The null hypothesis is that the introduction of posteriorly place

The null hypothesis is that the introduction of posteriorly placed implants into an

RPD has no effect on the load distribution. A Faro Arm FK866 cell line scan was used to extract the geometrical data of a human partially edentulous mandible. A standard plus regular neck (4.8 × 12 mm) Straumann® implant and titanium matrix, tooth roots, and periodontal ligaments were modeled using a combination of reverse engineering in Rapidform XOR2 and solid modeling in Solidworks 2008 FEA program. The model incorporated an RPD and was loaded with a bilateral force of 120 N. ANSYS Workbench 11.0 was used to analyze deformation in the IARPD and elastic strain in the metal framework. FEA identified that the metal framework developed high strain patterns on the major and minor connectors, and the acrylic was subjected to deformation, which could lead to acrylic fractures. The ideal position of the neutral axis was calculated to be 0.75 mm above the ridge. A potentially destructive mismatch of strain distribution was identified between the acrylic and metal framework, which could be a factor in the failure of the

acrylic. The metal framework showed high strain patterns on the major and minor connectors around the teeth, while the implant components transferred the load directly to the acrylic. “
“To analyze masticatory function after a short adaptation period relative to occlusal support length reduction in free-end removable partial VX-809 solubility dmso denture (RPD) wearers. Twenty-three patients (55.2 ± 8.4 years) were rehabilitated with maxillary complete and mandibular free-end RPDs extending to the second molars. Five occlusal support length conditions were determined by removing artificial teeth from the RPDs: full occlusal support (control); occlusal support to

the first molars, second premolars, and first premolars; and no occlusal support. To explore a probable short-term adaptation to occlusal support length reduction, participants wore their dentures at each condition for a period of 1 week before starting masticatory function assessment. For this purpose, masticatory performance, masticatory efficiency, chewing rate, selection chance, and breakage function were evaluated at each condition using the sieving method. Data were analyzed using repeated-measures ANOVA and post hoc Dunnett tests (α = 0.05). Masticatory performance Pembrolizumab and masticatory efficiency for 2 to 4 mm particles under the condition of occlusal support to the first molars and second premolars were similar to control values (p > 0.05). Masticatory efficiency relative to particles smaller than 2 mm was also seen at the condition of support length to the first premolars (p > 0.05). Chewing rates showed adaptation only at the condition of support length to the first molars (p > 0.05). A similar trend was noted for the selection chance of 8-mm particles, and breakage function for 8- and 2.4-mm particles (p > 0.05).

Samples were normalized using Significance Analysis of Microarray

Samples were normalized using Significance Analysis of Microarrays (SAM), and differentially expressed genes were identified at a nominal P ≤ 0.05. Unsupervised cluster analysis was performed using Cluster and TreeView programs.2. Only genes with a fold change ≥2 were included in the analyses. Functional classification and network analysis were performed using Ingenuity Pathway Analysis tool (Ingenuity Systems Inc.) and the GeneGo microarray tool. Microarray data from 139 HCC samples[21] were used for the survival

analysis according to the SIRT6 signatures. SIRT6 expression was selleck products investigated in a subcontingent of 53 HCC tumor specimens.[22] The Oncomine Cancer Microarray database (http://www.oncomine.org) was used to study gene expression of the SIRT6 signature in human HCC and conduct a meta-analysis for the predictive value of the SIRT6 signature in more than 40 different cancer types. Expression values of tumor samples were log-transformed and median-centered and standard deviation was normalized to one per array before comparison to their normal tissue counterparts as described

recently.[23] Statistical analysis was performed using Student t test or analysis of variance as indicated. P ≤ 0.05 was considered statistically significant. Results are presented as the mean ± SD or mean ± SEM as indicated. Univariate and multivariate analysis were performed using a chi-squared test and NVP-BEZ235 order Cox proportional hazard regression, respectively. For the multivariate analyses, only significant variables with sufficient data points were included. To investigate the relevance of SIRT6 for primary human HCC, we first used publically available gene expression data of liver cancer patients from the Oncomine Cancer Microarray database.[23] A significant reduction of SIRT6 expression was revealed in cirrhotic livers and HCC specimens (P < 0.001) compared with levels observed in noncirrhotic

