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R H Bell

Publications and source records attributed to R H Bell.

At least 37 records · Page 2Linked to original sources
PubMed1994

Thermal injury of the posterior duodenum during laparoscopic cholecystectomy.

While complications of laparoscopic cholecystectomy occur in 3-7% of cases, bowel injuries are uncommonly reported. Bowel injuries appear to be of two types: penetrating bowel injury from either the Veress needle or trocar, and thermal bowel injury from either contact or conductive burn. The duodenum is usually spared from Veress needle or trocar injury because of its posterior location. However, during dissection in the triangle of Calot, the duodenum is at risk for direct contact burn or energy conduction burn. In this report we describe a presumed conductive burn injury of the posterior second portion of the duodenum which followed laparoscopic cholecystectomy. This unrecognized injury resulted in full-thickness necrosis of the duodenal wall with delayed perforation. This injury was successfully managed with pyloric exclusion. The diagnosis and management of this previously unreported injury are described.

Aged↗
PubMed1994

Novel expression of gastrin (CCK-B) receptors in pancreatic carcinomas and dysplastic pancreas from transgenic mice.

Transgenic mice bearing the elastase I promoter--SV40 T-antigen fusion gene (ELSV) develop pancreatic acinar cell carcinomas by 3 to 6 months of age. The purpose of the study was to determine if pancreatic carcinomas and dysplastic pancreas from the Tg (Ela-1, SV40E + Ela-1, neo) Bri19 strain of ELSV transgenic mice express gastrin (CCK-B) receptors. To accomplish this, we utilized iodine 125 (125I)-gastrin binding studies, reverse transcription-polymerase chain reaction (RT-PCR), and Southern blot analysis to examine pancreatic carcinomas from 26-week-old male ELSV transgenic mice, dysplastic pancreas from 8-week-old male ELSV transgenic mice, and normal pancreas from 30-week-old nontransgenic male mice (SJL/J) and from 8-week-old nontransgenic male mice (B6SJLF1/J). No saturable gastrin binding to normal nontransgenic mouse pancreas was found. In contrast, saturable gastrin binding was detected at pH 6.5, 22 degrees C, in 9 of 13 pancreatic carcinomas and all 5 dysplastic pancreata. Competitive inhibition 125I-gastrin binding assays showed gastrin bound to a single class of high-affinity receptors (receptor binding affinity [Kd] 0.11 +/- 0.02 nM, binding capacities ranging from 1 to 60 fmol/mg protein for pancreatic carcinomas; Kd: 0.15 +/- 0.04 nM, binding capacities ranging from 1 to 9 fmol/mg protein for dysplastic pancreas). RT-PCR and Southern blot analysis confirmed 125I-gastrin binding studies by demonstrating gastrin (CCK-B) receptor mRNA expression in pancreatic carcinomas and dysplastic pancreas but an absence of mRNA expression in normal nontransgenic mouse pancreas. In conclusion, pancreatic carcinomas and dysplastic pancreas in ELSV transgenic mice novelly express gastrin (CCK-B) receptors. This expression may provide a growth advantage to acinar cells as part of the multistage process of carcinogenesis.

Animals↗
PubMed1994

Stimulation of in vivo pancreatic growth in the rat is mediated specifically by way of cholecystokinin-A receptors.

