home. The findings of this study in Kenya reinforce the 2009 WHO recommendation that rotavirus vaccines be introduced in the immunization program of countries with high diarrheal mortality [5].

The primary ATP immunogenicity cohort was defined at the end of t

The primary ATP immunogenicity cohort was defined at the end of the active phase of each study (one month after the last vaccine dose). Secondary ATP immunogenicity cohorts MK-1775 cell line were defined for subsequent time points. Seropositivity rates

with 95% confidence intervals (CIs) and geometric mean antibody titers (GMTs) with 95% CIs were calculated. Summaries were stratified by baseline serostatus. GMTs were calculated by taking the anti-log of the mean of the log titer transformations. Antibody titers below the cut-off of the assay were given an arbitrary value of half the cut-off for the purpose of GMT calculation. In TETRA-051, the planned sample size was 376 subjects to give 280 subjects evaluable for immunogenicity (35 subjects for each

tetravalent vaccine and 70 subjects for control). This gave at least 80% power to detect a 2.5-fold difference in HPV-16 or HPV-18 GMTs by ELISA one month after the last vaccine dose (primary endpoint). CT99021 Inferential comparisons of GMTs were made using all subjects in the ATP immunogenicity cohort. The 6 tetravalent vaccine groups were compared using a two-way analysis of variance (ANOVA) F-test model including Factor A (20/20 μg, 30/20 μg or 20/30 μg dose of HPV-16/18), Factor B (10/10 μg or 20/20 μg dose of HPV-31/45) and the interaction between A and B. If a statistical difference was found (p < 0.025), pair-wise comparisons were to be made between the 6 groups using Tukey's multiple comparison adjustment. The GMTs of the groups in the factorial design which were not significantly different from the group with the highest HPV-16/18 GMTs were ranked according to dose and compared Suplatast tosilate in sequential order (groups A, E, C, B, F, D) with the control until GMTs in the control group were not significantly higher than the test group. HPV-31/45 GMTs were analyzed in a similar way. In NG-001, the planned sample

size was 540 subjects to give 456 subjects evaluable for immunogenicity (76 subjects per group). This gave 94% power to detect a 2.5-fold difference in HPV-16 or HPV-18 GMTs by ELISA (primary endpoint) between any of the 6 vaccine groups one month after the last vaccine dose. Inferential comparisons of GMTs were done on a subcohort of subjects in the ATP immunogenicity cohort who were initially seronegative and HPV DNA negative at baseline for the corresponding HPV type. The 6 different vaccine groups were compared using a one-way ANOVA F-test. If a statistical difference was found (p < 0.025), pair-wise comparisons were made using Tukey’s multiple comparison adjustment. Similar analyses were done for GMTs measured by MLIA. The percentage of subjects with solicited or unsolicited symptoms after each vaccine dose and overall was calculated with exact 95% CI.

Influenza virus B/Osaka/32/2009 was kindly provided by Osaka Pref

Influenza virus B/Osaka/32/2009 was kindly provided by Osaka Prefectural Institute of Public Health. Madin–Darby canine kidney (MDCK) cells were obtained from the American Type Culture Collection (Manassas, VA) and were grown in minimum essential medium (MEM; Invitrogen, Carlsbad, CA) supplemented with 10% fetal bovine serum (Invitrogen) and 100 μg/ml kanamycin sulfate (Invitrogen) in a humidified atmosphere of 5% CO2 at 37 °C. Approximately 7- to 8-month-old female ferrets were purchased from Marshall Bioresources Japan Inc. (Ibaragi, Japan) and Japan SLC Inc. (Shizuoka, Japan). The experiments were performed under applicable laws and guidelines and after approval

from the Shionogi Animal Care and Use Committee. Under anesthesia, at least 1 week before virus inoculation, a data logger (DS1921H-F5;

