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Overlap of functional heartburn and gastroesophageal reflux disease with irritable bowel syndrome

World Journal of Gastroenterology 2013年第35期19卷 5787-5797页

作者： Nicola de Bortoli Irene Martinucci Massimo Bellini Edoardo Savarino Vincenzo Savarino Corrado Blandizzi Santino Marchi division of Gastroenterology University of Pisa division of Gastroenterology University of Padua division of Gastroenterology University of Genoa division of Pharmacology and chemotherapy University of Pisa

Several studies indicate a significant degree of overlap between irritable bowel syndrome(IBS)and gastroesophageal reflux disease(GERD).Likewise,both functional heartburn(FH)and IBS are functional digestive disorders that may occur in the same ***,data establishing a solid link between FH and IBS are lacking,mainly because the clinical definition of FH has undergone substantial changes over the *** available literature on the overlap between GERD or FH and IBS highlights considerable heterogeneity in terms of the criteria and diagnostic procedures used to assess heartburn and *** particular,several epidemiological studies included patients with concomitant IBS and GERD without any attempt to distinguish FH(as defined by the RomeⅢcriteria)from GERD via pathophysiological *** of these critical issues,there is preliminary evidence supporting a significantdegree of FH-IBS *** underscores the need for studies based on updated diagnostic criteria and accurate pathophysiological classifications,particularly to distinguish FH from *** distinction would represent an essential starting point to achieving a better understanding of pathophysiology in the subclasses of patients with GERD and FH and properly assessing the different degrees of overlap between IBS and the subcategories of *** present review article intends to appraise and critically discuss current evidence supporting a possible concomitance of GERD or FH with IBS in the same patients and to highlight the pathophysiological relationships between these disorders.

关键词： Functional gastrointestinal disorders Gastroesophageal reflux disease/Gastro-oesophageal reflux disease Irritable bowel syndrome Acidity(esophageal) Hypersensitivity

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Lansoprazole prevents experimental gastric injury induced by non-steroidal anti-inflammatory drugs through a reduction of mucosal oxidative damage

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World Journal of Gastroenterology 2005年第26期11卷 4052-4060页

作者： Corrado Blandizzi Matteo Fornai Rocchina Colucci Gianfranco Natale Valter Lubrano Cristina Vassalle Luca Antonioli Gloria Lazzeri Mario Del Tacca division of Pharmacology and chemotherapy Department of Oncology Transplants and Advanced Technologies in Medicine University of PisaPisaItaly Department of Human Morphology and Applied Biology University of Pisa Pisa Italy Institute of Clinical Physiology National Research Council Pisa Italy division of Pharmacology and chemotherapy Department of Oncology Transplants and Advanced Technologies in Medicine University of Pisa Pisa Italy

AIM:This study investigated the mechanisms of protection afforded by the proton pump inhibitor lansoprazole against gastric injury induced by different non-steroidal anti-inflammatory drugs (NSAIDs) in rats. METHODS: Male Sprague-Dawley rats were orally treated with indomethacin (100 μmol/kg), diclofenac (60 μmol/kg), piroxicam (150 μmol/kg) or ketoprofen (150 μmol/kg). Thirty minutes before NSAIDs, animals were orally treated with lansoprazole 18 or 90 umol/kg. Four hours after the end of treatments, the following parameters were assessed: gastric mucosal PGE2, malondialdehyde (MDA), myeloperoxidase (MPO) or non-proteic sulfhydryl compounds (GSH) levels; reverse transcription-polymerase chain reaction (RT-PCR) of mucosal COX-2 mRNA; gastric acid secretion in pylorus-ligated animals; in vitro effects of lansoprazole (1-300 μmol/L) on the oxidation of low density lipoproteins (LDLs) induced by copper sulphate. RESULTS: All NSAIDs elicited mucosal necrotic lesions which were associated with neutrophil infiltration and reduction of PGE2 levels. Increments of MPO and MDA contents, as well as a decrease in GSH levels were detected in the gastric mucosa of indomethacin- or piroxicam-treated animals. Indomethacin enhanced mucosal cyclooxygenase-2 expression, while not affecting cyclooxygenase-1. At the oral dose of 18 μmol/kg lansoprazole partly counteracted diclofenac-induced mucosal damage, whereas at 90 μmol/kg it markedly prevented injuries evoked by all test NSAIDs. Lansoprazole at 90 μmol/kg reversed also the effects of NSAIDs on MPO, MDA and GSH mucosal contents, without interfering with the decrease in PGE2 levels or indomethacin-induced cyclooxygenase-2 expression. However, both lansoprazole doses markedly inhibited acid secretion in pylorus-ligated rats. Lansoprazole concentration-dependently reduced the oxidation of LDLs in vitro. CONCLUSION: These results suggest that, besides the inhibition of acid secretion, lansoprazole protection against NSAID-induced gastr