BACKGROUND/AIMS: Cholecystokinin (CCK) and gastrin stimulate growth of rodent pancreas in vivo. However, it remains unclear whether these growth effects are mediated specifically by CCK-A receptors, CCK-B receptors, or both. To clarify this issue, the present study examined the effect of highly selective and biologically active CCK agonists on pancreatic growth. METHODS: Rats were subcutaneously injected with either (1) CCK-8, a nonselective CCK agonist (2.50 micrograms/kg body wt); (2) A-71623, a selective CCK-A agonist, tert-butyl-oxycarbonyl-Trp-Lys (epsilon-N-2-methylphenylaminocarbonyl)-Asp-(N-methyl)-Phe-NH2 (1.84 micrograms/kg body wt); (3) SNF-8815; a selective CCK-B agonist, [(2R,3S)-beta-MePhe28, N-MeNle31]CCK26-33 (2.40 micrograms/kg body wt); or (4) saline (control) for 21 days. Rats were killed, and pancreatic weight, protein content, RNA content, DNA content, protein-DNA ratio, RNA-DNA ratio, pancreatic area per nucleus, and number of mitoses per 10,000 acinar cells were determined. RESULTS: Nonselective CCK agonist significantly increased pancreatic weight, protein, RNA, and DNA contents, and number of mitoses per 10,000 acinar cells. Likewise, selective CCK-A agonist significantly increased pancreatic weight, protein, RNA, and DNA contents, protein-DNA ratio, RNA-DNA ratio, pancreatic area per nucleus, and number of mitoses per 10,000 acinar cells. In contrast, selective and biologically active CCK-B agonist had no effect. CONCLUSION: These findings indicate that pancreatic growth is mediated specifically by CCK-A receptors in the rat in vivo.

Animals↗
PubMed1994

Aggressive fibrous tissue lesions in the upper extremity: treatment and results.

The oncologic and functional results of treatment of aggressive fibromatosis were reviewed in 16 patients. Five had undergone previous resections. Complete surgical excision, the recommended primary treatment modality for aggressive fibromatosis tissue lesions, could only be performed in five patients. Radiation was administered in 13 patients and mainly used when the resection margins were positive. One patient required reoperation for recurrence. Complete detailed follow-up data were available in 15 patients. Functional analysis revealed 11 good-excellent, 2 fair, and 2 poor results using the Enneking classification. Local control was achieved with a combination of surgery and radiation, maintaining good-excellent function in most patients. The local nature of this tumor can be controlled with surgery and radiation while preserving function in the upper extremity.

Adult↗
PubMed1994

Cholecystokinin receptor characterization and cholecystokinin-A receptor messenger RNA expression in transgenic mouse pancreatic carcinomas and dysplastic pancreas.

Transgenic mice bearing the rat elastase I promoter - SV40 T-antigen (ELSV) fusion gene develop pancreatic acinar cell carcinomas by 3-6 months of age. In other animal models of pancreatic cancer, cholecystokinin (CCK) has been shown to be a tumor promoter. Therefore, we characterized CCK binding properties and CCK-A receptor mRNA expression in pancreatic carcinomas and dysplastic pancreata from the Tg(Ela-1, SV40E+Ela-1, neo)Bri19 strain of ELSV transgenic mice. To accomplish this, we utilized 125I-Bolton-Hunter-labeled-cholecystokinin octapeptide (125I-BH-CCK-8) binding studies, reverse transcription-polymerase chain reaction (RT-PCR), and Southern blot analysis to examine pancreatic carcinomas from 26-week-old male ELSV transgenic mice, dysplastic pancreata from 8-week-old male ELSV transgenic mice, and normal pancreas from 30-week-old nontransgenic male mice (SJL/J) and 8-week-old nontransgenic male mice (B6SJLF1/J). Optimal saturable CCK-8 binding was detected at pH 6.5, 22 degrees C. Competitive inhibition 125I-BH-CCK-8 binding assays performed on all four mouse pancreatic tissues showed that CCK-8 bound to two classes of CCK binding sites: a high affinity, lower capacity CCK binding site and a low affinity, higher capacity CCK binding site. RT-PCR and Southern blot analysis confirmed the 125I-BH-CCK-8 binding studies by demonstrating CCK-A receptor mRNA expression in the ELSV transgenic pancreatic carcinomas and dysplastic pancreas, as well as in normal nontransgenic mouse pancreas. In conclusion, pancreatic carcinomas and dysplastic pancreas from ELSV transgenic mice and normal nontransgenic mouse pancreas all bind 125I-BH-CCK-8 and express mRNA for the CCK-A receptor. In contrast to chemically-induced pancreatic tumors in the rat, ELSV transgenic mouse pancreatic tumors do not appear to significantly overexpress CCK-A receptors.

Animals↗
PubMed1994

Candida in pancreatic infection: a clinical experience.

