As reported by many authors [15, 40], majority of patients in the present study presented late in poor general condition. This was found to be the most important factor influencing the outcome of surgical procedure as also emphasized by a number of authors [15, 23, 29, 30, 36, 40]. In resource-poor countries, difficulties in diagnosis, patient transfer, and sub-therapeutic antibiotic treatment often result in delayed presentation to a hospital [3, 15, 28]. In agreement with other studies [15, 23, 28, 40], the diagnosis of typhoid intestinal perforation in this study was made from clinical evaluation, laboratory

investigation, identification of free air under the diaphragm on abdominal and chest radiographs and operative findings such as typical perforation on antimesenteric check details border, purulent collection and adhesion of bowel loops with friable pussy flecks. The value of the radiological investigation has been compared with other writers and with current radiological techniques; 80-90% of cases are correctly diagnosed. Findings from our study demonstrated free gas under the diaphragm on abdominal and chest radiographs in more click here than seventy percent of cases which is consistent with other studies [41, 42]. A plain abdominal or chest radiograph with free air under the diaphragm is a fairly frequent but variable finding signifying perforated hollow viscus, but its absence does not exclude the diagnosis. Abdominal ultrasonography has also

been found to be superior to plan radiographs in the diagnosis of free intra-peritoneal air as confirmed by the present study [43]. For the accurate diagnosis of typhoid intestinal perforation, blood for culture and sensitivity, urine for culture and sensitivity and stool for culture and sensitivity or bone marrow are required. None of these laboratory investigations was performed Glutathione peroxidase in our study mainly because of lack of facilities capable of performing these tests. It is very difficult to isolate Salmonella typhi from urine and stool specimens in most developing countries. This is often

due to lack of culture media, expertise and sometimes previous exposure to inadequate doses of antibiotics. Another major problems selleck products relating to the laboratory is the abuse of the Widal’s test. It is therefore recommended to carry out studies of baseline value of typhoid agglutinins in our setting as has been done in some areas to know the diagnostic utility of the Widal’s test. The clinical picture of typhoid intestinal perforation may be complex when typhoid fever occurs with HIV infected patients [44]. We could not find any study in the literature that shows the effect of HIV infection on outcome of patients with typhoid intestinal perforation. This observation provides room for research on this topic. The prevalence of HIV infection among patients with typhoid intestinal perforation in the present study, was 10.2% which is higher than 6.5% [45] in the general population in Tanzania.

Data are presented as the mean of the values for the right and the left side of the nose. Nasal reactivity was defined as a significant increase in nasal symptoms of ≥3 Smad inhibitor points in total symptom score (Kronholm Diab et al. 2009) and/or a significant decrease in AR measures of the anterior part of the nasal cavity (Hilberg and Pedersen 2000). A BMS-907351 nasal lavage was performed twice before the first challenge and 20 min after

the second one directly after the rhinometric measurement. The first lavage (Time 0) was performed to wash out mediators due to the general environmental exposure before the challenge. The second lavage (Baseline) before the challenge was used as the baseline for the post-challenge samples. The lavage procedure was made as earlier described in Kronholm Diab et al. (2009). Quality of life questionnaires The study participants filled in the Short Form 36 Health PR-171 manufacturer Survey (SF-36) (Ware and Sherbourne 1992; Ware et al. 1993) and the Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ) (Juniper and Guyatt 1991; Juniper et al. 1996) before the medical examination to avoid influence from the questions posed by the physician.

The participants were instructed according to the guidelines defined by the designers of the questionnaires. As proposed by several authors, we used a combination of generic and disease specific quality of life scales (Leong et al. 2005; Terreehorst et al. 2004). The study participants were asked if any serious or dramatic event had happened during the observation period to exclude response shift (van Gerth Wijk 2002). In the comparison analyses for quality of life, the number of participants in the S− group is 18, due to missing questionnaires from one hairdresser at the study find more end. SF-36 The SF-36 was given to analyze the hairdressers last 4 weeks. We used the Swedish self-administered

version (Sullivan et al. 2002). SF-36 comprises 36 items within eight health domains related to physical and mental health dimensions: PF (Physical Functioning, 10 questions), RP (Role Physical Functioning, 4 questions), BP (Bodily Pain, 2 questions), GH (General Health, 5 questions), VT (Vitality, 4 questions), SF (Social Functioning, 2 questions), RE (Role Emotional, 3 questions) and MH (Mental Health, 5 questions). The domains are scored on a scale of 0 (worst) to 100 (best) points and calculated for each domain using a standardized scoring system (Sullivan et al. 2002; Ware et al. 1993). On the basis of the eight scales, it is also possible to estimate a physical (PCS) and a mental component summary (MCS) score (Ware et al. 1995). The Swedish version of the SF-36 has shown good psychometric values in different studies (Taft et al. 2004), and there are norms for the Swedish population available (Sullivan and Karlsson 1998). RQLQ Rhinoconjunctivitis quality of life questionnaire (RQLQ) evaluates QoL in a particular disease state (Juniper and Guyatt 1991).

