For tuning of the MSD in EI mode perfluorotributylamine (PFTBA) was used as tuning compound. Mass spectra were taken at 2235 EMvolts APO866 mouse and fragments from 40 to 550. Interpretation of the mass spectrum of GC-MS was conducted using the database of National Institute Standard and Technology (NIST) which consists of more than 62,000 patterns. The spectrum of the unknown component was compared with the spectrum of the known component inherent in the NIST library. The name, molecular weight and structure of the components of the test materials were ascertained. Data are represented by Mean ± S.E.M. Significance of mean values

of different parameters between the treated groups were analysed using one way analysis of variances (ANOVA) after ascertaining the homogeneity of variances between the treatments. Paired comparisons were done by calculating the least significance. Statistical CFTR activator tests were performed using Microcal Origin 7.0 for Windows. Each experiment was repeated at least three times with different rats. Figure 1 shows that aqueous curry leaf extract provides protection to the gastric

mucosa against piroxicam induced damage in a dose-dependent manner. Aqueous curry leaf extract pre-administered at 100 mg/kg body weight dose reduced ulcer index by 86.7% against piroxicam fed animal group (**P≤ 0.001), but almost complete protection was rendered when 200 mg/kg BW and 300 mg/kg BW doses were administered. This is clearly indicating that the extract at 200 mg/kg BW dose is sufficient to provide protection against piroxicam induced gastric ulceration in rats. Figure 1A and 1B are representative photographs Thymidylate synthase of macroscopic and microscopic

changes in the rat stomach clearly indicating ulcerative damages on feeding rats with piroxicam at 30 mg/kg BW dose orally. Haematoxylin–eosin stained sections reveal that mucosal bleeding occurred on piroxicam feeding, which was protected when graded doses of the aqueous extract was administered before piroxicam feeding. Photographs of the inner surface of stomach show no ulcer spots in the rats fed 200 mg/kg BW and 300 mg/kg BW doses of the aqueous extract. Biomarkers of oxidative stress altered in piroxicam induced gastro-toxicity. Lipid peroxidation level and reduced glutathione content were also protected in a dose dependent manner by aqueous curry leaf extract. In figure 1D and 1E curry leaf extract shows reduction in lipid peroxidation level by 53.7% (**P≤0.001 Vs piroxicam fed group) and 1.4 fold increase (**P≤0.001 Vs piroxicam fed group) in reduced glutathione content on administration of 200 mg/kg BW dose prior to oral administration of 30 mg/kg body weight dose of piroxicam.

06 ng/mL, 2.38 mg/L, and 129 pg/mL for the prediction of 6-month mortality ( Table 2). Using the upper limit of normal of 0.5 ng/mL for PCT and 5 mg/L for CRP, the sensitivity was 41.0% and 69.2%, and the specificity was 94.5% and 62.0%, respectively. Higher PCT, CRP, and sTREM-1 levels as well as age, a lower albumin level, and the presence of cavitary lesion and pleural effusion were associated with 6-month mortality in the univariate Cox proportional hazards model (Table 3). In multivariate regression analysis, only PCT, sTREM-1, and albumin levels remained independently associated

with 6-month mortality. With a cutoff of 0.5 ng/mL serum buy Daporinad PCT, patients with ≧0.5 ng/mL had significantly shorter survival than those with <0.5 ng/mL (Fig. 3A). Similarly, patients

with a serum sTREM-1 level of 129 pg/mL or above had significantly poor prognosis (Fig. 3B). Table 4 shows the characteristics of patients with dichotomous levels of PCT (≧0.5 vs. <0.5 ng/mL) and sTREM-1 (≧129 vs. <129 pg/mL). Patients with PCT ≧0.5 ng/mL or sTREM-1 ≧129 pg/mL were more likely to have disseminated TB and to die within 2 or 6 months. Table 5 shows the dichotomous levels of PCT and sTREM-1 in each cause of death. Because of limited patient number, only patients succumbed to multi-organ failure and progressive respiratory failure could be analyzed. selleck We observed that sTREM-1 ≧129 pg/mL seemed to be better at predicting mortality due to multi-organ failure than PCT ≧0.5 ng/mL. In this prospective study of 243 patients diagnosed with PTB, we compared the potential of serum PCT, CRP, and sTREM-1

