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Metastatic type 1 gastric carcinoid:A real threat or just a myth?

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World Journal of Gastroenterology 2013年第46期19卷 8687-8695页

作者： Simona Grozinsky-Glasberg Dimitrios Thomas Jonathan R Strosberg Ulrich-Frank Pape Stephan Felder Apostolos V Tsolakis Krystallenia I Alexandraki Merav Fraenkel Leonard Saiegh Petachia Reissman Gregory Kaltsas David J Gross neuroendocrine tumor Unit Endocrinology and Metabolism ServiceDepartment of MedicineHadassah-Hebrew University Medical Center Endocrine Unit Department of PathophysiologyNational University of Athens Moffitt Cancer center Tampa Department of Internal Medicine Division of HepatologyGastroenterologyEndocrinology and MetabolismCharité Universit tsmedizin Department of Medical Sciences Section of Endocrine OncologyUppsala University Institute of endocrinology Soroka Ben Gurion University Hospital Department of Surgery Shaare-Zedek Medical CenterThe Hebrew University School of Medicine

AIM:To describe disease characteristics and treatment modalities in a group of rare patients with metastatic gastric carcinoid type 1(GCA1).METHODS:Information on clinical,biochemical,radiological,histopathological findings,the extent of the disease,as well as the use of different therapeutic modalities and the long-term outcome were ***’data were assessed at presentation,and thereafter at 6 to 12 monthly intervals both clinically and biochemically,but also endoscopically and *** were evaluated for the presence of specific symptoms;the presence of autoimmune disorders and the presence of other gastrointestinal malignancies in other family members were also *** evaluation of response to treatment was defined using established WHO ***:We studied twenty consecutive patients with a mean age of 55.1 *** mean follow-up period was 83 *** patients had regional lymph node metastases and 8 patients had liver *** primary tumor mean diameter was 20.13±10.83mm(mean±SD).The mean Ki-67 index was 6.8%±11.2%.All but one patient underwent endoscopic or surgical excision of the *** disease was stable in all but 3 patients who had progressive liver *** patients remained alive during the follow-up ***:Metastatic GCA1 carries a good overall prognosis,being related to a tumor size of≥1 cm,an elevated Ki-67 index and high serum gastrin levels.

关键词： Metastatic gastric carcinoids Gastrin Chro-mogranin A Somatostatin analogues Stomach neuro-endocrine tumor

Transcriptome and Proteome Expressions Involved in Insulin Resistance in Muscle and Activated T-Lymphocytes of Patients with Type 2 Diabetes

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Genomics, Proteomics & Bioinformatics 2007年第3期5卷 216-235页

作者： Frankie B.Stentz Abbas E.Kitabchi division of endocrinology Diabetes and MetabolismDepartment of MedicineThe University of Tennessee Health Science CenterMemphisTN 38163USA.

We analyzed the genes expressed （transcriptomes） and the proteins translated （pro- teomes） in muscle tissues and activated CD4^＋ and CD8^＋ T-lymphocytes （T-cells） of five Type 2 diabetes （T2DM） subjects using Affymetrix microarrays and mass spectrometry, and compared them with matched non-diabetic controls. Gene expressions of insulin receptor （INSR）, vitamin D receptor, insulin degrading enzyme, Akt, insulin receptor substrate-1 （IRS-1）, IRS-2, glucose transporter 4 （GLUT4）, and enzymes of the glycolytic pathway were decreased at least 50% in T2DM than in controls. However, there was greater than two-fold gene upregulation of plasma cell glycoprotein-1, tumor necrosis factor a （TNFα）, and gluconeogenic enzymes in T2DM than in controls. The gene silencing for INSR or TNFα resulted in the inhibition or stimulation of GLUT4, respectively. Proteome profiles corresponding to molecular weights of the above translated transcriptomes showed different patterns of changes between T2DM and controls. Meanwhile, changes in transcriptomes and proteomes between muscle and activated T-cells of T2DM were comparable. Activated T-cells, analogous to muscle cells, expressed insulin signaling and glucose metabolism genes and gene products. In conclusion, T-cells and muscle in T2DM exhibited differences in expression of certain genes and gene products relative to non-diabetic controls. These alterations in transcriptomes and proteomes in T2DM may be involved in insulin resistance.