Although the emphasis of this study was on corrosion

processes, we also identified the presence of bacterial virulence factors and antibiotic resistance genes, suggesting that these systems are reservoirs of microbial populations of public health relevance. Acknowledgements We thank Jarissa Garcia, John Sullivan, and James Weast of the Metropolitan Sewer District of Greater Cincinnati for the technical support provided during the collection of samples, to Dan Murray (USEPA) for discussions on concrete corrosion, to Brandon Iker for laboratory technical support, and to Robin Matlib for bioinformatics support. This manuscript was approved for publication by the United States Environmental Protection Agency (USEPA). Any opinions expressed in this manuscript AZD7762 datasheet are of the authors and do not necessarily

reflect the official positions and policies of USEPA. Any mention of products or trade names does not constitute endorsement or recommendation Bioactive Compound Library for use. Electronic supplementary material Additional file 1: Figure S1. Distribution (%) of sequences identified to particular subsystems (SEED) in selleck compound metagenomes of wastewater biofilms. Figure S2. Distribution of bacterial classes on concrete wastewater pipes as determined by taxonomic identification of 16S rRNA genes recovered from metagenome libraries. Numbers in brackets represent percentage of each group from the total number of sequences. Legend: 1. unclassified Bacteria domain, 2. Actinobacteria, 3a. Bacteroidia, 3b. Flavobacteria, 3c. Sphingobacteria, 4. Chloroflexi, 5a. Bacilli, 5b. Clostridia, 6. Fusobacteria, 7a. Alphaproteobacteria, 7b. Betaproteobacteria, 7c. Deltaproteobacteria, 7d. Epsilonproteobacteria, 7e. Gammaproteobacteria, 8. Synergistia and 9. other classes each representing <1%. Groups

(phylum): 3. Bacteroidetes, 5. Firmicutes, 7. Proteobacteria . Figure S3. UPGMA cluster analysis Methamphetamine of Bray-Curtis similarity coefficients for biofilms in wastewater systems. Sample types were classified by their taxonomic dominant group within the sulfur biogeochemical cycle: sulfur-reducing bacteria (SRB) and sulfur/sulfide-oxidizing bacteria (SOB). Location of biofilm: bottom (a), middle (b), top (c) and outdoor (d). Figure S4. Phylogenetic affiliation of phylotypes identified as Bacteroidetes from each biofilm: top pipe (TP, gray) and bottom pipe (BP, black). Clones were identified by genus or order (*) and percentage of each representative sequence in their respective libraries is provided in the brackets. The tree was inferred using maximum likelihood analysis of aligned 16S rRNA gene sequences with bootstrap values from 100 replicates. Box indicates the two most dominant phylotypes. Figure S5. Phylogenetic affiliation of Deltaproteobacteria phylotypes identified as sulfate-reducing bacteria (SRB) from each biofilm: top pipe (TP, gray) and bottom pipe (BP, black).

We report a functional germline mutation (polymorphism) in the galectin-3 gene at position 191 (rs4644) Selleckchem Milciclib substituting proline with histidine (P64H), which results in susceptibility to matrix metalloproteinase (MMP) cleavage and acquisition of resistance

to drug-induced apoptosis. This substitution correlates with incidence of breast cancer and racial disparity. Of note, Cleavage of galectin-3 by MMPs is related to progression of breast and prostate cancer. We show that galectin-3 regulated functions like chemotaxis, chemoinvasion, heterotypic aggregation, epithelial-endothelial cell interactions and angiogenesis are dependent in part on cleavage of the N terminus of galectin-3 followed by its release in the tumor microenvironment. Breast carcinoma cells harboring cleavable galectin-3 species showed JAK inhibitor increased chemotaxis towards collagen IV, invasion through Matrigel and heterotypic interactions with endothelial cells resulting in angiogenesis and 3-D morphogenesis in vitro compared to cells harboring non-cleavable galectin-3. Wound healing studies employing a novel cell culture insert showed

