34 Finally, the active ingredients of bipolar psychotherapy are d

34 Finally, the active ingredients of bipolar psychotherapy are difficult to ascertain. There are few or no identified differences in effectiveness between the modalities described above and, thus far, there have been no “dismantling” studies as have been conducted in psychotherapy for depression. Among the most often mentioned candidates as an active ingredient (and therapeutic outcome) is the enhancement of medication adherence. In the next section, we will briefly review the literature on medication adherence in bipolar disorder and we will Inhibitors,research,lifescience,medical present a model to enhance it. Focus on medication adherence The therapeutic

approaches described above are divergent, in their methods to a certain extent, but each involves education about, bipolar disorder and its treatment, and each has some content oriented toward enhancing medication adherence. Inhibitors,research,lifescience,medical Nonadherence is likely one of the greatest reasons why medications may not work as well in the community as they do in efficacy studies evaluating Inhibitors,research,lifescience,medical pharmacotherapy.35 Of course, adherence, in and of itself,

is not a guarantee of good outcome, but medication remains the backbone of treatment, for most people with bipolar disorder. Suboptimal adherence to medications for bipolar disorder is common. Estimates for the prevalence of nonadherence in bipolar disorder vary greatly by study population and instruments used to assess adherence. However, it is estimated that 20% to 60%, with a mean of 40%, of individuals Inhibitors,research,lifescience,medical with bipolar disorder arc nonadherent

to prescribed medications at any given time.36 A longitudinal study found that, among people who initiated lithium, Inhibitors,research,lifescience,medical the median time to discontinuation was only 76 days.37 In that same study, the probability of hospitalization was twice as high among discontinues versus continuers. Other studies have indicated that the consequences of nonadherence in bipolar disorder include greater propensity to relapse, higher hospitalization rates, and greater health care costs.36,38,39 Types of nonadherence GSK-3 Nonadherence is a complex phenomenon with a variety of distinctions and risk factors. There no is definition as to what the optimal level of adherence is in bipolar disorder, as there is in pharmacotherapy for the infectious diseases (eg, HIV). Furthermore, nonadherence is a not. a unitary or steady state phenomenon; nonadherence can be intermittent or continuous, and it can be specific to a single medication or to multiple medications. Moreover, nonadherence may be voluntary, such as deliberately not taking medication due to perceptions about, its ineffectiveness, or it can be involuntary, such as forgetting or misinterpreting instructions. Nonadherence may also involve table 1 consuming too much medication.

We paid particular attention to unintended consequences as they

We paid particular attention to unintended consequences as they revealed the strength of mutual dependencies between the social and technical elements that hold this new way of working together [64] and, provided an opportunity to investigate their role in shaping the outcomes of this organisational change [65]. In this case, it helped us to understand how space, time and information technology can be manipulated and mobilised. From there, we described a process by which they shape and are shaped, locally, as the new arrangements struggle to reach a consensus around the wait target

and the ED consolidates itself as a Inhibitors,research,lifescience,medical ‘modern’ emergency department. Reducing selleck chem maximum waiting times in ED has been the focus for this policy, as they are known to be important to patients, and are easily measurable, understandable (unlike, for instance, quality and safety) and easier to achieve (unlike average waiting times) [66]. On the other hand, the ED has traditionally

been a resource-poor and comparatively neglected area of the hospital, despite its high public Inhibitors,research,lifescience,medical profile. This is partly Inhibitors,research,lifescience,medical due to the low status of ED work within the wider medical profession [67], and a perception that, despite the major emergencies, much of the ED’s work consists of minor injuries and illnesses. The target meant that the ED, often for the first time, became the focus of managerial attention and resources [68]. The system of performance management in the NHS meant that hospital Chief Executives and Boards Inhibitors,research,lifescience,medical were directly accountable

for the performance of the ED against the target, and therefore took a much closer interest in the ED than had been the case hitherto. There was a concomitant expansion Inhibitors,research,lifescience,medical in the resources available to EDs. For instance, though the redesign had happened prior to the introduction of the 4 hour wait target in 2005, its announcement in 2000 and the subsequent work of emergency departments on fast track care made the reconfiguration of space a necessity. Likewise, the introduction of the IS system, and the streaming processes were all originally introduced in order to meet the target, but collectively led to a revolution in working in the ED. In particular, the redesign Entinostat of the built environment, towards compartmentalisation, signifies an important paradigm shift on the way healthcare organisations understand the practical value of space in the mediation of work. They acknowledged, perhaps for the first time, that spaces are not just neutral containers of social action. Therefore, if the aim is to implement a certain model of healthcare delivery, the configuration of the physical environment becomes a precondition, as “function follows form”. Likewise, time is not fixed and absolute. It too exerts meaning and it is embedded in local contexts and processes, structuring actions, events and behaviours.

