MUAPs were manually selected using signal trigger averaging with the patient exerting a weak to moderate effort so as to activate 2 to 5 MUAPs clearly seen on the baseline. Every effort was made to improve sharpness. The filters were set between 2 Hz to 10 kHz; the acquisition sensitivities were set at 100-500 μv/division and 5 ms/division. The duration of the MUAPs was determined manually after averaging at 100 μv/division and 5 ms/division. Polyphasic MUAPs, but not satellite potentials, were included in the analyses. MUAPs with

amplitude lower than 50μV and rise time longer than 500μsec were rejected. Twenty MUAPs were obtained from each muscle from 4-5 insertion points. The original stored data consisting of 20 averaged MUAPs from Inhibitors,research,lifescience,medical each muscle were re-analyzed Inhibitors,research,lifescience,medical for the purpose of this study using the mean duration and outlier methods and the results correlated with biopsy findings in the contralateral muscle. For the mean duration method, the duration of 20 MUAPs from each muscle were averaged

and the mean compared with normal values for age (3, 11). A muscle was categorized as neuropathic or myopathic if the mean MUAP duration was 20% above Inhibitors,research,lifescience,medical or below the mean normal values for age respectively. The 20 MUAPs were also analyzed by the outliers method (12). Outliers as defined by Stalberg are the upper or lower MUAP amplitude or duration values beyond which a normal Inhibitors,research,lifescience,medical individual has no more than 2 MUAPs. For the outliers method we used the upper and lower limit values of Oh (13). MUAPs less than 6μsecs in duration and /or less than 300μV in amplitude were defined as myopathic, while MUAPs longer than 17msec in duration and/or larger than 3,5mV in amplitude as neuropathic. Muscles with more than 2 MUAPs outside the limits

were considered check details abnormal. Muscle biopsies Open muscle biopsies were obtained from 20 vastus lateralis and 19 biceps brachii Inhibitors,research,lifescience,medical muscles. The biopsy was obtained from the contralateral muscle to that examined by QEMG. The selected muscle had a Medical research council (MRC) score more than 3. The pathologist reading the biopsies was not aware of the EMG result. Muscle biopsy findings were classified for the purpose of the study SB-3CT as myopathic; M1, increased variability in muscle fibre size involving both fibre types, M2, the presence of necrosis and/or regeneration, M3, the presence of endomysial fibrosis indicating chronicity and fibre loss and M4 alterations in the fibre architecture without significant fibre loss or variability in fibre size. Such abnormalities included ragged red and cytochrome c oxidase deficient fibres (Fig. 1). Biopsies were classified as neurogenic if there were angular atrophic fibres of both fibre types and/or the presence of type grouping, indicative of reinnervation (Fig. 1). Figure 1. Myopathic (M1, M2, M3, M4) and neuropathic (N1,N2) biopsy findings. For details see text. Asterix in M4 indicates a ragged red fibre.

The importance of such a resistance was revealed when a number of studies reported that resistance to clarithromycin was equal to the whole therapeutic

regime failure.28 Conclusion The high rate of clarithromycin resistance in the isolates in the present study is a serious alarm, and in agreement with clinical colleagues’ views that many of their patients do not respond to clarithromycin anymore. Point mutations in 23s rRNA are closely related to such a resistance. With daily increase in the use of clarithromycin in therapeutic regime for H. pylori in Iran, the rate of Inhibitors,research,lifescience,medical H. pylori resistance rate to the drug is increasing. Therefore, it seems necessary to do antibiotic susceptibility tests for H. pylori before therapy begins. Acknowledgment The authors would like to thank the Research Council of Inhibitors,research,lifescience,medical Kerman University of Ruxolitinib in vitro Medical Sciences for their financial supports. Conflict of Interest: None declared
Self-reactive lymphocytes can be dangerous to the body when they attack themselves and cause autoimmune diseases under certain conditions. Inhibitors,research,lifescience,medical Hence, the immune system has evolved several mechanisms to prevent this from occurring. The most well-documented mechanisms are the so-called clonal

deletion in the thymus, anergy and ignorance. There is evidence that self-reactive T cells are dominantly suppressed by newly identified T-cell subpopulations called regulatory T cells (Treg), which play important roles in the maintenance of immune homeostasis and the control of adaptive immune response.1 Among the reg cells, naturally occurring CD4+ and CD25+ regulatory T cells (nTregs) have been best characterized. Many subsets of Treg cells Inhibitors,research,lifescience,medical have been described that can suppress T cell response via different mechanisms. Recent studies showed that CD69+, CD4+CD25– T cells are a new subset of CD4+ Treg cells.2 Naturally occurring Tregs have been the object of this study,