increased migration and phosphorylation of focal adhesion selleck kinase inhibitor kinase in endothelial cells migrating towards H64 cells compared to P64 cells. Using 3- dimensional co-cultures of endothelial cells with breast cells harboring galectin-3 peptides, we show that amino acids 1-62 and 33–250 stimulate migration and interaction of cells with the endothelial cells. Immunohistochemical

analysis of blood vessel density and galectin-3 cleavage in a breast cancer progression tissue array support the in vitro findings. These results indicate that cleavage of galectin-3 in tumor microenvironment leads to breast cancer angiogenesis and progression. In conclusion, Meloxicam we provide novel data implicating a galectin-3 germline nonsynonymous functional polymorphism in breast cancer progression and metastasis. O4 Extracellular Matrix Remodeling Forces Tumor Progression Valerie Marie Weaver 1 1 Department of Surgery, UCSF, San Francisco, CA, USA Tumor progression is accompanied by a desmoplastic response that is characterized by significant extracellular matrix (ECM) remodeling. We have been studying the role of matrix metalloproteinase and lysyl oxidase-mediated collagen cross-linking in ECM remodeling and tissue desmoplasia during breast tumor progression. Thus far we have established a positive association between lysyl oxidase-dependent collagen cross-linking, the accumulation of linear, oriented collagen fibrils, tissue fibrosis and tissue stiffening during breast transformation. We have demonstrated that either pharmacological or antibody-mediated inhibition of lysyl oxidase-induced collagen cross-linking prevents tissue fibrosis, reduces tissue stiffening, enhances tumor latency and decreases tumor incidence in both the MMTV-Neu and PyMT transgenic mouse models of breast cancer.

On the contrary, there was an insignificant tendency towards better prognosis when basal keratins or vimentin were detected in a primary tumour. This observation remains to some extent in contrast with observations made by Cheang et al. [25], Liu et al. [31], and by Rakha et al. [32]. However, Jumppanen et al. have found that the clinical outcome of basal tumours is similar

to non-basal ER-negative tumours [33]. Moreover, they have observed that basal keratins expression significantly affected survival only during the first 5 years of follow-up and lost its significance later on. In our study the median follow-up period in a group of surviving patients was 7.5 years and our observation corresponds well with observations made by Jumppanen and colleagues [33]. Indeed,

Tischkowitz et al. have found that the difference in survival rate between triple negative and non-triple negative CB-5083 molecular weight breast cancer is reduced with longer follow-up period [34]. When basal phenotype markers like CK 5/6 and HER1 (EGFR) were analyzed without consideration of steroid receptors status, the reduction in survival of patients expressing these markers was more pronounced at 10 years of observation that at 3 Selleck Repotrectinib years. Our results, although restricted by a relative small number of patients with triple negative phenotype, confirm these findings. The present study also supports our previous analysis which showed that basal cytokeratins (CK5/6 and CK17) expression had not any impact on survival in patients with breast cancer [35]. The possible association of vimentin with clinically aggressive behaviour of tumours described by others [7–9, 11] may be explained by the correlation of vimentin expression with lack of steroid receptors and poor differentiation of cancer. We can confirm this observation (Table 1). However, we cannot offer a better indicator of basal type breast cancers by adding vimentin to the diagnostic panel when overall survival is a primary end-point.

Also, Terminal deoxynucleotidyl transferase an immunopanel find more defined as CK5/6 or 14 or 17-positivity did not show any significant prognostic value in survival analysis in a triple negative group. Five marker method proposed by Cheang et al. [25] showed superior prognostic value than only triple negative phenotype. In their analysis, triple negative, CK5/6-positive and EGFR-positive tumours were selected. Taken into consideration a strong positive correlation between EGFR and vimentin expression [4], we have taken an effort to construct an immunopanel defining basal-type tumours as triple negative tumours that are vimentin-positive or basal cytokeratin-positive. In a comparison with Cheang’s study, our analysis was based on a smaller number of patients and instead of EGFR, vimentin expression was applied. However, in our study, the median follow-up period in a group of living patients almost reached 8 years.

