4C), amygdala (F(3–16) = 2 451;

The acute administration did not alter the mitochondrial complex II–III activity in the prefrontal cortex (F(3–16) = 0,759; p = 0,53 Fig. 4C), amygdala (F(3–16) = 2.451; Selleckchem Tenofovir p = 0.10 Fig. 4C) and hippocampus (F(3–16) = 1.519; p = 0,24 Fig. 4C). The chronic treatment increased the mitochondrial complex II-III activity in the prefrontal cortex (F(3–15) = 4.175; p = 0,03 Fig. 4C) and hippocampus (F(3–13) = 10.168; p = 0.001 Fig. 4C) with imipramine at the dose of 30 mg/kg and in the amygdala (F(3–14) = 10.512; p = 0.001 Fig. 4C) with all treatments, but did not alter in the prefrontal cortex (F(3–15) = 4.175; p > 0.05 Fig. 4C) and in the hippocampus

(F(3–13) = 10.168; p > 0.05 Fig. 4C). The acute administration increased Selisistat the mitochondrial complex IV activity in the hippocampus (F(3–13) = 18.471; p < 0,001 Fig. 4D) with all treatments, compared with saline, but did not alter in the prefrontal cortex (F(3–12) = 0.828; p = 0.50 Fig. 4D) and amygdala (F(3–11) = 4,514; p = 0,27 Fig. 4D). The chronic treatment did not alter the mitochondrial complex IV activity in the prefrontal cortex (F(3–13) = 0.689; p = 0.57 Fig. 4D), amygdala (F(3–16) = 3.666; p = 0.35 Fig. 4D) or hippocampus (F(3–11) = 2.317; p = 0.13 Fig. 4D). The acute treatment decreased the Bcl-2 protein levels in the

prefrontal cortex (F(3–12) = 106.818; p < 0,001 Fig. 5A) and in the hippocampus (F(3–12) = 265,226; p < 0,001 Fig. 5A) with imipramine at the dose of 30 mg/kg and lamotrigine at the dose of 20 mg/kg, and also in the amygdala (F(3–12) = 87.304; p < 0.001 Fig. 5A) with all treatments, compared with saline. The chronic treatment decreased the Bcl-2 protein levels in the prefrontal cortex (F(3–12) = 310.093; p < 0.001 Fig. 5A), amygdala (F(3–12) = 238.818; p < 0.001

Fig. 5A) and hippocampus (F(3–12) = 557.669; p < 0.001 Fig. 5A) with all treatments. The acute treatment Non-specific serine/threonine protein kinase increased the AKT protein levels in the prefrontal cortex (F(3–12) = 49.088; p = 0.000 Fig. 5B) with imipramine at the dose of 30 mg/kg, in the amygdala (F(3–12) = 70.335; p < 0.001 Fig. 5B) with lamotrigine at the dose of 20 mg/kg and in the hippocampus (F(3–12) = 21.011; p = 0.009 Fig. 5B), with imipramine at the dose of 30 mg/kg and with lamotrigine at the dose of 20 mg/kg, compared with saline. The acute treatment also decreased the AKT protein levels in the amygdala with imipramine at the dose of 30 mg/kg (F(3–12) = 70.335; p = 0.04 Fig. 5B) and in the hippocampus with lamotrigine at the dose of 10 mg/kg (F(3–12) = 21.011; p = 0.04 Fig. 5B). The chronic treatment increased the AKT protein levels in the prefrontal cortex (F(3–12) = 121.938; p < 0,001 Fig. 5B), amygdala (F(3–12) = 83.853; p < 0.001 Fig.