关键词： genomics proteomics T-lymphocytes activation muscle Type 2 diabetes

Vitamin K and hepatocellular carcinoma: The basic and clinic

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World Journal of Clinical Cases 2015年第9期3卷 757-764页

作者： Xia Jinghe Toshihiko Mizuta Iwata Ozaki division of Hepatology Diabetology and EndocrinologyDepartment of Internal MedicineSaga Medical SchoolSaga University Department of Medicine Imari-Arita Kyoritu Hospital Health Administration center Saga University

Vitamin K(VK), which was originally identified as a cofactor involved in the production of functional coagulation factors in the liver, has been shown to be involved in various aspects of physiological and pathological events, including bone metabolism, cardiovascular diseases and tumor biology. The mechanisms and roles of VK are gradually becoming clear. Several novel enzymes involved in the VK cycle were identified and have been shown to be linked to tumorigenesis. The VKs have been shown to suppress liver cancer cell growth through multiple signaling pathways via the transcription factors and protein kinases. A VK2 analog was applied to the chemoprevention of hepatocellular carcinoma(HCC) recurrence after curative therapy and was shown to have beneficial effects, both in the suppression of HCC recurrence and in patient survival. Although a large scale randomized control study failed to demonstrate the suppression of HCC recurrence, a meta-analysis suggested a beneficial effect on the long-term survival of HCC patients. However, the beneficial effects of VK administration alone were not sufficient to prevent or treat HCC in clinical settings. Thus its combination with other anti-cancer reagents and the development of more potent novel VK derivatives are the focus of ongoing research which seeks to achieve satisfactory therapeutic effects against HCC.

关键词： Hepatocellular carcinoma Vitamin K Steroid and xenobiotic receptor Nuclear factor-kappa B Protein kinase A Protein kinase C Drug repositioning

Disease dependent qualitative and quantitative differences in the inflammatory response to ascites occurring in cirrhotics

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World Journal of Hepatology 2014年第2期6卷 85-91页

作者： Bashar M Attar Magdalena George Nicolae Ion-Nedelcu Guilliano Ramadori David H Van Thiel division of Gastroenterology and Hepatology John H Stroger Hospital of Cook County Rush University Medical center Victor Babes Infectious and Tropical Disease Clinic Department of Gastroenterology and endocrinology August Georg University

AIM:To assess differing patterns and levels of ascitic fluid cyctokine and growth factors exist between those with a high risk and low risk of spontaneous bacterial peritonitis(SBP). METHODS: A total of 57 consecutive patients with ascites requiring a large volume paracentesis were studied. Their age, gender, specific underlying disease conditions were recorded after a review of their clinical records. Each underwent a routine assessment prior to their paracentesis consisting of a complete blood count, complete metabolic profile and prothrombin time/international normalized ratio(INR) determination. The ascitic fluid was cultured and a complete cellcount and albumin determination was obtained on the fluid. In addition, blood and ascitic fluid was assessed for the levels of interleukin interleukin(IL)-1A, IL-1B, IL-2, IL-4, IL-8, IL-10, monocyte chemotactic protein(MCP)-1, tumor necrosis factor(TNF)-α, interferon(IFN)-γ, vascular endothelial growth factor(VEGF) and epidermal growth factor(EGF) utilizing the Randox Biochip platforms(Boston, MA). A serum-ascites gradient, for each cytokine and growth factor was calculated. The results are reported as mean ± SEM between disease groups with statistical analysis consisting of the student t-test(two tailed) with a P value of 0.05 defining significance. RESULTS: No clinically important demographic or biochemical differences between the 4 groups studied were evident. In contrast, marked difference in the cytokine and growth factors levels and pattern were evident between the 4 disease groups. Individuals with alcoholic cirrhosis had the highest levels of IL-1A, IL-1B, IL-4, IFNγ. Those with malignant disease had the highest levels of IL-2. Those with hepatitis C virus(HCV) associated cirrhosis had the highest value for IL-6, IL-8, IL-10, MCP-1 and VEGF. Those with cardiac disease had the highest level of TNF-α and EGF. The calculated serum- ascites gradients for the cardiac and malignant disease groups had a greater frequenc