because their function appears critical in maintaining self-tolerance and preventing Inhibitors,research,lifescience,medical autoimmune disease. This is illustrated by the finding that their removal leads to spontaneous development of autoimmune disease, such as autoimmune gastritis, thyroiditis, and diabetes type one and their 17-DMAG (Alvespimycin) HCl reconstitution prevents such diseases.3-5 Rheumatic heart disease (RHD) is the most common cardiovascular disease affecting children and young adults in the world. It is considered a major public health problem causing about 400,000 deaths annually worldwide, especially in developing countries. Molecular mimicry between heart tissue proteins and streptococcal antigens such as the M protein has shown that this protein, which is the major component of the streptococcal cell surface and the most important virulence factor, may act as the triggering factor leading to autoimmunity in RHD patients.

Finally, It would also be Interesting to study the above strategies in conjunction with pharmacogenomic approaches. Selected abbreviations and acronyms ACTH adrenocorticotropic hormone CRH corticotropin-releasing hormone DA dopamine DST dexamethasone suppression test GH growth hormone HPA hypothalamic-pituitary-adrenal (axis) HPT hypothalamic-pituitary-thyroid

(axis) NA noradrenaline PRL prolactin SSRI selective serotonin Inhibitors,research,lifescience,medical reuptake inhibitor T3 triiodothyronine T4 thyroxine TRH thryotropin-releasing hormone (protirelin) TSH thyroid-stimulating hormone (thyrotropin) Notes We would like to thank the nursing staff of Sector VIII and Françoise Fleck and Gabrielle Wagner, pharmacists, for performing the hormone analyses.
Pharmacopsychiatry and psychotherapy are beneficial for many patients with depression. Evidence-based and clinical experience collected Inhibitors,research,lifescience,medical during the past decades has allowed the introduction of guidelines and UMI-77 recommendations from experts in the field1-3 to optimize antidepressant pharmacotherapy. However, partial response and nonresponse are frequent,4 despite the introduction of new psychotropic Inhibitors,research,lifescience,medical agents, including ”third-generation

antidepressants,“5 and amelioration and remission rates are still far from optimal. The efficacy of available drugs can be increased, not only by the use of augmentation strategies6,7 and other combination treatments,8,9 but also by analysis of antidepressant drug concentrations in blood plasma.10 Recently, a group of psychiatrists, clinical pharmacologists, biochemists, and clinical chemists, all members of the AGNP (Arbeitsgemeinschaft fur Neuropsychopharmakologie und Inhibitors,research,lifescience,medical Pharmakopsychiatrie; www.agnp.de), worked out consensus guidelines for therapeutic drug monitoring (TDM) in psychiatry, after

Inhibitors,research,lifescience,medical they had compiled information from the literature.11 These guidelines were mainly based on the hypothesis that some inadequate or insufficient treatments of psychiatric patients can be explained by the fact that psychotropic drugs not only differ in their pharmacological profile, but also in their metabolism and pharmacokinetics in the individual patient. Treatment should therefore be adapted accord_ isothipendyl ing to this situation by using TDM and pharmacogenetic tests. This combined strategy takes into consideration the fact that the fate of the drug depends on both environmental (diet, smoking habits, comorbidities, and cornedications) and genetic factors. Pioneering work in this field was mainly carried out in Sweden, where the first study on the plasma concentration–clinical effectiveness relationship of an antidepressant (nortriptyline)12 was performed. This was an outstanding demonstration of the usefulness of the combination of TDM and pharmacogenetic tests (CYP 2D6) in a pharmacovigilance case situation.

45 However, little evidence currently exists as to whether reduction of hippocampal volume is directly due to elevated levels of Cortisol, though it has been postulated that elevated Cortisol may influence

cognitive performance and mood state.46 MS patients are known to have a chronically activated HPA axis,47 and HPA axis activity correlates with progression ratings and cognitive impairment over 3 years.48 In addition, MRI studies28 have shown an association between depression in MS and temporal lobe atrophy (though not specifically hippocampal atrophy). Given the association between depression and both HPA activity and Inhibitors,research,lifescience,medical hippocampal atrophy, the chronic activation of the HPA axis in MS may be one source of these patients’ increased susceptibility to the development of depression. Steroid treatment Consistent with a role for the HPA axis in the mechanism of depression, exogenous corticosteroids have been shown to have powerful mood-altering effects. Inhibitors,research,lifescience,medical Corticosteroids are often used in high doses to treat exacerbations in MS. They are associated with a great number of side effects, including effects on mood.49 Their short-term Inhibitors,research,lifescience,medical use often produces an activated state characterized