Anxiety, irritability, and interpersonal friction, in addition to

Anxiety, irritability, and interpersonal friction, in addition to specific depressive symptoms, appear to be common residual symptoms. The rollback phenomenon and state-trait dichotomy Detre and Jarecki92 Ponatinib manufacturer provided a model for relating prodromal and residual symptomatology, defined

as the rollback phenomenon: as the illness remits, it progressively recapitulates (though in a reverse order) many of the stages and symptoms that were seen during the time it, developed. According to the rollback model, there Inhibitors,research,lifescience,medical is also a temporal relationship between the time of development of a disorder and the duration of the phase of recovery. For example, if an illness begins with occasional anxiety attacks that are superseded some weeks Inhibitors,research,lifescience,medical later by depressive symptoms

which then find FAQ become progressively more severe until, after several months, the patient develops total insomnia and confusion, the symptoms tend, as the condition improves, to remit in reverse order, the confusion and insomnia diminishing first, and the depressed mood next. After the depression lifts, the patient may again experience anxiety attacks for several weeks, until finally these symptoms, too, disappear. “92 The rollback phenomenon-or, at least, a strong relationship between prodromal and residual symptomatology-has been substantiated in the treatment of major depression.84 Inhibitors,research,lifescience,medical In one study,84 almost 70% of the residual symptoms that were found to occur in 40 remitted depressed patients were also present at, the prodromal phase of illness. This percentage increased to almost, 90% of cases Inhibitors,research,lifescience,medical for residual

generalized anxiety and irritability. These results achieved independent, replication,93 and are also supported by several lines of evidence. In a prospective study94 which examined the possibility that, episodes of major depression result, in lasting personality changes that persist beyond recovery (the scar hypothesis), there was no evidence of negative change Inhibitors,research,lifescience,medical from premorbid to postmorbid assessment. These findings were replicated by Ormel et al.78 Further, a 10-year follow-up study after severe depression93 suggested that residual symptoms were common and persistent, with considerable fluctuations. This would Cilengitide suggest continuity-whether we rate it in characterological or symptomatological terms-between the prodromal and residual phases. Another line of evidence is based on recognition of specific temporal courses of change during treatment of depression.96-99 Different types of treatment may affect the temporal course of change in depression,100 and the use of pattern analysis may differentiate true drug and placebo responses early in treatment.101 Patients do not suddenly become well, but tend to gradually lose their depressive symptoms over the months following treatment.

22,23 The symptoms provoked by these agents can closely resemble

22,23 The symptoms provoked by these agents can closely resemble naturally occurring attacks.19,24 Unfortunately, many of these provocation challenges have been studied too little to ascertain their selleck chem inhibitor mechanisms of action and relative potency.19,25 Interestingly, one twin study found a high concordance rate for CO2 sensitivity,26 suggesting a genetic #especially randurls[1|1|,|CHEM1|]# etiology, although much remains to be learned about the heritability of panicogen sensitivity. Rodent models of panic provocation challenges The technology revolutionizing neurobiological research in rodents is rapidly expanding knowledge of mechanisms underlying behavior.

The ability to explore panicogens Inhibitors,research,lifescience,medical in animal models provides a powerful Inhibitors,research,lifescience,medical research opportunity. However, progress in this area has been limited in comparison with the advancements made in other behavioral models. Yet, several examples are notable. Shekhar and colleagues have developed rodent models

of lactate-evoked panic27,28 and have found that orexin-expressing neurons in the hypothalamus play a critical role.29 In another example, doxapram potentiated fear and anxiety-related behaviors in rats and induced expression of the immediate early gene c-Fos in the amygdala.30 A few investigators have also begun Inhibitors,research,lifescience,medical to explore the effects of CO2 on fear and anxiety in rodents.31-33 For example, Mongeluzi et al found that high CO2 concentrations can serve as an unconditioned stimulus