关键词： Ascites Cirrhosis Growth factors Inflammation Procalcitonin

Lipoic acid suppresses portal endotoxemia-induced steatohepatitis and pancreatic inflammation in rats

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World Journal of Gastroenterology 2013年第18期19卷 2761-2771页

作者： Yu-Feng Tian Chih-Tsueng He Yu-Ting Chen Po-Shiuan Hsieh division of General Surgery Department of Surgery Yung Kung Campus Chi-Mei Medical Center Department of Health and Nutrition Chia Nan University of Pharmacy and Science Tainan 717 Taiwan division of endocrinology and Metabolism Department of Internal Medicine Tri-Service General Hospital Taipei 114 Taiwan Department of Physiology and Biophysics National Defense Medical Center Department of Medical Research Tri-Service General Hospital Taipei 114 Taiwan

AIM: To examine the effect of α-lipoic acid (LA) on mild portal endotoxemia-induced steatohepatitis and associated pancreatic abnormalities in fructose-fed rats. METHODS: Rats were randomly assigned into two groups with a regular or 60% fructose-enriched diet for 8 wk. After fructose feeding for 4 wk, rats were further divided into four subgroups: with intraportal saline (F PV ), with intraportal saline plus administration of LA (F PV + LA ), with lipopolysaccharide (LPS) infusion (F PLPS ), and with LPS infusion plus administration of LA (F PLPS + LA ). Rats were treated with LPS using intraportal infusion while LA was administered orally. Metabolite levels, superoxide levels, inflammatory markers, malondialdehyde content, glutathione content and toll-like receptor 4 (TLR4 ) gene expression were all measured using standard biochemical techniques. Pancreatic insulin secretion was evaluated by a hyperglycemic clamp technique. Histology of liver and pancreas tissues were evaluated using hematoxylin and eosin staining and immunohistochemistry. RESULTS: Fructose-induced elevation in plasma C-reactive protein, amylase, superoxide, white blood cell count as well as in hepatic and pancreatic contents of malondialdehyde, tumor necrosis factor alpha and interleukin-6 were increased in animals treated with LPS and reversed with LA administration. The augmented hepatic gene expression of TLR4 in fructose-fed rats was further increased in those with intraportal LPS infusion, which was partially reversed by LA administration. Pathological examination showed inflammatory changes and leukocyte infiltration in hepatic and pancreatic islets of animals treated with LPS but were rarely observed in those with LA treatment. In addition to affects on the liver, impaired pancreatic insulin secretion seen in fructose-fed rats was deteriorated in with LPS treatment and partially reversed with LA administration. CONCLUSION: These data suggest LA could significantly suppress mild portal-endot

关键词： Lipoic acid Oxidative stress Steatohepatitis Portal endotoxemia Insulin secretion Fructose

Somatostatin receptor scintigraphy in the follow up of neuroendocrine neoplasms of appendix

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World Journal of Clinical Cases 2020年第17期8卷 3697-3707页

作者： Jelena Saponjski Djuro Macut Dragana Sobic-Saranovic Sanja Ognjanovic Ivana Bozic Antic Djordje Pavlovic Vera Artiko center for Nuclear Medicine Clinical Center of SerbiaBelgrade 11000Serbia Clinic for endocrinology Diabetes and Metabolic DiseasesClinical Center of SerbiaFaculty of MedicineUniversity of BelgradeBelgrade 11000Serbia center for Nuclear Medicine Clinical center of Serbia Faculty of Medicine University of BelgradeBelgrade 11000Serbia University Children's Clinic Belgrade 11000Serbia

