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It is found that the novel and unique numerical representation of a protein can reduce computational complexity of protein sequence search to the tune of O(log(n)). It may also help implementation of various other similarity-based operation possible, such as clustering, phylogenetic analysis and classification of proteins on the basis of the properties used to build this numerical representation of protein.Apnea is one of the three cardinal findings in brain death (BD). Apnea testing (AT) is physiologically and practically complex. We sought to review described modifications of AT, safety and complication rates, monitoring techniques, performance of AT on extracorporeal membrane oxygenation (ECMO), and other relevant considerations regarding AT. We conducted a systematic scoping review to answer these questions by searching the literature on AT in English language available in PubMed or EMBASE since 1980. Pediatric or animal studies were excluded. A total of 87 articles matched our inclusion criteria and were qualitatively synthesized in this review. A large body of the literature on AT since its inception addresses a variety of modifications, monitoring techniques, complication rates, ways to perform AT on ECMO, and other considerations such as variability in protocols, lack of uniform awareness, and legal considerations. Only some modifications are widely used, especially methods to maintain oxygenation, and most are not standardized or endorsed by brain death guidelines. Future updates to AT protocols and strive for unification of such protocols are desirable.Background Early systolic blood pressure (SBP) reduction is believed to improve outcome after spontaneous intracerebral hemorrhage (ICH), but there has been a limited assessment of SBP trajectories in individual patients. We aimed to determine the prognostic significance of SBP trajectories in ICH. Methods We collected routine data on spontaneous ICH patients from two healthcare systems over 10 years. Unsupervised functional principal components analysis (FPCA) was used to characterize SBP trajectories over first 24 h and their relationship to the primary outcome of unfavorable shift on modified Rankin scale (mRS) at hospital discharge, categorized as an ordinal trichotomous variable (mRS 0-2, 3-4, and 5-6 defined as good, poor, and severe, respectively). Ordinal logistic regression models adjusted for baseline SBP and ICH volume were used to determine the prognostic significance of SBP trajectories. Results The 757 patients included in the study were 65 ± 23 years old, 56% were men, with a median (IQR) Glasgow come scale of 14 (8). FPCA revealed that mean SBP over 24 h and SBP reduction within the first 6 h accounted for 76.8% of the variation in SBP trajectories. An increase in SBP reduction (per 10 mmHg) was significantly associated with unfavorable outcomes defined as mRS > 2 (adjusted-OR = 1.134; 95% CI 1.044-1.233, P = 0.003). Compared with SBP reduction 40 mmHg may be harmful in ICH patients. For early SBP reduction to have an effective therapeutic effect, both target levels and optimum SBP reduction goals vis-à-vis hematoma volume should be considered.Purpose Laparoscopic sleeve gastrectomy (LSG) has rapidly become increasingly popular in bariatric surgery. However, in the long-term follow-up, intractable severe gastroesophageal reflux disease (GERD) after primary LSG can necessitate further investigations. The purpose of this study was to evaluate the endoscopic results at 5-year follow-up, on a cohort of patients who underwent LSG, the correlation GERD-esophagitis, and the results of pH-metry studies. Materials and methods Forty-eight patients that underwent LSG (same surgeon) in our center between 2010 and 2015 were included. These patients were identified during the regular annual follow-up visit between January and July 2018 and systematic upper endoscopy was proposed. A pH-metry was carried out for the 13 patients who presented QoL altering GERD symptoms. Results Twenty-two patients (45.8%) with abnormal endoscopic results were identified at a mean follow-up of 62.4 months following LSG. GERD symptomatology was identified for only 13 patients (27.1%)etry should be used. Equally, the latter should be used in case of decision to conversion for patients with severe reflux to RYGBP in order to objectify the operative indication and to achieve a reference point for follow-up.Introduction Literature on long-term (> 10 years) outcomes in terms of weight loss, resolution of co-morbidities, and quality of life (QoL) after bariatric surgery is limited. The aim of this study was to investigate the excess weight loss (EWL), resolution of comorbidities, and QoL more than 10 years after laparoscopic Roux-en-Y gastric bypass (LRYGB) using the Bariatric Analysis and Reporting Outcome System (BAROS). Methods Data on patient demographics, weight, body mass index (BMI), comorbidities, type of surgery, complications, and QoL were collected from a prospectively maintained database. Results A total of 92 patients out of 104 who underwent LRYGB during the study period and completed a median follow-up of 130 months were successfully contacted. The median age was 48 years (IQR 42-54 years) and 85.9% had a BMI of more than 40. The median excess weight loss (EWL) was 46.5% (IQR 27.9-64.3%). Type 2 diabetes mellitus reduced from 56.5 to 23.9% (p less then 0.001), hypertension from 51.1 to 39.1% (p = 0.016), and obstructive sleep apnoea from 33.7 to 12.0% (p less then 0.001). Participants reported feeling better (median 0.2, IQR 0.2-0.4), engaging in more physical activity (0.1, IQR 0.1-0.3), having more satisfactory social contacts (0.4, IQR 0.2-0.5), a better ability to work (0.3, IQR - 0.1-0.5), and a healthier approach to food (0.2, IQR - 0.3-0.3) at the end of follow-up. Conclusion LRYGB leads to positive outcomes in terms of weight loss, reduction in comorbidities, and improvement in QoL at a follow-up of more than 10 years.The pathogenesis of