livers (Fig. 1A). In confirmation of these findings, a down-regulation of SIRT6 in HCC tissues compared with nondiseased normal livers was also observed in around 45% (24/53) using independent gene expression data from our recently published cohort of 53 human acetylcholine HCCs (Fig. 1B, upper panel).[22] Consistently, around 42% (16/38) of the tumor samples showed SIRT6 levels below the median center of the expression data of all samples (normalized expression units < 0) of patient samples analyzed in Fig. 1A (Fig. 1B, lower panel). These data indicate a stepwise reduction of SIRT6 in both premalignant and malignant stages of hepatocarcinogenesis. To investigate the gene expression pattern deregulated by SIRT6 loss, we established a SIRT6 KO gene expression signature. To obtain a hepatocyte-specific transcriptome analysis, we isolated primary mouse hepatocytes from wild-type (WT) and Sirt6-deficient livers at 3 weeks of age.

02% This abnormality can present with epigastric pain, dyspepsia

02%. This abnormality can present with epigastric pain, dyspepsia, and upper gastrointestinal bleeding, or can be found incidentally. Our patient has remained asymptomatic after treatment of the gastric LBH589 price ulcer and discovery of the fistula during routine follow-up endoscopy. Patients respond well to conservative treatment for peptic ulcers. Accessory pylorus channels persist for life in the majority of patients. In some patients, however, such channels close or connect with the true pylorus to form a single channel, as observed in our patient. Surgical intervention is not typically considered a treatment option, although it should be considered in patients

with refractory symptoms and other complications. To prevent this complication, early diagnosis and appropriate treatment of the peptic ulcer are necessary. Contributed by “
“A 58 year-old Caucasian man, with a history of hyperlipidemia and benign prostate hypertrophy, complained of 3-week rectal bleeding. find more He also had a 6-month history of left lower quadrant pain, diarrhea, unintentional 14-pound weight loss, and urticaria. Examination revealed no lymphadenopathy, palpable mass, or organomegaly.

Abnormal laboratory results were as follows: gamma globulin 1.7 (normal: 0.6–1.6 g/dL), immunoglobulin A 439 (50–400 mg/dL). Other studies included white blood cell, hemoglobin, albumin, lactate dehydrogenase, uric acid, beta-2 microglobulin, C-reactive protein, C1 esterase inhibitor, and other immunoglobulins were within normal limits. Computed topographic (CT) colonography (Figure 1, left) and colonoscopy (Figure 1, right) demonstrated innumerable sessile polyps (2–4 mm) throughout the entire colon. Esophagogastroduodenoscopy Dolichyl-phosphate-mannose-protein mannosyltransferase and video capsule endoscopy also revealed

multiple small nodules in the duodenal bulb and ileum, respectively. Immunohistochemical staining of excised colonic polyps was positive for Cyclin D1 (Figure 2, 200x). The chest and abdomen CT scans showed no hepatosplenomegaly or lymphadenopathy, and the bone marrow examination was normal. The patient decided to return to his native state for further treatment. Mantle cell lymphoma (MCL) is a subtype of the B-cell non-Hodgkin lymphomas (NHL) and comprises about 7% of adult NHL. MCL is characterized by the chromosomal translocation t(11:14), resulting in overexpression of Cyclin D1. Cyclin D1 is a nuclear protein that promotes cell proliferation. Positive immunohistochemical staining for this protein is diagnostic for MCL. Approximately 25% of patients with MCL present with extranodal disease. Extranodal sites include bone marrow (>60%), liver and spleen (45–60%), Waldeyer’s ring, and gastrointestinal tract (20%). Multiple lymphomatous polyposis (MLP) is a rare primary gastrointestinal (GI) manifestation of MCL. It occurs predominately in male (65%) with mean age of 63 years. Endoscopy shows small polyps (0.5–2 cm) along one or more segments of the GI tract.

