From Darwin’s statement (above) about the superiority of natural selection over the argument from design, we might imagine that Ray’s questions about reproduction would have been answered soon after the publication the Origin in 1859. Not so. Natural selection was, and still is, a better conceptual framework for

thinking about the natural world, and provided a compelling and straightforward explanation for the existence of parasites and parasitoids. Sex, however, continued to be a mystery, and because Darwin largely avoided questions about the Crenolanib supplier number of sperm and copulation behaviour, it was almost a century before anyone tackled these questions and offered a convincing answer. Retrospectively, biologists such

as Smith (1984, 1998) attributed Darwin’s lack of interest in promiscuity to a statement in Descent: ‘It is shown by various facts, given hereafter, and by the results fairly attributable to sexual selection, that the female, though comparatively passive, generally exerts some choice and accepts one male in preference to the others’ (Darwin, 1871). The emphasis here being on one male, a clear indication that Darwin assumed females at least to be sexually monogamous. I have suggested that Darwin made this assumption as a way of avoiding embarrassment, both with the public and within his learn more family, especially his wife Emma and daughter Etty (Henrietta), the latter who helped him correct the proofs of Descent (Birkhead, 1997). Darwin’s desire to avoid offending his family, undoubtedly Chloroambucil reinforced by Victorian prudery, inhibited his writing on sexual matters. When he felt it necessary to discuss the sexual swellings of female primates, for example in Descent he wrote the passage in Latin knowing that Etty would be unable to read it. Darwin was well aware of female promiscuity, from the literature, from his correspondents and from personal observation (Barrett et al., 1987; Smellie, 1790). With reference to the pigeons he kept and bred, Darwin (1868) wrote: ‘even when a male does break his marriage-vow, he does not permanently desert his

mate’. Notice here that the emphasis is the male rather than the female breaking the marriage vow. Most pigeon breeders, however, including Girton (1765), whose book Darwin owned, recognized the existence of extra-pair copulations, pointing to the fact that selective breeding could easily be disrupted by a ‘false tread’ (an extra-pair copulation). Even more significantly, Darwin was aware of the extensive literature on so-called ‘thief pigeons’ in which particularly attractive males could cause paired females to abandon their partner in favour of themselves – even during the incubation period (Darwin, 1871; Birkhead, 2008). Darwin also knew that whatever it was that made these males irresistible to females was inherited, for pigeon breeders could select for it.

When responses to questions about sexual or personal grooming practices were discordant between partners, responses were recoded for presence rather than absence of the practice. The study was approved

by the Institutional Review Boards of the University of California at San Francisco, Blood Centers of the Pacific, California Pacific Medical Center, Kaiser Permanente Northern California, St. Louis University, and the Centers for Disease Control and Prevention. Serum samples from index subjects were tested for anti-HCV via enzyme immunoassay (EIA 2.0) (Abbott https://www.selleckchem.com/products/c646.html Laboratories, Abbott Park, IL) and for HCV RNA via qualitative polymerase chain reaction (PCR) with detection limit ≤50 IU/mL (Roche Amplicor, Roche Molecular Diagnostics, Pleasanton, CA) (if not documented in medical records in prior 6 months). Serum samples from partners

were tested for anti-HCV via EIA and positive results confirmed via recombinant immunoblot assay (RIBA 3.0, Chiron Corporation, Emeryville, CA). RIBA-positive samples were tested for HCV RNA via qualitative PCR. Serotyping of the antibody based on RIBA methodology was used in anti–HCV-positive click here concordant couples with HCV RNA–negative partners.10 Genotype was determined in samples from anti–HCV-positive, HCV RNA–positive concordant couples using the InnoLipa assay (Innogenetics, Ghent, Belgium). HCV RNA–positive specimens from genotype-concordant couples were amplified via reverse-transcription nested PCR, and the HCV consensus sequences were determined by directly sequencing uncloned PCR products

from the 897-nucleotide-long NS5B region for genotype 1a and 1b samples and from a 944-nucleotide-long NS5B region for the 2b samples employing ABI dye-termination techniques.11 The 1a and 1b sequences correspond to H77 positions 7479 to 8375 (with genotype 1b sequences missing three nucleotides relative Cell press to the 1a sequences, resulting in a gap corresponding to 7566 to 7568 in the H77 sequence). These 1a/1b alignments cover the region of the ORF coding for the last 42 amino acids of NS5A and the first 258 amino acids of NS5B.The genotype 2b alignments correspond to the H77 sequence 8326-9269, encoding NS5B from amino acid 242 to 556.To evaluate the relatedness between isolates from genotype-concordant partners, the consensus sequences from their isolates were compared with corresponding regions from reference sequences of the same subtype downloaded from the Broad Institute or from the National Center for Biotechnology Information; this included 99 genotype 1a and 97 genotype 1b sequences. The sequences were imported into the MEGA 4 sequence analysis package, and the pairwise distances and number of differences were calculated for each pair. These nucleotide sequences have been submitted to GenBank under accession numbers HQ022864-HQ022879.

