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Biomedical subjects

J Mueller

Publications and source records attributed to J Mueller.

At least 37 records · Page 2Linked to original sources
PubMed1997

Bombesin-like peptides stimulate somatostatin release from rat fundic D cells in primary culture.

In several species, bombesin-like neuropeptides stimulate somatostatin release in in vitro preparations of gastric mucosa. We sought to determine if this response is due to a direct effect on fundic D cells. Rat fundic mucosal cells were isolated by pronase E (1% D cells). D cells were separated by counterflow elutriation and subsequent density-gradient centrifugation (Nycodenz) (15% D cells) and grown in primary culture for 48 h (46% D cells). Cultured cells were double stained with affinity-purified rabbit-anti-gastrin-releasing peptide (GRP) receptor antibody and mouse monoclonal antibody to human somatostatin. After incubation with rhodamine-labeled anti-rabbit and fluorescein isothiocyanate-labeled anti-mouse antibodies, reactions were visualized by fluorescence microscopy. All cells positive for somatostatin had GRP receptors, whereas all non-D cells showed no expression in this G cell-free culture system. Somatostatin release from cultured cells was stimulated by sulfated cholecystokinin octapeptide (CCK-8; EC50 3 X 10(-10) M) and epinephrine (EC50 4 X 10(-8) M), which are established stimuli for canine fundic D cells. Bombesin (EC50 6 X 10(-11) M), its mammalian analog GRP-27, and neuromedin C (GRP-10) (EC50 1 X 10(-10) M, for both) were almost equally potent stimuli of somatostatin release, eliciting maximal response at 10(-9) M (400-550% above basal). Neuromedin B was less potent and effective (maximal response at 10(-8) M, 230% above basal). [D-Phe6]bombesin-(6-13)-OMe, a specific bombesin receptor antagonist, inhibited bombesin-stimulated somatostatin release in a competitive manner (IC50 9 X 10(-8) M). Potentiating interactions were observed between bombesin and dibutyryladenosine 3',5'-cyclic monophosphate (DBcAMP) or epinephrine, but not between bombesin and CCK-8. We conclude that bombesin-like peptides directly stimulate somatostatin release by interacting with specific receptors on rat fundic D cells. Bombesin-like peptides appear to induce Ca(2+)-phospholipid-dependent signal-response transduction, as is indirectly suggested by potentiating interactions with DBcAMP or epinephrine.

Animals↗
PubMed1997

Ductuloendocrine cell proliferation in the pancreas of two young dogs with diabetes mellitus.

Two cases of diabetes mellitus in juvenile dogs (a 3-4 month-old Golden Retriever and a 2-month-old Labrador Retriever) are described here in terms of their clinical, histologic, and immunohistologic findings. Only very few insulin-positive cells were demonstrated immunohistochemically in one dog. In the second dog, the alterations of the pancreas consisted of hydropic vacuolar degeneration of B cells in the islets of Langerhans. In both cases, hyperplasia of the vacuolated cells was prominent. These cells formed tubular structures and were immunohistochemically positive for cytokeratin and proliferating cell antigen (MIB-1). Furthermore, within these vacuolated areas, some cells were positive to varying degrees for insulin, glucagon, somatostatin, and pancreatic polypeptide. Apoptotic cells could be seen in the exocrine pancreas, in vacuolated areas, and occasionally in the islets of both dogs. We interpret these alterations as ductuloendocrine cell proliferation, probably as an idiopathic compensatory response.

Age Factors↗
PubMed1996

Analysis for microsatellite instability and mutations of the DNA mismatch repair gene hMLH1 in familial gastric cancer.