BACKGROUND neuroendocrine tumors of appendix(ANETs)known as carcinoids,are rare endocrine neoplasms originated from enterochromaffin cells of gastrointestinal *** are the third most frequent(16.7%)gastrointestinal neuroendocrine tumors,with the incidence of 0.08-0.2 cases/100000 during one *** ANETs occur in 0.2%-0.7%of emergency surgical resections because of suspected appendicitis which is usually the first manifestation of *** there are a lot of papers about application of somatostatin receptor scintigraphy in gastrointestinal neuroendocrine tumors,there are very rare sporadic cases described about ANETs *** To establish the role of somatostatin receptor scintigraphy(SRS)in the management of patients with neuroendocrine tumors of appendix(ANET).METHODS The total of 35 patients was investigated,23 females and 12 males,average age(43.7±17.3 years).All patients had histological diagnosis of ANET(34 carcinoids of appendix and one tubular carcinoid).Majority of tumors have been found incidentally during surgery of:Acute appendicitis(n=15),perforated appendicitis(n=2),ileus(n=3),hysterectomy(n=3),ruptured ovarian cyst(n=2),caecal volvulus(n=1),while 9 patients had diagnosis of appendiceal tumor before the *** patients had tumor grade(G)G1,12 G2 and 6 *** right hemicolectomy was performed in 13,while the rest of the patients had appendectomy *** was done early(2 h)and late(24 h)after *** of 740 MBq technetium-99 m ethylenediamine-N,N’-diacetic acid Hydrazinonicotinyl-Tyr3-Octreotide(technetium-99 m-Tektrotyd,Polatom,Poland).SRS was performed for restaging in all the patients after *** There were 12 true positive(TP),19 true negative,3 false positive and 1 false negative SRS *** of the method was 92.31%,specificity was 86.36%,positive predictive value was 80.00%,negative predictive value was 95.00%and accuracy 88.57%.Receiver operating characteristics analysis showed t

关键词： Somatostatin receptor scintigraphy carcinoid Appendix Follow up Nuclear medicine Radionuclide

MKRN3 regulates the epigenetic switch of mammalian puberty via ubiquitination of MBD3

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National Science Review 2020年第3期7卷 671-685页

作者： Chuanyin Li Wenli Lu Liguang Yang Zhengwei Li Xiaoyi Zhou Rong Guo Junqi Wang Zhebao Wu Zhiya Dong Guang Ning Yujiang Shi Yinmin Gu Peng Chen Zijian Hao Tianting Han Meiqiang Yang Wei Wang Xuehui Huang Yixue Li Shan Gao Ronggui Hu Department of Pediatrics Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine State Key Laboratory of Molecular Biology CAS Center for Excellence in Molecular Cell Institute of Biochemistry and Cell Biology Chinese Academy of Sciences University of Chinese Academy of Sciences CAS Key Laboratory of Computational Biology CAS-MPG Partner Institute for Computational BiologyShanghai Institute of Nutrition and HealthShanghai Institutes for Biological SciencesUniversity of Chinese Academy of SciencesChinese Academy of Sciences College of Life Sciences Shanghai Normal University center for Pituitary tumor Ruijin Hospital Affiliated to Shanghai Jiao Tong University Shanghai Institute of Endocrine and Metabolic Diseases Shanghai Key Laboratory for Endocrine Tumors and E-Institute for EndocrinologyRuijin Hospital Shanghai Jiao Tong University School of Medicine division of endocrinology Diabetes and Hypertension Department of Medicine Brigham and Women's Hospital Harvard Medical School CAS Key Laboratory of Bio-medical Diagnostics Suzhou Institute of Biomedical Engineering and Technology Chinese Academy of Sciences Cancer center Shanghai Tenth People's HospitalSchool of Medicine Tongji University

Central precocious puberty(CPP) refers to a human syndrome of early puberty initiation with characteristic increase in hypothalamic production and release of gonadotropin-releasing hormone(Gn RH). Previously, loss-of-function mutations in human MKRN3, encoding a putative E3 ubiquitin ligase, were found to contribute to about 30% of cases of familial CPP. MKRN3 was thereby suggested to serve as a ‘brake’ of mammalian puberty onset, but the underlying mechanisms remain as yet ***, we report that genetic ablation of Mkrn3 did accelerate mouse puberty onset with increased production of hypothalamic Gn RH1. MKRN3 interacts with and ubiquitinates MBD3, which epigenetically silences GNRH1 through disrupting the MBD3 binding to the GNRH1 promoter and recruitment of DNA demethylase TET2. Our findings have thus delineated a molecular mechanism through which the MKRN3–MBD3 axis controls the epigenetic switch in the onset of mammalian puberty.