Pancreatic infection remains a significant clinical problem, with substantial morbidity and mortality. Published case reports of Candida species identified in these infections prompted a review of 17 consecutive patients recently treated for peripancreatic infection by scheduled relaparotomy. Six patients were transferred from other hospitals, all having undergone prior operative intervention (median stay elsewhere: 58 days). The 11 other patients underwent initial operation an average of 14 days after admission. Candida species were identified in the initial operative cultures of 5 patients (29%), three of whom had undergone previous drainage at other hospitals. Two patients (11.7%) had Candida identified at subsequent operation. Six patients were treated with Amphotericin B for a median of 12 days (range 6-32) and a median dosage of 420 mg (range 225-830 mg). All patients were cleared of their Candida infection, but three subsequently died, for an overall mortality of 17.6%. Candida infected patients suffered a 42 per cent mortality. Our series supports the suspicion that Candida is much more frequent (41% of patients) than previously recognized in peripancreatic sepsis, and is commonly acquired after the initial operation. Amphotericin B therapy is effective in clearing Candida infection, but affected patients have a high associated mortality.

Acute Disease↗
PubMed1993

4,5-Dihydro-1-phenyl-1H-2,4-benzodiazepines: novel antiarrhythmic agents.

A series of 4,5-dihydro-1-phenyl-1H-2,4-benzodiazepines has been identified as potential antiarrhythmic agents that interact with sodium and potassium channels and prolong the ventricular effective refractory period (ERP) in anesthetized guinea pigs. Concomitant displacement of radiolabeled bactrachotoxin from site II in Na+ channels and of radiolabeled dofetilide from delayed rectifier K+ channels was evident with all members of this chemical series at a concentration of 10 microM. Structure-activity relationship (SAR) studies using a paced guinea pig model to assess prolongation of the ERP indicated that methyl or ethyl at the 1-position had little effect on activity, while larger groups caused a diminution of activity. Compounds with substituents at either the 3- or 4-position that increased lipophilicity generally were more potent; however, too many lipophilic substituents simultaneously at positions 1, 3, and 4 resulted in less active compounds. Substituents on either aromatic ring had little influence on activity, and phenyl at the 5-position resulted in a significant reduction in antiarrhythmic activity. When two sets of enantiomerically pure compounds were tested in the guinea pig, chirality was shown to be important for activity of 8, where the (R)-enantiomer was the more active, but not in the case of 15, where the enantiomers were equiactive. Several compounds in this series increased the threshold for ventricular fibrillation and refractoriness in myocardially-infarcted anesthetized cata and delayed the onset of aconitine-induced arrhythmias in anesthetized guinea pigs following intravenous dosing. Moreover, these compounds possessed oral antiarrhythmic activity in conscious myocardially-infarcted dogs. Compound R-15 has been advanced for further biological and toxicological evaluations.

Animals↗
PubMed1993

Stimulation of growth of azaserine-induced putative preneoplastic lesions in rat pancreas is mediated specifically by way of cholecystokinin-A receptors.

Cholecystokinin (CCK) has been shown to stimulate the growth of both normal pancreas and azaserine-induced putative preneoplastic pancreatic lesions in the rat. The present study was performed to determine whether these effects are mediated by way of CCK-A receptors, CCK-B receptors, or both. Sixteen-day-old male Lewis rats were given i.p. injections of azaserine at 30 mg/kg body weight. Starting on day 21, rats were given s.c. injections, 5 days/week for 16 consecutive weeks, of either (a) CCK octapeptide (nonselective CCK agonist) (2.50 micrograms/kg body weight, n = 17), (b) tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2-methylphenylaminocarbonyl++ +)-Asp- (N-methyl)-Phe-NH2 (highly selective CCK-A agonist) (1.84 micrograms/kg body weight, n = 18), (c) [(2R,3S)-beta-MePhe28,N-MeNle31]CCK26-33 (highly selective CCK-B agonist) (2.40 micrograms/kg body weight, n = 18), or (d) normal saline solution (control, n = 17). Rats were subsequently sacrificed, pancreatic weights were determined, and quantitative morphometric analysis of atypical acinar cell foci and nodules was performed. Both CCK octapeptide and the selective CCK-A agonist tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2- methylphenylaminocarbonyl)-Asp-(N-methyl)-Phe-NH2 stimulated pancreatic growth and the development of acidophilic atypical acinar cell foci and nodules. Furthermore, the effect produced by the selective CCK-A agonist tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2- methylphenylaminocarbonyl)-Asp-(N-methyl)-Phe-NH2 was greater than that produced by CCK octapeptide. In contrast, the selective CCK-B agonist [(2R,3S)-beta-MePhe28,N-MeNle31]CCK26-33 had no effect. These findings suggest that the growth of putative preneoplastic lesions (acidophilic atypical acinar cell foci and nodules) in the rat pancreas during the early stages of azaserine-induced pancreatic carcinogenesis is mediated specifically by way of CCK-A receptors.