Anacetrapib levels to predict an unfavorable outcome for PTB patients. We report five major findings. First, a significant proportion of patients with PTB had serum CRP levels above the normal cutoff; however, serum levels of PCT above the upper limit of normal were observed in only few PTB patients. Second, PCT, CRP, and sTREM-1 levels on the diagnosis of PTB were significantly higher in 6-month nonsurvivors than in survivors. Third, PCT, CRP, and sTREM-1 exhibited comparable discriminative power in predicting 6-month mortality in patients with PTB. Fourth, higher PCT and sTREM-1 levels and a lower albumin level were independent associated with a poor 6-month outcome. Fifth, a PCT level over the normal cutoff (0.5 ng/mL) and an sTREM-1 level above the best cutoff (129 pg/mL) were also associated with higher 2-month mortality and the presence of disseminated TB. It has been reported that sTREM-1 is poorly expressed in pneumonia or pleuritis caused by TB compared with in those caused by bacteria.8, 13, 14 and 18 Although the reasons why the TREM-1 response in TB is poor remain to be clarified, there are two possible explanations. One is that TREM-1 expression is strongly upregulated by extracellular bacteria; in contrast, intracellular microorganisms, such as MTB, have no effect.

“
“This editorial concerns the joint issue of human numbers and failure of food supply, and focuses on the fact that coral reefs, if fished less intensively and destructively, can support much more biomass (food) than they do now. It starts with HTS assay correcting some misconceptions about the supply of food globally, before focussing on some reasons why reefs cannot do what they are being asked to do. It also tries to show

that failing to admit to some clear points is leading to a worsening situation. It has become fashionable to claim that Malthus’ predictions of mass famine have been wrong. After all, it has been argued, the world population today is 7 billion, and is likely to rise to least 9 billion within a human generation. Two examples: at one end of the spectrum we have a journalist best left unnamed who said: “…Malthus was wrong as he failed to foresee the great boom in agriculture and technology.” At the other end we

read in the President’s Foreword to a Royal Society report (no less!) which says: “But despite devastating regional famines, prognostications of mass starvation have not been fulfilled, even though the population has risen around sixfold since Malthus’s time” (Rees, 2009). It is not clear why the President of such an august body (which must contain an ecologist or two who could have been consulted) thinks ‘devastating regional famines’ are not ‘mass starvation’, and nor does it say why the two things are different anyway – they would be identical for the people in an affected region. Therefore, when is famine selleck chemicals llc not a famine? What is mass starvation, if different? Table 1 grimly lists several defined famines, detailing Cytidine deaminase locations, dates and estimated numbers of those who died. This simply tries to illustrate what numbers of deaths constitute ‘famine’ in conventional terms. It does not enumerate

those who had lives blighted by food shortages and which resulted in devastating consequences for human health and society, and it does not attribute any one particular cause to each case. Such situations persist in many countries today, with chronic undernourishment affecting almost one billion people worldwide (FAO, 2012), and many political wars are underlain by resources shortages too. Coastal people in the tropics are amongst the vulnerable. Present day data on food shortages and on deaths that arise from this are available, though difficult to measure. A decade ago, Black et al., (2003) asked in The Lancet: “Why and where are 10 million children dying each year?” Two years later in the same journal these co-authors report on World Health Organisation estimates of the causes of death in children (Bryce et al., 2005), stating: “Under-nutrition is an underlying cause of 53% of all deaths in children younger than age 5 years” (Fig. 1).

Clearly

the Vallee Professorship was extremely valuable for my scientific career. At the core of the Vallee Visiting Professor program is its collaborative mentality. Academic-social interactions play a key role in generating new ideas and are thus a central focus for VVPs. Such was the case for Torsten Wiesel, who came in May 2010, to renew contact with the Department of Neurobiology, where he had previously been find more a member for twenty years, serving as chair for ten of them. Having left his research career for various administrative roles, he was interested to get an insider’s view of his old department. In Torsten’s words, my experience as a Vallee Visiting Professor was intellectually rich and wonderful. I met with nearly the entire faculty of the department individually, which turned out to be a

very enriching and enjoyable experience. The faculty members described their research programs, followed by intense and detailed discussions about various aspects of their work. It was not until later, when attending a dinner for Torsten – the Foundation hosts a festive dinner near the end of each visit both to celebrate the Vallee Visiting Professor, and to recognize the contributions of his/her colleagues and friends during the visit – that it was learnt of the intangible consequences of Torsten’s visit that had widely impacted his host department. Senior members of the Department of Neurobiology said that Torsten’s presence learn more in the department had incited a palpable energy that stirred ideas and renewed drive not just among principal investigators, but also throughout the ranks in their laboratories. When Malcolm Green came in 2004 to Jeremy Knowles’ laboratory in the Department of Chemistry, the visit provided a much-needed opportunity

