He began his study of medicine at the University of Wilno in East

He began his study of medicine at the University of Wilno in Eastern Poland (now part of Lithuania) under Soviet occupation where he completed the first trimester, and joined the Polish Army and spent World War II from 1940 to 1945 as a prisoner of war in Germany and France, an experience he speak sparingly of except about when he escaped from his imprisonment in Hamburg, Germany and recaptured in Strasbourg, France. He resumed his medical education at the University of Brussels, Belgium after the CP-673451 molecular weight war and graduated with a M.D. degree in 1949. As a student, he listed

seven papers, wherein he is a co-author or author, pertaining to the effects of hormone on vaginal cytology from the Research Laboratory of the Department of Obstetrics and Cytology. He FG-4592 chemical structure emigrated to Canada in 1951 where he was

in private practice, served a year residency in medicine at the University Hospital in Saskatoon, and joined its faculty where he obtained a research fellowship in the laboratory of Dr. E.R. Yendt in the Department of Medicine, University of Toronto to study metabolic bone disease, parathyroid, kidney stones and renal hypertension. Dr. Yendt spent time with Dr. John E. Howard at John Hopkins University, a former member of Fuller Albright’s team in Massachusetts General Hospital. George moved to the University of Ottawa in 1963 from Saskatoon where he was involved in the first hospital to introduce maintenance hemodialysis and kidney transplantation in Canada. In late 1960, George decided to spend his sabbatical years working in calcified tissue laboratories. He wrote about his sabbatical in the Medical Research Council of Canada short summary of research accomplishment and personalized biography of their most

talented senior award winner in Canada as follows: “Subsequently the work of two investigators influenced my research. First, that of Dr. Harold Frost, head of Orthopedics at Henry Ford Hospital in Detroit, originator of a method of studying lamellar bone turnover system by means of bones labeled in vivo with tetracycline. Second that of Dr. Webster S.S. Jee, Anatomy professor at the University of Utah in Salt Pyruvate dehydrogenase Lake City in whose laboratory I familiar myself with the study of cell kinetics by means of tritiated thymidine”. Originally he was to stay 3 months in Frost’s laboratory but he extended it to 9 months where he came in contact with other “Frostians” which included Pierre Meunier, Eimei Takahashi, Bruce Epker, Bob Hattner and others. George spent a short 3 months in my laboratory in which he enhanced my research by critiquing our manuscripts and mentoring my postdoctoral trainees and summer dental student investigators.

8 μg, p < 0 05 2-way RM ANOVA) ( Fig  3b) The DOI induced increa

8 μg, p < 0.05 2-way RM ANOVA) ( Fig. 3b). The DOI induced increase in mechanical evoked neuronal response was reversed back

towards baseline levels by spinal application of ketanserin (1 μg). The effect of DOI on the thermal evoked responses was more variable. Spinal application of DOI on the evoked response to 40 °C and 45 °C heat in 2 of the 6 cells resulted in a clear and sustained buy MDV3100 inhibition with one or both doses of DOI. Furthermore, in some instances, a transitory reduction was seen at the early (10 min.) time point to the evoked response to 40 °C and 45 °C stimuli; these inhibitory effects of DOI on these thermal stimuli were dwarfed by a marked facilitation of the neuronal response at the later time points (30 and 50 min.) post DOI administration. By contrast the evoked neuronal response to 48 °C was clearly facilitated (significant at 17.8 μg, p < 0.05 LBH589 2-way ANOVA). The increased heat evoked neuronal responses produced by DOI were reversed back towards baseline levels by spinal application of ketanserin ( Fig. 3c). There is considerable evidence for the critical role for serotonin (5-HT) in the modulation of spinal nociceptive transmission. A number of early studies observed inhibition and subsequent analgesia following blockade of the 5-HT system; more recently, however, a pronociceptive/hyperalgesic

action has also emerged for the 5-HT system (for review see Bannister et al. (2009)). These contrary reports can, in part, be accounted Staurosporine datasheet for by the multiplicity of neuronal targets and receptor subtypes upon which 5-HT acts (Knight et al., 2004). To date, seven distinct families of