关键词： Lansoprazole Gastric injury Non-steroidal anti-inflammatory drugs

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EXPERIMENTAL ANIMAL TUMOR IMMUNOTHERAPY WITH BACTERIAL POLYSACCHARIDE

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中华医学杂志(英文版) 1981年第6期94卷 375-378页

作者：赵家琪 Kazuo Nitta 新田和男 On leave from Immunology Section Dongzhimen HospitalBeijing. chemotherapy division National Cancer Center Research InstituteTokyo

A carboxymethyl-polysaccharide of bacterialorigin,CM-TAK,exhibits very strong antitumoractivity in a subcutaneous sarcoma 180(S180)sclid tumor,when intraperitoneally injected at20 mg/kg/day every other day,starting on day1 and totalling up to 5 times or by 1 shotcf 100 mg/kg either on day 1,day 7 or day *** ratios of tumor growth are nearly100% by any mode of injection *** manymice,tumors completely disappear after treat-ment with CM-TAK.

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Expression of the Apoptosis Inhibitor Survivin and its correlation with Thymidine Kinase and Axillary Lymph Node Metastasis in Breast Cancer

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生物医学工程学杂志 2005年第S1期22卷 133-134页

作者： Jian-Ping WU Yun-Feng ZHOU Zhi-Guo LUO Ming-Sheng ZHANG(Dept of Radio-chemotherapy, Zhongnan Hospital,Cancer Research Center, Wuhan University,Wuhan 430071,China) Dept of Radio-chemotherapy Zhongnan Hospital Cancer Research Center Wuhan University Wuhan 430071 China

1 IntroductionMany molecular factors have been demonstrated to interfere with cellular proliferation and programmed cell death. One of these factors is a recently discovered member of the 'inhibitor of apoptosis protein(IAP)' called survivin. Survivin is abundantly expressed in most solid and hematologic malignancies, but undetectable in normal adult tissues. Interference with survivin function induces pleiotropic cell-division defects and apoptosis. Cytosolic thymidine kinase (TK) is a marker for proliferating cells and TK is one of several key enzymes involved in DNAmetabolism that phosphorylates thymidine to thymidine mono-phosphate. This study was aimed to detect the expression of suvivin and TK in breast cancer, and to explore a possible relationship between survivin expression and axillary lymph node metastasis.

关键词： Expression of the Apoptosis Inhibitor Survivin and its correlation with Thymidine Kinase and Axillary Lymph Node Metastasis in Breast Cancer IAPs

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ACTIVATION OF NATURAL KILLER CELLS WITH 3,6-BIS (2-PIPERIDINOETHOXY) ACRIDINE TRIHYDROCHLORIDE (CL 246, 738)

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中华医学杂志(英文版) 1987年第3期100卷 192-197页

作者： Bosco Shang Wang Araceli L. Lumanglas Jillian Silva Veronica M. Ruszala-Mallon Frederick E. Durr Laboratory of Tumor Immunology Department of Chemotherapy Research Medical Research Division American Cyanamid Company Lederle Laboratories Pearl River New York 10965

The mechanism of action of 3,6-bis(***-thoxy) acridine trihydrochloride (CL 246,738) in the potentiation of natural killer (NK) cells was investigated. Orally administered CL 246,738 consistently produced enhancement of NK cell activity in mice. Using anti-asialo GM-1 (ASGM-1) antibody as an NK cell marker, it was determined that the compound increased the number of ASGM-1 positive cells in mice as indicated by immunofluorescence staining. The compound at concentrations of 0.02-0.2 μg/ml also induced NK cell activity in vitro. This effect was dependent upon the presence of macrophages and was inhibited by anti-IFN (alpha+beta), but not anti-lFN (beta) antibody. Taken together, it is postulated that the compound functions by stimulating macrophages to release IFN (alpha) which subsequently activates NK cells. As an effective stimulator of IFN and NK cells, CL 246,738 may prove clinically useful in the immunotherapy of certain types of malignancy.