关键词： ubiquitin MKRN3 DNA methylation MBD3 DNA demethylase central precocious puberty

Late-onset non-islet cell tumor hypoglycemia: A case report

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World Journal of Clinical Cases 2021年第1期9卷 163-169页

作者： Shunichi Matsumoto Eijiro Yamada Yasuyo Nakajima Naoki Yamaguchi Takashi Okamura Toshiki Yajima Satoshi Yoshino Kazuhiko Horiguchi Emi Ishida Masashi Yoshikawa Jun Nagaoka Sho Sekiguchi Mai Sue Shuichi Okada Izumi Fukuda Ken Shirabe Masanobu Yamada Department of Medicine and Molecular Science Gunma University Graduate School of MedicineMaebashi 371-8511GunmaJapan division of General Thoracic Surgery Integrative Center of General SurgeryGunma University HospitalMaebashi 371-8511GunmaJapan Department of endocrinology Diabetes and MetabolismGraduate School of Medicine Nippon Medical SchoolTokyo 1138602Japan

BACKGROUND Hypoglycemia due to non-insulin-producing tumors is referred to as non-islet cell tumor hypoglycemia(NICTH).As NICTH is a rare lesion,the natural course of NICTH is not well *** report a case of NICTH that was observed 30 years before the onset of *** SUMMARY A 50-year-old man was diagnosed with an abnormal right chest shadow during a routine X-ray examination,but no further examination was undertaken because the lesion appeared *** years after the tumor discovery,the patient was admitted to the hospital with symptoms of severe hypoglycemia,which was diagnosed as NICTH based on a complete *** tumor was resected and found to be a solitary fibrous mass(15.6 cm×13.7 cm×10.4 cm);thereafter,the patient’s blood glucose levels normalized and he completely *** NICTH can have an acute onset,even if the tumor has been present and asymptomatic over a long time period.

关键词： Hypoglycemia Non-islet cell tumor hypoglycemia Blood glucose Solitary tumor Late onset Case report Insulin-like growth factor II

Long term omeprazole therapy for reflux esophagitis:follow-up in serum gastrin levels,EC cell hyperplasia and neoplasia

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World Journal of Gastroenterology 2000年第6期6卷 789-792页

作者： Pankaj Singh Anant Indaram Ronald Greenberg Vernu Visvalingam Simmy Bank division of Gastroenterology Albert Einstein Colege of MedicineLong Island Jewish Medical CenterNew Hyde ParkNew York

AIM To evaluate the long-term safety ofomeprazole in patients of gastroesophagealreflux disease resistant to treatment with H2receptor *** We prospectively followed 33patients on omeprazole therapy for severeerosive esophagitis for 5-8 years,with periodicgastrin levels,*** infection,gastricbiopsies for incidence of ECL cell hyperplasia,carcinoids,gastric atrophy and *** 185 patient follow-up years and 137 gastricbiopsies were *** Among the 33 patients,36% reachedtheir peak gastrin levels in an average of 8months to one year,then drifted Down slowlyover 1-2 year period to just above their baselinelevel,24% of the patients had a peak gastrinlevel above 400ng·L^1 and one patient had apeak level above 1000 ng·L^*** patient had amild ECL cell hyperplasia which was self limitingand did not show any dysplastic *** percent of patients were positive *** *** gastric biopsies did notshow gastric atrophy,intestinal metaplasia orneoplastic *** In a series of 33 patients followed for 5 - 8 years on omeprazole therapy for severe reflux esophagitis, we did not observe any evidence of significant ECL cell hyperplasia, gastric atrophy, intestinal metaplasia, dysplasia or neoplastic changes.

关键词： gastroesophageal reflux proton pump inhibitors enterochromaffin cell hypergastrinemia carcinoid tumor biopsy