For the detection of differentially expressed genes, we used the Limma package. Adjustment of p-values was done by the determination of false discovery rates (FDR). Functional analysis was conducted using the R/Bioconductor package GOstats and the GO database. Unsupervised clustering analysis revealed a unique gene expression signature of livers with AH, which was markedly distant to NASH and control groups. We next identified the pathways that were only overexpressed in patients with AH compared to NASH and control livers. The “structural molecule activity” was the most significant up-regulated pathway

in AH (p= 7.5 x10-9). Within this family, we identified cytokeratin 23 (KRT23), an intermediate filament, and one of the most up-regulated genes in the whole transcrip-tome (94-fold increased compared to normal livers). Next, we confirmed by qPCR that hepatic expression Ibrutinib in vitro of KRT23 was markedly up-regulated in patients with AH compared to other liver disease such as HCV, compensated alcoholic cirrhosis and NASH. Serum levels of KRT23 were also found elevated only in Wnt inhibitor patients with AH. Importantly, the baseline hepatic mRNA expression of KRT23 correlated with disease severity and 90-day survival (AUROC: 0.72). Immunohistochemistry

studies showed that KRT23 was expressed at the areas of ductular reaction and progenitor cell expansion. Next, we explored the expression of KRT23 in experimental models of acute-on-chronic liver injury and in models progenitor cell expansion in mice. We found that hepatic KRT23 was induced by an acute injury (either by LPS orethanol) on a fibrotic liver. Interestingly, KRT23 was expressed in two models of progenitor cells expansion

in liver injury (DDC and CDE diets) and was detected in progenitor cells. In summary, human and experimental data indicate that KRT23 is a novel marker of progenitor cell Doxorubicin price expansion and potential molecular driver of alcoholic hepatitis. Loss-of-function studies in animal models of AH should investigate the role of KRT23. Disclosures: Vicente Arroyo – Speaking and Teaching: GRIFOLS The following people have nothing to disclose: Gemma Odena, Juan José Lozano, Jose Altamirano, Daniel Rodrigo-Torres, Oriol Morales-Ibanez, Silvia Affò, Malika Humphries, Pau Sancho-Bru, Juan Caballeria, Ramón Bataller Background: In our established chronic alcohol exposure model, progressive liver injury is associated with microvesicular steatohepatitis, early fibrosis, hepatic insulin resistance, and increased hepatic ER and oxidative stress. Previous studies showed that limited low-level exposures to dietary nitrosamines also cause steatohepatitis with hepatic insulin resistance and oxidative stress. Epidemiologic data indicate that in humans, heavy alcohol abuse that leads to alcoholic liver disease (ALD) is associated with binge drinking and cigarette smoking.

Key Word(s): 1. Tumor suppressor; 2. alkB gene; 3. DNA methylation; 4. Lentivirus; Presenting Author: ZHONGQIU WANG Additional Authors: PU WANG, BO JIANG Corresponding Author: BO JIANG Affiliations: Department of Gastroenterology, Nanfang Hospital, Southern Medical University; Department of Gastroenterology, Nanfang Hospital, Southern Medical University Objective: Microbial translocation from the gastrointestinal

tract has been implicated in many fetal diseases, such as SIRS, MOFS etc. Syndecan-1 (Sdc1) is the predominant cell surface heparan sulfate proteoglycan expressed on intestinal epithelia, and there is substantial evidence that heparin sulfate participates in binding a wide variety of microbes to mammalian cells to mediate microbial adherence and internalization, but few studies have focused AZD2281 mouse on their translocation and the potential mechanismis unknown.

