Blood samples were collected from 147 (98%) participants 14 days post dose 3 for the immunogenicity evaluation of PRV (Table 2). The results of efficacy and immunogenicity have been reported previously [21]. During the study, 39 SAEs, including 6 deaths, occurred among study participants

and there were no deaths due to gastroenteritis. The most common SAEs were pneumonia (Table 3). PRV/placebo was received 8 times from the sponsor, and stool/blood was shipped to the sponsor 18 times. PRV/placebo was stored initially in the cold room at the ICDDR, B Dhaka and transferred to Matlab from time to time selleck (17 times). From Matlab, the vaccine was taken to the field in cold boxes. The temperature of the PRV/placebo was monitored continuously during each shipment, during storage in Dhaka and Matlab, and during transport to the field. There were no excursions of temperature during storage and transportation of vaccine at any time. This clinical trial was the first Phase III efficacy study of a rotavirus vaccine conducted in Bangladesh. It involved identifying all infants who were eligible to receive vaccine at a very early age from this demographically defined population, obtaining written informed consent form a parent, providing

vaccine on schedule along with the other standard EPI vaccines, collection of blood samples from a sub-set for determination of immunogenicity and maintaining clinical surveillance for gastroenteritis learn more among the study

participants in the entire study area over an extended period of time. It also included follow up of subjects in their homes or through telephone (when mothers were away due to social visit), and collection of stool specimens when they reported to the diarrhoea treatment centres. All of these activities were conducted following procedures consistent with good clinical Modulators practices. While this type of study has been carried out in other developing countries, the study in Bangladesh was notable that all children were enrolled from an area where there is an ongoing HDSS, 99.6% MTMR9 of the participants completed follow up for at least one year, and 99.9% of the required stool specimens were actually collected. (The one missed stool sample occurred when a child was re-hospitalized and it was not clear if this was a separate episode.). However, some children (about 10%) were not enrolled in the study as their mothers reported that they could not be available during follow up period. This was possible because the availability of the participants could be known beforehand with the support of the existing HDSS and is important for any vaccine trial because availability of the participants for follow up is crucial for vaccine efficacy assessment. Also, the cold chain was consistently maintained for the vaccine, and all SAEs were reported on time as required.

51 Other groups have demonstrated alterations in trigeminal nerve diffusion in trigeminal neuralgia52–55 and

in temporomandibular disorder.56 Figure 3 Somatotopically Organized Activation Patterns of the Human Trigeminal Ganglion Evoked by Noxious Heat to the Ophthalmic (V1), Maxillary (V2), and Mandibular (V3) Facial Regions. Taken together, these studies demonstrate that, at Inhibitors,research,lifescience,medical least for cranial nerves, functional and diffusion MRI can provide mechanistic insight into pain processes at the interphase of the peripheral and central nervous system. SPINAL CORD PAIN IMAGING Positron Emission Tomography (PET) The metabolic rate of glucose increases in the spinal cord during nociceptive in-flow,57,58 affording a mechanism to image spinal pain signaling using 18F-fluorodeoxyglucose. We found no studies demonstrating altered spinal PET ligand uptake in pain, but such

an endeavor appears possible if there is massive peripheral Inhibitors,research,lifescience,medical signaling. FDG is routinely used in oncological staging, and a retrospective analysis of cancer pain patients might demonstrate elevated FDG uptake in corresponding segments of the spinal cord. Ideally, such a study would utilize high-resolution PET in combination with MR or CT to delineate the spinal cord cross-section in multiple voxels, allowing assessment of anterior and Y-27632 posterior segments, and possibly lateralization effects. To illustrate Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical PET imaging of the spine, we present mean FDG standardized uptake values (SUV) obtained from two studies of 92 patients59 and 30 patients60 without spinal malignancy (Figure 4). Figure 4 Midline 18F-FDG PET/CT of a Healthy Spinal Cord. Magnetic Resonance Imaging Structural MRI is used routinely to assess spinal cord injuries, but due to the spine’s small cross-section, and noise sources such as motion, cerebrospinal fluid (CSF) pulsation, and magnetic susceptibility, functional imaging of the spine is technically challenging. Recent developments in MR sequences and post-processing have opened up the field, and

it is possible to define structure and function Inhibitors,research,lifescience,medical with greater specificity.61 The first functional spinal cord imaging results were published in 1999, indicating that 3-tesla imaging of the cervical click here spinal cord showed that repeated hand exercise led to a blood-oxygenation level dependent (BOLD)-like increase in spinal cord signal, predominantly on the ipsilateral spinal cord between C6 and T1.62 Since then, spinal fMRI has been reported using multiple paradigms (pain, motor, vibration, light touch) in healthy subjects and in patient populations including carpal tunnel syndrome, spinal cord injuries, and multiple sclerosis. These studies, along with methodological advances, are the subject of two excellent reviews on state-of-the-art spinal cord imaging methods63 and applications64 that we refer the reader to for full details.