Meanwhile, the Au nanoparticles on the surface of LED devices

could increase the roughness of the surface. So the enhancement of optical output power may also originate Mocetinostat from the surface scattering effect. When comparing the Au nanoparticles from the 5-nm Au-CNT system with the LEDs that had Au nanoparticle arrays from the 2-nm Au-CNT system, the latter showed more enhanced light emission Optical microscopy images of the LEDs with and without the Au nanoparticles with an injection current of 100 mA are shown in the inset of Figure  3. Further optimization of the particle-forming conditions would lead to an even higher increase in the efficiency of the LEDs with nanoparticles from the metal-CNT system in the future. Figure 3 EL spectra of LEDs. The LEDs are with Au nanoparticles from the 2- and 5-nm Au-CNT systems BMS202 datasheet with an injection current of 100 mA measured at room temperature, using a planar LED as a reference. The inset shows optical microscope images of the LEDs (a) without any Au nanoparticles, (b) with Au nanoparticles from the 5-nm Au-CNT system, and (c) with Au nanoparticles from the 2-nm Au-CNT system.

All of the devices were operated with an injection current of 100 mA. Figure  4a shows the optical output power for the LEDs with and without Au nanoparticles on p-GaN surfaces versus the injection current (L-I) characteristics for all of the devices. The enhancement factor in the optical output power increased as the injection current increased. The voltage–current (I-V) characteristics for the LEDs with and without an Au nanoparticle layer are shown in Figure  4b. The forward voltage for LEDs with Au nanoparticles on the p-GaN surface was 2.7 V, which is almost the same as that of the planar LEDs without any Au nanoparticles, indicating that fabricating Au nanoparticles on the p-GaN surfaces did not

cause the electrical properties to deteriorate. Figure 4 Optical output power and I – V characteristics. (a) Optical output power as a function of the injection current with Au nanoparticles from the 2- and 5-nm Au-CNT systems, compared with a planar LED. (b) I-V characteristics of GaN LEDs with Au nanoparticles (-)-p-Bromotetramisole Oxalate from the 2- and 5-nm Au-CNT systems compared with a planar LED. To further confirm these results, photoluminescence (PL) spectra measurements were taken for all of the LEDs. The samples were pumped at a normal incidence angle with light from a He-Cd laser source (λ = 325 nm) with an excitation laser power of 10 mW at room temperature. The polarization direction of the laser was buy AZD3965 perpendicular to the Au nanoparticle chains. The laser beam penetrated through an attenuator and then was focused on the sample from the top using a 40 × UV objective lens with a focused spot diameter of approximately 5 μm.

Intraperitoneal rectal injuries will cause

peritonitis, sepsis and even death if not detected early. Intraperitoneal free air (IFA) is usually diagnosed by an erect Chest X-ray [2]. If the erect chest X-ray was normal, then an abdominal CT scan is recommended. Point-of-care ultrasound has been recently used to detect IFA [3, 4]. Hereby, we report an unusual case of trans-anal rectal injury in which point-of-care ultrasound was of a great help for an early diagnosis. Case presentation A 45-year-old male presented to the Emergency Department complaining of lower abdominal pain and dysuria of two days duration. His blood pressure was 120/80 mmHg, his pulse was 107 beat per minute and his temperature learn more was 36.8°C. Abdominal examination revealed tenderness and

guarding in the lower selleck products abdomen. Surgeon-performed portable point-of-care ultrasound as an extension of the abdominal examination was done immediately and revealed an inflamed omentum with hypoechoic stranding in the right upper quadrant (Figure 1A), thickened non compressible small bowel (Figure 1B), and free fluid in the pelvis. A transverse abdominal section of the right upper quadrant showed free intraperitoneal air (Figure 2). Rectal examination revealed a large longitudinal rectal tear 8 cm from the anal verge with an inflamed floppy mucosa. The patient admitted that he has inserted a glass bottle through his anus two days before, which was associated with sudden Demeclocycline lower abdominal pain and a small

amount of rectal bleeding. Erect chest X-ray confirmed the presence of air under the diaphragm (Figure 3). C-reactive AZD1480 research buy protein was 418 mg/L (Normal less than 0.7 mg/L), serum creatinine was 139 micromol/L (normal less than 107 micromol/l) and white blood cell count was 13.8 × 109/L. Arterial blood gas has shown an arterial oxygen tension of 50 mmHg on normal air. Laparotomy has confirmed the sonographic findings with thickened omentum, an edematous small bowel, pelvic abscess, and a 12 cm intraperitoneal tear of the anterior wall of the rectum which was necrotic (Figure 4). The rectum was dissected and transected 8 cm from the anus. Low mesorectal excision of the necrotic rectum and a Hartman’s procedure was performed. Two surgical drains without suction were left in the pelvis. Postoperatively, the patient was ventilated in the ICU. His arterial oxygen tension was 80 mmHg using an oxygen concentration of 50%. The patient received Tazocine intravenously 4.5 gms 8 hourly and Clexane 40 mg subcutaneously daily for one week. His respiratory and renal functions became normal within 4 days. The patient was discharged home on day 10 with good general condition and he is planned for reconnection of the colon after 3 months.