check details Our experiments were designed to clarify the ability and mechanism of Sdc1 on mediating the translocation of enteric flora with intestinal epithelium. Methods: Expression of Sdc1 in different colon intestinal cell lines was detected by RT-PCR, Western blot and immunofluorescence. Bacterial translocation and epithelial permeability assays were performed using transwell polyester membrane filters. After the confluent cells reached a TER of almost 300 omegas measured using an epithelial tissue voltohmmeter, bacteria suspensions were taken from the basolateral chamber and TER was measured at the same time point. Ectopic expressions of Sdc1 were

obtained by transfecting Sdc1 overexpresstion plasmid or Sdc1 siRNA and the corresponding PtdIns(3,4)P2 bacterial translocation and epithelial permeability assays were performed. Coorperation between Sdc1 and tight junction (TJ) proteins was conformed via co-IP, western blot and immunofluorescence. Results: High Sdc1 expression on HT-29 and low Sdc1expression on Caco-2 enterocytes both appeared concentrated on the cell borders, while high expressions on SW480 and low expression on LoVo were on cytoplasm and nucleus respectively. It demonstratedSdc1 inhibited translocation of E.coli across HT-29 monolayer, but not Caco-2 for both the TER reduction (28.2% ± 4.1% vs. 54.9% ± 5.8%) and E.coli translocation (57.5 ± 6.1% vs.90.6% ± 14.4%) across HT29 were significantly less (P < 0.01). Ectopic expression of Sdc1 by transfecting Sdc1 overexpresstion plasmid notably inhibited TER reduction (40.2% ± 5.0% vs. 60.4% ± 6.3%) and E.coli translocation (57.4% ± 4.8% vs. 77.0% ± 11.1%)(P < 0.01). And blocking Sdc1expression by transfecting Sdc1 siRNA significantly increased TER reduction (40.9% ± 5.6% vs. 13.4% ± 5.3%) and E.coli translocation (88.5 ± 4.3% vs. 21.6% ± 5.8%)(P < 0.01). Moreover, Sdc1 colocalized with TJ proteins on the membrane of intestinal epithelial cells. Co-IP and western blot also demonstrated Sdc1 bound to TJ proteins, and altered expressions of Sdc1 affects expression of TJ proteins.

“
“p38α mitogen-activated protein kinases (MAPK) may be essential in the up-regulation of proinflammatory cytokines and can be activated by transforming growth factor β, tumor necrosis factor-α, interleukin-1β, and oxidative stress. p38 MAPK activation results in hepatocyte growth arrest, whereas increased proliferation has been considered a hallmark of p38α-deficient cells. Our aim was to assess the role of p38α in the progression of biliary cirrhosis induced by chronic cholestasis as an experimental model of chronic inflammation associated with hepatocyte proliferation, apoptosis, oxidative stress, and fibrogenesis. Cholestasis was induced

in wildtype and liver-specific p38α knockout selleck mice by bile duct ligation and animals were sacrificed at 12 and 28 days. p38α knockout mice exhibited a 50% decrease in mean life-span after cholestasis induction. MK0683 MK2 phosphorylation was markedly reduced in liver of p38α-deficient mice upon chronic cholestasis. Hepatocyte

growth was reduced and hepatomegaly was absent in p38α-deficient mice during chronic cholestasis through down-regulation of both AKT and mammalian target of rapamycin. Cyclin D1 and cyclin B1 were up-regulated in liver of p38α-deficient mice upon chronic cholestasis, but unexpectedly proliferating cell nuclear antigen was down-regulated at 12 days after cholestasis induction and the mitotic index was very high upon cholestasis in p38α-deficient mice. p38α-knockout hepatocytes exhibited cytokinesis failure evidenced by an enhanced binucleation rate. As chronic cholestasis evolved the binucleation rate decreased in wildtype animals, whereas it remained high in p38α-deficient mice. Conclusion: Our results highlight a key role of p38α in hepatocyte proliferation, in the development of hepatomegaly, and in survival during chronic inflammation such as biliary cirrhosis. (HEPATOLOGY 2013) Mitogen-activated protein kinases (MAPKs) are essential for the cellular response against injury and for regulation of cell death and tissue homeostasis. p38 MAPKs are a family of serine/threonine

protein kinases activated by environmental and genotoxic stress that have key roles in the Aspartate control of cell proliferation, differentiation, and survival, as well as in the regulation of the inflammatory response.1 p38α is the most abundant kinase within the p38 MAPK family and displays relevant biological roles in pathophysiology. Increased proliferation and impaired differentiation have been considered hallmarks of p38α-deficient cells.2 Mice with liver-specific deletion of p38α exhibited enhanced hepatocyte proliferation after partial hepatectomy2 and developed more liver tumors with increased numbers of proliferative tumor cells.3 p38α may repress cell proliferation by antagonizing the c-Jun N-terminal kinase (JNK)/c-Jun pathway.