in Pavlovian fear conditioning.31 Johnson et Inhibitors,research,lifescience,medical al observed that CO2 inhalation can induce c-Fos expression in fear circuit structures and may thus activate brain regions thought to be responsible for panic.33 Despite these examples, the mechanisms underlying Inhibitors,research,lifescience,medical panicogen action and panic attacks remain largely unknown. Clinical clues about panicogen action Perhaps the most well-studied panicogens are CO2 and lactate. CO2 provocation challenges vary between investigators, but generally consist of breathing single or multiple breaths of CO2 at concentrations ranging from 5% to 35%.24 Protocols for lactate provocation challenges typically include intravenous infusion of 0.5 M sodium D,L-lactate up to 10 mg/kg body weight over 20 minutes or until panic occurs.12,19,34 Several observations led investigators to suggest that CO2 and lactate may share mechanisms of action.35 For example, most CO2-sensitive Drug_discovery panickers are also lactate-sensitive.36 In addition, CO2 and lactate produce stereotypic responses. In particular both induce prominent ventilatory symptoms, suggesting a degree of neuro anatomical or physiological overlap.37,38 Interestingly, both CO2 and lactate may be more likely to affect panic disorder patients who report strong respiratory symptoms during their naturally occurring attacks.

This complex process, schematically depicted in Figure 1, can be

This complex process, schematically depicted in Fluoro-Sorafenib Figure 1, can be broken down in three major events: (1) vascular transport of stem cells; (2) near-wall dynamics and vascular adhesion of stem cells; and (3) intratissue migration of stem cells. Figure 1 The vascular transport of stem cells, from the site of injection to the damaged area, can be broken down in three major steps: Inhibitors,research,lifescience,medical (1) vascular transport of stem cells; (2) near-wall dynamics and vascular adhesion of stem

cells; and (3) intratissue migration … Over the years, the author and his collaborators have developed a hierarchical computational model to predict the wall and tissue accumulation of injectable agents, such as circulating cells, nanoparticles, and small and macromolecules.26-36 This hierarchical computational model comprises three modules, each focusing on different scales and biological compartments. The first module deals with the macroscopic transport of the stem cell solution in patient-specific Inhibitors,research,lifescience,medical vascular networks (Figure 1A); the second module analyzes the near-wall dynamics and blood vessel wall adhesion of the injected solution of stem cells (Figure 1B); and the third module focuses on the Inhibitors,research,lifescience,medical transport in the extravascular space and migration

within the damaged tissue of the Inhibitors,research,lifescience,medical injected stem cells (Figure 1C). The modules are all connected together so that information can be transferred efficiently and accurately over multiple temporal and spatial scales but can also be used separately depending on the aim of the study. Module 1: Vascular

Transport of Stem Cells Blood flow and vascular transport are influenced by authentic, Inhibitors,research,lifescience,medical patient-specific vascular geometry and endothelial wall properties. A critical step in developing accurate predictive tools is the precise reconstruction of the vascular geometry, from the site of injection to the infarcted area, using magnetic resonance imaging (MRI) or computed tomography.36 This requires preprocessing for improving the quality of the clinical images, geometrical segmentation, and solid and mesh constructions for the computational analysis. Brefeldin_A The resulting three-dimensional (3D) vascular geometry is then used for solving the transport problem by coupling a Navier-Stokes solver for the blood flow with a linear scalar advection-diffusion equation for studying the time-dependent evolution of the system.34 Following this approach, the temporal and spatial distribution of several biophysical sellekchem parameters—such as the wall shear rate (WSR), wall shear stress (WSS), oscillatory index (OSI), velocity profile, pressure field, and volumetric concentration of any injected agents—can be predicted within the authentic, patient-specific vascular network.

Fat is present in tumours like

Fat is present in tumours like lipoma or teratoma, but we could not explain the fat deposition, peritumoural and distant to the tumour. This fat was well encapsulated and we removed the peritumoral quantity intact with the tumour, but we removed the fat piece meal around the portal traid. The gallbladder along with the fatty clumps were removed during hepatectomy. We were apprehensive about Inhibitors,research,lifescience,medical leaving behind small macroscopic amount of fat around