3A) In contrast to NIs, these molecules have shown a restricted

3A). In contrast to NIs, these molecules have shown a restricted spectrum of activity against the various HCV genotypes26 and present a very low barrier to emergence of resistance.27 The hallmark of all allosteric HCV NNIs described so far is that, in contrast to active site NIs, they are noncompetitive with nucleotide triphosphate substrates and inhibit the polymerase at a stage preceding the elongation reaction.1 Different NNI binding

sites are illustrated in Fig. 3B. These include thumb site I (benzimidazole-binding site), thumb site II (thiophene-binding site), palm site I (benzothiadiazine-binding site), and palm site II (benzofuran-binding site). Significant variability in the amino acid sequence is observed at these sites, making it difficult to achieve antiviral efficacy against different genotypes or even HCV isolates within the same genotype. As a result, most reported NNIs are rather specific for genotype 1 or 1b.14 Several structurally related NNIs have been shown to bind to the thumb site I.31 This class of inhibitors interrupts the intramolecular contacts between the thumb and the finger loop, thereby preventing the formation of a productive enzyme/RNA complex.32 These agents are also known as finger loop inhibitors and are characterized by having a

common benzimidazole or indole chemical core (Fig. 3B). HCV variants resistant to these agents carry mutations at positions P495, P496, and T38933, 34 (Fig. 3A). Clinically, agents belonging to this class of NNIs display reduced activity against genotype 1a compared with genotype 1b.35 Several thumb I NNIs are currently being investigated in phase 2 www.selleckchem.com/products/DMXAA(ASA404).html clinical trials, including

BI 207127, TMC647055, and BMS791325. Thumb II NNIs bind to a cavity located at the base of the thumb domain of NS5B (Fig. 3A). Mutations at positions L419, M423, and I482 in the viral polymerase have been shown to confer resistance to this class of compounds.36 Lomibuvir/VX-222 (Fig. 3B), a tiophene carboxylic acid, and filibuvir/PF-868554, a dihydropyranone derivative, are currently in phase 2 clinical trials. The palm I NNI-binding site is located at the junction of the palm and the thumb domain of NS5B, in proximity to the catalytic site. Benzothiadiazine compounds such as setrobuvir/RG7790 (formerly ANA598; Fig. 3B), ABT-333, and Interleukin-2 receptor ABT-072 bind to this NNI site. The most frequently resistant mutations selected by these agents are C316Y, M414T, Y448H/C, and S556G (Fig. 3A).37 These compounds are currently in phase 2 clinical trials. Acylpyrrolidines are yet another class of palm I-binding compounds.38 In this class, GSK625433 was advanced into phase 1 clinical trials, but this study was halted because of adverse effects noted in preclinical carcinogenicity studies.39 The palm II NNI-binding site partially overlaps with the palm I site and is located proximal to the junction between the palm and thumb domain.

In constructing the model, we made several assumptions based on d

In constructing the model, we made several assumptions based on data available

in the literature17–24 or justifiable clinical opinions (Table 1). The dropout probability from the WL of our reference HCC case receiving no bridging therapies (Strategy B) was calculated from four major studies,17–20 and this probability was confirmed in recent data from the UNOS database,6, 21, 22 where only a minority of patients had locoregional R788 cell line bridging therapies and the median time to LT was relatively short. The median time to transplant was used, rather than the median time on the WL, to calculate the daily probability of getting a transplant, as in other recent models,21, 22 because the latter excludes the time spent on the list with an inactive status. As mentioned above, we assumed that the conventional dropout probability of HCC patients was modified linearly by the specific sorafenib HR on time to progression.11, 12 In the base-case scenario,

we assumed an HR = 0.47, which is the value obtained in subgroup analyses on the efficacy of sorafenib for intermediate HCCs.23 Because there are no robust data in the literature on the tumor stage of WL patients at the moment of dropout, in our model we assumed that patients with compensated cirrhosis removed from the WL due to tumor progression were Barcelona clinic liver cancer (BCLC) B and C patients in equal proportions, whereas those with decompensated cirrhosis and tumor progression were assumed to be in BCLC D stage. According to recently buy C646 published guidelines,24,