by increased energy, decreased sleep, and variable euphoria, which can be quite destabilizing to a patient’s mood state. With initial dosing, longterm use, and discontinuation, steroid administration can result in new depressive symptoms as well as dramatic and even life-threatening worsening of mood in those already suffering from depression.50 The effects Inhibitors,research,lifescience,medical of steroids on mood regulation provides further support for a role of the HPA axis in precipitating depression. The role of inflammation in MS depression The increased incidence of depression in MS may be directly related to the inflammation which is the hallmark of this autoimmune disease. Alterations in the immune function

of depressed patients have been observed for many years, although the precise nature of the changes has been variable, with some reflecting suppression Inhibitors,research,lifescience,medical and others activation Dipeptidyl peptidase of the immune system.51-53 Recent work has demonstrated that depression is associated with an activation of inflammatory pathways, as evidenced by increases in C-reactive screening assay protein and other changes.54-57 In MS, depression scores are higher in patients with increased CSF white blood cell counts, in vitro interferon (IFN)-γ production, increased messenger ribonucleic acid (mRNA) for tumor necrosis factor (TNF)-α and IFN-γ, and central nervous system (CNS) inflammation as demonstrated by gadolinium-enhancing lesions on T1-weighted MRI.5,21,58 Cytokines Proinflammatory cytokines are chemical messengers that are produced by immunocompetent cells and mediate communication between cells of the immune system, and are elevated in MS.

It is of note that two of these studies referred to drug-naïve patients who had been medicated for only 6 weeks with antipsychotic agents, and they developed MetS in response to this [Akt inhibitor Saddichha et al. 2007, 2008], and the third study referred to a very rare population of drug-naïve, unmedicated patients with an extremely low prevalence of MetS, as discussed above [Padmavati et al. 2010]. A German study explored the prevalence of MetS in patients

with treated or untreated Inhibitors,research,lifescience,medical schizophrenia at baseline and at 3 months after initiation or switch of antipsychotic treatment. The authors reported an increase from 44.3% to 49.6%, and also described the lowest Inhibitors,research,lifescience,medical baseline MetS prevalence (24.7%) in previously unmedicated patients [Kraemer et al. 2011]. The lack of further studies on drug-naïve patients is an anticipated source of

bias in any effort to explore the role of antipsychotic medication in the development of MetS. However, numerous studies attempted to compare various antipsychotics or groups of antipsychotics (FGAs versus SGAs) in terms of their contribution to MetS [Almeras et al. 2004; Kato et al. 2004; Straker et al. 2005; Correll et al. 2006, 2007; Hagg et al. 2006; L’Italien et al. 2007; Suvisaari et al. 2007; Tirupati et al. 2007; Inhibitors,research,lifescience,medical Cerit et al. 2008; De Hert et al. 2008b; Meyer et al. 2008; Saddichha et al. 2008; Huang et al. 2009; Rezaei et al. 2009; Schorr et al. 2009; Lee et al. 2011]. Consistent findings across these studies found that MetS was more likely with SGAs over FGAs, polypharmacy over monopharmacy and high-potency over low-potency agents. Inhibitors,research,lifescience,medical For individual antipsychotics, clozapine

and olanzapine appeared to be related to higher MetS rates than other antipsychotic agents. Metabolic syndrome and ethnicity Inhibitors,research,lifescience,medical Very few studies attempted to address the issue of ethnicity when MetS rates are calculated [Basu et al. 2004; Kato et al. 2004; McEvoy et al. 2005; Straker et al. 2005; Correll et al. 2006; Lamberti et al. 2006]. Black African and Hispanic patients appeared to present with higher rates of MetS, however some studies found rates to be similar to white populations. However, outcomes appeared to be quite inconsistent. It is of note that despite Indian and Asian populations having a predisposition to develop diabetes, studies of patients with schizophrenia ADAMTS5 originating from these populations usually reported lower prevalence rates of MetS compared with white and black patients. Of course this observation can also reflect the lower rates of prescribing atypical antipsychotics in developing versus developed countries. Metabolic syndrome and duration of pscyhotic illness or type of psychiatric setting Only three studies were identified which looked at duration of psychotic illness in the calculation of MetS rates.

