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Biomedical subjects

Stjepan Mise

Publications and source records attributed to Stjepan Mise.

10 recordsLinked to original sources
PubMed2006

The presentation and organization of adaptive cytoprotection in the rat stomach, duodenum, and colon. Dedicated to André Robert the founder of the concept of cytoprotection and adaptive cytoprotection.

BACKGROUND: Adaptive cytoprotection could be demonstrated in lesion attenuation within the whole gastrointestinal tract, in particular sequences, with onset and duration longer than the initial short-lasting period (i.e. one hour) defined by Robert in the stomach only. MATERIAL/METHODS: Adaptive cytoprotection possibly appeared and lesions were attenuated when the stomach, duodenum or colon, in various combinations and sequences, were challenged with initial (mild) and/or final (strong) irritants over a two-week period. Rats were challenged with the mild or strong irritants 25% or 96% ethanol intragastrically 1 ml/rat (stomach) and cysteamine 40 mg or 400 mg/kg subcutaneously (duodenum), or intrarectally (colon). To postulate the prostaglandin relationship known in Robert's cytoprotection and adaptive cytoprotection, indomethacin (1 mg/kg subcutaneously) was given simultaneously with the second challenge. RESULTS: Administering the mild and strong irritant protocols within the same part of the gastrointestinal tract, adaptive cytoprotection presents in the stomach (1 h to 14 days), duodenum (2 h to 14 days), but not in the colon. With these protocols applied to different parts of the gastrointestinal tract, adaptive cytoprotection cross-reaction was evident in the stomach-duodenum, duodenum-stomach (1 h-14 days and 2 h-14 days), stomach-colon, and duodenum-colon (both 2-24 hours), but not in the colon-stomach or colon-duodenum. This protection was fully antagonized with indomethacin. CONCLUSIONS: As observed for a day and even weeks, stomach-duodenum-colon adaptive cytoprotection is an important new defensive phenomenon.

Adaptation, Physiological↗
PubMed2006

An experimental model of prolonged esophagitis with sphincter failure in the rat and the therapeutic potential of gastric pentadecapeptide BPC 157.

We report a simple novel rat model that combines prolonged esophagitis and parallel sphincters failure. The anti-ulcer gastric pentadecapeptide BPC 157, which was found to be stable in gastric juice, and is being evaluated in inflammatory bowel disease trials, is an anti-esophagitis therapy that recovers failed sphincters. Twelve or twenty months after the initial challenge (tubes sutured into sphincters for one week and then spontaneously removed by peristalsis), rats exhibit prolonged esophagitis (confluent hemorrhagic and yellowish lesions, thinner epithelium and superficial corneal layer, with stratification derangement); constantly lowered pressure of both sphincters (assessed by using a water manometer connected to the drainage port of a Foley catheter implanted into the stomach either through esophageal or duodenal incision); and both lower esophageal and pyloric sphincter failure. Throughout the esophagitis experiment, BPC 157 was given at either 10 micro g/kg, i.p., once a day (last application 24 h before assessment) or alternatively, it was given continuously in drinking water at 0.16 micro g/ml (12 ml/rat). This treatment recovers i) esophagitis (macroscopically and microscopically, at either region or investigated time period) and ii) pressure in both sphincters (cmH2O). In addition, BPC 157 (10 micro g/kg) or saline (1 ml/rat, 5 ml/kg) was specifically given directly into the stomach; pressure assessment was performed at 5 min thereafter. The effect of BPC 157 is specific because in normal rats, it increases lower esophageal sphincter-pressure, but decreases pyloric sphincter-pressure. Ranitidine, given as the standard drug using the same protocol (50 mg/kg, i.p., once daily; 0.83 mg/ml in drinking water; or 50 mg/kg directly into the stomach) had no effect.

Animals↗
PubMed2005

Multidose activated charcoal in the treatment of carbamazepine overdose with seizures: a case report.

Serious complications after carbamazepine poisoning, such as coma, seizures, respiratory failure, cardiac conduction abnormalities, and death are more likely with serum levels greater than 170 micromol L(-1). We report a case of a single massive carbamazepine overdose in a 19-year-old male, following attempted suicide, without prior history of seizure disorder. On admission, three hours after ingestion, serum carbamazepine concentration was 179 micromol L(-1) and Glasgow Coma Scale scored 6. The patient was intubated and treated with multiple doses of activated charcoal for 48 hours. Twelve hours after ingestion, two repeated generalised myoclonic seizures were noted when serum carbamazepine levels peaked at 181 micromol L(-1), and were successfully treated with diazepam. Carbamazepine serum level fell within the therapeutic range 63 hours after ingestion and the patient was discharged without any long-term sequelae. As there is no antidote for carbamazepine poisoning, supportive treatment remains the only, but usually potent option.