PD symptoms reportedly occur in over 50% of all elderly patients receiving these agents and the cumulative annual incidence of TD in middle-aged and elderly patients is over 25%.56 The likelihood of reversing this potentially debilitating condition diminishes with age. Other adverse effects of these agents that are often intolerable in the older population include orthostatic hypotension and anticholinergic effects. Orthostasis is estimated

to occur in 5% to 30% of geriatric patients and is a major contributing factor to the occurrence of falls.57 The Inhibitors,research,lifescience,medical elderly are also more prone to the consequences of falls, such as bone fractures, injuries, and dependency. Low-potency antipsychotics and clozapine are more likely to cause significant drops in orthostatic blood pressure. Anticholinergic effects in the elderly may cause side effects, such as check details constipation, dry mouth, urinary retention, and cognitive impairment. The elderly are especially sensitive to these effects and the Inhibitors,research,lifescience,medical use of laxatives or stool softeners is already

particularly high in nursing homes. Cognitive impairments may lead to decreased independence, and a more rapid decline in cognitive functioning may occur in the elderly treated with antipsychotics than in the younger adult population. Clozapine has been used successfully in the elderly Inhibitors,research,lifescience,medical population at lower doses than adult patients. Mean dosages range from 50 to 300 mg/day with a much slower rate of titration. Inhibitors,research,lifescience,medical This may be a good choice for treating psychotic elderly patients with preexisting

PD, because of its lower affinity for D2 receptors in the striatum. Clinically, however, it is a poorly tolerated antipsychotic in geriatric patients and should Inhibitors,research,lifescience,medical be used with caution. The risk for agranulocytosis appears to be about 4% in the elderly population with older women being at highest risk.58 The risk for seizure activity is increased in the elderly59 and sedation is one of the major reasons for discontinuation.60 Clozapine therapy should be initiated at 12.5 to 25 mg/day given in two divided doses, titrating by increments of 12.5 STK38 mg over 5 to 7 days. Controlled studies examining the efficacy of clozapine in the elderly specifically for patients with schizophrenia are rare. Howanitz and colleagues61 studied clozapine (maximum 300 mg/day) compared with chlorpromazine (maximum 600 mg/day) in a 12-week, double-blind fashion in patients with chronic schizophrenia. Patients on clozapine tended to do better than the chlorpromazine group, although this did not reach significance, probably due to the sample size.62 Tachycardia and weight gain were problematic for clozapine-treated patients, while those treated with chlorpromazine were highly sedated. Clozapine should be used as a last resort in geriatric patients with schizophrenia and at least one trial of an SGA should be made first.

Sex hormone-binding globulin (SHBG) increased at 1.6% per year. The increase in SHBG likely results

in a further decline in testosterone levels. Dehydroepiandrosterone, dehydroepiandrosterone sulfate, cortisol, and estrone showed significant declines, whereas dihydrotestosterone, follicle-stimulating hormone, luteinizing hormone, and prolactin increased over time.54 Another recent study from the MMAS cohort controlled for confounding factors such as chronic illness, body mass index (BMI), medications, and lifestyle when analyzing testosterone levels. The authors report that chronic disease and high BMI significantly decreased testosterone concentrations, Inhibitors,research,lifescience,medical whereas smoking tended to increase total, free, and bioavailable testosterone Inhibitors,research,lifescience,medical concentrations.55 Finally, declining testosterone may cause decline in libido, ED, and difficulty achieving ejaculation. The level of testosterone does appear to influence sexual function. Testosterone replacement therapy was found to improve erectile function for hypogonadal men in a randomized, placebo-controlled, double-blind, Inhibitors,research,lifescience,medical parallel group, multicenter study,56 although exogenous testosterone obviously has severe adverse effects on spermatogenesis. Birth Defects There is concern that the increased