to think about my future research program. But, apart from Olopatadine working on research, Malcolm established or renewed many friendships, often over dinner at Jeremy and Janey Knowles’ home, with prominent figures such as Alan Davison, Dick Schrock, Dietmar Seyferth, Dan Nocera, Steve Lippard, Dick Holm, George Whitesides, John Deutsch, and Samuel P. Huntington. Likewise, Jesper Haeggström, who visited the lab of Charles Serhan at Brigham and Women’s Hospital, recalls being particularly stimulated by all the informal meetings and discussions with distinguished colleagues both inside and outside my own immediate fields of interest. I remember spending one morning in K. Frank Austen’s laboratory, sharing thoughts on intracellular lipid receptors with Peter Weller, and learning the latest new developments regarding in vivo imaging from Ulrich von Andrian. In addition to these meetings, being in Charles Serhan’s lab allowed ample opportunities to interact with all members of a world-leading team in the field of lipid mediator research.

8 (1 ml final volume), and centrifuged

at 15000g for 15 min. The supernatant was worked up with a Sigma/Aldrich assay kit (Catalog Number FLAA) according to the manufacturer’s instructions and measured using a SIRIUS Luminometer (Berthold, Pforzheim, Germany). Mitochondrial ATPase activity was measured in intact-uncoupled and freeze–thawing-disrupted mitochondria according to the protocol of Bracht et al. (2003), with modifications. Intact mitochondria (1 mg protein/ml) were incubated in a medium containing 125 mM sucrose, 65 mM KCl, and 10 mM HEPES-KOH, pH 7.4, plus 0.2 mM EGTA and 5 mM ATP for 20 min at 37 °C, in the presence of 1 μM carbonyl cyanide m-chlorophenyl hydrazone (CCCP), in a final volume of 0.5 ml. When disrupted mitochondria were used as the enzyme source, the medium contained 20 mM TRIS–HCl (pH this website 7.4). The reaction was started by the addition of 5 mM ATP and stopped by the addition of ice-cold 5% trichloroacetic Epigenetics inhibitor acid. ATPase activity was evaluated by measuring released inorganic phosphate, as described by Fiske and Subbarow (1925), at 700 nm using a DU-800 spectrophotometer (Beckman Coulter, Fullerton, CA). Results were expressed as nmol Pi. min−1. mg protein−1. Sensitivity to oligomycin (1 μg/ml) was tested in all mitochondrial suspensions. The activity of NADH and succinate

dehydrogenases was measured spectrophotometrically according to Bracht et al. (2003), using a DU-800 spectrophotometer (Beckman Coulter, Fullerton, CA). The reaction medium (final volume 1.5 ml) contained 20 mM TRIS, pH 7.4, and 1 μM Antimycin A. Disrupted mitochondria (0.2 mg/ml) were added along with one of four abamectin concentrations (5, 10, 15 and 25 μM), either 1 mM NADH or 10 mM succinate, and 0.4 mM potassium ferricyanide as electron acceptor. The amount of ferricyanide reduced was determined by the decrease in absorbance at 420 nm and enzyme activity was represented as nmol. min−1. mg protein−1, using 1.04 mM−1 as the molar extinction coefficient of ferricyanide. Inhibition of ADP-induced depolarization of Δψ

was performed as described Vitamin B12 (O’Brien et al., 2008) with modifications. Freshly isolated mitochondria were pre-incubated in the presence of 5–25 μM ABA or 5 μM carboxyatractyloside (cATR) and then energized with 5 mM succinate for 1.5 min before adding 400 nmol ADP. ADP-induced depolarization describes the change and recovery in Δψ upon addition of ADP. The amplitude of depolarization induced by ADP was measured in the presence and absence of the test compounds. Data are expressed as the mean ± S.E. mean, and statistical differences were calculated using one-way analysis of variance (ANOVA) followed by the Dunnett´s test using GraphPad Prism, v 4.0 for Windows (GraphPad Software, San Diego, CA, USA). Mitochondrial oxygen consumption was monitored in the presence of varying concentrations of ABA.