Functional MRI (fMRI) provides measures of relative cerebral blood flow (rCBF) during SB431542 chemical structure memory or other cognitive

task performance, and has the advantages of high resolution in space and time and lack of radiation exposure.29 Thirty middle-aged and older subjects with mild memory complaints but normal memory performance received APOE genotyping. The 14 subjects with the APOE-4 genetic risk for AD did not differ significantly from the 16 subjects without APOE-4 group in age, prior educational achievement, or rates of AD family history. During fMRI scanning on a 3-tesla unit, subjects performed an unrelated paired associate learning task. Brain activation Inhibitors,research,lifescience,medical patterns were determined during both learning and retrieval task periods and analyzed using both between-group and within-subject approaches. Compared with subjects without APOE-4, those at genetic risk showed significantly greater magnitude and spatial extent of rCBF during memory retrieval in regions Inhibitors,research,lifescience,medical affected by AD: left medial temporal and bilateral parietal

and prefrontal. Longitudinal data indicated that baseline brain activation correlated with Inhibitors,research,lifescience,medical verbal memory decline assessed 2 years later. Relative cerebral blood flow responses to a memory challenge may reflect compensatory cognitive efforts for emerging functional deficits in people at genetic risk for AD. These results suggest that combining brain activation and genetic risk measures may provide information that eventually predicts future cognitive decline. PET imaging of plaques and tangles in AD New research is under way to develop additional early detection strategies with greater sensitivity and specificity, including studies aimed at imaging the neuropathological hallmarks of AD. Intraneuronal NFTs and extracellular Inhibitors,research,lifescience,medical P-amyloid-rieh senile plaques (SPs) have been implicated as central components of the pathogenic cascade in AD, which

highlights the Inhibitors,research,lifescience,medical importance of noninvasive in vivo assessment of SP and NFT deposition. A hydrophobic radiofluorinated derivative of 1,1-dicyano2-[6-(dimethylamino)naphthalen-2-yl]propene (FDDNP) was used in conjunction Cediranib (AZD2171) with PET to determine the localization and load of NFTs and SPs in the living brain of AD patients (n=7) and controls (n=3).30 Fluorescence microscopy also was used to determine SP and NFT binding in AD brain specimens. Greater accumulation and slower FDDNP clearance was observed in SP/NFTrieh brain areas, particularly the hippocampus-amygdalaentorhinal complex, but also temporal and parietal cortex in advanced disease stages. In vitro fluorescence microscropy showed excellent visualization of NFTs, SPs, and diffuse amyloid in AD, matching results with thioflavin T obtained in the same specimens. The availability of this noninvasive technique may allow longitudinal evaluation of SP and NFT deposition, permitting more accurate diagnosis and evaluation of therapies.

For a group of patients subjected to preoperative radiochemotherapy for locally advanced rectal carcinoma, however,

there was no correlation between the level of Bax Olaparib cell line expression and tumor recurrence (56). Contrary to our findings, results of studies performed in vitro demonstrate that CRC cell lines with high Bax expression responded well to long-term 5-FU exposure, which induced apoptosis (57),(58). Inhibitors,research,lifescience,medical Additionally, studies performed in vitro have indicated that antioxidants, such as N-acetylcysteine and vitamin E, are required to augment Bax expression to elicit 5-FU-induced apoptosis (59). Nevertheless, there were no such findings in clinical studies or in experimental studies Inhibitors,research,lifescience,medical performed in vivo. Based on our findings, however, the low levels of Bax may exert less intrinsic resistance to the complex cascade of intracellular signals of apoptotic pathways triggered by chemotherapeutic agents. Thus, there are apparently distinct mechanisms of Bax involvement in the manifestation of apoptosis. Molecular markers have different functional roles, similar to the Bax expression observed here. A recent investigation by Tsuji et al (60) demonstrated that high expression of dihydropyrimidine dehydrogenase (DPD) in Stage II and III CRCs was an effective indicator Inhibitors,research,lifescience,medical of oral 5-FU-based adjuvant therapy; however, low expression of tumor DPD predicted poor survival for patients undergoing surgery Inhibitors,research,lifescience,medical alone. The prognostic

value of high Bax expression observed for the surgery-alone group might be useful for a sub-set of Stage I and Stage II patients; in contrast, the predictive