We examined 30 gastric-cancer patients with a varying degree of family history of stomach cancer and/or synchronous gastric tumors for microsatellite instability. We observed microsatellite instability at at least 1 of 8 loci tested in tumors of 14/30 patients; of these 14, 8 had single locus alterations and 6 had alterations at at least half of the 8 loci. Among the patients with microsatellite instability at > or = 4 loci, 3 patients showed a strong familial clustering of gastric cancer. Mutation analysis of the DNA mismatch repair gene hMLHl on paired non-tumorous and tumor DNA from 10 patients, 6 with microsatellite instability at > or = 4 loci and 4 with an alteration at one locus, revealed a novel missense mutation, present in the normal and tumor DNA of one patient with microsatellite instability at multiple loci in his tumor. His family history of cancer included one second-degree relative affected with gastric cancer. These data suggest that germline mutations in the hMLHl gene occur in some gastric-cancer patients and that in the majority of cases microsatellite instability in gastric tumors may be due to defects in other genes responsible for DNA replication fidelity than the hMLHl.

Adaptor Proteins, Signal Transducing↗
PubMed1996

Expression of bcl-2 and p53 in de novo and ex-adenoma colon carcinoma: a comparative immunohistochemical study.

The development of colorectal carcinoma from adenomas is recognized as the dominant mechanism of colon carcinogenesis. However, early colon carcinomas are being increasingly detected which have no adenomatous elements in their vicinity, and which, despite their small size, already show submucosal invasion. Such tumours (so-called 'de novo' carcinomas) have renewed consideration of the de novo colorectal carcinogenesis pathway. The goal of this study was to evaluate the expression of tumour suppressor gene p53 and apoptosis control gene bcl-2 in de novo carcinomas, compared with early carcinomas developing in the background of an adenoma (ex-adenoma). Fifty cases each of de novo and ex-adenoma carcinomas (pT1) were studied. p53 expression was significantly higher in the de novo carcinomas than in the ex-adenoma carcinomas (62 per cent vs. 42 per cent), while bcl-2 tended to be weaker in the de novo than in the ex-adenoma carcinomas. These differences' support the concept that de novo carcinomas are a unique pathological entity, with a phenotype reflecting their more aggressive behaviour.

Adenocarcinoma↗
PubMed1996

Epidemiology of erythema exsudativum multiforme majus, Stevens-Johnson syndrome, and toxic epidermal necrolysis in Germany (1990-1992): structure and results of a population-based registry.

The severe skin reactions erythema exsudativum multiforme majus (EEM with mucosal involvement, EEMM), Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN) are difficult to study as they are very rare diseases with an incidence of about two cases per 1 million inhabitants per year. We report on the structure of a registry with the aim of ascertaining all hospitalized cases of EEMM, SJS, and TEN in western Germany and Berlin. The registry is structured as an intensive reporting system, regularly contacting more than 1500 departments including 100% of the burn units (n = 34), departments of pediatrics (n = 241), departments of dermatology (n = 106), and 100% of all internal medicine departments in hospitals with intensive care facilities or with more than 200 beds (n = 1161). With a coverage rate up to 95% based on the number of responding departments between April 1, 1990 and December 31, 1992, from a total of 767 reported cases 353 patients with EEMM, SJS, and TEN were finally included in the registry. Most of these patients were directly reported to the registry; only 2.54% (9 of 353) were primarily registered by the German spontaneous reporting systems. Assuming an average population of 64.5 million for western Germany and Berlin an incidence up to 1.89 per 1 million inhabitants per year could be calculated for SJS and TEN.

Epidemiologic Methods↗
PubMed1996

Three teams improving thrombolytic therapy.

BACKGROUND: The American Heart Association (AHA) standard for delivering thrombolytic therapy to chest pain patients is 30 to 60 minutes after patient presentation to the emergency department. Three acute care hospitals in an integrated health system in northern California shortened the time of administration of thrombolytic agents to appropriate patients presenting with chest pain in the emergency department. FINDING THE SOLUTIONS: Physician-led multidisciplinary teams developed algorithms to reduce variation and decrease the thrombolytic administration process to 30 minutes. Changes were made to prehospital and hospital thrombolytic policies and staff practices. REALIZING RESULTS: Each of the three acute care hospitals reduced their thrombolytic administration time by 48% to 59% to levels within the AHA standard. LEARNING FROM THE PROCESS: Internal benchmarking for clinical processes promotes a synergy between hospitals and medical staffs for the improvement of patient care. Multidisciplinary teams, which include community representatives, achieve a thorough understanding of a process, which in turn reduces variation in practice and improves quality.