25 patients with compensated cirrhosis and a tumor progressing beyond the MC (BCLC B and C patients) should be treated with chemoembolization (standard care for BCLC B patients) or sorafenib (standard care for BCLC C patients). We assumed that the BCLC B patients had a mean of selleck chemicals three TACE treatments, whereas the BCLC C patients were given systemic therapy with sorafenib. As reported in recent studies,11, 12, 24, 25 we set the median survival of treated patients at 20 months for BCLC B patients, and 10 months for BCLC C patients (Table 1). As mentioned above, we assumed that Strategy A patients developing a BCLC C tumor after dropout did not receive further sorafenib therapy. We set the median survival of untreated BCLC C patients at 7 months, whereas that of untreated BCLC D patients at 4 months.11, 12, 24, 25 In the sensitivity analysis simulating the introduction of locoregional treatments in Strategy B patients after the first 6 months on the WL, we assumed that patients underwent one percutaneous ablation and one TACE. As in recently published Markov models,16, 17 we considered an early transplant-related mortality of 5% and a long-term 5-year survival rate of 72% for patients transplanted for HCC meeting the MC. Our analysis included all direct health-related costs (in Euros in 2008) associated with each strategy, assessed from a payer’s perspective and discounted at 3% a year.

Our results are of further relevance considering that most patien

Our results are of further relevance considering that most patients with HCC are diagnosed at an advanced stage and that this group included the majority of patients

who were candidates for sorafenib treatment. By contrast, BCLC B patients who failed or were not suitable for locoregional treatments are a heterogeneous group of patients, representing a small subgroup of HCC patients who are candidates for sorafenib treatment, and not fully representative of the entire BCLC B spectrum. The robustness of these results was confirmed buy BKM120 in the probabilistic sensitivity analysis, showing that the probability of dose-adjusted sorafenib providing a cost-effective alternative to BSC was about 70% for advanced and 10% for intermediate HCC at a willingness-to-pay threshold of €38,000 per QALY.

The cost-effectiveness of dose-adjusted sorafenib in both advanced and intermediate HCC was sensitive to the BSC survival rate, sorafenib treatment duration, and the choice of parametric model used to predict survival gain. It is important to highlight that dose-adjusted sorafenib remains cost-effective in BCLC C HCC patients under a wide range of survival of untreated patients. This issue is very relevant, given the high heterogeneity and the unpredictability Cisplatin solubility dmso of clinical behavior of advanced HCC. 3 On the efficacy side of the cost equation, identification of robust predictive biomarkers would increase the overall efficacy of sorafenib for HCC by treating only those patients most likely to respond. This is not a trivial point, because sorafenib therapy is costly and still in search of optimization due to the lack of serum biomarkers of early response that are deemed necessary to generate see more response-guided therapeutic algorithms. Moreover, the identification of stopping rules based on predictors of mortality (such as early radiologic progression)

could assist the clinician in the cost-effective management of patients with HCC. Unfortunately, stopping sorafenib in patients with early radiologic progression only marginally improves the cost-effectiveness ratio. Therefore, the identification of the optimal sorafenib dose, effective but not toxic, remains to date the only strategy to substantially improve the ICER. Modeling the indication for treatment of advanced/intermediate HCC with dose-adjusted sorafenib clearly improves its cost effectiveness. In this line, the role of dose-adjusted sorafenib should be taken into account also for the future perspectives in the adjuvant setting after resection/ablation or after transarterial chemoembolization and for the design of future comparative trials versus novel targeted therapies. Although the proposed algorithms are useful tools for decision making, the treatment strategy should be carefully agreed upon with the patient, taking into account all the different factors, particularly the safety profile, that can interfere with treatment response.