There are several immune evasion mechanisms,

which might explain the ability of the virus to escape the immune responses and establish a persistent infection. These immune evasion strategies include: virus mutation, primary T cell response failure, impairment of antigen presentation, suppression of T cell function by HCV proteins, impairment of T cell maturation and a tolerogenic environment in the liver [6]. Nevertheless, the immunological basis for the inefficiency of the cellular immune response in chronically infected persons is not well understood. Cellular immune responses play a critical role in liver damage during the clinical course of hepatitis C infection. HCV-specific CD4+ T cells are involved in eradication of the virus in acute infection but their responses are weak and insufficient in chronic hepatitis Dinaciclib [7]. However, there is no clear evidence that CD4+ T cells play a direct role in the liver injury observed during chronic HCV infection. CD4+ T cells activate

the CD8+ cytotoxic T lymphocyte (CTL) response, which eradicates the virus-infected cells either by inducing apoptosis (cytolytic mechanism) or by producing interferon-gamma (IFN-γ), which suppresses the viral replication (non-cytolytic mechanism) [8]. Enhanced hepatocyte apoptosis leads to liver damage in chronic HCV infections [9]. HCV-specific CD8+ CTL responses are compromised in most patients who fail to clear the infection. In addition, Ilomastat order those cells have a diminished capacity to proliferate and produce less IFN-γ in response to HCV antigens [10]. Those inefficient selleck screening library CD8+ T cell responses mediate HCV-related liver damage and are inadequate at clearing the chronic infection. The mechanisms responsible for immune-mediated liver damage associated with HCV are poorly understood. One of the mechanisms for liver damage is that the HCV-activated T cells express the Fas ligand at the cell surface, which will bind with the Fas receptor on hepatocytes, initiatiating Fas-mediated signaling, which may then lead to cell death [11]. HCV core protein increases the

expression of Fas ligand on the surface of liver-infiltrating T cells leading to the induction of hepatic inflammation and liver damage [12, 13]. Another important Selleck VS-4718 mechanism of immune-mediated liver damage is through CD8+ T cell-mediated cytolysis. Previous studies on concanavalin-A-induced hepatitis have demonstrated that CD8+ T cells can kill the target cells in vivo by cytolytic mechanisms mediated by perforin [14] or requiring IFN-γ [15]. This may also involve additional molecules such as TNF-α [16]; therefore, the level of cytolytic activity or expression of cytolysis mediators from the infiltrating lymphocytes could be a determinant for induction of immune-mediated liver damage. It is still controversial whether the liver damage associated with hepatitis C infection is due to the viral cytopathic effects or due to the immune response mediated damage.

Understanding the changes in generated nanotips will help us pick the right combinations of laser parameters to grow the desired amount and kind of nanotips over the large surface area of dielectric targets. Methods The experiments were performed on plain microscopic slide glass with composition of 60% to 75 wt.% SiO2, 5% to 12 wt.% CaO, PR-171 cell line and 12% to 18 wt.% Na2O. A direct-diode-pumped Yb-doped fiber amplifier/oscillator

system (wavelength, λ = 1,030 nm) capable of delivering a maximum average output of 16 W was used as a femtosecond laser source to irradiate targets with thickness of 0.90 to 1.0 mm. The laser intensity profile beam was focused into a spot (full width at half-maximum) diameter of 10 μm on the target surface using a telecentric lens of 100-mm effective focal length. The same setup was used to perform these experiments as reported in a previous paper done by our research group [16]. However, for these experiments, a square bracket was placed in front of the target surface which holds six nozzles providing continuous flow of nitrogen gas. The machining was performed in the form of 26 × 26 arrays of

microholes for various femtosecond laser parameters. We JNK inhibitor investigated the effect of three different pulse widths (214, 428, and 714 fs) on the generation of nanotips for a repetition rate of 13 MHz at a dwell time of 0.5 ms. The effect of various selleck laser JAK inhibitor pulse repetition rates (4, 8, and 13 MHz)