Anseriformes, the fastest-flying birds in our sample, exhibit only moderate

eye sizes, while the Accipitridae, grouped within the Falconiformes, are the largest-eyed birds measured but have only moderate flight speeds. We, therefore, conclude that Leuckart’s Law as a simple expression of flight speed is not useful for explaining bird eye sizes. “
“In many polygynous mammals, sexual size dimorphism (SSD) is thought to have evolved through sexual selection, because larger males prevail in male–male combat and secure access to estrous females. SSD is often correlated with higher age-specific mortality of males than FDA-approved Drug Library of females, possibly because males have higher nutritional requirements and riskier growth and reproductive tactics. www.selleckchem.com/products/MK-1775.html In adult chamois Rupicapra rupicapra, sexual dimorphism in skeletal size was about 5%, but dimorphism in body

mass was highly seasonal. Males were about 40% heavier than females in autumn but only 4% heavier in spring. For a given skeletal size, males were heavier than females only in autumn. Chamois sexual dimorphism appears mainly due to greater summer accumulation of fat and muscle mass by males than by females. Male mass declines rapidly during the rut. Limited dimorphism in skeletal size combined with substantial but seasonal dimorphism in mass has not been reported in other sexually dimorphic ungulates. Seasonal changes in mass allow males to achieve large size for the rut by accumulating body resources during summer. The use of these resources over the rut may reduce mortality associated with sustaining

a large size over the winter. “
“Optimal escape theory predicts that animals should moderate their flight responses according to the level of risk represented by a potential predator. This theory should apply even when organisms are habituated Histidine ammonia-lyase to disturbance, and how animals respond to human presence is likely to determine their success exploiting urban habitats. Therefore, urban animals should be sensitive to cues that inform them about levels of risk, allowing them to reduce costs by not overreacting to innocuous stimuli, while ensuring that they are nevertheless reactive to genuinely threatening stimuli. We tested this at a highly urbanized site in New York City, where eastern grey squirrels appear to pay little attention to humans. Squirrels were approached tangentially on a trajectory that took the observer within ∼2 m of them and we measured alert distance, flight initiation distance (FID), and distance fled for each focal individual. Squirrels showed little sign of being alerted to the pedestrian if he remained on the footpath and did not look at them (only 5% of individuals moved away), but 90% of squirrels moved away, with longer FID and flight distance, when approached by a pedestrian that moved off the footpaths and looked at them. Squirrels therefore modulate their reactions when pedestrians behave in a predictable manner (i.e.

Reliable measurements were defined as: median value of 10 (TE, ARFI) LS measurements with a success rate≥60% and an interquartile range interval<30%, values expressed in kPa (TE) or m/s (ARFI). Reliable LS measurements by means of SSI were definied PD-332991 as the median value of 5 LS measurements expressed in kPa. Results: The etiology of liver disease was: chronic hepatitis C – 99 patients (57.6%), chronic hepatitis B – 67 patients (38.9%), coinfection (B+C virus or B+D virus) – 6 patients (3.5%). Reliable LS measurements were obtained in a significantly higher percentage of patients by means of ARFI elastography as compared with TE and SSI:

92.5% vs. 79.1%, (p=0.0007) and 92.5% vs.81.9%, (p<0.0001), respectively. The rate of reliable LS measurements was similar for TE and SSI: 79.1% vs. 81.9%, (p=0.60). Conclusion: The most feasible shear-waves ultrasound elastographic method for non-invasive assessment of liver fibrosis in chronic viral hepatitis patients was ARFI. Key Word(s): 1. liver fibrosis; 2. liver stiffness; 3. elastography; 4. shear wave; Presenting Author: IOAN SPOREA Additional

Authors: OANA GRADINARU-TASCAU, SIMONA BOTA, ANA JURCHIS, ALINA POPESCU, MADALINA POPESCU, ROXANA SIRLI, MILANA SZILASKI Corresponding Author: IOAN SPOREA Affiliations: Department of Gastroenterology and Hepatology,”Victor Alisertib nmr Babes” University of Medicine and Pharmacy, Timisoara, Romania Objective: To identify if experience plays a role in the liver stiffness (LS) measurements by means of SSI. Methods: The study included 371 consecutive subjects with or without hepatopathies, in which LS was MG-132 datasheet evaluated with an AixplorerTM ultrasound system (SuperSonic Imagine S. A., Aix-en-Provence, France). Reliable LS measurements by means of SSI were definied as the median value of 5 LS measurements expressed in kilopascals (kPa). The SSI measurements were performed by a novice (with less than 300 abdominal ultrasounds performed) or by a more experienced