5-HT receptors have been identified (5-HT1–5-HT7), and several of these have been further sub-classified. Among them, the 5-HT2 receptor is thought to play an important role in spinal pain modulation; however, as is the case for other 5-HT receptor subtypes, opposing data exist as to the direction of effect (pro- or antinociceptive) produced by 5-HT2 receptor modulation. Our electrophysiological data show that the 5-HT2A antagonist, ketanserin (10–100 μg/50 μl), and the 5-HT2A/2C antagonist, ritanserin (2 mg/kg), at these doses, have an overall inhibitory effect on spinal neuronal activity with selectivity for the higher intensity responses; furthermore, the 5-HT2A/2C receptor agonist, DOI, produced an overall facilitation of spinal neuronal responses with significant effects seen on the mechanical and thermal evoked neuronal responses. These increased neuronal responses were reversed by spinal application of ketanserin. Thus, our data support a pronociceptive role for the 5-HT2 receptor, most likely through targeting the 5-HT2A receptor subtype, on spinal nociceptive transmission under normal conditions.

Kettering Prize presented by the General Motors Cancer Research F

Kettering Prize presented by the General Motors Cancer Research Foundation in 1987. In 1997 the Basil I.

Hirschowitz Endowed Chair in Gastroenterology was established at the University of Alabama at Birmingham and was awarded to Dr. Charles Elson. He also has a named lectureship each year at the ASGE plenary session. As the only other two Directors of the Gastroenterology Lumacaftor research buy Division at UAB since its creation in 1959, we will miss his uncompromising commitment to excellence, insatiable quest for knowledge, unmistakable professionalism, and warm generous heart. “
“Biliary strictures are one of the most common adverse events after liver transplantation, particularly with living donors, occurring in as many as 40% of patients in the postoperative period.1 and 2 The classification of biliary strictures as anastomotic or nonanastomotic is useful both anatomically and to define response to nonsurgical interventions, with nonanastomotic biliary strictures responding less favorably to endoscopic therapy than anastomotic biliary strictures (ABSs).3, 4 and 5 The endoscopic management of ABSs has dramatically improved over the past decade, by using balloon dilation (BD) and the increasing number of plastic stents (PSs) with successful selleck stricture resolution in 64% to 100% of orthotopic liver transplantation (OLT)

patients.6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19 and 20 However, ABSs after living donor liver transplantation (LDLT) remain refractory to endoscopic therapy in most case series.21, 22, 23 and 24 Although the optimal strategy for treating these strictures remains to be defined, serial BD and PS exchanges over an extended period have become the preferred method, especially in OLT patients.25 and 26 Covered self-expandable metal stents (SEMSs) have been used to treat malignant strictures and, more recently, Niclosamide benign conditions including post-transplantation ABSs. Because covered SEMSs have a greater likelihood of migration and a small risk of nonremovability, their overall safety and efficacy have yet

to be defined in the transplantation setting.26 and 27 The purpose of this study was to conduct a systematic review to compare the efficacy and safety of SEMSs versus multiple plastic stents (MPSs) in the management of ABSs after both OLT and LDLT. A comprehensive search was performed with the assistance of a research librarian. EMBASE (1974 to present) and MEDLINE (1948 to present) were searched from inception until October 2012 by using the following search terms: endoscopy, endoscopic retrograde cholangiopancreatography, liver transplantation, and biliary and/or anastomotic biliary stricture. Electronic searches were supplemented by manual searches of references of included studies and review articles. A single reviewer (D.K.) screened titles and abstracts. By using inclusion and exclusion criteria, full articles on potentially relevant studies were assessed by 2 pairs of independent reviewers (D.K./S.Z.G., D.K./P.T.).

For this purpose body temperature and weight were measured immedi

For this purpose body temperature and weight were measured immediately before treatment and body temperature was measured again 4 h post-injection. An additional measurement of body weight was taken 21 h post-injection

after the animals had been subjected to the open field (OF) test (n = 8). In a separate experiment (experiment 2.2), mice were euthanized 3 h after injection of PRR agonists ( Fig. 1) and the brains were collected for immunohistochemical visualization of c-Fos expression in select brain regions (n = 3–5). Following euthanasia the brains were removed, put on dry ice and stored at −70 °C Pictilisib until use. Protocol 3 was used in 3 separate experiments (Fig. 1) in which the effects of MDP and FK565 in combination with the lower dose of LPS (0.1 mg/kg) were investigated. In experiment 3.1 body temperature and weight were measured before treatment and the body temperature was measured again 4 h post-injection. The OF test was conducted 21 h after the treatment