This finding suggests that most preterm infants are able to mount

This finding suggests that most preterm infants are able to mount a specific cellular immune response [24]. In the present study, the time of immune evaluation, three months after the booster dose, could be stated as a limitation. It is possible that the antibody titers

and numbers of circulating tetanus-specific T cells may have decayed from peak levels three months after vaccination. Antibody levels following a booster dose usually peak after 15 and 30 days. The antigen-specific IFN-producing cells most probably are found among circulating Peripheral blood mononuclear cells 1–2 weeks after vaccination very transiently, thereafter, they rapidly reach the lymph nodes and then decay with time [24], [25], [26] and [27]. With the increase in the survival rate of premature infants at progressively younger gestational ages and the growing use of therapeutic resources, Gefitinib premature infants currently exhibit different characteristics from those of past decades [28] and [29] and factors other than prematurity itself may learn more be involved in the immune response. Thus, apart from the direct comparison of antibody levels between groups, linear and logistic regression analyses were performed to control for variables that may affect the response to vaccination. It should be

pointed out that the same independent variables were incorporated into all multiple linear and logistic regression models, which DNA ligase contributes to the consistency of the findings. Breastfeeding for more than six months was associated with a 3.5 fold increase in the chance of having optimal protective antibody levels against tetanus at 15 months of age, and a 0.96 IU/mL (95% CI: 0.08–1.83) increase of antibody levels 3 months after the booster dose. However, given the significantly lower rates of breastfeeding in premature infants, the effect observed of breastfeeding could be a confounding of other factors (e.g. gestational age, affinity maturation, etc.) that could influence the antibody response levels in these infants. However, this effect has also been

described by Greenberg et al. [30], who found high levels of antibodies among children who received a conjugated vaccine against H. influenzae type b and tetanus toxoid and had been breastfed until at least six months of age. Jeppesen et al. [31] found a correlation between breastfeeding and the population of T CD8+ cells. It is suggested that breastfeeding contributes to the structural and functional development of the thymus and the control of the apoptosis of immature thymocytes, which subsequently transform into CD4+ T and CD8+ T cells [32]. The use of antenatal corticosteroids, nutritional status and erythrocyte transfusions were not associated with the humoral response to the tetanus vaccine at 15 and 18 months, which is in agreement with findings described in previous studies [5], [8], [9], [10] and [33].

, 1997 and Roozendaal et al , 2009) Stressors activate the HPA-a

, 1997 and Roozendaal et al., 2009). Stressors activate the HPA-axis through the release of corticotropin-releasing hormone (CRH) from the paraventricular nucleus (PVN) of the hypothalamus. When CRH reaches the anterior pituitary gland, it elicits adrenocorticotropic hormone (ACTH) release, which prompts glucocorticoid synthesis in the adrenal glands. Finally, glucocorticoids are released into the bloodstream where they travel and bind to receptors throughout the body and brain (McEwen et al., 1986,

de Kloet, 2004 and Sapolsky et al., 2000). Glucocorticoid release follows a slower time course than rapidly released catecholamines, peaking check details 10–20 min after the onset of stress exposure (Sapolsky et al., 2000). Glucocorticoids are often characterized as a recovery hormone that adapts an organism to the neurophysiological changes that occur during stress (Lupien et al., 2007). Collectively, these two systems interact and function in a complementary manner to mobilize energy and help an organism cope with stressful experiences. Despite the inability of peripheral catecholamines to cross the blood–brain barrier, noradrenaline is projected throughout

the brain by way of the locus coeruleus (LC). The LC serves as the brain’s primary source of noradrenaline and shares reciprocal connections with brain regions that are critical to the acquisition and regulation of conditioned fear, such find more as the amygdala, hippocampus and PFC (Benarroch, 2009). The high proportion of noradrenaline receptors in the amygdala and PFC render these brain regions found especially sensitive to the effects of stress (McEwen et al., 1986). Circulating glucocorticoids can influence brain function by readily crossing the blood–brain barrier and binding to high-affinity mineralocorticoid and low-affinity glucocorticoid receptors distributed throughout the amygdala, hippocampus and prefrontal cortex (Joels et al., 2012 and Lupien et al., 2007). The effects