operator (with approximately 500 ultrasounds performed). Results: The study group included 371 consecutive subjects, 42% men and 58% women, with a median age of 48 years (ranging between 17-85 years). The novice performed 57.4% and the more experiecend operator 42.6% of the SSI measurements. The more experienced operator had a higher rate of reliable examinations compared with the novice : 87.4% vs. 72.8% (p =0.001). The rate of reliable measurements was similar for novice and experienced operator in patients with a normal weight (BMI < 25 kg/m2) and in overweight patients (BMI between 25.1 – 29.9 kg/m2), 92.3% vs. 97.5%, p=0.24, respectively 71.1% vs 80.4%, p=0.39. For obese patients (BMI ≥ 30 kg/m2) the rate of reliable LS measurements was significantly higher for the more experienced operatos as compared with the novice: 73.4% vs 45.9%, p=0.

In most of these discrepant cases, the factor VIII levels are reduced by 50% or more when measured by a two-stage assay as compared with a one-stage assay and this can lead to missing the diagnosis of mild haemophilia A when a one-stage assay is used as a screening method. The reverse situation, higher factor VIII levels

with a two-stage method than with a one-stage method, is less frequent. Mutations and molecular mechanisms of many of these discrepant cases have been resolved [12–14]. However, it remains unclear which assay is the best reflection of the bleeding phenotype. Using thrombin generation assays in patients with the more common discrepancy pattern (FVIII lower by two-stage assay), the most significant correlation was www.selleckchem.com/screening/gpcr-library.html found between the one-stage FVIII assay and thrombin generation [12]. In two families with the

‘reversed discrepancy’ (FVIII higher by two-stage assay) and contrasting clinical www.selleckchem.com/products/poziotinib-hm781-36b.html histories (one family bleeding and one non-bleeding), impaired thrombin generation reflected the bleeding phenotype [15]. Characterization of the molecular mechanisms resulting in low FVIII levels have helped to identify regions of the factor VIII gene critical for proper factor VIII biosynthesis, thrombin activation, intramolecular stability as well as binding regions for important partners such as von Willebrand factor, factor IXa and the phospholipid surface [16]. In patients with the common presentation of mild haemophilia A with reduced FVIII activity in a two-stage assay as compared with a one-stage assay, a number of missense mutations mainly clustered within the A domains have been described that lead to defective stability

of FVIIIa. Conversely, mutations impairing FVIII activation by thrombin result in higher FVIII activity in a two-stage than in a one-stage assay [14]. Some particular FVIII missense mutations, mainly located within the region encoding for the light chain of factor VIII, contribute to an unexpectedly high incidence of inhibitors in mild haemophilia A [16,17]. Genetic testing might thus become an important key feature in the management of mild haemophilia A patients. Most patients with mild haemophilia A respond well to the administration of desmopressin which typically results in a 2–6-fold increase of FVIII levels Selleckchem Forskolin over baseline [18]. The peak postdesmopressin levels of FVIII depend on the patient’s basal FVIII level [19] and postdesmopressin FVIII half-life, typically around 5–8 h, is positively related to basal and peak von Willebrand Factor Antigen levels and patient age [20]. Young children often have a markedly lower response to desmopressin than adults [21]. Postdesmopressin FVIII levels >0.30 IU mL−1 are considered clinically adequate at least for the treatment of spontaneous or posttraumatic bleeding, whereas a postdesmopressin FVIII level of at least 0.50 IU mL−1 is required for the treatment of major surgery.

Conclusion: When colonizes in esophagus, H. pylori increases the severity of esophageal inflammation and the incidence of BE and EA. The process may involve in the activation of NF-kB signaling pathway. Key Word(s): 1. esophagus; 2. NF-kB; 3. Helicobacter pylori; Presenting Author: SHU-JUN WANG Additional Authors: WEI-HONG WANG, YUN-XIANG CHU, GUI-GEN TENG Corresponding Author: WEI-HONG WANG