rate of DNA fragmentation previously discussed leads to an increase in fetal abnormalities. It is difficult to demonstrate the effects that DNA fragmentation and UMI-77 supplier paternal age have on genetic disorders Inhibitors,research,lifescience,medical for several reasons. Genetic disorders are rare, which makes studying them difficult. Although more men are having children at later ages, the number of older fathers is still relatively small, further impeding studying these rare outcomes. Many studies do not control for maternal age or lifestyle and health issues, which may confound their results. One study that showed an association between

paternal age and a genetic mutation examined men aged 22 to 80 years. The results Inhibitors,research,lifescience,medical revealed associations between age and the frequencies of sperm with DNA fragmentation and fibroblast growth factor receptor 3 gene (FGFR3) mutations. FGFR3 mutation causes achondroplasia. The study found no associations between male age and sperm with aneuploidies or diploides. Specifically, isothipendyl there was no link between paternal age and Down syndrome, Klinefelter syndrome, Turner syndrome, XYY syndrome, Apert syndrome (FGFR2 mutation), or sex ratio.57 There is ongoing debate in the literature regarding the contribution of paternal age to trisomies in the offspring. A study of 3419 offspring with trisomies showed a paternal age effect only when the maternal age was ≥ 35 years. This effect was strongest when maternal age was > 40 years. When maternal age was > 40 years, the paternal contribution to Down syndrome was as important as the maternal age effect.58 There has been recent evidence of increased rate of first trimester spontaneous abortion with older paternal age.

The need for further international collaboration between interested specialists was emphasised and the goals of the International Myositis Assessment and Clinical Modulators studies (IMACS) group noted [37]. I am told that in the 1970s the rheumatologists at a large London teaching hospital were wont to use the abbreviation SSOM–some sort of myositis. I assume that this was an honest attempt to indicate ignorance about cause and that they felt more comfortable “lumping” cases with many common features together, rather than “splitting” up into

subcategories when there was no clear rationale to do so. Are we now any the wiser? I think that the answer is definitely yes, but note again the wise words of my colleague who R428 in vivo warned against rigid definitions in that they may lead us to assume we know more than we Selumetinib mouse do. The major development relates to our increased understanding of the immunopathogenesis of

DM and PM, although it is clear that we do not understand all of the relevant mechanisms. It is salutary to remember why we are trying to achieve a system of classification, and how we might go about doing so. The critical relationship between establishing diagnostic criteria and any system of classification has been emphasised. The main benefits of classification are in aiding the diagnostic

approach, defining specific subgroups that have a similar natural history and response to treatment, and leading on from that are helpful for epidemiological studies. Arguably, definitive classification depends upon identifying the specific cause of each disorder. A comparison can be made with limb-girdle muscular dystrophy. In the 1950s we were able to define LGMD by clinical features and certain histological features. We could see that some patients had particular associated features whereas others did not–e.g. cardiomyopathy or early ventilatory muscle involvement. Now we can define individual subtypes at a Phosphoprotein phosphatase molecular level and note which are associated with such complications. For the myositides we are somewhere between these two stages. Box 4 is essentially a synthesis of previous classifications that is intended to be useful clinically–in other words, most patients can, on the basis of clinical and laboratory features, be placed in a specific category. The first part of Box 4 lists conditions with either a known cause (rather few) or those in which myositis is associated with another definable entity, although the pathogenic relationship between the two may be uncertain. The second part includes what are frequently referred to as the IIM.

104 Impaired glutamate reuptake from the synaptic cleft by astroglia prolongs synaptic activation by glutamate.105 Accordingly, increased glutamatergic activityhas been observed in patients with depression.106 Neuroprotective and neurotoxic metabolites of the tryptophan-kynurenine metabolism in psychiatric disorders In contrast to microglial cells which produce QUIN, astrocytes play a key role in the production of KYNA in the CNS. Astrocytes are the main source of KYNA.107 The cellular 5FU localization of the kynurenine metabolism is primarily in macrophages and microglial cells, but also in astrocytes.108 Inhibitors,research,lifescience,medical KMO, a critical enzyme in the kynurenine metabolism, is absent in human astrocytes, however.109 Accordingly,