and body weight was measured after the OF test (Fig. 1). Subsequently the animals were subjected to the tail suspension test (TST) for 6 min (25.5 h post-injection) and euthanized 30 min after start of the TST. Blood was sampled to measure the plasma levels of cytokines, corticosterone, kynurenine and tryptophan (Fig. 1). In addition, the brains were collected, frozen in −70 °C cold 2-methyl butane (Fisher Scientific, Leicestershire, UK) and stored at this temperature until measurement of cytokines (n = 7–8). In experiment 3.2 mice (Fig. 1) were euthanized CAL-101 clinical trial 3 h after injection of PRR agonists to record the levels of circulating and brain cytokines and circulating corticosterone without interference by any behavioral test (n = 7–8). In a further experiment (experiment 3.3) singly housed mice were subjected to the forced swim test (FST) 21 h post-injection, since depression-like behavior has been shown to be modified by different housing conditions (Painsipp et al., 2011) (n = 7–8). All compounds were dissolved in pyrogen-free sterile saline (0.9% NaCl) and pyrogen-free

sterile saline injected intraperitoneally (i.p.) at the same volume (50 μL/10 g body weight) was used as vehicle (VEH) control. For the analysis of the interaction between NOD agonists and LPS, two doses of LPS were examined. First, the widely used PR171 dose of 0.83 mg/kg LPS inducing the full spectrum of sickness (Frenois et al., 2007 and Painsipp et al., 2011) was used. Since, in combination with the NOD agonists, this dose of LPS led to a marked decrease in body temperature and locomotion, while a ceiling effect was observed with other parameters, a lower dose of 0.1 mg/kg LPS was also tested. The doses of the NOD agonists (see below) were chosen on the basis of their immunological effects in vivo ( Parant et al., 1995 and Shikama et al., 2011) and the results of pilot experiments. Thus, doses of 1 mg/kg (LabMaster studies) and 3 mg/kg (ex LabMaster studies) of MDP and 0.001 mg/kg (LabMaster studies) and 0.

1C) Rarely, parasite-positive areas were seen during the chronic

1C). Rarely, parasite-positive areas were seen during the chronic phase PLX3397 supplier (data not shown). Histopathological analyses revealed that in T. cruzi-infected C3H/He mice, brain inflammation was restricted to the acute phase of infection, when inflammatory cells were seen in the parenchyma and perivascular cuffs with one or more layers of infiltrating cells ( Fig. 1D). In the acutely infected C3H/He mice, several CNS areas were affected including hippocampus ( Fig. 1D), a brain region involved in depression in mouse models ( Bahi and Dreyer, in press). In contrast, no inflammatory infiltrates were detected in the brain of acutely and chronically T. cruzi-infected C57BL/6

mice ( Fig. 1D), resembling the CNS of NI controls. These data are summarized in Table S1. Therefore, these models allowed us to test whether behavioral alterations were induced during chronic T. cruzi infection and whether they were a long-term consequence of acute CNS inflammation. To test whether behavioral alterations are present in T. cruzi infection, we initially subjected infected

mice to the open-field test and analyzed the numbers AZD6244 cost of peripheral and central crossed lines and rearing episodes. Acutely infected C57BL/6 mice exhibited a significant (p < 0.001; t (11) > 5.124) decrease in locomotor/exploratory activity compared with the NI controls in five-, ten- and thirty-minute sessions ( Fig. S1A). Chronically T. cruzi-infected C57BL/6 mice also presented a significant decrease in locomotor/exploratory activity expressed as the reductions in the number of crossed peripheral (p < 0.0001; t (9) = 11.89) and central (p < 0.01; t Phloretin (9) = 4.107) lines and rearing episodes (p < 0.0001; t (9) = 8.888) in five-minute sessions ( Fig. S1B). This finding confirms our previous data ( Silva et al., 2010). Conversely, when T. cruzi-infected C3H/He mice were compared with sex- and age-matched NI controls, there were no significant differences (p > 0.05; t (6) < 1.500)

in the numbers of crossed peripheral and central lines or rearing episodes during the acute (30 dpi; Fig. 2A) or chronic (90 dpi; Fig. 2B) phases of infection in five-minute sessions of the open-field test. Furthermore, no significant (p > 0.05; t (11) < 1.000) behavioral alterations were detected in acutely ( Fig. S2A) or chronically ( Fig. S2B) T. cruzi-infected C3H/He mice when their performances in ten- and thirty-minute sessions of the open-field test were analyzed. Considering that sickness features may contribute to behavioral alterations such as decreases in spontaneous locomotor/exploratory activity ( Rogers et al., 2001), we further assessed sickness behavior by checking body weight loss (which reveals loss of appetite), apathy and increase in temperature (indicative of fever). During the recorded interval (from 7 to 150 dpi), apathy, characterized as prostration, was not detected in C3H/He and C57BL/6 mice infected with a low-level inoculum of the Colombian T. cruzi strain.