the portal triad and its effect on Navitoclax clinical trial recurrence of the tumour. We have followed up for 24 months and the patient is tumour free till now. Table 1 Reports of pancreatic and hepatic MCNs Hepatic MCN is found in about 5% of cystic hepatic lesions (2). It is common in women like its pancreatic counterpart, commonly symptomatic and single. Both the pathologists concurred that the tumors in the pancreas and the liver were histologycally similar and were in favour of the diagnosis of simultaneous occurrence of mucinous cystic neoplasm in Inhibitors,research,lifescience,medical two organs. One of the proposed pathogenesis is these tumours are derived from the detached cells covering the gonads which is in close proximity of the liver and pancreas in the fetal period (2). But this fails to explain the presence of these tumours in men and in tumours Inhibitors,research,lifescience,medical where there is no ovarian-like stroma. Conclusions Liver and pancreatic mucinous cystic neoplasm occurring together is extremely rare.

The presence of these tumors in a male patient puts the current hypothesis of pathogenesis in doubt. The unusual amount of fat occurred selleck probably as a response to the tumour and it is not involved with the recurrence of the tumour as appears from the followup of the discussed patient. Inhibitors,research,lifescience,medical Acknowledgements Disclosure: The authors declare no conflict of

interest.
Patients with pancreatic cancer are often diagnosed after progression to Inhibitors,research,lifescience,medical a locally advanced or metastatic stage. Medical students are taught to recognize the classic “painless jaundice” from malignant obstruction of the distal common bile duct in the setting of this dreaded disease, which continues to have dismal Dacomitinib survival rates of only 5% (1). Endoscopic placement of a biliary stent is a standard palliative measure for patients with metastatic disease, to relieve jaundice and associated pruritus during the last months of life. Self-expanding metal stents (SEMS) have been found to be more cost-effective than plastic stents for patients whose life expectancy exceeds 6 months (2). In contrast, for patients who present with resectable disease, a multicenter randomized controlled trial has shown that placement of a biliary stent prior to pancreaticoduodenectomy leads to increased rates of complications, and that these patients should proceed directly to surgery (3). This trial did not address the population of patients who undergo neoadjuvant therapy, in an attempt to downstage locally advanced disease and make curative resection possible.

An elastic polymer tube is interposed between the leaflet and th

An elastic polymer tube is interposed between the leaflet and the free myocardial wall and secured to the epicardial

surface by an Vorinostat msds adjustable knot. The MitraFlex (TransCardiac Therapeutics, Atlanta, GA, USA) places an anchor in the inner LV myocardium and another on the leaflet via a thoracoscopic transapical approach and connects the two with a synthetic chord; it can also perform an edge-to-edge repair at the same time. The NeoChord (NeoChord, Inc., Minnetonka, Inhibitors,research,lifescience,medical USA)25 uses a mini-thoracotomy transapical access to capture the leaflet, and the chords are then exteriorized, adjusted, and tightened to the left ventricular myocardium. The V-Chordal (Valtech Cardio Ltd, Or-Yehuda, Israel)26 system uses a slow rotation of a helical element to fixate the chorda to the papillary muscle (Figure 2). Currently, the chordae are then sutured to the leaflets by direct vision through a mini-thoracotomy left atriotomy approach, Inhibitors,research,lifescience,medical but a clip-attaching

mechanism is already under development, to allow transfemoral access. Figure 2 The V-Chordal Device, Inhibitors,research,lifescience,medical a Surgically Implantable Adjustable Chordae Device. Alternative techniques for leaflet repair have been proposed. The Percu-Pro (Cardiosolutions, Stoughton, USA) is a space-occupying “buoy” anchored at the LV apex through a transseptal approach that should fill the gap between leaflets. The Thermocool irrigation ablation electrode (Biosense Webster, Inc., Diamond

Bar, CA, USA) delivers, in the context of degenerative disease, radiofrequency energy to the leaflets to provoke shrinking and reduced motion.27 ANNULOPLASTY PROCEDURES Annuloplasty is a fundamental step Inhibitors,research,lifescience,medical to achieve effective and durable results after surgery.28 To achieve similar outcomes, transcatheter procedures should probably incorporate annular remodeling. In addition, the lack of a reliable annuloplasty device is impacting the eligibility for transcatheter interventions. Up to a third of patients screened for MitraClip are refused Inhibitors,research,lifescience,medical due to unfavorable anatomy, including annular dilatation.29 Transcatheter annuloplasty may therefore Dacomitinib both improve outcomes and expand therapeutic indications. Different devices to reduce and reshape the mitral http://www.selleckchem.com/products/MG132.html annulus are at different stages of research and development, addressing different anatomical and pathophysiological concepts. Indirect Annuloplasty (Sinoplasty) The coronary sinus (CS) encircles the posterior mitral annulus, and it may allow devices to be delivered to affect indirectly the posterior mitral annulus geometry. Although the CS approach is a consolidated procedure, it has important limitations: the CS is variably located at a certain distance from the mitral annulus (frequently increased in case of severe MR with annular dilation),30 and circumflex coronary artery compression has been frequently observed.