Key Word(s): 1 Ursodeoxycholic acid; 2 colorectal adenomas; 3

Key Word(s): 1. Ursodeoxycholic acid; 2. colorectal adenomas; 3. colorectal cancer; 4. systematical review; Presenting Author: CHAN SEO PARK Additional Authors: BYUNG IKBYUNG IK, KYEONG OKKYEONG OK, SI HYUNGSI HYUNG, SUNG BUMSUNG BUM Corresponding Author: BYUNG IKBYUNG IK Affiliations: Yeungnam PLX4032 mw University College of Medicine Objective: Rectal carcinoid tumors ≤1 cm in size can be treated by endoscopic resection. The aim of this study was to investigate the clinical feature and to clarify the treatment outcome

of a technique named endoscopic submucosal resection with a ligation device (ESMR-L) in a large number of rectal carcinoid tumors. Methods: Between March 2007 and February 2013, 66 cases of carcinoid tumors in colorecum were detected and 55 cases of carcinoids estimated at 10 mm or less in diameter. 59 cases were treated endoscopically. 7 cases were removed by endoscopic biopsy, 13 cases were removed by conventional endoscopic mucosal resection (EMR) and 39 cases were removed by endoscopic submucosal resection with a ligation device (ESMR-L). The clinical feature, selection of treatment, complete resection rate, local recurrence, distant metastases and complications associated with the procedure were analyzed. Results: Of

66 cases were 37 males and 29 females with a mean age of 50.70 ± 12.53 years. Tumor size ranged from 0.3 to 2 cm in diameter, with an average

size of 0.83 ± 0.41 cm. Carcinoids were located in rectum (62 cases), sigmoid click here colon (3 cases) and cecum (1 case). Distribution of rectal carcinoids were located in the 6.63 ± 2.98 cm Torin 1 concentration from anal verge. 52 cases of rectal carcinoids were treated by EMR or ESMR-L. The mean lengths of hospital stay were 2.7 days. Complete resection of the lesions was obtained in 88.5% (46/52). The complete resection rates were 61.5% (8/13) by conventional EMR and 97.4% (38/39) by endoscopic submucosal resection with a ligation device. ESMR-L was superior to conventional EMR in terms of complete resection (p = 0.003). Minor bleeding associated with the ESMR-L occurred in two lesions (5.1%), but all cases were successfully managed with hemoclips. Histopathologically, all tumors were confined to submucosal layer. 2 cases were with lymphovascular invasion, 1 case was with perineural invasion and 7 cases were with remnant tumor cells at resection margin. But, neither local recurrence nor distant metastasis of all rectal carcinoids was detected during a median follow-up period of 49.6 ± 14.6 months. Conclusion: In our studies, ESMR-L proved to be a safe and effective procedure to resect rectal carcinoid tumors measuring less than 1 cm in a diameter. And ESMR-L is decidedly superior to conventional endoscopic polypectomy. Key Word(s): 1. Carcinoid tumor; 2. Rectum; 3.

there was significant diferrence in level 2

to level 1 an

there was significant diferrence in level 2

to level 1 and level 3 to level 1 (P < 0.05). 2) pathological grade on mucosal inflammation: there were 7 level 1,11 level 2 and 50 level 3. there was significant diferrence between level 3 to level 1 and level 3 to level 2 (P < 0.05)3) Montreal grade: 15 patients was E1 (22.1%), 27 patients MK-2206 chemical structure was E2 (39.7%) and 26 patients wsa E3 (38.2%). there was no significant diferrence between three groups. 5. follow-up observation: 24 patients carried out follow-up colonoscopy, 1 patient’s moderate dysplasia developed to severe dysplasia, other patients’dysplasia disappeared with the improvement of inflammation. Conclusion: middle-aged and male UC patients have dysplasia Alectinib supplier more easily, and mild dysplasia accounts for most