and different dwell times was also investigated on glass samples. All the aforementioned experiments were done by circular polarization of laser pulses. We also examined how different (linear, p-) polarizations would change the growth of nanotips on the target surface. The linear (p-) polarization of the beam was achieved by placing a half-wave plate in front of the focusing lens. The laser-irradiated glass samples have been analyzed by SEM. Results and discussion It is found that laser conditions have great effect on the nanotip growth. They control the population and the shape of the synthesized nanotips. Table 1 summarizes the observations. Table 1 Summary of effects of laser conditions to tip growth Laser parameters Effects on nanotip growth Pulse width Short pulses yield narrow long tips Repetition rate Higher repetition rate promotes the growth of dense, oriented narrow nanotips Dwell time Longer dwell time increases the population of nanotips. However, beyond an optimum dwell time, over heating will remelt the newly formed nanotips Polarization Linear (p-) polarization increases the population of nanotips Effect of pulse width There are two mechanisms responsible for laser-induced optical breakdown of materials: multiphoton absorption and avalanche ionization.

Minor sequence variants are underlined in the sequences. This applies to all sequence drug discovery tables Screening of Hypocrea gelatinosa. A single strain

(ICMP 5417) of this species has previously been screened positive Aib and Iva by a GC/MS-based approach (Brückner et al. 1991). From the specimen of H. gelatinosa, 14 compounds 14−27, six 18-residue and eight 19-residue peptaibols, were sequenced. All of them but compounds 14 and 18 are new (Tables 6 and 7, Table S2a and S2b; Fig. 2a). The 18-residue sequences, compounds 19−21, 23, 25, and 27, named gelatinosins B 1−6, resemble hypomurocins6 or neoatroviridins7. Two of the 19-residue sequences, compounds 14 and 18, are identical with the recently described hypopulvins from H. pulvinata (Röhrich et al. 2012). The selleck compound new compounds 15−17, 22, and 24, named gelatinosins A 1−5, exhibit a partially new building scheme − the residue in position 5 of the peptide chain was assigned as Phe, based upon HR-MS/MS data. gelatinosa was shown to produce three minor 11-residue SF4-peptaibols, compounds 6, 29, and 33, and nine gelatinosins B (compounds, 19, 20, 25, 27, 28, 30−32, and 34), 18-residue selleck products peptaibols of the hypomurocin/neoatroviridin-type.

However, 19-residue peptaibols have not been detected (Tables 6 and 7, Table S2a and S2b; Fig. 2b). tR [min] [M + H]+   Residuea 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 14 37.1–37.3 1866.0929 Ac Aib Ala Ala Ala Aib Gln Aib Lxx Aib Gly Lxx Aib Pro Vxx Aib Aib Gln Gln Pheol 15 37.7–37.8 Nintedanib molecular weight 1895.1067 Ac Aib Ala Aib Aib Phe Gln

Aib Aib Aib Gly Lxx Aib Pro Vxx Aib Aib Glu Gln Lxxol 16 38.0–38.2 1908.1358 Ac Aib Ala Aib Aib Phe Gln Aib Aib Aib Gly Lxx Aib Pro Lxx Aib Aib Gln Gln Lxxol 17 38.8–38.9 1909.1186 Ac Aib Ala Aib Aib Phe Gln Aib Aib Aib Gly Lxx Aib Pro Lxx Aib Aib Glu Gln Lxxol 18 39.5–39.6 1880.1083 Ac Aib Ala Ala Ala Aib Gln Aib Lxx Aib Ala Lxx Aib Pro Vxx Aib Aib Gln Gln Pheol 19 40.2–40.4 1762.0856 Ac Aib Ser Ala Lxx Aib Gln Aib Lxx Aib Gly Vxx Aib Pro Lxx Aib Aib Gln – Lxxol 20 40.9–41.1 1762.0840 Ac Aib Ser Ala Lxx Aib Gln Vxx Lxx Aib Gly Vxx Aib Pro Lxx Aib Aib Gln – Vxxol 21 41.2–41.4 1776.1023 Ac Aib Ser Ala Lxx Vxx Gln Aib Lxx Aib Gly Vxx Aib Pro Lxx Aib Aib Gln – Lxxol 22 41.9 1952.1674 Ac Aib Ala Aib Aib Phe Gln Aib Aib Aib Ser Lxx Aib Pro Lxx Vxx Aib Gln Gln Lxxol 23 42.1–42.3 1776.1023 Ac Aib Ser Ala Lxx Vxx Gln Vxx Lxx Aib Gly Vxx Aib Pro Lxx Aib Aib Gln – Vxxol 6 42.3 1203.8117 Ac Vxx Gln Lxx Lxx Aib Pro Lxx Lxx Aib Pro Lxxol                 24 42.9 1953.