it has been pointed out that astrocytes cannot produce the product 3-hydroxykynurenine (3-HK), but they

are able to produce large amounts of early kynurenine metabolites, such as KYN and KYNA.109 This supports the observation that inhibition of KMO leads to an increase Inhibitors,research,lifescience,medical in the KYNA production in the CNS.110 The complete metabolism of kynurenine to QUIN is observed mainly Inhibitors,research,lifescience,medical in microglial cells, only a small amount of QUIN is produced in astrocytes via a side-arm of the kynurenine metabolism. Therefore, due to the lack of kynurenine-hydroxylase (KYN-OHse),in case of high tryptophan breakdown to KYN, KYNA may accumulate in astrocytes. A second key player in the metabolization of 3-HK are monocytic Inhibitors,research,lifescience,medical cells infiltrating the CNS. They help astrocytes in the further metabolism to QUIN.109 However, the low levels of sICAM-1 (ICAM-1 is the molecule that mainly mediates the penetration of monocytes and lymphocytes into the CNS) in the serum and in the CSF of nonmedicated schizophrenic patients,22 and the increase of adhesion molecules during antipsychotic therapy indicate that the Inhibitors,research,lifescience,medical penetration of monocytes may be reduced in nonmedicated schizophrenic patients.57 Quinolinic acid as a depressiogenic and neurotoxic substance Apart from certain liver cells, only macrophage-derived cells are able to convert tryptophan into quinolinic acidolonic

acid.111 Interestingly, in a model of infection, the highest concentrations of QUIN are found in the gray and white matter of the cortex, not in subcortical areas. This finding points out that high levels of QUIN therefore may be associated with cortical dysfunction.112 The strong about association between cortical QUIN concentrations and local IDO activity supports the view that the induction of IDO is an important event in initiating the increase of QUIN production.113 In the CNS, invaded macrophages and microglial cells are able to produce QUIN111 During a local inflammatory CNS process, the QUIN production in the CNS might increase without changes of the peripheral blood levels of QUIN. The local QUIN production correlates with the level of β2 microglobulin, an inflammatory marker. Local CNS concentrations of QUIN are able to exceed the blood levels by far.

Central administration of Y2R agonists have failed to alter anxiety-like behavior in a number of studies (Broqua and et al, 1995, Heilig and et al, 1989, Britton and et al, 1997 and Sorensen and et al, 2004). However, agonism of Y2R in the locus coeruleus and lateral septum produces anxiolytic effects, whereas Y2R are required for NPY-mediated anxiolysis in the hippocampus (Kask et al., 1998a, Kask et al., 1998b, Kask et al., 1998c, Trent and Menard, 2013 and Smialowska and et al, 2007). Y2R agonism in the basolateral Modulators amygdala has bidirectional effects on anxiety in the social interaction test, with low agonist doses generating anxiety and high doses decreasing anxiety (Sajdyk et al., 2002). A recent study

indicates that knockout of the Y2R in GABAergic neurons located CFTR modulator in the central nucleus of the amygdala was anxiogenic specifically in female mice (McCall et al., 2013). Contrasting reports indicate that Y2R antagonism in the central nucleus of the amygdala is anxiolytic (Kallupi et al., 2013), and that ablation of Y2R in either the basolateral or central nucleus of

the amygdala find more produces an anxiolytic phenotype (Tasan et al., 2010). Global deletion of Y2R reduces anxiety in the elevated plus maze, light–dark, open-field, and marble burying tests (Tasan and et al, 2009, Painsipp et al., 2008, Painsipp and et al, 2008 and Tschenett and et al, 2003), and Y2R deficient mice exhibit reduced neuronal activation upon exposure to an anxiogenic environment (Nguyen et al., 2009). Taken together, this evidence very suggests that Y2R may function in a regionally specific and neurochemically selective fashion. The Y4R and Y5R also have putative roles in rodent anxiety-like behavior. Similar to Y2R mutant mice, deletion of the Y4R also reduces anxiety-like behavior in a number of rodent paradigms