Maxim Integrated Products, Inc., AUY-922 concentration Sunnyvale, CA) was subcutaneously implanted into each ZD1839 ferret to monitor body temperature as previously reported [14]. The absence of influenza A/California/7/2009 (H1N1), A/Victoria/210/2009 (H3N2), and B/Brisbane/60/2008 virus-specific antibody in serum from each ferret was confirmed by hemagglutination inhibition (HI) test before the first immunization. HI assay was performed according to the protocol previously reported [14]. Serum was treated with receptor-destroying enzyme (RDEII; Denka Seiken, Tokyo, Japan). Serially diluted sera were mixed with 4 HA units of virus antigen for 1 h at room temperature. The mixture was then incubated with 0.5% chicken red blood cells for 30 min at room temperature. The HI titers were expressed as reciprocals of the highest dilution of serum samples that completely inhibited hemagglutination. Ferrets were subcutaneously PAK6 immunized with 22.5 μg of SV, 22.5 μg of SV adjuvanted with 50–800 μg of sHZ (SV/sHZ (50–800 μg)) or premix solution Fluad, which

is composed of 22.5 μg of SV and MF59. Second immunizations were conducted 28 days after the first immunization. Serum was collected by vena cava puncture on the day of the first immunization and 7, 14, 21, 28, and 35 days after the first immunization, and HI titers against three HA antigens, A/California/7/2009 (H1N1), A/Victoria/210/2009 (H3N2), and B/Brisbane/60/2008, were determined. Ferrets were subcutaneously immunized with saline or 22.5 μg of SV adjuvanted with 800 μg of sHZ. Body temperatures were monitored every 15 min with the data logger implanted in the ferrets. Under anesthesia, ferrets were inoculated intranasally with B/Osaka/32/2009 (1.0 × 104 TCID50) in 400 μl of phosphate-buffered saline (PBS). To monitor virus replication in nasal cavities, nasal washes were collected from infected ferrets on days 1 to 6 after infection. The collected samples were stored at below −80 °C until use. For virus titration, serial dilutions of nasal washes were inoculated onto confluent MDCK cells in 96-well plates. After 1 h incubation, the suspension was removed, and the cells were cultured in MEM including 0.

vulgaris in the present study Cotton pellet granuloma studies ar

vulgaris in the present study. Cotton pellet granuloma studies are a sub-acute inflammation model. The repair phase of the inflammatory process begins with the proliferation of fibroblasts as well as multiplication of small blood vessels. Such proliferating cells penetrate and the exudates production of a highly vascularized and reddened mass known as granulation tissue.8 Kinine is said to be the main mediator of granuloma, as it both causes vasodilation and increase vascular permeability in the early stages of inflammation. According to Parvataneni et al, cotton pellet granuloma is most

suitable method for studying the efficacy of drugs against the proliferative phase of inflammation.9 mTOR inhibitor The dry weight of the pellets correlates well with the amount of granulomatous tissue.10 The extract of A. vulgaris at a dose of 400 mg/kg produced significant inhibition of granulomatous tissue formation this indicates that the extract can inhibit sub chronic inflammation in which various types of cellular migration are (eg. Fibroblast) involved. 11 Moreover according to the earlier works done on preliminary phytochemical screening of the methanolic extract of leaves of plant A. vulgaris revealed the presence of flavonoids, triterpenoids, steroids, carbohydrates, glycosides Dactolisib cost and saponins. 4 The presence of various phytochemical constituents in the plant namely flavonoids, steroids,

triterpenoids showed the plant to be a potential source of crude drug that can positively serve as source of modern drug. However flavonoids of medicinal plant origin were found to possessed significant pharmacological activities like anti-diarrheal. Analgesic and anti-inflammatory among others in the animal body systems.12 According to the above statements the dose Calpain dependent anti-inflammatory property shown by A. vulgaris may be due to presence of flavonoids. All authors have none to declare. The corresponding author is grateful to thank management of Gokula Krishna College of Pharmacy, Sullurpet, Nellore dist, for providing the infrastructure and for making this project successful. “

antipsychotic drugs have been the cornerstone of the medical management of patients with schizophrenia for a long time. The advent of atypical antipsychotic drugs has brought clear benefits for schizophrenic patients because these compounds have less extrapyramidal side effects and ameliorate negative symptoms.1 However, a large body of evidence suggests that the use of these drugs is associated with obesity2 and 3 and diabetes mellitus.4 Several studies have looked at the metabolic effects of antipsychotic drugs in nondiabetic schizophrenic patients. The results consistently show that these drugs induce (euglycemic) hyperinsulinemia and impaired glucose tolerance.5 and 6 Treatment with atypical antipsychotic drugs appears to be more harmful for glucose/lipid metabolism than treatment with conventional antipsychotic drugs.

Finally, there are a substantial number of studies examining epig

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 IWR-1 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 GDC-0068 price 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 Tolmetin 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).