3,507 research outputs found

    Synchronous double primary malignant tumor of the gallbladder and liver: a case report

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    We report a case of synchronous double primary tumor of gallbladder and liver. A 63-year-old male was admitted to the hospital complaining of abdominal discomfort. Enhanced computed tomography of the abdomen showed acute cholecystitis with tiny gallbladder stones and a 2.2 cm size enhanced nodule in the left lobe of the liver. Under the impression of acute cholecystitis with gall bladder stones and hepatocellular carcinoma of the left Liver, the patient underwent a laparotomy. At laparotomy, a mass was palpated on the surface of the neck portion of the gall bladder. Intraoperative frozen diagnosis revealed adenocarcinoma of the gall bladder. The patient was diagnosed as having gall bladder cancer and hepatocellular carcinoma, so extended cholecystectomy with dissection of regional lymph nodes and left hemihepatectomy were performed. Histological examination revealed moderated differentiated adenocarcinoma of gallbladder and hepatocellular carcinoma of liver. To our knowledge, the simultaneous occurrence of primary malignant tumor of the gallbladder and liver has never been published before. The patient is doing well with no evidence of recurrence 17 months after surgery

    Bilateral herpetic keratitis presenting with unilateral neurotrophic keratitis in pemphigus foliaceus: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>We report a case of bilateral herpetic keratitis developing after rapid oral corticosteroid tapering in a patient with pemphigus foliaceus, which was followed by unilateral neurotrophic keratitis that was treated with amniotic membrane transplantation.</p> <p>Case presentation</p> <p>A 71-year-old Korean man developed bilateral herpetic keratitis one week after rapid tapering of systemic corticosteroid. He had been on high-dose oral corticosteroid and azathioprine therapy for six months for treatment of pemphigus foliaceus. Topical acyclovir ointment was prescribed. A week later, our patient's right eye had healed, but his left eye showed increased stromal edema with enlarged epithelial defects. He was prescribed oral acyclovir with topical broad-spectrum antibiotics applied to his left eye. The stromal edema cleared within a week but the epithelial defect remained unchanged. An amniotic membrane transplantation was performed on our patient's left eye, and his epithelial defect had totally healed three weeks later.</p> <p>Conclusions</p> <p>Patients with autoimmune disease or who are on immunosuppressive therapy have a higher chance of developing bilateral herpetic keratitis. Although rare, the condition may be followed by unilateral neurotrophic keratitis. Rapid corticosteroid tapering may act as a triggering factor for viral infection or reactivation of herpes.</p

    Differentially altered social dominance- and cooperative-like behaviors in Shank2- and Shank3-mutant mice

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    Background: Recent progress in genomics has contributed to the identification of a large number of autism spectrum disorder (ASD) risk genes, many of which encode synaptic proteins. Our understanding of ASDs has advanced rapidly, partly owing to the development of numerous animal models. Extensive characterizations using a variety of behavioral batteries that analyze social behaviors have shown that a subset of engineered mice that model mutations in genes encoding Shanks, a family of excitatory postsynaptic scaffolding proteins, exhibit autism-like behaviors. Although these behavioral assays have been useful in identifying deficits in simple social behaviors, alterations in complex social behaviors remain largely untested. Methods: Two syndromic ASD mouse models—Shank2 constitutive knockout [KO] mice and Shank3 constitutive KO mice—were examined for alterations in social dominance and social cooperative behaviors using tube tests and automated cooperation tests. Upon naïve and salient behavioral experience, expression levels of c-Fos were analyzed as a proxy for neural activity across diverse brain areas, including the medial prefrontal cortex (mPFC) and a number of subcortical structures. Findings: As previously reported, Shank2 KO mice showed deficits in sociability, with intact social recognition memory, whereas Shank3 KO mice displayed no overt phenotypes. Strikingly, the two Shank KO mouse models exhibited diametrically opposed alterations in social dominance and cooperative behaviors. After a specific social behavioral experience, Shank mutant mice exhibited distinct changes in number of c-Fos+ neurons in the number of cortical and subcortical brain regions. Conclusions: Our results underscore the heterogeneity of social behavioral alterations in different ASD mouse models and highlight the utility of testing complex social behaviors in validating neurodevelopmental and neuropsychiatric disorder models. In addition, neural activities at distinct brain regions are likely collectively involved in eliciting complex social behaviors, which are differentially altered in ASD mouse models. © 2020, The Author(s).1

    Multidisciplinary approach for hepatocellular carcinoma arising from cirrhotic liver with Budd-Chiari syndrome: a case report

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    Budd-Chiari syndrome (BCS) is defined by the obstruction of the hepatic venous outflow between the small hepatic veins and the junction of the inferior vena cava (IVC) with the right atrium. BCS with IVC obstruction occasionally progresses to hepatocellular carcinoma (HCC). Here, we report the case of a patient with HCC arising from a cirrhotic liver with BCS, in whom the hepatic portion of the IVC was obstructed, and who had a favorable outcome with a multidisciplinary approach and IVC balloon angioplasty

    Protocol for Quantitative Analysis of Synaptic Vesicle Clustering in Axons of Cultured Neurons

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    Clustering of synaptic vesicles along the neuronal axons is a critical mechanism underpinning proper synaptic transmission. Here, we provide a detailed protocol for analyzing the distribution of synaptic vesicles in presynaptic boutons of cultured neurons. The protocol covers preparation of cultured neurons, expression of synaptic vesicle-enriched proteins, and quantification procedures. Utilizing neurons from postnatal transgenic mice, this method can be applied to investigate the roles of synaptic genes in regulating vesicle dynamics at synaptic sites. For complete details on the use and execution of this protocol, please refer to Han et al. (2020a). © 2020 The Author(s)1

    PPM1A Controls Diabetic Gene Programming through Directly Dephosphorylating PPAR?? at Ser273

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    Peroxisome proliferator-activated receptor gamma (PPAR gamma) is a master regulator of adipose tissue biology. In obesity, phosphorylation of PPAR gamma at Ser273 (pSer273) by cyclin-dependent kinase 5 (CDK5)/extracellular signal-regulated kinase (ERK) orchestrates diabetic gene reprogramming via dysregulation of specific gene expression. Although many recent studies have focused on the development of non-classical agonist drugs that inhibit the phosphorylation of PPAR gamma at Ser273, the molecular mechanism of PPAR gamma dephosphorylation at Ser273 is not well characterized. Here, we report that protein phosphatase Mg2+/Mn2+-dependent 1A (PPM1A) is a novel PPAR gamma phosphatase that directly dephosphorylates Ser273 and restores diabetic gene expression which is dysregulated by pSer273. The expression of PPM1A significantly decreases in two models of insulin resistance: diet-induced obese (DIO) mice and db/db mice, in which it negatively correlates with pSer273. Transcriptomic analysis using microarray and genotype-tissue expression (GTEx) data in humans shows positive correlations between PPM1A and most of the genes that are dysregulated by pSer273. These findings suggest that PPM1A dephosphorylates PPAR gamma at Ser273 and represents a potential target for the treatment of obesity-linked metabolic disorders
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