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Acute pancreatitis in aging animals:Loss of pancreatitis-associated protein protection?

World Journal of Gastroenterology 2012年第26期18卷 3379-3388页

作者： Sophia Fu Albert Stanek Cathy M Mueller Nefertti A Brown Chongmin Huan Martin H Bluth michael e zenilman Department of Surgery SUNY Downstate Medical SchoolBrooklynNY 11203United States Department of Pathology Wayne State UniversityDetroitMI 48202United States Department of Surgery Johns Hopkins School of Medicine and SUNY Downstate School of Public HealthBethesdaMD 20814United States

AIM:To investigate the effect of age on severity of acute pancreatitis(AP) using biochemical markers,histology and expression of the protective pancreatitisassociated proteins(PAPs).MeTHODS:AP was induced via intraductal injection of 4% sodium taurocholate in young and old *** and pancreata were assayed at 24 h for the parameters listed above;we also employed a novel molecular technique to assess bacterial infiltration using polymerase chain reaction to measure bacterial genomic ribosomal ***:At 24 h after induction of AP,the pancreata of older animals had less edema(mean ± Se histologic score of young vs old:3.11 ± 0.16 vs 2.50 ±-0.11,P ecreased local inflammatory response(histologic score of stromal infiltrate:3.11 ± 0.27 vs 2.00 ± 0.17,P eased bacterial infiltration(174% ± 52% increase from sham vs 377% ± 4%,P ecreased expression of PAP1 and PAP2 was demonstrated by Western blotting analysis and immunohistochemical *** were no differences in serum amylase and lipase activity,or tissue myeloperoxidase or monocyte chemotactic protein-1 ***,in the most-aged group,serum C-reactive protein levels were higher(young vs old:0.249 ± 0.04 mg/dL vs 2.45 ± 0.68 mg/dL,P er animals,there is depressed PAP expression related to a blunted inflammatory response in AP which is associated with worsened bacterial infiltration and higher C-reactive protein level;this may explain the more aggressive clinical course.

关键词：急性胰腺炎相关蛋白动物保护聚合酶链反应单核细胞趋化蛋白1 血清淀粉酶 PAPS

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Invasive amebiasis and ameboma formation presenting as a rectal mass: An uncommon case of malignant masquerade at a western medical center

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World Journal of Gastroenterology 2007年第42期13卷 5659-5661页

作者： Rosemarie e Hardin George S Ferzli michael e zenilman Pratap K Gadangi Wilbur B Bowne Department of Surgery The State University of New York Health Science Center of Brooklyn NY 11203 United States Department of Surgery Lutheran Medical Center Brooklyn NY 11203 United States Department of Surgery SUNY-Health Science Center of Brooklyn United States Department of Surgery Lutheran Medical Center Brooklyn NY 11203 United States Department of Surgery Coney Island Hospital Brooklyn NY 11203 United States Department of Surgery The State University of New York Health Science Center of Brooklyn NY 11203 United States Department of Surgery Department of Veteran's Affairs New York Harbor Health Care System Brooklyn NY 11203 United States

A 54-year-old man presented with rectal pain and bleeding secondary to ulcerated,necrotic rectal and cecal masses that resembled colorectal carcinoma upon *** masses were later determined to be benign amebomas caused by invasive entamoeba histolytica,which regressed completely with medical *** Western countries,the occurrence of invasive protozoan infection with formation of amebomas is very rare and can mistakenly masquerade as a *** surprisingly,there have been very few cases reported of this clinical entity within the United ***,we report a patient that had an extremely rare occurrence of two synchronous lesions,one involving the rectum and the other situated in the *** review the current literature on the pathogenesis of invasive *** infection and ameboma formation,as well as management of this rare disease entity at a western medical center.