Affiliations: Peking University First Hospital Objective: To compare the efficacy of concomitant therapy for 7 days with standard triple therapy for 7 or 10 days in H. pylori eradication in China. Methods: 246 patients who were diagnosed as H. pylori infection by rapid urease test or 13C-urea breath test were included. All patients had never received Raf inhibitor eradication therapy. Patients were randomly divided into concomitant therapy for 7 days and standard triple therapy for 7 or 10 days. Concomitant therapy composed of esomeprazole (20 mg),

amoxicillin (1000 mg), clarithromycin (500 mg) and tinidazole (500 mg); all drugs were given twice a day. Standard triple therapy consisted of esomeprazole (20 mg), amoxicillin (1000 mg) and clarithromycin (500 mg); the drugs were given twice a day. The eradication rates were determined 4 weeks after the end of the treatment by 13C-urea ICG-001 in vivo breath test. The incidence of adverse reaction were recorded. Results: 242 of the 246 patients completed the follow-up. The intention-to-treat analyse (ITT) and the per-protocol analysis (PP) indicated that the concomitant therapy (91.4% and 92.5%) was superior to standard triple therapy for 7 days (79.3% and 81.2%) and 10 days (79.5% and 80.5%) (P < 0.05). The difference for the eradication rate between the standard triple therapy for 7 days and 10 days was not

significant (P > 0.05). There were no significant difference for the adverse reactions between the concomitant therapy (8.8%), standard triple therapy for 7 days (7.5%) and 10 days (9.8%) (P > 0.05). Conclusion: Concomitant therapy for 7 days is an effective and a safe strategy for H. pylori eradication and deserves consideration for the Selleck Gemcitabine initial eradication treatment in China. Key Word(s): 1. Helicobacter pylori; 2. eradication; 3. Concomitant therapy; Presenting Author: MARA BARBOSA Additional Authors: CARLA MARINHO, JOSE COTTER Corresponding Author: MARA BARBOSA Affiliations: Centro Hospitalar Do Alto Ave Objective: BACKGROUND: Subclinical hepatic encephalopathy (SHE) is characterized by a mild cognitive impairment. It is controversial if Helicobacter pylori infection has a role in SHE by contributing to the hyperammonemia that exists in cirrhosis. AIM: To assess the relationship between H. pylori infection, hyperammonemia and the presence of SHE in cirrhotic patients. Methods: METHODS: A prospective study was conducted. One-hundred and two cirrhotic outpatients were evaluated.

“
“Menkes disease (MD) is an infantile—onset X-linked recessive neurodegenerative disorder caused by deficiency or dysfunction of a copper-transporting ATPase, ATP7A. The effect of altered transportation of copper may affect various

enzymatic functions differently. Among all enzymatic functions, lysyl-oxidase enzymatic activity, which is crucial in the formation of the lysine-derived cross-links in collagen and elastin, is the most sensitive to the copper transport alterations. Trametinib order Pili torti, tortuous intracranial vessels and bladder diverticula are clinical aspects strictly related to the connective tissue alterations dependent on the lysyl-oxidase deficiency. Despite a pleiotropic clinical appearance of MD patients, we observed tortuous intracranial vessels and bladder diverticula in 4 consecutive Menkes patients at different stages of the disease. We speculate that these findings are present at early stages and could be considered suggestive findings in MD. “
“We retrospectively reviewed neuroradiology database

at our tertiary-care hospital to search for patients with metaphoric or descriptive signs on brain computed tomography or FDA-approved Drug Library chemical structure magnetic resonance imaging. Only patients who had clinical or pathological definitive diagnosis were included in this review. “
“This study aimed to identify clinical and ultrasound imaging predictors of progression of carotid luminal narrowing in subjects with asymptomatic moderate internal carotid artery (ICA) stenosis.

A total of 571 subjects with asymptomatic moderate (50-69%) ICA stenoses were enrolled. They underwent ultrasound examination at baseline and after 12 months. Demographics, vascular Avelestat (AZD9668) risk factors, medications, plaque characteristics (surface and echogenicity) and common carotid intima-media thickness (IMT) were collected. At the follow-up examination, any change of ICA stenosis was graded in three categories (i) ≥70% to near occlusion, (ii) near occlusion, and (iii) occlusion. Progression of stenosis was defined as an increase in the stenosis degree by at least one category from baseline to follow-up. At 12 months, progression occurred in 142 subjects (prevalence rate 25%). At the multivariable logistic model, pathological IMT values (considered as binary variable: normal: ≤1 mm vs. pathologic: >1 mm) significantly predicted the risk for plaque progression after adjusting the model for possible confounders (OR 2.28, 95% CI 1.18-4.43, P = .014, multivariable logistic model). Our results confirm the role of carotid wall thickening as a marker of atherosclerosis. Carotid IMT measurement should be considered to implement risk stratification in patients with asymptomatic carotid disease. “
“Basilar artery fenestration aneurysms are rare aneurysms, posing unique challenges for endovascular treatment.