After 4 weeks of observation, a second cohort was assigned randomly to group 3 (BMS-791325 150 mg twice Selleckchem Veliparib daily for 24 weeks) or group 4 (BMS-791325 150 mg twice daily for 12 weeks). Patients were stratified by genotype 1a/1b, with 1b patient enrollment targeted between 25% and 38% or less of the total number of patients

in each group. The primary end point was an HCV-RNA level less than 25 IU/mL at SVR12. Other end points included analysis of HCV RNA at various time points during and after treatment, rates of viral breakthrough and relapse, and assessment of safety and tolerability. In the event of viral breakthrough (defined as confirmed increase in HCV-RNA level >1 log10 from nadir or confirmed HCV RNA level >25 IU/mL on or after week 8), patients were eligible to receive treatment intensification, defined as peginterferon alfa-2a (180 μg subcutaneously, once weekly) and ribavirin (1000 mg orally per day if patient weighed <75 kg, or 1200 mg orally per day if patient weighed >75 kg) in addition to continuation of the direct-acting antivirals for up to an additional 48 weeks. Blood samples were drawn at baseline, days 1-7, days 9, 11, 14, 21, 28, every week through week 8, then every 2 weeks until the end of

treatment, and post-treatment weeks 4, 12, 24, 36, and 48. HCV-RNA level was determined at a central laboratory using the COBAS TaqMan v2 assay (Roche Molecular Diagnostics, Pleasanton, CA), with a lower limit of quantitation selleckchem of 25 IU/mL and a lower limit of detection of approximately 10 IU/mL. HCV genotypes were determined by polymerase chain reaction amplification and sequencing using the VERSANT HCV Amplification 2.0 Kit (LiPA) (Siemens, Munich, Germany). Phosphoprotein phosphatase The host interleukin

(IL)28B genotype (rs12979860 single-nucleotide polymorphism) was determined by Monogram Biosciences (South San Francisco, CA) using a real-time polymerase chain reaction assay. All baseline samples were analyzed for polymorphisms in HCV NS3, NS5A, and NS5B associated with drug resistance using population sequencing (sensitivity, ≈20%). Safety and tolerability were measured by serious adverse events, treatment-emergent adverse events, discontinuations owing to adverse events, severity grade 3/4 adverse events, and severity grade 3/4 laboratory abnormalities. Vital sign and electrocardiographic measurements, physical examinations, and clinical laboratory results were assessed throughout the study. Binary antiviral activity end points were assessed using modified intent-to-treat methodology. Patients prescribed a different treatment as assigned for the whole treatment duration were analyzed based on actual treatment (as treated).

012) lower compared with UT-SCC-34 xenografts. CA IX is considered as a promising endogenous hypoxia-related marker, and a significant but weak correlation has been reported between CA IX staining and the distribution of the exogenous hypoxic cell marker pimonidazole [22]. However, also, other microenvironmental factors, such as pH homeostasis, affect the expression of CA IX [23]. In a number of studies, CA IX has been shown to be associated with a poorer locoregional control, overall survival, and aggressive phenotype [24] and [25]

Our Buparlisib in vivo finding that [18F]EF5 uptake, in addition to hypoxia, also reflects an adverse phenotype is further supported by previous studies depicting a relationship between unlabeled EF5 binding and tumor aggressiveness [19] and [20]. We also found a higher, with a trend toward significance (P = .082), expression pattern of Hif-1α in UT-SCC-34 xenografts ( Figure 2 and Table 2) compared to UT-SCC-8, whereas the Hif-1α expression was significantly lower AZD2281 in UT-SCC-74A xenografts (P = .012). In other words, we did not observe any relationship between Hif-1α expression and the uptake of [18F]EF5

( Figure 1). Our results are in line with earlier studies reporting a limited, or nonexisting, colocalization of Hif-1α with pimonidazole [26] and [18F]FMISO ([18F]fluoromisonidazole) [27]. Vucovic et al. [28] described a significant correlation between Hif-1α expression and EF5 staining in cervical cancer xenografts. However, the percentages of Hif-1α–positive cells staining for EF5 and vice versa ranged between 10% to 20%, pointing to a rather low association between these two markers. Moreover, declines in Hif-1α levels and Hif-1 activity in the later phase of tumorigenesis have been reported by Lehmann et al. [27]. In comparison PRKACG to UT-SCC-8 xenografts, the uptake of [18F]FDG was also higher, although not statistically significantly, in UT-SCC-34 and UT-SCC-74A xenografts (Figure 1). This finding further supports our conclusion that the phenotype of UT-SCC-34 and UT-SCC-74A xenografts