of glucocorticoids include dampening glucose transport within cortical neurons and glia cells, which may further influence brain function by diminishing processing and amplifying the effects of early catecholamine release by slowing their clearance from synaptic space (Grundemann et al., 1998, Ferry et al., 1999 and Roozendaal et al., 2002). The release of glucocorticoids is controlled through negative feedback mechanisms housed within the PFC, suggesting that this region is targeted both for glucocorticoid binding under stress and for the regulation of glucocorticoid release (Diorio et al., 1993). Consistent with this, both chronic exposure to stress and affective psychopathology have been shown to be related to deficits in HPA regulation and inhibition (Cacioppo et al., 1998, Nyklicek et al., 2005 and Radley et al., 2006). Learning to respond appropriately to cues that signal danger is critical to survival and can facilitate adaptive behavior.

31 Oxygen therapy should be titrated to achieve oxyhaemoglobin sa

31 Oxygen therapy should be titrated to achieve oxyhaemoglobin saturation (SpO2) between 88 and 92%,31 and is usually administered via nasal prongs or a venturi mask. Oxygen can also be delivered using high flow nasal cannulae, which may better Everolimus ic50 meet the

inspiratory flow demands of severely dyspnoeic patients and is more tolerable than a face mask. Such systems can also provide humidification, which may be important to prevent sputum retention in patients with excess secretions; however, there is no evidence to guide practice in this area. Non-invasive ventilation is highly effective as a supportive therapy for people with AECOPD complicated by type-II respiratory failure. It unloads the respiratory muscles, restores acid-base balance and provides time for pharmaceutical therapies to be effective. A systematic review and meta-analysis showed that in patients with COPD and acute hypercapnic respiratory failure (PaCO2 > 45 mmHg, pH < 7.35), non-invasive ventilation reduced mortality compared to usual care

(RR 0.52, 95% CI 0.36 to 0.76) and reduced the need for intubation selleck chemicals (RR 0.41, 95% CI 0.33 to 0.53).32 There are also benefits for the health system, with reduced length of stay in those treated with non-invasive ventilation (MD – 3.24 days, 95% CI –4.41 to –2.06).32 Physiotherapists are frequently involved in the delivery of non-invasive ventilation, including assessment and referral of appropriate patients, establishing patients on treatment, titration of pressures, optimising patient

Tryptophan synthase tolerance and monitoring treatment effects.33 Non-invasive ventilation may assist in delivery of other physiotherapy treatments such as early mobilisation. In a group of hospitalised patients who were recovering from acute-on-chronic respiratory failure, most of whom had COPD, the use of non-invasive ventilation and oxygen during walking resulted in clinically significant improvements in walking distance, oxyhaemoglobin saturation and exercise-induced dyspnoea compared to walking on oxygen alone.34 Non-invasive ventilation also improved endurance time for unsupported upper limb exercise. These results were obtained from patients who were as early as 2 days into their hospital admission, using inspiratory positive airway pressure ranging from 15 to 18 cmH2O and expiratory positive airway pressure ranging from 4 to 5 cmH2O. Physiotherapists frequently use breathing exercises to relieve dyspnoea, improve thoraco-abdominal co-ordination and enhance functional capacity in people with acute exacerbations of COPD. Commonly used techniques include breathing control (also known as diaphragmatic or abdominal breathing) and pursed lip breathing (gentle exhalation through lips that are pressed together).