In the SPICOSA work package ‘observational techniques’, the use o

In the SPICOSA work package ‘observational techniques’, the use of remote sensing as diagnostic tool was investigated. First, the main policy issue in Himmerfjärden was identified. Secondly, suitable indicators were identified which could be implemented into management models. Thirdly, a conceptual model was developed that explored how to use remote sensing and bio-optics in integrated coastal zone management. One of the work packages in the SPICOSA project High Content Screening was academic training. In this work package, Stockholm University was instructed to develop on-line teaching material in

the field of remote sensing and bio-optics. This material was published on the SPICOSA teaching and dissemination platform SETnet at the end of the SPICOSA project in 2011. The material included the film ‘The Science of Ocean Color’, a film consisting of 5 chapters filmed and directed by Roland Doerffer. It can be downloaded directly on the SETnet web page [36]. The article presented here may be regarded as supportive material for the bio-optics and remote sensing lectures published on the SETnet web page. The starting point

for developing remote sensing as diagnostic tool was the main ‘Impact’ and ‘Policy Issue’ for the study U0126 clinical trial site Himmerfjärden. Following the SPICOSA launch meeting in February 2007 the members of work task (WT) 10.3 (observational techniques) were instructed to make a list of ‘human activities’

and ‘main impacts’ for their respective sites, based on a given table of possible coastal impacts. Table 1 lists the relevant impacts and human activities for Himmerfjärden. The table was prepared by the Himmerfjärden Stockholm University SPICOSA scientific team. On 13 Nov 2007 the Swedish SPICOSA participants arranged the first Himmerfjärden stakeholder meeting in Södertälje, Sweden. During this meeting, eutrophication, caused by increased Phosphoribosylglycinamide formyltransferase loads of nitrogen, was identified as the major environmental problem in Himmerfjärden, as in general for the Baltic Sea. After identifying nitrogen management as the major policy issue, the next step was to identify the key indicators of eutrophication that can be simulated within the ESE Assessment box [21], and that also could be monitored by remote sensing. Secchi depth was found to be the link between the ecological and the economic component of the ESE: In the economic model, questionnaires were used to evaluate the monetary value that the residents in the Himmerfjärden area, or visitors/tourists put on improved water clarity (e.g. a Secchi depth increase by one meter). The ecological model estimated Secchi depth according to empirical relationship between nitrogen concentration and Secchi depth. Besides nitrogen loads water exchange rates were also included in the model. Nitrogen reduction e.g.

In our present study we have demonstrated that measuring IMT in

In our present study we have demonstrated that measuring IMT in

postmortem arterial specimens by US is a reliable and reproducible method, which could be used for US standardization in subsequent studies. Hence, in vitro US measured IMT could be used to develop, improve, compare or validate new imaging techniques (e.g. fast three dimensional imaging techniques), automated IMT measurement algorithms, or new softwares for ultrasound methods. Carotid IMT is strongly determined by genetic factors acting independently of traditional cardiovascular risk factors [35] and [36]. A heritability range of 20–40% has been estimated by studies in unselected subjects, twins, and people with type II diabetes [36], [37], [38], [39] and [40]. Genes related to hemostasis, lipid and lipoprotein levels, extracellular matrix remodeling, antioxidation, renin–angiotensin system, endothelium function, Nintedanib datasheet Selleck Tyrosine Kinase Inhibitor Library inflammation have been associated with

carotid IMT changes [34] and [41]. On the other hand, laminar flow and oscillatory shear stress trigger diverse local endothelial responses and altered gene expressions and result in an atherogenic phenotype [26], [42], [43] and [44] which may vary in different carotid segments with a possible impact on IMT. Our results implicate that in vitro US including IMT provide valuable information about autopsied arterial specimens. These, afterwards, can be stored and made available in tissue banks for a wide O-methylated flavonoid range of ‘-omics’ investigations. In addition, in vitro US of arterial specimens could serve as a guide to identify the most appropriate region of an intact autopsied vascular tissue for histological sampling. Furthermore, Liao et al. (2008) applied the gene risk score (GRS) to estimate a cumulative effect of genes significantly associated with IMT and emphasize

