Mucinous tubular and spindle cell carcinoma with papillae: A report of 5 cases and comparison with 18 cases of papillary renal cell carcinoma.

As its descriptive name indicates, mucinous tubular and spindle cell carcinoma (MTSCC) is composed of tubules, spindle cells, and extracellular mucinous stroma. Papillary architecture in MTSCC is regarded as infrequent finding and often is described as papillation or pseudopapillary appearance since bona fide papillary structures with fibrovascular cores are not seen. In this study, we report five cases of MTSCC with papillary formation and compare those with 18 cases of former type 1 papillary renal cell carcinoma (PRCC).

Charting New Territory With a Novel WHO Provisional Category: A Case Study of a Low-Grade Oncocytic Tumor (LOT) in the Kidney.

A low-grade oncocytic tumor of the kidney (LOT) is a distinctive entity categorized under the 2022 World Health Organization (WHO) classification as "Other oncocytic tumors of the kidney." It represents a unique subset of oncocytic tumors, distinct from oncocytoma and chromophobe renal cell carcinoma. Characterized by bland oncocytic cells that diffusely express CK7 and lack CD117 expression, LOT typically manifests as a solitary, small lesion with a low stage.

Solitary Intraosseous Myofibroma of the Mandible in a Nine-Year-Old Child: A Case Report and Literature Review.

Myofibroma (MF) is a benign neoplasm derived from myofibroblasts. While they are infrequent, these tumors are predominantly found in the pediatric group and seldom manifest as intraosseous mandibular tumors. Herein, we present a 9-year-old female with a radiolucent lesion in the left mandible associated with malposed left lower canine and 1st premolar teeth.

Activation of AMP-activated protein kinase attenuates ethanol-induced ER/oxidative stress and lipid phenotype in human pancreatic acinar cells.

Primary toxicity targets of alcohol and its metabolites in the pancreas are cellular energetics and endoplasmic reticulum (ER). Therefore, the role of AMP-Activated Protein Kinase (AMPKα) in amelioration of ethanol (EtOH)-induced pancreatic acinar cell injury including ER/oxidative stress, inflammatory responses, the formation of fatty acid ethyl esters (FAEEs) and mitochondrial bioenergetics were determined in human pancreatic acinar cells (hPACs) and AR42J cells incubated with/without AMPKα activator [5-aminoimidazole-4-carboxamide ribonucleotide (AICAR)]. EtOH treated hPACs showed concentration and time-dependent increases for FAEEs and inactivation of AMPKα, along with the upregulation of ACC1 and FAS (key lipogenic proteins) and downregulation of CPT1A (involved β-oxidation of fatty acids).

Linking Dysregulated AMPK Signaling and ER Stress in Ethanol-Induced Liver Injury in Hepatic Alcohol Dehydrogenase Deficient Deer Mice.

Ethanol (EtOH) metabolism itself can be a predisposing factor for initiation of alcoholic liver disease (ALD). Therefore, a dose dependent study to evaluate liver injury was conducted in hepatic alcohol dehydrogenase (ADH) deficient (ADH) and ADH normal (ADH) deer mice fed 1%, 2% or 3.5% EtOH in the liquid diet daily for 2 months.

Plexiform Schwannoma of the Tongue in a Pediatric Patient with Neurofibromatosis Type 2: A Case Report and Review of Literature.

Introduction: Plexiform schwannoma is a rare variant of schwannoma that accounts for only 5% of all schwannomas. Herein, we present a rare case of plexiform schwannoma of the tongue in a pediatric patient with neurofibromatosis type 2 (NF2).

Case Presentation: A 13-year-old female presented with a growing left-sided tongue mass.

Hepatic alcohol dehydrogenase deficiency induces pancreatic injury in chronic ethanol feeding model of deer mice.

The single most common cause of chronic pancreatitis (CP, a serious inflammatory disease) is chronic alcohol abuse, which impairs hepatic alcohol dehydrogenase (ADH, a major ethanol oxidizing enzyme). Previously, we found ~5 fold greater fatty acid ethyl esters (FAEEs), and injury in the pancreas of hepatic ADH deficient (ADH) vs. hepatic normal ADH (ADH) deer mice fed 3.

Proteomic Profiling of Liver and Plasma in Chronic Ethanol Feeding Model of Hepatic Alcohol Dehydrogenase-Deficient Deer Mice.

Background: Chronic alcohol abuse, a major risk factor for such diseases as hepatitis and cirrhosis, impairs hepatic alcohol dehydrogenase (ADH; key ethanol [EtOH]-metabolizing enzyme). Therefore, differentially altered hepatic and plasma proteomes were identified in chronic EtOH feeding model of hepatic ADH-deficient (ADH ) deer mice to understand the metabolic basis of alcoholic liver disease (ALD).

Methods: ADH deer mice were fed 3.

Proteins Differentially Expressed in the Pancreas of Hepatic Alcohol Dehydrogenase-Deficient Deer Mice Fed Ethanol For 3 Months.

Objectives: The aim of this study was to identify differentially expressed proteins in the pancreatic tissue of hepatic alcohol dehydrogenase-deficient deer mice fed ethanol to understand metabolic basis and mechanism of alcoholic chronic pancreatitis.

Methods: Mice were fed liquid diet containing 3.5 g% ethanol daily for 3 months, and differentially expressed pancreatic proteins were identified by protein separation using 2-dimensional gel electrophoresis and identification by mass spectrometry.