4) At experimental pH, Amlodipine besylate form strong 1:1 compl

4). At experimental pH, Amlodipine besylate form strong 1:1 complexes with Ca2+ ion. Absorbance differences at pH 1.2, 2.2, 6.4 and 7.4 were (Fig. 5, Fig. 6, Fig. 7 and Fig. 8) IWR-1 chemical structure indicated as “ˆ” shaped curves

and the break points were found at absorbance difference of 0.15, 0.16, 0.17 and 0.18 at pH 1.2, 2.2, 6.4 and 7.4 respectively. It confirmed the formation of 1:1 complexes of Amlodipine besylate with Ca (II) ion. Ardon’s plot confirmed the formation of 1:1 complex of Amlodipine besylate with Ca (II) ion at pH 1.2, 2.2, 6.4 and 7.4, since the method is valid for only 1:1 complexes. The Ardon’s plots gave straight lines intercept which are presented in Fig. 9, Fig. 10, Fig. 11 and Fig. 12 indicate the formation of 1:1 complexes at experimental pH. The value of stability constant check details for the complexation of Amlodipine besylate with Ca (II) ion at pH 1.2, 2.2, 6.4 and 7.4 were obtained from the spectral data using Ardon’s plot. The values of stability constant were given as [(Intercept)/(slope)] by using Ardon’s equation. The values of stability constants for the drug–metal system at pH 1.2, 2.2, 6.4 and 7.4 presented in Table 1 The in vitro determination of percentage of protein binding of Amlodipine besylate and their 1:1 mixture with Ca (II) ion was done by equilibrium dialysis method at physiological temperature (37 ± 0.5)°C and at pH 7.4. The observed values of protein

binding for drug alone and with metal are given in Fig. 13. The spectra of drug molecules alone and (1:1) mixture of drug and metal showed significant change in their absorption intensities. This may be due to interaction of Ca2+ with drug that may alter the absorption intensities but the position of the compound does not shift. Job’s plots showed, for a constant total concentration of drug and metal, the complex was at its greatest concentration at a point where the species of drug and metal are combined in the ratio in which they occur in complex. The straight lines which cross each other showed a break at nearly 5 mol fractions indicating the 1:1 complexes for all the systems. At experimental pH, Amlodipine besylate forms

strong 1:1 complexes with Ca2+ indicated as ‘ˆ’ shaped curves. These curves may indicate strong kinetics of complexation between Amlodipine besylate with else Ca2+. The stability constants obtained from the Ardon’s plot for Amlodipine–Ca2+ system was remain quite close at all pH systems except at pH 7.4. At pH 7.4 the stability constant was 0.11, higher than all other systems. So, we can conclude that a stable complex was formed at pH 7.4 i.e. in blood. In protein binding studies it was found that at a low drug concentration the percentage of protein binding attains a steady state plateau condition (84%). This indicated the saturation of the sites of protein by the drugs or its complexes as observed by other investigators.

“Figure options Download full-size image Download high-qua

“Figure options Download full-size image Download high-quality image (377 K) Download as PowerPoint slideIt is with great sorrow that I inform the Scientific Community of Cardiovascular Pathologists that Marcos A. Rossi, Professor of Pathology in Ribeirao Preto, Brazil, passed away prematurely due to acute myocardial infarction on May 9, 2013. He graduated at the Faculty of Medicine in Ribeirao Preto, which is under the rule of the University of Sao Paulo and where he did all his career: PhD in 1970,

Lecturer in 1977, Associate Professor in 1981, Full Professor (“Professor Titular”) in 1986 at the early age of 42. In 1971–72 he spent a Post-Doc period in the Department of Pathology at the Mount Sinai School of Medicine in New York, led by Prof. Hans Popper, the discoverer of liver architecture, where he learnt the technique of electron microscopy. BMS 354825 Back in Ribeirao, he set up a laboratory

of ultrastructure, then became an outstanding electron mycroscopist under the mentorship of Professor Fritz Koberle, an Austrian pathologist, colleague of Prof. Popper in Wien, who advanced the neurogenic theory of Chagas disease accounting for megaesophagus, megacolon and dilated cardiomyopathy. By the way this was the topic of Marcos Rossi’s Ph.D. thesis. www.selleckchem.com/products/cilengitide-emd-121974-nsc-707544.html The experience at the Mount Sinai in New York was a breakthrough for his career as experimental cardiovascular scientist in a developing country. Marcos Rossi was very productive