(Tasan and et al, 2009 and Painsipp and et al, 2008). Knockout of the Y4R with the Y2R enhances the anxiolytic phenotype observed following deletion of either receptor alone (Tasan et al., 2009). Finally, pharmacological studies indicate that Y5R ligands may have promising anxiolytic properties. A Y5R antagonist blocked the anxiolytic effects of a Y2R agonist in the basolateral amygdala (Sajdyk et al., 2002), while i.c.v. delivery of a Y5R agonist produced anxiolytic effects (Sorensen et al., 2004). Y5R can form heterodimers with Y1R (Gehlert et al., 2007), and these receptor subtypes are colocalized in the basolateral amygdala, hippocampus, and hypothalamus (Wolak and et al, 2003, Longo and et al, 2014, Oberto and et al, 2007 and Fetissov et al., 2004). Y1 and Y5 receptors act synergistically in the regulation of energy homeostasis (Mashiko et al., 2009). Although the combined effects of Y1 and Y5 receptor agonists have not been tested in the context of anxiety thus far, the notion of co-activating these receptors could be valuable in the development of pharmacotherapeutics for enhanced anxiolytic effects.

139 While overexpression #selleck compound randurls[1|1|,|CHEM1|]# of the ε4 allele might be expected in MCI compared with normal controls,

its frequency would not be likely to reach the levels seen in AD, since MCI cases comprise not only preclinical AD, but also other more benign conditions predisposing to cognitive impairment. In one large study, the prevalence of nondemented persons with at least one copy of the £4 allele was 22%, while in AD the frequency was 64%.140 Values intermediary between these estimates were found in several studies of nondemented memory impaired individuals who appear to satisfy criteria for the diagnosis of MCI14,18,141,142 Two large population-based studies found that ε4 status was a significant risk factor for Inhibitors,research,lifescience,medical MCI.143,144 Most studies have found e4 to exert a cognitive impact on nondemented older adults. In community samples of nondemented elderly, although one cross_sectional study did

not find a significant relationship between £4 status and cognition,145 other longitudinal Inhibitors,research,lifescience,medical studies found ε4 to be a predictor of accelerated cognitive decline.146-148 According to one report,149 nondemented subjects who carried an e4 allele were more likely to have subjective memory Inhibitors,research,lifescience,medical complaints than those without ε4. In studies of cognitively normal persons with high MMSE scores, the impact of age on memory performance (and memory change over time) was more pronounced in e4 homozygotes relative to those without ε4.150-152 These latter reports indicate that ε4 may subtly influence cognitive Inhibitors,research,lifescience,medical performance even before the onset of MCI; it is unknown whether this influence can precede the emergence of AD pathology. Although epidemiological and longitudinal clinical

data support ε4 as a risk factor for dementia Inhibitors,research,lifescience,medical and cognitive decline, its utility as a predictor of clinical outcome in MCI populations needs to be compared with imaging, biomarker, and neuropsychological variables. Treatment of MCI The treatment of MCI is reviewed in detail by Gauthier later in this issue.153 Currently, there are no pharmacological treatments for MCI with proven efficacy or regulatory approval. However, clinically there appears to be growing use in MCI of the marketed AD treatments, donepezil, rivastigmine, galantamine, and memantine. A number of clinical trials in MCI patients have been conducted, thus far with L-NAME HCl mixed results. For example, a 6-month, placebo-controlled trial of donepezil failed to show significant efficacy on the primary end points, but did show efficacy on some secondary cognitive measures.154 Since a high proportion of “amnestic” MCI patients (presumably representing cases of prodromal AD) progress to an AD diagnosis within several years, 2- to 4-year “survival” clinical trial designs have been conducted with MCI patients in which “conversion” to AD is the primary outcome. Such studies are used to determine if a treatment can slow the progression of symptoms.

However, even for those patients found to have very low-risk cancers, AS remains underutilized as a primary treatment strategy due to acknowledged rates of under-grading and understaging. The result is the current

over-treatment of many thousands of men who would not have experienced any symptoms or loss of life had their cancers never been diagnosed. A significant proportion of these men likely experienced long-term adverse effects of surgery, radiation therapy, androgen ablation, and other treatments that ultimately were Inhibitors,research,lifescience,medical unnecessary, and the costs of these avoidable treatments are calculable in the billions of dollars. A clear need therefore exists for novel biomarkers that can help generate improved predictions,