value of Bax expression might be useful in predicting the efficacy of 5-FU-based therapy, particularly for patients with advanced stage disease (Stage III or IV), who routinely receive 5 -FU-based adjuvant therapy. Larger studies determining the clinical usefulness of Bax expression in CRCs according to pathologic stage may confirm these findings. In the current investigation, increased Bcl-2 expression in CRCs Inhibitors,research,lifescience,medical was not predictive of 5 -FU-based adjuvant therapy; however, increased Bcl-2 expression was an indicator of prolonged survival for patients who had surgery alone. The prognostic value of Bcl-2 expression in CRCs has been demonstrated (8),(61). The association between increased these Bcl-2 expression and patient overall survival was stronger in early-stage CRCs (62)-(64) and for CRCs located in the distal colorectum (11). Similar to our findings, other studies demonstrated that, for patients receiving 5-FU-based chemotherapy, Bcl-2 expression did not influence response to chemotherapy and did not affect overall survival(55),(65),(66). Our multivariate survival analysis, however, demonstrated a better survival of patients whose tumors had low a Bax/Bcl-2 ratio (i.e., Bax was low) and who received 5-FU-based adjuvant chemotherapy. Furthermore, the expression of these two apoptotic markers was not associated with p53nac.

86,92-95 Biochemical studies have shown that PS1 and PS2 both have eight membranespanning segments with a large hydrophilic loop between the transmembrane domains 6 and 7, and the N-tcrminal and C-terminal both face the cytoplasm.96-100 This unique structure confers their capacity to

interact with other cytoplasmic proteins. Both of these hypotheses have been supported experimentally: γy-secretase is an oligomeric complex containing presenilin91,101-105; and presenilin itself acts as a γ-secretase.103,106-110 Indeed, compelling evidence has emerged to support a role for PS1 and PS2 Inhibitors,research,lifescience,medical in the y-secretase proteolysis of APP, Notch (a transmembrane protein essential for neurogenesis), and other substrates.105,107,107,109,111-116 For example, PS1 facilitates the proteolysis of APP C-terminal fragments Inhibitors,research,lifescience,medical by a- and P-secretase,106,109,116-119 which produces Aβp peptides, including Aβ42.84,89,120 Loss of presenilin function results in diminished Aβ production.109,121-123 The PS1 or PS2 mutations found in AD do not result in loss of function. 111,120,121,124,125

Instead, these missense mutants significantly and specifically enhance γ-secretase cleavage to generate amyloidogenic Aβ42 peptides.69,89,90,126,127 All these findings point to a central role for Inhibitors,research,lifescience,medical PS1 and PS2 in both APP processing and AD pathogenesis. However, a critical question here is why so many different kinds of mutation in either PS1 or PS2 produce gain of

function to enhance y-cleavage. Recently, it has been reported that polymorphisms in PS1 and PS2 increase risk of Inhibitors,research,lifescience,medical developing late-onset AD.128 The pathway by which these polymorphisms predispose to AD is not clear. These findings make it extremely difficult to understand the role of presenilin-regulated APP metabolism in the pathogenesis of AD. Moreover, we have recently found that PS1 plays an important role in adult neurogenesis in the brain.129 On the basis of the fact that neuronal loss in the brain is a hallmark of AD, it is possible Inhibitors,research,lifescience,medical that the loss of function associated with presenilin mutations, and hence neurogenesis, is another molecular pathway by which presenilin mutation leads to AD. It should be noted that, although PS1 mutations are all more common in FAD, the PS1 and PS2 mutations combined are only implicated in about 8% of cases of earlyonset FAD.32,130-132 The majority of AD is late-onset, and the determination of the contribution of genetic PLX4032 supplier variations in these patients is fundamental to our understanding of the pathogenesis of AD. Apolipoprotein E Apolipoprotcin H (APOL) was originally reported as a risk factor for cardiovascular disease. First, a weak linkage was found between a locus of chromosomal region 19q and FAD,133 and then a stronger association between APOE and late-onset AD was reported in 1993.