dysplasia. Dysplasia is most found in ulcer and erosion which has severe inflammation and in all-colitis type and left semi-colitis type. most patients’dysplasia disappears with the vanishing of the inflammation, we consider that most dysplasia is relatted to inflammation, frequent follow-up was needed to UC with dysplasia. Key Word(s): 1. ulcerative colitis; 2. dysplasia; 3. canceration; Presenting Author: KATJA GRUBELIC RAVIC Additional Authors: MARKO BRINAR, SILVIJA CUKOVIC CAVKA, NADA BOZINA, BORIS VUCELIC, MARTINA ROJNIC KUZMAN, ZELJKO KRZNARIC, NADAN RUSTEMOVIC Corresponding Author: KATJA GRUBELIC RAVIC, MARKO BRINAR, SILVIJA CUKOVIC CAVKA, NADA BOZINA, BORIS VUCELIC, MARTINA ROJNIC KUZMAN, ZELJKO KRZNARIC, NADAN RUSTEMOVIC Affiliations: University Hospital Zagreb; University check details Hospital Centre Zagreb Objective: Serotonin

(5-HT) is an important factor in gut function, playing key roles in intestinal peristalsis, secretion, vasodilatation and sensory signalling. The serotonin-selective reuptake transporter protein (SERT) terminates the action of 5-HT. Human SERT is encoded by a single gene on chromosome 17q11; 2 important polymorphic sites in the SERT gene are: variable number tandem repeats in the gene’s second intron (SERTin2), and an insertion/deletion in the promoter region (SERTPR). Consistent with the effects of 5-HT in the gut, SERT polymorphisms could potentially be involved in the development of different CD phenotypes. The aim of this study was to evaluate the relationship between SERT polymorphisms in CD patients vs. controls. Methods: A total of 193 CD patients (phenotyped in 3 group according to Vienna classification) and 217 control were subjected to genotyping. DNA of all subjects was analysed by polymerase chain reaction (PCR-RT). The association of genetic polymorphic variant SERTPR/rs 25531 and SERTin2 polymorphic loci with the CD patients vs. controls was tested using program SPSS 13.0, UNPHASED ver. 3.0. 10. A test for Hardy – Weinberg equilibrium using Markov chain method implemented in Arlequin ver. 3.0.

there was significant diferrence in level 2

to level 1 an

there was significant diferrence in level 2

to level 1 and level 3 to level 1 (P < 0.05). 2) pathological grade on mucosal inflammation: there were 7 level 1,11 level 2 and 50 level 3. there was significant diferrence between level 3 to level 1 and level 3 to level 2 (P < 0.05)3) Montreal grade: 15 patients was E1 (22.1%), 27 patients Quizartinib purchase was E2 (39.7%) and 26 patients wsa E3 (38.2%). there was no significant diferrence between three groups. 5. follow-up observation: 24 patients carried out follow-up colonoscopy, 1 patient’s moderate dysplasia developed to severe dysplasia, other patients’dysplasia disappeared with the improvement of inflammation. Conclusion: middle-aged and male UC patients have dysplasia selleck kinase inhibitor more easily, and mild dysplasia accounts for most