and by extension, better-informed decision-making about timing and intensity of treatment. Many candidate biomarkers have been proposed for this purpose. However, the majority correlate closely with Gleason grade or other established characteristics, and therefore offer little independent Inhibitors,research,lifescience,medical information. Even among those that show particular promise in initial studies, fewer still prove valuable on rigorous external validation. For this reason, PSA, stage, and Gleason score remain the only prognostic factors assayed Inhibitors,research,lifescience,medical in routine clinical practice. Several presentations at this year’s annual meeting have addressed this critical unmet need. Certainly the ultimate measure of the success of prostate cancer Cyclopamine chemical structure therapy is a reduction in all-cause mortality (ACM). Isariyawongse and colleagues34 examined ACM and prostate cancer-specific mortality Inhibitors,research,lifescience,medical (PCSM) in 10,429 men treated with RP

external beam radiotherapy or brachytherapy between 1995 and 2005. Median follow-up was 5.5 years with 14.7% of survivors followed for > 10 years. Twelve percent of men died with 1.7% of deaths due to PCSM. Age, treatment modality, PSA Inhibitors,research,lifescience,medical biopsy Gleason score, and comorbidity predicted ACM. PCSM was foretold by age, PSA biopsy Gleason score, and clinical T stage. A nomogram demonstrating good concordance was created and may be found in the abstract. Does early biochemical recurrence after RP alter survival? This was the subject of a presentation by Ta and colleagues.35 Men undergoing RP in Victoria, Australia, between 1995 and 2000 were studied by linking cancer and death registries. Biochemical recurrence (BCR) was defined as two consecutive ADAMTS5 readings > 0.2 ng/mL; 2116 men had BCR, 250 men died, and 3.8% of these men died from prostate cancer. The time to BCR strongly predicted death in men with adverse disease but did not correlate with PCSM in those with low-risk disease. Punnen and colleagues36 performed a multi-institutional analysis of the Cancer of the Prostate Risk Assessment-Post Surgical (CAPRA-S) score to predict outcome after RP.

15) The focus was set at the level of the mitral annulus and was moved to an appropriate level

when necessary. According to each coronary artery territory, the position of the transducer was adjusted to locate the region of interest in the center of the image sector, and MCE was repeated by adjusting the triggering interval. If perfusion defects were consistent with a typical Cell Cycle inhibitor ischemic territory of a coronary artery, observed in the subendocardial area, or associated Inhibitors,research,lifescience,medical with wall motion abnormalities of the same area, or if the severity of perfusion defects improved according to the lengthening triggering interval, perfusion defects were regarded as true myocardial perfusion defects and not artifacts.16) Myocardial perfusion defects present in at least one coronary territory were considered positive (Fig. 1A). MCE results were interpreted by different reviewers blinded to the clinical data. Fig. 1 Myocardial contrast echocardiography using power Inhibitors,research,lifescience,medical harmonic Doppler imaging with a dual-frame triggering (A). Left, perfusion frame

was generated when the first packet of pulses encountered microbubbles in the myocardium and destroyed them. Right, post-destruction … Myocardial perfusion imaging with technetium-99m sestamibi As soon as possible after Inhibitors,research,lifescience,medical MCE, all patients underwent resting MPI with technetium-99m sestamibi. For SPECT imaging, 64 projections were obtained for 20 seconds, each at >180° using a dual-head rotating gamma camera. Image reconstruction was performed using standard back-projection algorithms. Short-axis slices of the left ventricles were normalized to peak heart rate. Circumferential Inhibitors,research,lifescience,medical count profiles were generated for five short-axis slices from apex to base. Scintigraphic results were analyzed by an experienced

nuclear medicine Inhibitors,research,lifescience,medical physicians who were blinded to patients’ clinical and laboratory data. Perfusion images were evaluated without gating in 35 (36%) patients and with gating in 63 (64%) patients, allowing assessment of regional function. Positive MPI was defined as a mild or definite perfusion defect on SPECT MPI performed Astemizole without gating, and a definite perfusion defect with associated abnormality in wall motion and thickening on gated MPI. Quantitative coronary angiography Coronary angiography was performed in all patients by standard techniques. Quantitative analysis of coronary angiography was done by experienced investigators using a quantitative analyzer (Ancor 2.0, Siemens, Erlangen, Germany). Significant stenosis that required urgent revascularization was defined as critical stenosis (diameter stenosis ≥90%) with the potential to affect coronary blood flow at rest and stenosis associated with ulceration or thrombus (Fig. 1B). Statistical analysis Continuous variables are presented as mean±SD.