2; Elekta, Helsinki, Finland) SSS efficiently separates brain si

2; Elekta, Helsinki, Finland). SSS efficiently separates brain signals from external disturbances based on the fundamental properties of magnetic fields (Taulu et al. 2004; Taulu and Simola 2006). The data were obtained 1500 msec before and 1000 msec after application of each trigger for MRCFs and SEFs elicited by PM. The averages of approximately 60 CAL-101 epochs for MRCFs and SEFs following PM were obtained separately. SEFs accompanying Inhibitors,research,lifescience,medical median nerve stimulation were obtained

50 msec before and 300 msec after stimulation, and 300 epochs were averaged. For analysis of MRCFs and SEFs elicited by PM, the band-pass filter was set from 0.2 to 60 Hz. The data 500 msec before and 500 msec after movement onset were used to analyze MRCFs following active movement and SEFs following PM, and the first 200 msec (−500 to −300 msec) were used for baseline data. To analyze SEFs elicited by median nerve stimulation, the band-pass filter was set from 0.5 to 100 Hz, and the 20-msec period preceding the stimulus was used for Inhibitors,research,lifescience,medical the

baseline data. We first calculated the magnitude of the response at each sensor to find the location with the largest response. This was obtained by squaring MEG signals for each of two planar-type gradiometers at a sensor’s location, summing the squared signals, and then calculating the root of the Inhibitors,research,lifescience,medical sum (Kida et al. 2006, 2007). We used the root sum square (RSS) waveforms to look for a peak channel showing the largest amplitude. Then, the peak amplitude and Inhibitors,research,lifescience,medical latency

of the prominent response in the RSS waveform were measured at the peak channel to compare MRCFs and SEFs elicited by PM. As several cortical activities following PM overlapped temporally, we attempted to use multiple Inhibitors,research,lifescience,medical source model analysis for the active and passive movements. We used the Brain Electrical Source Analysis (BESA) software package (NeuroScan Inc., Mclean, VA) for the analysis of multiple source locations and time courses of source activities (Inui et al. 2003, 2004; Wang et al. 2004). This method allows spatiotemporal modeling of multiple simultaneous sources over defined intervals. The location and orientation of the dipoles were calculated by an iterative least-squares fit. The goodness-of-fit Entinostat (GOF) indicated the percentage of the data that could be explained by the model. We used GOF for selleck compound individual data for a period from 10 to 100 msec after movement onset to determine whether the model was appropriate. GOF (10–100 msec) values >80% were considered to indicate a good model. First, the best location and orientation of a source for explaining the major magnetic field components was estimated using the one-source model at a point of peak waveform from 10 to 50 msec after movement onset in all subjects.

10 The present review aimed to study the epidemiology of IBDs in

10 The present review aimed to study the epidemiology of IBDs in Iran in comparison to Asian Tipifarnib mechanism countries. There have been several epidemiologic studies on IBDs in Iran with respect to such variables as age, gender, family history, common risk factors (e.g. genetics, family aggregation, appendectomy, and smoking), less common risk factors, and clinical features. In each section of this Inhibitors,research,lifescience,medical review, data on IBDs Iran will be compared with those in Asian countries. Materials and Methods PubMed, Medline, and Persian databases-including SID and IranMedex were searched from 1970 to 2012. The keywords used

in this search were inflammatory bowel Inhibitors,research,lifescience,medical disease, Iran, ulcerative colitis, Crohn’s disease, epidemiology, risk factors, genetics,

extra-intestinal manifestations, Asia, Middle East, and ethnicity. OR, AND or NOT were applied during search by MeSH, appropriately. Due to restrictions, only the Persian and English languages were used as limitation (Persian for references in Iran). Only the epidemiological aspects assessed in Iranian articles Inhibitors,research,lifescience,medical were compared with the same subjects in other Asian countries. Articles in the form of clinical trials, case reports, case series, and radiologic and surgical procedures were excluded. Each article was surveyed twice by two authors, and the obtained data were Inhibitors,research,lifescience,medical recorded in a pre-prepared checklist. Of all the articles on the subject in Iran (available in above indices), two were duplicated and just one was used in the present study. Asian countries