the importance of future gene-IMT association studies on different populations. The use of the GRS may simplify an assessment of multiple gene effects in complex diseases and may provide a better estimate of individual susceptibility to atherosclerosis [26]. The accuracy and utility of GRS can possibly be improved by including an US artifact free postmortem IMT measurements of different parts of arterial wall (e.g. ‘far wall, near wall’, etc.). GRS combined with IMT could improve the precision and reliability of prognosis determination models for a complex disease like atherosclerosis. In the present study we measured arterial IMT applying in vitro US and compared it to in vivo determined IMT, histological IMT and average arterial wall thickness. We demonstrate that for microscopic IMT determination purposes cutting and processing frozen arterial sections after in vitro US is a suitable histological technique which has advantages compared to use of formalin fixed paraffin embedded (FFPE) slides.

, 2010) After surgical procedures involving skin and deeper stru

, 2010). After surgical procedures involving skin and deeper structures, pain occurs both at rest and during stimuli such as pressure and touch, which are usually not painful. These exaggerated responses can be measured by using pressure (eg, pressure algometry after hysterectomy and thoracotomy) or touch methods (eg, von Frey filament-induced pain after hysterectomy, colectomy, and nephrectomy). By examining some of the fundamental basis of incisional pain, it may be possible to develop a link between animal models of pain and clinical postoperative pain (Brennan et al., 2005). Several studies have focused on the development of novel analgesic

drugs that inhibits voltage-sensitive Ca2+ channels (VSCCS). The ω-conotoxin MVIIA is a selective, reversible and potent blocker of N-type Ca2+ channels this website www.selleckchem.com/products/dorsomorphin-2hcl.html (NCCs) that inhibits both neuronal excitability and neurotransmission (Miljanich and Ramachandran, 1995). ω-Conotoxin MVIIA was originally isolated from the cone snail Conus magnus and was subsequently synthesized and called ziconotide. Ziconotide has also been shown to bind and block cloned human NCCs. In fact, intrathecal administration of ziconotide in humans likely facilitates its binding to these

channels in the dorsal horn reducing pain signaling and inducing potent analgesia ( Smith and Deer, 2009). However, ziconotide has a narrow therapeutic window and produces some serious side effects even with analgesic doses ( Smith and Deer, 2009). The side effects tend to occur more commonly at higher doses and include: nausea, vomiting, confusion, postural hypotension, abnormal gait, urinary retention, nystagmus/amblyopia, drowsiness/somnolence, dizziness or lightheadedness, weakness, visual problems, elevation

of serum creatine kinase, or vestibular side effects. Another alternative for the treatment of severe pain are opioids. Morphine is used in moderate or severe acute pain unresponsive to less potent analgesics. Morphine is highly effective but has several unwanted effects such as constipation, nausea, vomiting, hypotension, bradycardia and respiratory depression that limit its use (Hoskin and Hanks, 1991). Thus, in order to improve the quality of pain management, it is necessary to investigate new analgesic agents with less adverse side effects. Chlormezanone Toxins obtained from the venom of the spider Phoneutria nigriventer, popularly known as armed spider have been extensively investigated. These toxins have a broad range of actions, including activation of Na+ channels, blockade of K+ and Ca2+ channels ( Gomez et al., 2002). One purified fraction of the venom, called PhTx3, contains six neurotoxins peptides isoforms, PnTx3-1 to 6 ( Cordeiro Mdo et al., 1993). The neurotoxin PnTx3-6, here called as Phα1β, reversibly and non-specifically inhibits VSCCS, namely l-(Cav1.2), N-(Cav2.2), P/Q-(Cav2.1), and R-(Cav2.3) type, with different potency (N > R > P/Q > L) in heterologous and native systems ( Vieira et al.

aureus strains already seem to have acquired mecA [1] Various fu

aureus strains already seem to have acquired mecA [1]. Various functional genes of diverse metabolic pathways are found carried by SCC in the staphylococcal oriC environ. Some examples are; pbp4, encoding penicillin-binding protein 4 (PBP4) in the cell-wall synthesis pathway [8], arginine catabolic pathway genes (ACME) [9], and hdc encoding histidine decarboxylase [10]. However, the genes much more frequently found in