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Carcinoid tumor of the duodenum and accessory papilla associated with polycythemia vera

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World Journal of Gastroenterology 2005年第24期11卷 3794-3796页

作者： Horng-Yuan Wang Ming-Jen Chen Tsen-Long Yang Ming-Chih Chang Yu-Jan Chan division of Gastroenterology Department of Surgery division of Hematology Department of Pathology

Carcinoid tumors have been reported in a wide range of organs but most frequently involve the gastrointestinal tract; however, duodenal carcinoid tumors are rare. We report a 50-year-old male patient complaining of multiple melenas for 3 wk. The panendoscopy and endoscopic retrograde cholangiopancreaticography revealed swelling accessory papilla with an ulcer. The biopsy taken showed a carcinoid tumor. The lesion was removed by wide resection. Patient was found to have an abnormal blood cell count during the follow-up period with elevated levels of hemoglobin and hematocrit of 21.2 g/dL and 63.5%,respectively, thrombocytosis of 501 000/μL, and leukocytosis of 20 410/μL. He was diagnosed as a polycythemia vera by a hematologist after further evaluation. He received periodic phlebotomy and hydroxyurea treatment. The response was good and his hematocrit was stabilized by periodic phlebotomy in the range of 44-49% during the last 2 years. The possible origin of UGI bleeding by a duodenal carcinoid tumor, although rare, should be considered. There has been one case report of a duodenal carcinoid tumor that involved accessory papilla of the pancreas divisum and one case report of metastatic carcinoid tumor associated with polycythemia vera. It is different in our patient as compared with the latter report, which mentioned a polycythemia vera patient who was found to have a metastatic carcinoid in the 17 years follow-up period. chemotherapy had been given before the carcinoid tumor was revealed. Our patient had no previous chemotherapy for polycythemia vera before he was found to have duodenal carcinoid tumor; this excludes the possibility of chemotherapy induced carcinoid tumor, although it had been suspected in the previous report. In our patient, the existence of both diseases may be by predisposition of each other since both diseases have an increased incidence of other neoplasm, or they may be coexistent incidentally.

关键词： Carcinoid tumor Accessory papilla Polycythemia vera

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Endoscopic stenting-Where are we now and where can we go?

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World Journal of Gastroenterology 2008年第24期14卷 3798-3803页

作者： Mark Terence McLoughlin Michael Francis Byrne UBC division of Gastroenterology

Self expanding metal stents (SEMS) play an important role in the management of malignant obstructing lesions in the gastrointestinal tract. Traditionally,they have been used for palliation in malignant gastric outlet and colonic obstruction and esophageal malignancy. The development of the polyflex stent,which is a removable self expanding plastic stent,allows temporary stent insertion for benign esophageal disease and possibly for patients undergoing neoadjuvant chemotherapy prior to esophagectomy. Potential complications of SEMS insertion include perforation,tumour overgrowth or ingrowth,and stent migration. Newer stents are being developed with the aim of increasing technical and clinical success rates,while reducing complication rates. Other areas of development include biodegradable stents for benign disease and radioactive or drug-eluting stents for malignant disease. It is hoped that,in the future,newer stents will improve our management of these diffi cult conditions and,possibly,provide prognostic as well as symptomatic benefi t in the setting of malignant obstruction.

关键词： Endoscopy Stent Palliation Bowel obstruction Malignancy

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Liver transplantation for metastatic neuroendocrine tumor: A case report and review of the literature

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World Journal of Gastroenterology 2005年第48期11卷 7676-7683页

作者： Wojciech C Blonski K Rajender Reddy Abraham Shaked Evan Siegelman David C Metz Department of Gastroenterology and Hepatology division of Gastroenterology Department of Surgery Department of Magnetic Resonance Imaging division

Neuroendocrine tumors are divided into gastrointestinal carcinoids and pancreatic neuroendocrine tumors. The WHO has updated the classification of these lesions and has abandoned the term ＂carcinoid＂. Both types of tumors are divided into functional and non-functional tumors. They are characterized by slow growth and frequent metastasis to the liver and may be limited to the liver for long periods. The therapeutic approach to hepatic metastases should consider the number and distribution of the liver metastases as well as the severity of symptoms related to hormone production and tumor bulk. Surgery is generally considered as the first line therapy. In patients with unresectable liver metastases, alternative treatments are dependent on the type and the growth rate. Initial treatments consist of long acting somatostatin analogs and/or interferon. Streptozocin-based chemotherapy is usually reserved for symptomatic patients with rapidly advancing disease, but generally the therapy is poorly tolerated and its effects are short-lived. Locoregional therapy directed such as hepatic-artery embolization and chemoembolization, radiofrequency thermal ablation and cryosurgery, is often used instead of systemic therapy, if the disease is limited to the liver. However, liver transplantation should be considered in patients with neuroendocrine metastases to the liver that are not accessible to curative or cytoreductive surgery and if medical or Iocoregional treatment has failed and if there are life threatening hormonal symptoms. We report a case of liver transplantation for metastatic neuroendocrine tumor of unknown primary source and provide a detailed review of the world literature on this controversial topic.