were defined according to the latest confirmed map by the United Nations (UN) (United Nations Statistics Division, 2011). Among the articles, only those review articles whose references were used in our references were selected in order to complete our reference list.10 In total, there were 21 documented articles on IBD epidemiology in Iran and 170 in Asia. The articles will be described in the following section (figure 1). Figure 1 This Inhibitors,research,lifescience,medical flow chart depicts the inclusion and exclusion criteria applied in the present review Incidence and Prevalence According to a recent systematic Drug_discovery review that has assessed the trend of incidence and prevalence of IBDs around the world, the incidence and prevalence rates of IBDs have increased in the last 4-5 decades. The annual incidence rates were 0.6-24.3, 0.1-6.3, and 0-19.2 per 100,000 chemical information individuals for UC and 0.3-12.7, 0.04-5.0, and 0-20.2 per 100,000 individuals for CD in Europe, Asia and Middle East, and North America-respectively. Also, the prevalence ranges were 4.9-505, 4.9-168.3, and 37.5-248.6 per 100,000 persons for UC and 0.6-322, 0.88-67.9, and 16.7-318.5 per 100,000 persons for CD in Europe, Asia and Middle East, and North America-respectively.

The data were coded and entered into a computer using Statistical

The data were coded and entered into a computer using Statistical Package for Social Sciences (SPSS) version 15.0. Results were expressed as number, percentiles and medians. Categorical variables were compared using chi-square tests. Survival functions (OAS) were estimated using Kaplan Meier test, comparison between survival curves was achieved by the Log Rank test. P-value of <0.05 taken to indicate statistical significance. Results Patient’s Inhibitors,research,lifescience,medical characteristics The characteristics of the 91 patients of groups I, II

and III are shown in Table 1. The three patient groups were balanced; the most common pathological type was squmous cell carcinoma 60% in GI, 48.6% in GII and 53.8% in GIII, followed by adenocarcinoma, all patients had dysphagia, 14.3% had metastasis and the most common sites of metastasis were lung and liver. Table 1 Patient’s characteristics There was no significance difference between Inhibitors,research,lifescience,medical the median radiation dose given for GI and GIII, it was 24.66 and 26.29 in G1and GIII respectively, stent migration occurred in 3 patients of GII and in 1 patient Inhibitors,research,lifescience,medical of GIII. All patients inhibitor KPT-330 underwent stent had complications included transient chest pain after stent placement and gastroesophageal

reflux. The median overall survival (OAS) was 169 days (95% CI, 96.53-241.46) in GI, 119 days (95% CI, 106.48-131.51) in GII and 237 days (95% CI, 107.07-366.92) in GIII. The difference between GI &II was statistically insignificant (P=0.86) while the difference between GI &III was significant (P=0.01) (Figures 1,​,22). Figure 1 OAS among radiotherapy group and stenting group Figure 2 OAS among radiotherapy group and radiotherapy + stenting group Inhibitors,research,lifescience,medical Discussion Esophageal cancer is increasing in last few years, unfortunately the majority

of patients will present with locally advanced or metastatic disease which is difficult to control. Considering this fact, it is important to offer treatment providing adequate and rapid palliation of symptoms especially the obstructive symptoms which reflect on the quality of life. Radiotherapy for esophageal Inhibitors,research,lifescience,medical cancer is a relatively effective GSK-3 treatment and provides survival benefits. In the present study 91 patients enrolled 30 patients received radiotherapy, 35 patients underwent stent and 26 patients underwent stent and received radiotherapy, relief of dysphagia occurs rapidly in stent groups than in radiotherapy alone group (8) and was more standing in stent plus radiotherapy group, recurrence of dysphagia occurs in 8.5% in GII and 3.8% in GIII this is due to tumor over growth on the stent in GII. The median overall survival time was 169 days for patients receiving radiotherapy and this comparable to reported by Slabber et al. (13), who reported 144 days median over all survival, the median radiation dose was 24.66±5.07 in GI and 26.29±6.17 GIII, doses more than 40 Gy increase toxicity.