and wrote 261 full papers (and others in press) and 23 book chapters. His research has been consistently supported from Brazilian Agencies by nearly 60 grants. Worth to be mentioned are his contributions on Chagas cardiomyopathy, with special references on coronary microvasculopathy and PDK4 progression of Chagas myocarditis towards chronic dilated cardiomyopathy, on myocardial damage and subcellular events occurring during sepsis (a phenomenon which he called “septic cardiomyopathy”) and, more recently, on molecular mechanisms of cardiotoxicity by anthracycline. At the first International Symposium on Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D) in 1996, held in Paris, his group presented the pathology of Chagas cardiomyopathy, which may affect the right ventricle with aneurysms, thus mimicking ARVC/D. Later on, in 1997, I met him for the first time when he came to my Institute as Visiting Professor (March 24, 1997) and delivered a lecture on Chagas disease. He had the opportunity to see the famous Anatomical Theatre of Fabrici ab Acquapendente, built in 1594, an experience which fascinated him. On October 2010, he invited me to Sao Paulo at the Biennial Meeting of the International Academy of Pathology, where he was committed to organize a Symposium on Advances on Cardiovascular Pathology and gave me the task to cover the topic of Molecular Pathology of Sudden Cardiac Death.

To determine whether

PVM-specific memory CD8+ T-cells may

To determine whether

PVM-specific memory CD8+ T-cells may confer immune protection, mice were immunized with GM-CSF-expanded BM-DC loaded with synthetic P261–269 (DCp) and then challenged with PVM. As shown in Fig. 3A and B, numbers of P261–269-specific CD8+ T-cells detected in the BAL of immunized mice were substantially higher than in non-immunized controls (Fig. 3A and B). Over the duration of the infection, DCp-primed mice lost less weight (Fig. 3C), displayed significantly reduced total-cell influx in the BAL (Fig. 3D), viral loads were significantly lower than in non-immunized mice (Fig. 3E), and peribronchial and interstitial cellular infiltrates were reduced (Supplementary Fig. GW-572016 mw 2), indicating an enhanced control of disease and viral loads. Since vaccination with FI-PVM elicits an enhanced Th2 response upon PVM infection [40], we investigated the effect of DCp immunization on CD4 T-cell differentiation

during PVM challenge. Compared with FI-PVM-immunized controls, mice immunized with P261–269-loaded DC displayed elevated amounts of IFNγ mRNA and cytokine levels in the lungs following challenge, indicating that they had developed a Th1-skewed immune response (Fig. 4A and B; upper panels). In contrast, FI-PVM immunized mice developed a Th2-skewed response, as indicated by the relatively high levels of IL-4 in the lungs see more (Fig. 4A and B; lower panels) and eosinophilia in two out of four mice (Fig. 4C and D). Thus, the presence of memory CD8+ T-cells specific for a single PVM-epitope led to enhanced control of virus replication and prevented Th2 skewing of PVM-induced CD4 T-cell responses upon PVM challenge, leading to a reduction of PVM-induced disease. Since immunization with P261–269-loaded DC provided partial protection, we decided to assess the protective capacity of the total PVM-specific CD8+

T-cell response, targeting multiple epitopes. A mix of CD8+ T-cells enriched from the spleen, MLN and lungs of PVM-infected or uninfected mice were adoptively transferred into recipient mice that then were infected with PVM. At d. 7 p.i. a clear population of P261–269-tetramer+ over cells was detectable in the lungs of mice that had received CD8+ T-cells of PVM-infected donors, but not in the lungs of recipients that had received naïve CD8+ T-cells of uninfected controls (Fig. 5A and B). In addition, recipients receiving immune cells from infected mice showed significantly reduced weight-loss and viral load (Fig. 5C and D). These results show that PVM-specific CD8+ T-cells, despite being a major cause of pathology in pneumovirus infections, can provide protection against PVM infection. Despite the fact that hRSV is a major cause of disease in infants, there still are major gaps in our knowledge of the host response against this virus. There is an increasing interest in using the natural mouse pathogen PVM to mimic and study severe pneumovirus infections.