关键词： Liver metastases, Neuroendocrine tumors Liver transplantation

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Understanding and treating refractory constipation

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World Journal of Gastrointestinal Pharmacology and Therapeutics 2014年第2期5卷 77-85页

作者： Gabrio Bassotti Corrado Blandizzi Gastroenterology and Hepatology Section Department of MedicineUniversity of Perugia06156 PerugiaItaly division of Pharmacology and chemotherapy Department of Clinical and Experimental MedicineUniversity of Pisa56126 PisaItaly

Chronic constipation is a frequently encountered disorder in clinical practice. Most constipated patients benefit from standard medical approaches. However, current therapies may fail in a proportion of patients. These patients deserve better evaluation and thorough investigations before their labeling as refractory to treatment. Indeed, several cases of apparent refractoriness are actually due to misconceptions about constipation, poor basal evaluation (inability to recognize secondary causes of constipation, use of constipating drugs) or inadequate therapeutic regimens. After a careful reevaluation that takes into account the above factors, a certain percentage of patients can be defined as being actually resistant to first-line medical treatments. These subjects should firstly undergo specific diagnostic examination to ascertain the subtype of constipation. The subsequent therapeutic approach should be then tailored according to their underlying dysfunction. Slow transit patients could benefit from a more robust medical treatment, based on stimulant laxatives (or their combination with osmotic laxatives, particularly over the short-term), enterokinetics (such as prucalopride) or secretagogues (such as lubiprostone or linaclotide). Patients complaining of obstructed defecation are less likely to show a response to medical treatment and might benefit from biofeedback, when available. When all medical treatments prove to be unsatisfactory, other approaches may be attempted in selected patients (sacral neuromodulation, local injection of botulinum toxin, anterograde continence enemas), although with largely unpredictable outcomes. A further although irreversible step is surgery (subtotal colectomy with ileorectal anastomosis or stapled transanal rectal resection), which may confer some benefit to a few patients with refractoriness to medical treatments.

关键词： Chronic constipation Laxatives Medical treatment Refractory constipation Surgical treatment

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Identification of a dihydroorotate dehydrogenase inhibitor thatinhibits cancer cell growth by proteomic profiling

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Oncology Research 2023年第6期31卷 833-844页

作者： MAKOTO KAWATANI HARUMI AONO SAYOKO HIRANUMA TAKESHI SHIMIZU MAKOTO MUROI TOSHIHIKO NOGAWA TOMOKAZU OHISHI SHUN-ICHI OHBA MANABU KAWADA KANAMI YAMAZAKI SHINGO DAN NAOSHI DOHMAE HIROYUKI OSADA Biomolecular Characterization Unit Technology Platform DivisionRIKEN Center for Sustainable Resource Science(CSRS)Saitama351-0198Japan Chemical Resource Development Unit Technology Platform DivisionRIKEN Center for Sustainable Resource Science(CSRS)Saitama351-0198Japan Chemical Biology Research Group RIKEN Center for Sustainable Resource Science(CSRS)Saitama351-0198Japan Molecular Structure Characterization Unit Technology Platform DivisionRIKEN Center for Sustainable Resource Science(CSRS)Saitama351-0198Japan Institute of Microbial Chemistry(BIKAKEN) NumazuMicrobial Chemistry Research FoundationShizuoka410-0301Japan division of Molecular Pharmacology Cancer Chemotherapy CenterJapan Foundation for Cancer ResearchTokyo135-8550Japan Department of Pharmaceutical Sciences University of ShizuokaShizuoka422-8526Japan

Dihydroorotate dehydrogenase(DHODH)is a central enzyme of the de novo pyrimidine biosynthesis pathway and is a promising drug target for the treatment of cancer and autoimmune *** study presents the identification of a potent DHODH inhibitor by proteomic ***-based screening revealed that NPD723,which is reduced to H-006 in cells,strongly induces myeloid differentiation and inhibits cell growth in HL-60 cells.H-006 also suppressed the growth of various cancer *** profiling of NPD723-treated cells in ChemProteoBase showed that NPD723 was clustered with DHODH inhibitors.H-006 potently inhibited human DHODH activity in vitro,whereas NPD723 was approximately 400 times less active than H-006.H-006-induced cell death was rescued by the addition of the DHODH product orotic ***,metabolome analysis revealed that H-006 treatment promotes marked accumulation of the DHODH substrate dihydroorotic *** results suggest that NPD723 is reduced in cells to its active metabolite H-006,which then targets DHODH and suppresses cancer cell ***,H-006-related drugs represent a potentially powerful treatment for cancer and other diseases.

关键词： Anticancer agents Differentiating agents Drug target identification

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