Algorithms↗
PubMed1996

Miserable minority: emotional risk factors that influence the outcome of a mild traumatic brain injury.

Emotional risk factors are explored in four case studies, each of whom had sustained a mild traumatic brain injury (MTBI). Selected pre-existing personality traits that compounded the symptom presentation included over-achievement, dependency, grandiosity and borderline personality traits. Premorbid risk factors are described and their influence on co-morbid and post-morbid difficulties is discussed. We also touched upon the therapeutic issues involved in our cases. General treatment considerations are highlighted for dealing with grandiosity, narcissistic features and borderline traits. Over-achievement and perfectionism are discussed in the context of providing treatment for stress management. Finally, the effect of pre-existing emotional trauma combined with the MTBI is discussed.

Adult↗
PubMed1996

Stromelysin-3 (ST-3) mRNA expression in colorectal carcinomas. Localization and clinicopathologic correlations.

Stromelysin-3 (ST-3) mRNA expression was studied in 28 colorectal carcinomas and compared with that of adjacent nontumorous tissue. By Northern blot analysis, levels of ST-3 mRNA were significantly increased in the carcinomas compared with ST-3 expression was seen with degree of invasion, nodal or distant metastases, or histologic grade. In situ hybridization of nontumorous tissue showed no significant ST-3 expression. In tumor tissue, ST-3 mRNA was localized adjacent to colon carcinoma cells in irregular foci within the stoma. No significant difference in ST-3 expression was found between the center and periphery of the colon tumors. Most of the colon carcinomas (26 of 28) induced an expression of ST-3 in the directly adjacent stroma. No significant correlation between ST-3 mRNA expression and tumor stage and grade was seen. By Northern blot, we also saw expression of ST-3 in noncarcinomatous tissue, further supporting the concept that ST-3 expression is a tumor-induced but not a tumor-specific phenomenon.

Adult↗
PubMed1995

Liver transplantation for treatment of giant hepatocellular adenomas.

Giant hepatocellular adenomas are associated with a high incidence of rupture with intra-abdominal hemorrhage and may also undergo malignant transformation. If resection is not technically feasible, liver transplantation should be a treatment option. The aim of this report is to describe the indications, feasibility, and outcome of liver transplantation for hepatocellular adenomas. A 66-year-old man with a 17-cm hepatocellular adenoma originating in the left lobe but involving nearly the entire liver and a 35-year-old woman with a 20-cm tumor involving the right lobe of the liver and compressing the left lobe underwent liver transplantation without complication. In both cases, a histological diagnosis was made by core needle biopsy preoperatively, and resection was technically not possible. Hepatocellular adenoma involving nearly all of the liver with no evidence of malignant change was confirmed in the explant liver from both cases. Giant hepatocellular adenomas may be unresectable and require liver transplantation for complete removal to prevent potential rupture with hemorrhage or malignant transformation.

Adenoma, Liver Cell↗
PubMed1995

School-based AIDS education for adolescents.

PURPOSE: To describe a program which utilizes medical students and persons with AIDS (PWAs) to provide for adolescents school-based education about acquired immunodeficiency syndrome (AIDS). METHODS: Two 1.5 hour classroom sessions were conducted by medical students and persons with AIDS for seventh and eighth grade students (n = 1,161 students) at two urban middle schools. In addition, a two hour informational session was provided for parents. A 49 question student health survey was used to evaluate adolescents' HIV knowledge, tolerance of persons with AIDS, and intentions to engage in human immunodeficiency virus (HIV) safe behaviors. RESULTS: Significant (p < 0.01) increases in HIV knowledge and tolerance of persons with AIDS were observed, which persisted for three months. A significant (p < 0.01) improvement in intention to engage in HIV-safe behaviors was observed but did not persist for three months. CONCLUSIONS: Medical students and persons with AIDS can provide school-based AIDS education to early adolescents.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Microsatellite instability in adenocarcinomas of the upper gastrointestinal tract. Relation to clinicopathological data and family history.