is more aggressive. Membranous Glut-1 expression was detected in all three UT-SCC xenografts. The expression of Glut-1 did not relate to the uptake of [18F]FDG or [18F]EF5. The highest expression was seen in UT-SCC-8 and UT-SCC-34 xenografts, whereas the lowest expression was detected in UT-SCC-74A xenografts (Figure 2 and Table 2). Although tumors frequently overexpress Glut-1, the cellular uptake of [18F]FDG is not exclusively attributable to Glut-1 [16], which probably explains the previous contradictory studies on the relationship between Glut-1 and [18F]FDG. To further evaluate phenotype differences detected in the xenografts in vivo, we determined the uptake of [18F]EF5 and [18F]FDG in the cell lines in vitro. Cells were grown under normoxia and for 1, 3, 6, 12, and 24 hours of 1% of oxygen ( Figure 3 and Figure 4).

In terms of average water spread area for each category of wetland, man-made coastal wetlands have the highest area (Fig. 3). The aquatic vegetation in all the selleck chemicals llc wetlands put together, account for 1.32 m ha (9% of total wetland area) in post monsoon and 2.06 m ha (14% of total wetland area) in pre monsoon (SAC, 2011). Major wetlands types in which aquatic vegetation occur include lakes, riverine wetlands, ox-bow lakes, tanks and reservoirs. In terms of the proportion of the geographical area, Gujarat has the highest proportion (17.5%)

and Mizoram has the lowest proportion (0.66%) of the area under wetlands. Among Union Territories in India, Lakshadweep has the highest proportion (around 96%) and Chandigarh has the least proportion (3%) of geographical area under wetlands. Gujarat has the highest proportion (22.8%) and UT of Chandigarh has nearly negligible part

of the total wetland area in the country. Water-spread area of wetlands changes over seasons. The States of Sikkim, Nagaland, Mizoram, Meghalaya, and Jharkhand have more than 90% of the total wetland area as water spread area during post monsoon. Significant reduction in water spread area of wetlands from post monsoon to pre monsoon was selleck screening library found in the States of Uttar Pradesh (28%), Chhattisgarh (29%), Himachal Pradesh (29%), Tripura (29%), Sikkim (30%), Andhra Pradesh (31%), Jharkhand (32.5%), Punjab (33%), Bihar (34%), Gujarat (36%), Karnataka (38.5%), Maharashtra (53.5%), Tamil Nadu (55%), Madhya Pradesh (57%), and Rajasthan (57%). In terms of contribution of the total water spread area in the country, highest during post monsoon was observed in the State of Gujarat (13.5%) and lowest in Sikkim and Tripura (0.1% each). During pre-monsoon, highest was again in Gujarat (12.6%)

and lowest was in Sikkim and Tripura (0.1% each). As regards percentage area under aquatic vegetation, Andhra Pradesh, Delhi, Karnataka, Manipur, Orissa, Punjab, Tamil Nadu, Tripura, and West Bengal have 15–59% of the wetland area under Interleukin-3 receptor aquatic vegetation (Fig. 4). Further, Andhra Pradesh, Gujarat, Karnataka, Orissa, Tamil Nadu, Uttar Pradesh, and West Bengal account for nearly 3/4th of the total area under aquatic vegetation. In Andhra Pradesh, maximum amount of aquatic vegetation is found in reservoirs, aquaculture ponds and irrigation tanks. In Gujarat, it is found in rivers, reservoirs and creeks. In Karnataka, it is in irrigation tanks, ponds and reservoirs. In Orissa, aquatic vegetation was more in rivers, reservoirs, lagoons, irrigation tanks and ponds. In Tamil Nadu, it is in lakes and irrigation tanks. In Uttar Pradesh, most of the aquatic vegetation is found in rivers, lakes and riverine wetlands, whereas in West Bengal, most of it is in Mangroves.

All antibodies were used at the manufacturers’ recommended concentrations with matched isotype controls (from Serotec). Dead/dying cells were excluded from the analysis using DAPI (Sigma) and were normally less than 5%.