the oriC environ are drug-resistance genes. Besides mecA, such drug-resistance genes against mercury, cadmium, kanamycin, bleomycin, erythromycin, spectinomycin, and fusidic acid have been found in association with SCC elements in oriC environ [4] and [11]. Evidently, IPI-145 in vitro the oriC environ serves as the storehouse in support for achieving the multi-drug-resistance phenotype. S. aureus quickly acquired β-lactamase plasmids soon after the penicillin G was introduced in 1940s, but no plasmid carrying mecA has been found. Although the reason is not clear, SCC-mediated acquisition of a single copy of mecA gene on the chromosome might have been less effective against penicillin-G as compared to the plasmid-born multiple copies of beta-lactamase encoding blaZ genes. On the other hand, mecA encodes cell-wall

synthesis enzyme PBP2’ [12]. PBP2’ is a homolog of intrinsic S. aureus PBPs and considered to have inefficient transpeptidase activity [13] and [14]. As such, overproduction of PBP2’ may cause turbulence in the cell-wall synthesis and a big fitness cost especially during Florfenicol the growth in the absence of β-lactam antibiotics. Storage of mecA as a single gene copy in oriC Erastin nmr environ and multiple gene doses of blaI on the penicillinase plasmid would be the best way to maintain mecA in the repressed status in the drug-free growth condition. (Here, note that blaI gene

is the cognate repressor gene of blaZ. The BlaI also cross-represses mecA gene because the cognate mecA-gene repressor gene mecI is usually deleted or inactivated by mutations [15].) Apparently, oriC environ is suitable for the storage of foreign genes in single copies that may have a hazardous effect on the cell physiology if overexpressed. 2) The origin of mecA gene We previously identified a mecA-gene homolog mecB on the plasmids and chromosomes of Macrococcus caseolyticus isolates [16] and [17]. Macrococcal species, disseminated in nature as animal commensals, are immediate antecedents of staphylococcal species ( Fig. 2) [17]. The macrococcal mecB was distantly related to mecA (61.7% nucleotide identity), and was found disseminated among the macrococcal strains as a transposon, designated Tn6045 [16]. No complete form of SCCmec was found in macrococcal strains. However, many ccr genes are found on the plasmids and chromosomes of the macrococci, and tandem integration of an SCC element and a mecB transposon was observed in the oriC environ of a macrococcal strain [16].

Amongst others, the results from the SPACE study have encouraged

Amongst others, the results from the SPACE study have encouraged those claiming that restenosis might be a relatively benign pathology [16] and [44]. On the other hand, especially long-term follow-up

data raise concern that patients with ISR could be suffering from a higher complication rate in comparison to patients without ISR [30]. Since CAS is often recommended the treatment of choice in younger patients (<70a) [3], [4], [5] and [9] it is of greatest interest to evaluate the complication rates of ISR in the long run. By now, the results regarding the incidence and clinical complications www.selleckchem.com/products/INCB18424.html of ISR of the randomized controlled trials comparing CAS and CEA [4], [6] and [11] are eagerly awaited. The unresolved clinical impact of ISR further highlights the importance to identify independent risk factors which are predictive RG7420 price for an ISR. These would be helpful to detect those patients in which a tight follow up is necessary. Advanced age [17] and [19] has been found to be predictive for an ISR, which would further contribute to the recommendation of choosing a CEA as a first treatment of choice especially in elderly patients [3] and [5]. CAS is frequently recommended in patients with a restenosis after CEA because a redo-CEA sometimes appears to be technically difficult and might

bear a higher periprocedural risk than the initial operation [7] or in patients with a radiogenic stenosis [45]. When considering the optimal treatment option for those patient subgroups, one

should take into account though that a CAS procedure because of a CEA-restenosis or radiation-induced stenosis is also associated with a higher rate of ISR [20], [23], [34] and [35]. An insufficient result after a CAS procedure, e.g. due to insufficient stent adaptation, could be shown to be associated with a higher risk of ISR occurrence [19], [20] and [28]. Therefore, to ameliorate the long-term benefit of a CAS, it is a worthwhile aim to pursue a perfect stent adaptation to the vessel lumen. The fact that an aggressive postdilation bears the risk of distal embolization and microvascular injury, which may itself initiate neointimal hyperplasia complicates the procedure. Furthermore, the characteristics of the stent deployed are of special interest regarding the incidence of ISR. Usually, the selection MG-132 in vitro of the stent length and width are based on angiographic findings in order to appropriately cover the stenosis. However, narrower and longer stents were correlated with a higher ISR risk [28] and [30]. It is conceivable that a stent with a larger diameter results in a reduced flow-velocity, less turbulences and thus in less frequent ISR. A longer stent, which is used to cover longer lesions, probably represents the presence of a high plaque burden and has repeatedly been identified as an independent predictor for periprocedural complications [46] and [47].