dysplasia. Dysplasia is most found in ulcer and erosion which has severe inflammation and in all-colitis type and left semi-colitis type. most patients’dysplasia disappears with the vanishing of the inflammation, we consider that most dysplasia is relatted to inflammation, frequent follow-up was needed to UC with dysplasia. Key Word(s): 1. ulcerative colitis; 2. dysplasia; 3. canceration; Presenting Author: KATJA GRUBELIC RAVIC Additional Authors: MARKO BRINAR, SILVIJA CUKOVIC CAVKA, NADA BOZINA, BORIS VUCELIC, MARTINA ROJNIC KUZMAN, ZELJKO KRZNARIC, NADAN RUSTEMOVIC Corresponding Author: KATJA GRUBELIC RAVIC, MARKO BRINAR, SILVIJA CUKOVIC CAVKA, NADA BOZINA, BORIS VUCELIC, MARTINA ROJNIC KUZMAN, ZELJKO KRZNARIC, NADAN RUSTEMOVIC Affiliations: University Hospital Zagreb; University selleckchem Hospital Centre Zagreb Objective: Serotonin

(5-HT) is an important factor in gut function, playing key roles in intestinal peristalsis, secretion, vasodilatation and sensory signalling. The serotonin-selective reuptake transporter protein (SERT) terminates the action of 5-HT. Human SERT is encoded by a single gene on chromosome 17q11; 2 important polymorphic sites in the SERT gene are: variable number tandem repeats in the gene’s second intron (SERTin2), and an insertion/deletion in the promoter region (SERTPR). Consistent with the effects of 5-HT in the gut, SERT polymorphisms could potentially be involved in the development of different CD phenotypes. The aim of this study was to evaluate the relationship between SERT polymorphisms in CD patients vs. controls. Methods: A total of 193 CD patients (phenotyped in 3 group according to Vienna classification) and 217 control were subjected to genotyping. DNA of all subjects was analysed by polymerase chain reaction (PCR-RT). The association of genetic polymorphic variant SERTPR/rs 25531 and SERTin2 polymorphic loci with the CD patients vs. controls was tested using program SPSS 13.0, UNPHASED ver. 3.0. 10. A test for Hardy – Weinberg equilibrium using Markov chain method implemented in Arlequin ver. 3.0.

It provides a detailed analytical means of studying broader aspec

It provides a detailed analytical means of studying broader aspects of carnivoran feeding ecology, such as predation habits, carrying capacity, ecological hunting requirements and species interactions, which are important aspects of carnivoran management. “
“The Italian Peninsula was one of the main refugia in southern Europe during the climatic oscillations of the Pleistocene, and was considered a ‘hotspot’ of biodiversity. A number of phylogeographic analyses identified highly divergent lineages SB203580 cost in Italy that apparently did not contribute to the post-glacial

re-colonization of Europe, supporting the existence of refugia within refugia in the southern-most part of Italy. For the bank vole Myodes glareolus, genetic analyses highlighted a low variability for this species on the Italian peninsula, suggesting that cryptic refugia of central Europe were the main source of postglacial re-colonization in Europe.

In this work, we analysed the mtDNA phylogeography of M. glareolus with a special emphasis on the Italian refugium. We extended previous analyses by including new sequences from a wider range of samples across Daporinad in vivo the Italian peninsula. Our results suggest a high mitochondrial diversity of the bank vole in Italy and support the existence of an ancient and deeply divergent population in the Calabria region. This population did not participate to the recent re-colonization of Italy while we highlight the possible occurrence of multiple and more recent colonization events between Europe and Italy. The phylogeographic pattern observed in Italy appears compatible with refugia-within-refugia scenario. “
“Live-capture is a necessary component for the scientific study and management of most mammals, but it may negatively affect their health and physiology. We compared blood parameters related to the

stress response (nominal base levels) from red squirrels Tamiasciurus hudsonicus see more after capture of up to 4.5 h in five different live trap models (Hava-hart, Sherman, Tomahawk 102, Tomahawk 103 and ‘Special Squirrel’ trap) with true base levels (obtained in less than three minutes). In addition, we evaluated the capture rate in the five trap models. We found that (1) prolonged time in live traps altered stress hormone concentrations compared with true base levels, but maximum corticosteroid-binding capacity was unaffected; (2) squirrels captured in a trap model with reduced visibility (a roof cover – Hava-hart) had significantly lower (c.