This implies the product is tunable. The particle habit was needle-shaped. Two miscible fluids were used as the solvent (DMSO) and antisolvent (water). The effect of process pressure (determining the energy input), the NFN concentration, the supersaturation

ratio, and the presence of surfactant on the particle size and the crystallized material was investigated. Higher pressures resulted in smaller particle sizes, as did lowering NFN concentration and supersaturation ratios. The surfactant that was Inhibitors,research,lifescience,medical used (Solutol) did not affect the particle size. The crystalline structure was not affected by the shear rate of the process. It was identical to those formed in a beaker under low shear conditions. However, the crystallite size of the material decreased threefold from no shear to high shear conditions. CBZ was selected as a model system since it is known to exhibit polymorph multiplicity. Several solvents and antisolvents were Inhibitors,research,lifescience,medical used to determine their effect on the crystalline structure and particle size. CBZ is also known

to form hydrates, therefore both aqueous and nonaqueous solvent/antisolvent systems were used for comparison. Inhibitors,research,lifescience,medical They were Dichloromethane (DCM)/Hexane, Poly(ethylene-glycol) (PEG) 300/Water, and BMS-907351 mw Dimethyl sulfoxide (DMSO)/Water. The results obtained with respect to processing conditions are consistent with those of the NFN study. Particle sizes obtained with all bottom up experiments were consistently in the range of 250–320nm. Unfortunately, the results obtained with respect to polymorph selectivity

were not Inhibitors,research,lifescience,medical as definitive. What was observed is that the solvent/antisolvent system does matter, but it is unclear if the degrees of supersaturation or processing intensity had significant roles in that study. Inhibitors,research,lifescience,medical Three different morphologies were detected via XRD patterns and a hypothesis is given to explain the detailed observations presented there. Although not conclusive and thus more thorough studies must be performed, the explanations are consistent with those results. Although the emphasis in the previous paragraphs was in crystallization, other processes can be used to manufacture nanosized not materials with tailored properties. Encapsulation of functional ingredients in polymers is another method, which will be discussed in more detail in the sections that follow. Table 2 summarizes the processes used in the bottom up production of nanoparticles and the properties controlled via such methodologies. Table 2 List of various “bottom up” processes and influence on particle properties. 2.2. Simultaneous Targeting/Delivery Techniques Creative advances in nanotechnologies, coupled with systems biology, has led to novel chaperone systems for simultaneous targeting/delivery, and in certain instances, enhanced controlled release strategies.

The sinus, which did not respond to anti-Koch’s treatment or loads of antibiotics, healed completely in 11 (one application a day) applications of citric acid. Hence, we can safely suggest the use of citric acid in the treatment of a chronic sinus when other conventional modalities are exhausted.
Background: Peripheral vascular injury associated with lower limb trauma is a well-known Inhibitors,research,lifescience,medical emergency. The experience for the management of popliteal artery trauma

have mainly come from managing the traumas of military personnels during Iran-Iraq war. The present study compared the effects of two currently-used surgical techniques in the management of popliteal trauma, namley femoropopliteal bypass graft and interposition vein graft on limb salvage. Methods: A retrospective review of 40 click here patients with popliteal artery trauma admitted to the trauma unit of a university teaching hospital during 2003 to 2008. The patients had undergone femoropopliteal bypass graft (n=26) or interposition vein graft (n=14) for the management Inhibitors,research,lifescience,medical of popliteal trauma. Results: The amputation rate among patients managed by femoropopliteal bypass or interposition vein graft was 35.7% and 61.5%, respectively. Knee stability among patients managed

Inhibitors,research,lifescience,medical by interposition graft group was 57.7% and in those managed by femoropopliteal bypass graft was 85.7%. Conclusion: The rates of knee stability achieved by the employed techniques indicate that femoropopliteal Inhibitors,research,lifescience,medical bypass vein graft is superior, and therefore, preferable to the interposition vein graft in the management of popliteal artery trauma. Key Words: Vascular surgery, vascular trauma, interposition graft Introduction Car accidents may Inhibitors,research,lifescience,medical cause acute trauma to lower limbs, and lead to popliteal vessel damage resulting in a high amputation rate. Early revascularization is the usual approach to avoid the amputation of the legs, and increase their salvage. Interposition graft and femoropopliteal bypass are the two recent techniques. Vascular injuries to the leg caused by war

trauma have been reported to lead to three time more amputation than those caused by civilian accidental injuries.1 Vascular injuries to the legs costitute 15 to 20% of the Calpain battlefield arterial trauma. Blunt injuries of lower legs have also been included in several studies.2-4 Most of the studies on trauma to the peripheral vessels of the lower legs have been puplished by military surgeons using patients’ data from war fields.5-7 Although several case series studies describing popliteal vessel injuries from penetrating and blunt trauma have been published, we have a vast eperience stemming from managing trauma injuires of military personnel during eight years war between Iran and neoghboring Iraq.