Data were analysed on an LSRII flow cytometer equipped with DIVA software (BD Biosciences). The phenotypic identification 17-AAG purchase of the ‘ex-vivo MSC’ using the CD45−/lowCD271+ phenotype was first described by our group using ICBMA [27], [28] and [35] and has since been independently validated by others [29], [36] and [37]. MSC enumeration was performed by staining the aspirated MNC fraction with CD45-FITC (Dako UK Ltd, Ely, UK), CD271-PE (Miltenyi Biotec) and 7-AAD, as previously described [28]. A minimum of 5 × 105 events were acquired and analysed using an LSRII flow cytometer to establish the percentage of CD45−/lowCD271+ cells. The frequency of CD45−/lowCD271+

per ml of sample was then calculated based on the following formula: CD45−/lowCD271+ cells/ml = % CD45−/lowCD271+ cells × MNCs/ml. Bone marrow MNCs were isolated using Lymphoprep and cells were then re-suspended at 1 × 107 cells/ml in FACs buffer. Antibodies were added at the manufacturers’ recommended concentrations and the cells were incubated for 20 min. Antibodies used were: CD45-PECy7, CD73-PE, CD34-PerCP, CD19-PE, CD33-FITC, CD61-FITC (BD Biosciences), CD90-PE, CD105-PE, CD31-FITC (Serotec) and CD271-APC (Miltenyi Biotec). The cells were washed and re-suspended Navitoclax nmr in FACs buffer containing 100 ng/ml DAPI before analysing on an LSRII flow cytometer. Dead cells were excluded from the analysis using DAPI (usually < 5%) before gating on the CD45−/low CD271+ cell population and assessing the expression of all other markers. Statistical analysis

and graphing were performed using GraphPad Prism version 4 for Windows (San Diego, California, USA). Gaussian distribution could not be assumed given the number of samples and differences between donor-matched ICBMA and LBFBM groups were tested using Wilcoxon signed ranks test. The differences in the MSC content between different patient groups were analysed using Mann–Whitney test. Significance was assumed when p < 0.05. A standard CFU-F assay was acetylcholine first performed to measure the MSC content of ICBM aspirates in three groups of orthopaedic patients and healthy controls (Table 1). Consistent with previously reported findings [10], high donor-to-donor variation was observed, potentially due to factors related to donor age [38] or a variable degree of dilution of ICBM sample with blood during the aspiration procedure [39]. No significant differences in CFU-F abundance in ICBMA were found between all three groups of orthopaedic patients and healthy controls (Table 1).

Through the molecular modeling method employed in this study, several answers could be reaching about Pg-AMP1 structures. In fact, there are several possible conformations for Pg-AMP1, without a tendency to a specific fold type. In contrast to a previous report [28], the molecular model of Pg-AMP1 Autophagy inhibitor price here reported shows only the N-termini α-helix, indicating that the probable structure could be more flexible than previously described. The same scenario was assumed for the recombinant Pg-AMP1 structural prediction, in which extremely flexible structures were observed. Carson et al. [3] showed that the His6 tag normally does

not alter the structure of recombinant proteins. In our predictions, the His6 tag takes on a random coil conformation, as well as the C-terminal of predicted Pg-AMP1structure. Otherwise, ATR inhibitor despite the overall structure maintenance, the His6 tag seems to alter the Pg-AMP1 activity, since the recombinant protein is active against bacteria in which the native form is completely inactive, such as Gram-positive bacteria S. aureus and S. epidermides. These data indicate that the His6 tag may alter the mechanism of action of Pg-AMP1. The His6 tag probably increases the affinity

of recombinant Pg-AMP1 to bacterial membranes, providing an stronger interaction with anionic membranes, due to the increase in positive C-terminal charges. The net charge seems to be an essential property

to antimicrobial activity. Dathe et al. [5] had conducted an study generating several analogs of magainin. those The analogs were designed for keeping several properties such as hydrophobicity and helix propensity, changing only the net charge. The more active analogs were the ones with charges higher than +5. In this view, the His6 tag could generate a similar effect to observed in the magainin analogs developed by Dathe et al. [5]. Bearing this in mind, we propose that the N-terminal is responsible for membrane binding, independently of the helix being one or two residues longer as observed in some models of recombinant Pg-AMP1, acting as a membrane anchor mediated by the three arginine residues. Subsequently, the random coil starts to interact with phospholipids, destabilizing the membrane. Metaphorically, this peptide would acts like a chain whip, an Asian melee weapon. The recombinant protein would be a chain whip with a sharper metal dart, the His6 tag ( Fig. 4). In conclusion, it was observed that heterologous expression of Pg-AMP1 conserved its antimicrobial activity, enabling this peptide to be a candidate for production of antimicrobial compounds. Moreover, theoretical modeling clearly shows that the proposed structure is extremely variable due to flexibility of high glycine content.