It is a lipophilic derivative and crosses to the brain It modifi

It is a lipophilic derivative and crosses to the brain. It modifies MES (maximal electroshock) and inhibits PTZ (pentylenetetrazole) induced clonic seizures.3 NBV is a relatively new highly cardioselective, β-adrenergic receptor antagonist not attributed to blockade of α1-adrenergic receptors selleck kinase inhibitor on smooth muscle cells. NBV has antioxidative effect and is a highly lipophilic drug. Patients with epilepsy may have impaired cognitive abilities and AED therapy may

contribute to this impairment. Such patients would therefore need additional treatment, beside AED therapy to correct the accompanying neurological disorder. There is no effective treatment of seizures in stroke and hence treatment needs to be initiated in the context of the patient. The presence of co morbid conditions and the use of other drugs also complicate antiepileptic therapy, and the risk of drug interactions is a particular hazard in elderly patients on multiple co medication. So, the present study was an attempt to evaluate the antiepileptic efficacy of a combination of drug with antihypertensives which can CB-839 mouse be effective when associated with risk factors especially cerebrovascular risk factors, stroke which might precipitate epilepsy. Male albino swiss strain mice weighing 18–30 g were procured

from the Central Animal House Facility, I.T.S Paramedical College, Ghaziabad, India (approval no – 1044/C/07/CPCSEA/27th Feb 2007). Animals were housed in groups of 5–6% and maintained at 20–30 °C and 50–55% humidity in a natural light and dark cycle, with free access to food and water. Utmost care was taken to ensure that animals were treated in the most humane and ethically acceptable manner. The drugs used were NBV (Nebicard, Torrent Pharmaceuticals, India), GBP (Gabapin, Intas Pharmaceuticals, India) and a chemoconvulsant PTZ (Sigma, USA). NBV and GBP were suspended too in 0.25% of carboxy methyl cellulose (CMC) in 0.9% saline solution and were freshly prepared prior to administration. All the drugs were given

in volumes of 10 ml/kg. NBV was administered at a dose of 0.25, and 0.5 mg/kg p.o.4 while gabapentin was administered at a dose of 50 and 100 mg/kg p.o.5 PTZ was administered at a dose of 70 mg/kg i.p.6 The drug treatment was given for 4 days and observations were made at the 4th day after drugs treatment. The observations were made at the time of peak effect of the drugs (for NBV after 30 min for GBP after 2 h). The control animals received 0.25% CMC in 0.9% saline solution. All the parameters were performed to all groups i.e control as well as drugs treated. The seizures threshold and the latency to seizures was evaluated by Increasing Current Electroshock Seizure test7 and PTZ test.6 Spontaneous alternation method8 and rotarod9 test was performed for the evaluation of neurobehavioural impairment. Biochemical estimation was done by measuring the level of Lipid peroxidation10 and reduced glutathione11 in brain.

Familiarity with staff helped to ease anxiety associated with mov

Familiarity with staff helped to ease anxiety associated with moving to a new venue. Supervision, albeit in a less intensive form than during

pulmonary rehabilitation, was important for guiding components of the exercise programme for which participants lacked confidence – such as the cooldown – or for altering or progressing regimens. Cisplatin nmr Ongoing encouragement was important for maintaining participants’ confidence that they could safely exert themselves beyond usual limits. They give you confidence … to push yourself a bit, to try to do a bit more. Fellowship: Participants greatly valued the peer support found within pulmonary rehabilitation. Camaraderie contributed to a sense of enjoyment, which positively influenced attendance and physical effort exerted during the classes. The sociability encountered at pulmonary rehabilitation commonly provoked feelings of sadness when leaving the course. Despite attending ongoing exercise sessions supported by the pulmonary rehabilitation team, many participants in Group A expressed regret that pulmonary rehabilitation could not continue in its original form, largely due to the established social network. I didn’t really want to go anywhere else because we got used to the place, the people, it