关键词：寄生虫病阿米巴病直肠疾病阿米巴痢疾

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Pancreatic regenerating protein (regⅠ) and regⅠreceptor mRNA are upregulated in rat pancreas after induction of acute pancreatitis

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World Journal of Gastroenterology 2006年第28期12卷 4511-4516页

作者： Martin H Bluth Sameer A Patel Brian K Dieckgraefe Hiroshi Okamoto michael e zenilman Department of Surgery State University of New York-Downstate Medical CenterBrooklynNew YorkUnited States Department of Surgery Montefiore Medical Center and Albert Einstein College of MedicineBronxNew YorkUnited States Department of Medicine Division of GastroenterologyWashington University School of MedicineSt. LouisMissouriUnited States Department of Biochemistry Tohoku University Graduate School of MedicineSendaiJapan

AIM: Pancreatic regenerating protein (regⅠ) stimulates pancreatic regeneration after pancreatectomy and is mitogenic to ductal andβ-cells. This suggests that regⅠand its receptor may play a role in recovery after pancreatic injury. We hypothesized that regⅠand its receptor are induced in acute pancreatitis. MeTHODS: Acute pancreatitis was induced in male Wistar rats by retrograde injection of 3% sodium taurocholate into the pancreatic duct. Pancreata and serum were collected 12, 24, and 36 hours after injection and from normal controls (4 rats/group). RegⅠreceptor mRNA, serum regⅠprotein, and tissue regⅠprotein levels were determined by Northern analysis, enzyme-linked immunosorbent assay (eLISA), and Western analysis, respectively. Immunohistochemistry was used to localize changes in regⅠand its receptor. ReSULTS: Serum amylase levels and histology confirmed necrotizing pancreatitis in taurocholate treated rats. There was no statistically significant change in serum regⅠconcentrations from controls. However, Western blot demonstrated increased tissue levels of regⅠat 24 and 36 h. This increase was localized primarily to the acinar cells and the ductal cells by immunohistochemistry. Northern blot demonstrated a significant increase in regⅠreceptor mRNA expression with pancreatitis. Immunohistochemistry localized this increase to the ductal cells, islets, and acinar cells. CONCLUSION: Acute pancreatitis results in increased tissue regⅠprotein levels localized to the acinar and ductal cells, and a parallel threefold induction of regⅠreceptor in the ductal cells, islets, and acinar cells. These changes suggest that induction of reg I and its receptor may be important for recovery from acute pancreatitis.

关键词：胰腺再生蛋白急性胰腺炎病理机制治疗

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Dexamethasone mediates protection against acute pancreatitis via upregulation of pancreatitis-associated proteins

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World Journal of Gastroenterology 2006年第42期12卷 6806-6811页

作者： emad Kandil Yin-Yao Lin Martin H Bluth Hong Zhang Gabriel Levi michael e zenilman Department of Surgery State University of New York Downstate Medical Center Brooklyn New York United States Department of Pathology State University of New York Downstate Medical Center Brooklyn New York United States

AIM: To examine the influence of dexamethasone on pancreatitis-associated protein (PAP) gene expression using both in vitro and in vivo models of acute pancreati- tis and to study how PAP gene expression correlates with severity of pancreatitis. MeTHODS: In vitro, IL-6 stimulated pancreas acinar AR42J cells were cultured with increasing concentrations of dexamethasone and assayed for PAP expression (RT-PCR). In vivo , pancreatitis was induced in rats by retrograde injection of 40 g/L taurocholate into the pancreatic duct. Animals were pretreated with dexamethasone (2 mg/kg) daily or saline for 4 d. Pancreata and serum were harvested after 24 h and gene expression levels of PAPⅠ, Ⅱ and Ⅲ were measured by RT-PCR. Severity of pancreatitis was based on serum amylase, pancreatic wet weight, and histopathological score. ReSULTS: In vitro, dexamethasone and IL-6 induced a marked transcription of PAPⅠ, Ⅱ and Ⅲ genes in AR42J cells at 24 h (P eas mRNA levels of PAPⅠ, Ⅱ or Ⅲ increased by 2.6-fold, 1.9-fold, and 1.3-fold respectively after dexa- methasone treatment, compared with saline treated ani- mals. Serum amylase levels and edema were significantly lower in the dexamethasone group compared with the saline group. Histopathologic evaluation revealed less inflammation and necrosis in pancreata obtained from dexamethasone treated animals (P examethasone significantly decreases the severity of pancreatitis. The protective mechanism ofdexamethasone may be via upregulating PAP gene ex- pression during injury.

关键词：地塞米松保护作用胰腺炎病理机制

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