Adult↗
PubMed2005

[Viral hepatitis: Croatian consensus statement].

There has been a dramatic improvement in diagnostic procedures and therapy of viral hepatitis in the last 20 years. Improvements in therapy caused an increase in actual cost, however, with significant long-term savings through a decreased cost of treatment of advanced liver disease including liver transplantation. The Croatian National Board for Viral Hepatitis has decided to initiate the organization of consensus conference on viral hepatitis enabling the leading experts in the country to give the best possible recommendations for the diagnosis, prophylaxis and therapy in our circumstances. The Consensus Conference took place in Zagreb in June 2004, with update in March 2005, organized by the Croatian National Board for Viral Hepatitis, Reference Centers of the Ministry of Health for Chronic Liver Diseases, Infectious Diseases and AIDS, Croatian Society of Gastroenterology--Hepatology Section, Croatian Society for Nephrology, Dialysis and Transplantation, and Croatian Institute for Health Insurance. Invited experts provided written reports on the respective subjects that appear in this issue and their recommendations resulting in this consensus statement.

Consensus Statements as Topic↗
PubMed2005

[Factors influencing clinical course of viral hepatitis].

Hepatitis B and C are diseases characterized by a high global prevalence, complex clinical course and limited efficacy of currently available antiviral therapy. Hepatitis B: local factors have a significant influence not only on the disease prevalence but also on the disease course. Vertical transmission of the infection in the areas of high prevalence results in perinatal infection, which universaly leads to the development of chronic disease. Factors associated with an increased risk of cirrhosis are older age, persistent viremia, coinfection with HCV, HDV and HIV, and consumption of alcohol, while the role of viral genotype is uncertain. Predictors of HCC development in cirrhotic liver are older age, male sex, alcohol abuse, exposure to aflatoxin, coinfection with HCV and HDV, continuously active inflammation, and potentially viral genotype. Survival predictors in cirrhotic patients are age, serum albumin, platelet count and splenomegaly as a reflection of portal hypertension. Hepatitis C: the risk of cirrhosis is low. Risk factors for cirrhosis are infection in older age, alcohol abuse, and coinfection with HBV and HIV. Obesity has negative impact on treatment efficacy.

Disease Progression↗
PubMed2003

Different effect of antiulcer agents on rat cysteamine-induced duodenal ulcer after sialoadenectomy, but not gastrectomy.

The focus was on salivary glands in cysteamine-induced duodenal ulcer and the different effects of antiulcer agents on cysteamine-induced duodenal ulcer in sialoadenectomized but not gastrectomized rats. We tested antiulcer agents on cysteamine-induced duodenal ulcer in rats (agents/kg i.p.) simultaneously with cysteamine 400 mg/kg s.c., rat killed 24 h thereafter subjected to no surgery (normal), to gastrectomy (24 h before) or sialoadenectomy, acute (24 h before) or chronic (21 days before). (i) Ulcerogenesis: cysteamine-induced duodenal ulcer had the same severity and incidence in normal, gastrectomized or acutely or chronically sialoadenectomized rats. (ii) Antiulcer effect under normal conditions or following gastrectomy: in normal or gastrectomized rats all agents tested, gastric pentadecapeptide BPC 157 [currently in clinical trials for inflammatory bowel disease (PL-10, PLD-116, PL-14736, Pliva) (10.0 microg or 10.0 ng), ranitidine (10 mg), atropine (10 mg), omeprazole (10 mg)] inhibited cysteamine-induced duodenal ulcers, acting through gastric acid-independent mechanisms. Following sialoadenectomy, acute or chronic: ranitidine, omeprazole and atropine were completely ineffective, while pentadecapeptide BPC 157 could protect. Thus, we found that contrary to stomach, salivary glands are implicated in cytoprotective agent activity (standard agents were ineffective after sialoadenectomy). Also, gastric pentadecapeptide BPC 157 was consistently associated with a cytoprotective effect, suggesting a beneficial activity distinctive from that of H2-receptor blockers, proton-pump inhibitors and anticholinergics; but probably replacing missing salivary glands factors.

Animals↗