was like a little circle, family if you like and made quite a lot of friends. And then it suddenly stopped. And we had to consider going somewhere else … I was really upset at finishing … it was a sort Nutlin-3 chemical structure of emotional thing as well as a physical thing. Sharing experiences of living with COPD and the opportunity for social interaction was seen

to be an important aspect of both pulmonary rehabilitation and ongoing exercise options. The feeling of belonging to a group facilitated regular attendance at maintenance sessions. The people that I know at many the gym, we’ve all done pulmonary rehab and we all have a cup of tea after we exercise together and that encourages me to go, cos I think ‘Ooh if I don’t go today … they’ll wonder where I am’. Confidence: Social support from a disease-specific peer group helped to reduce feelings of isolation that can accompany a chronic disease. A sense of security was gained from exercising alongside others with similar symptoms, reducing feelings of self-pity and self-doubt. If you’re mixed with other people with the same complaints, same problems … you have a lot more confidence. Symptoms relating to COPD were commonly cited as a significant barrier to participation in physical activity. Breathlessness predominated due to its imposed physical restriction and associated psychological and emotional effects including feelings of embarrassment and defeat. If you can’t breathe properly, it’s very hard to do anything … You’re inclined to think, ‘Oh I can’t do it,’ so I don’t do it.

scale bar indicates 0 0001 substitutions per nucleotide position

scale bar indicates 0.0001 substitutions per nucleotide position ( Fig. 3). The fermentation rate of SSII2 (B. subtilis) strain for the alpha amylase production was investigated in 5 L submerge fermentor. The culture aliquots were withdrawn every 6 h, starting from 12 h aseptically and subjected to enzyme estimation up to 40 h of fermentation period. After submerged RGFP966 fermentation, the maximum activity of amylase was obtained in the enzyme extract harvested after 12 h at pH 7 and 32 °C temperature. During submerged fermentation process the production of amylase reached maximum of 4 U/ml at 10 h of incubation period. The enzyme production reached its maximum enzyme production 2.72 g/L at 12 h. 20 Partial

purification of amylase enzyme by ammonium sulfate precipitation showed maximum protein content of 54.54, which is mg/L up to 80% purification fold. Amylase assay showed maximum extracellular enzyme activity of 538 U/ml. Optimum parameters were identified in submerged fermentation which was carried out in a 5 L fermentor with a working volume of 3.5 L and the maximum protein content was estimated to be 2.72 mg/L. Ammonium sulfate precipitation was performed to partially purify the fermented product and it showed maximum protein content of 54.54 mg/L Etoposide manufacturer which is about 80%

higher than non purified enzyme. The SSII2 isolate was characterized by 16S rDNA sequencing and found to be B. subtilis. The partially purified protein can be further characterized by SDS-PAGE

analysis and column chromatography. By doing so, a stable amylase with higher enzyme activity can be identified which may have wide industrial applications and high amylase producing potential. All authors have none to declare. The researchers are thankful to the UGC (University Grant commission) for their encouragement and support, F No. 37-300/2009 (SR). “
“Control of population growth is very important in populated countries like India and China, population control is an issue of global and national public health concern. The rise in population may affect drastically the economic growth of the country. India within, few years of time span will be the leading country as far as the population is concerned. Since the population rising tremendously, this may affect drastically on the socio-economic growth of India. So Sodium butyrate in order to control population, family planning has been promoted through several methods of synthetic contraception. A verity of synthetic contraceptive agents is available in the market, but these contraceptives having side effects. Thus, there is a need to replace these drugs by safe and effective contraceptive agents such as plant based contraceptive agents. Many of our ancestors used the plants or plants extracts as antifertility agents without any side effects and toxic effects.1 So in resent research there was much attention has been given to screen plant based contraceptive agents.