We analyzed 66 adenocarcinomas arising in the upper gastrointestinal tract for microsatellite instability at eight microsatellite loci to investigate the role of these genetic alterations in the etiology of these tumors. We identified alterations in at least one locus in 11/46 adenocarcinomas of the stomach, in 2/15 adenocarcinomas arising in Barrett's esophagus, and in 1/5 adenocarcinomas of the duodenum and jejunum. Microsatellite instability in gastric tumors was found in 5/22 of intestinal, 1/3 of mixed, and 5/21 of diffuse type tumors. No relationship to the tumor stage (TNM), age, and survival time of the patients was observed. One patient had two synchronous gastric tumors both exhibiting microsatellite instability at multiple loci. His family history revealed four individuals in the maternal line afflicted with gastric carcinoma in three generations. Our data show that microsatellite instability is a genetic event in 11 to 24% of tumors of the upper gastrointestinal tract. The observation of microsatellite instability and a familial clustering of gastric tumors may suggest a genetic predisposition for a subset of gastric tumors, which may be identified by microsatellite analysis.

Adenocarcinoma↗
PubMed1994

In situ hybridization in pathology.

The technique of in situ hybridization (ISH) is presented with special reference to its use in the practice of pathology. Methodological and theoretical aspects of ISH are first considered with regard to tissue fixation, probe selection and preparation, various types of labeling reactions and aspects of hybridization conditions as they relate to hybridization protocols. This is followed by a discussion about the interpretation of the results of ISH with regard to sensitivity and specificity and the importance of, and various types of, controls. Lastly, specific applications of ISH in pathology are discussed, concluding with possible future applications for ISH in research and diagnosis.

Animals↗
PubMed1993

Charcot-Marie-Tooth disease type 1A. Association with a spontaneous point mutation in the PMP22 gene.

BACKGROUND: Charcot-Marie-Tooth disease (CMT) is the most common inherited peripheral neuropathy. CMT type 1A is associated with a 1.5-megabase DNA duplication in region p11.2-p12 of chromosome 17 in most patients. An increased dosage of a gene within the duplicated segment appears to cause the disease. The PMP22 gene, which encodes a myelin protein, has been mapped within the duplication and proposed as a candidate gene for CMT type 1A. METHODS: We analyzed DNA samples from a cohort of 32 unrelated patients with CMT type 1 who did not have the 1.5-Mb tandem duplication in 17p11.2-p12 for mutations within the PMP22 coding region. Molecular techniques included the polymerase chain reaction (PCR), heteroduplex analysis to detect point mutations, and direct nucleotide-sequence determination of amplified PCR products. RESULTS: A 10-year-old boy was identified with a point mutation in PMP22, which resulted in the substitution of cysteine for serine in a putative transmembrane domain of PMP22. Analysis of family members revealed that the PMP22 point mutation arose spontaneously and segregated with the CMT type 1 phenotype in an autosomal dominant pattern. The patients with the PMP22 point mutation had clinical and electrophysiologic phenotypes that were similar to those of patients with the 1.5-Mb duplication. CONCLUSIONS: The PMP22 gene has a causative role in CMT type 1. Either a point mutation in PMP22 or a duplication of the region including the PMP22 gene can result in the disease phenotype.

Amino Acid Sequence↗
PubMed1992

High-specificity in-situ hybridization. Methods and application.

We describe a technique of in-situ hybridization using oligonucleotide probes employing the expression of immunoglobulin VH genes as a model. Optimal conditions for hybridization with the 35S-labeled oligonucleotide probes were established with monoclonal B-cell lines that express VH genes of known nucleic acid sequence. The range of sensitivity and specificity achieved with this technique is documented. Under conditions of high stringency, this method can detect the expression of highly related VH hypervariable regions.

B-Lymphocytes↗