idiopathic membranous nephropathy is associated with autoantibodies, most often against the phospholipase A2 receptor (PLA2R) and with genetic factors, especially those involving human leukocyte antigen (HLA) genes. Idiopathic membranous nephropathy is not a typical inherited Mendelian disorder. Reports of idiopathic membranous nephropathy in twins are rare. Herein, we report on two twin sisters diagnosed with PLA2R-associated idiopathic membranous nephropathy. We identified the HLA-DRB1*0301, HLA-DRB1*1501, and HLA-DQB1*0602 alleles in the twin sisters, which were reported as independent risk alleles for idiopathic membranous nephropathy in the Asian population. This case report provides novel evidence for the role of predisposing HLA alleles in the pathogenesis of idiopathic membranous nephropathy.Morphine as an opioid is an important drug in the treatment of moderate to severe pain. Several stress factors via generation of nitric oxide (NO) and oxidative stress (OS) are responsible for the adverse effects of morphine-induced analgesia, addiction, and antinociceptive tolerance, including altered Ca2+ concentration, inflammation, OS, and release of apoptotic factors. TRPM2 is a Ca2+-permeable cation channel and it is activated by OS and NO. Hence, adverse effect of morphine addiction may occur via the OS and NO-induced TRPM2 activation. Because of the unclear etiology of morphine-induced adverse effects in the hippocampus, investigating the involvement of TRPM2 and NO synthetase (NOS) activations in the treatment of morphine-induced OS, apoptosis, and neuroinflammation is a major challenge. The hippocampal neuron of TRPM2 wild-type (TRPM2-WT) and knockout (TRPM2-KO) mice were divided into control, morphine, NOS inhibitor (L-NAME) + morphine, and TRPM2 channel blockers (ACA and 2-APB) + morphine. The morphine-induced increases of apoptosis, neuron death, OS, lipid peroxidation, caspase-3 and caspase-9, neuroinflammatory cytokines (IL-1β, TNF-α, IL-6), and Ca2+ levels in the hippocampal neuron of TRPM2-WT mouse were decreased by the L-NAME, ACA, and 2-APB treatments, although cell viability, neuron count, and reduced glutathione and glutathione peroxidase levels were increased by the treatments. However, the effects of morphine were not observed in the hippocampus of TRPM2-KO mice. Taken together, our data show that neurodegeneration adverse effects of morphine were induced by activation of TRPM2, and excessive generations of NO and OS. Thus, inhibition of TRPM2 may modulate morphine-induced neurodegeneration in the hippocampus.Human placenta-derived stem cells (hPSCs) with the therapeutic potential to recover from optic nerve injury have been reported. We have recently demonstrated that hPSCs have protective abilities against hypoxic damage. To improve the capacity of hPSCs, we established a hypoxia-preconditioned strain (HPPCs) using a hypoxic chamber. The hPSCs were exposed to short-term hypoxic conditions of 2.2% O2 and 5.5% CO2. We also performed in vivo experiments to demonstrate the recovery effects of HPPCs using an optic nerve injury rat model. Naïve hPSCs (and HPPCs) were injected into the optic nerve. After 1, 2, or 4 weeks, we analyzed changes in target proteins in the optic nerve tissues. In the retina, GAP43 expression was higher in both groups of naïve hPSCs and HPPCs versus sham controls. Two weeks after injection, all hPSC-injected groups showed recovery of tuj1 expression in damaged retinas. We also determined GFAP expression in retinas using the same model. In optic nerve tissues, HIF-1α levels were significantly lower in the HPPC-injected group 1 week after injury, and Thy-1 levels were higher in the hPSC-injected group at 4 weeks. There was also an enhanced recovery of Thy-1 expression after HPPC injection. In addition, R28 cells exposed to hypoxic conditions showed improved viability through enhanced recovery of HPPCs than naïve hPSCs. VEGF protein was a mediator in the recovery pathway via upregulation of target proteins regulated by HPPCs. Our results suggest that HPPCs may be candidates for cell therapy for the treatment of traumatic optic nerve injury.Immune-mediated ataxias account for a substantial number of sporadic otherwise idiopathic ataxias. Despite some well-characterised entities such as paraneoplastic cerebellar degeneration where diagnostic markers exist, the majority of immune ataxias remained undiagnosed and untreated. We present here our experience in the treatment of suspected primary autoimmune cerebellar ataxia (PACA) using mycophenolate. All patients reported attend the Sheffield Ataxia Centre on a regular basis and had undergone extensive investigations, including genetic testing using next-generation sequencing, with other causes of ataxia excluded. The diagnosis of PACA was strongly suspected based on investigations, pattern of disease progression, and cerebellar involvement. Patients were treated with mycophenolate and monitored using MR spectroscopy of the cerebellar vermis. Thirty patients with PACA are reported here. Of these, 22 received mycophenolate (group 1). The remaining 8 were not on treatment (group 2-control group). Out of the 22 treated patients, 4 underwent serial MR spectroscopy prior to starting treatment and thus were used as controls making the total number of patients in the control group 12. The mean change of the MRS within the vermis (NAA/Cr area ratio) in the treatment group was + 0.144 ± 0.09 (improved) and in the untreated group - 0.155 ± 0.06 (deteriorated). The difference was significant. We also demonstrated a strong correlation between the spectroscopy and the SARA score. We have demonstrated the effectiveness of mycophenolate in the treatment of PACA. The results suggest that immune-mediated ataxias are potentially treatable, and that there is a need for early diagnosis to prevent permanent neurological deficit. The recently published diagnostic criteria for PACA would hopefully aid the diagnosis and treatment of this entity.
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