Animals↗
PubMed1993

Overexpression of messenger RNA for cholecystokinin-A receptor and novel expression of messenger RNA for gastrin (cholecystokinin-B) receptor in azaserine-induced rat pancreatic carcinoma.

Using receptor binding assays, we have previously demonstrated the overexpression of the high-affinity cholecystokinin (CCK) receptor and the novel expression of the gastrin (CCK-B) receptor in the azaserine-induced rat pancreatic carcinoma DSL-6. Since cDNA of both the CCK-A receptor (classical pancreatic CCK receptor) coding region and the CCK-B receptor coding region have recently been cloned and sequenced, we investigated the expression of messenger RNA of these receptors in DSL-6 pancreatic carcinoma. Our results showed that the 32P-labelled cDNA probe of the CCK-A receptor coding region hybridized with an approximately 2.7 kb mRNA from both DSL-6 pancreatic carcinoma and normal rat pancreas. However, the relative expression of the CCK-A receptor mRNA in DSL-6 pancreatic carcinoma was approximately 8-fold of that in normal rat pancreas. The 32P-labelled cDNA probe of the CCK-B receptor coding region hybridized with an approximately 2.7 kb mRNA from DSL-6 pancreatic carcinoma; no hybridizing mRNA could be identified from normal rat pancreas. In summary, the CCK-A receptor mRNA is overexpressed approximately 8-fold and the gastrin (CCK-B) receptor mRNA is novelly expressed in DSL-6 pancreatic carcinoma as compared to normal rat pancreas. These results further confirm our previous findings based on receptor binding assays. The gene overexpression of the CCK-A receptor and the novel gene expression of the gastrin (CCK-B) receptor may be generated by alterations in gene regulation during carcinogenesis, and may play an important role in promoting tumor growth.

Animals↗
PubMed1993

Effect of streptozotocin diabetes on development of nitrosamine-induced pancreatic carcinoma when diabetes induction occurs after nitrosamine exposure.

Diabetes mellitus has been suggested as a possible risk factor for the development of pancreatic cancer in humans. Previous studies in our laboratory have shown, however, that streptozotocin (STZ) diabetes inhibits the development of cancer of the exocrine pancreas in hamsters when STZ is administered prior to treatment with the pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine (BOP). It has been reported by others that the concurrent administration of BOP and STZ enhances pancreatic carcinogenesis in hamsters. The purpose of the present study was to determine the effect of STZ diabetes on the development of BOP-induced pancreatic carcinoma when STZ is given following exposure to BOP. Groups of Syrian golden hamsters were treated with either BOP only (single s.c. injection, 40 mg/kg body wt at week 0), BOP (single s.c. injection, 40 mg/kg body wt at week 0) plus STZ (50 mg/kg body wt x3 daily i.p. doses at weeks 10, 20 or 30), STZ only (50 mg/kg body wt x3 daily i.p. doses at weeks 10, 20 or 30), or neither BOP nor STZ. The experiment was terminated at 40 weeks after BOP treatment. No significant difference was seen in the incidence of pancreatic cancer between those animals receiving BOP only at week 0 and those receiving BOP at week 0 plus STZ at weeks 10, 20 or 30 of the study. The results would appear to indicate that STZ diabetes, established after BOP tumor initiation, plays no apparent role in the modulation of pancreatic carcinogenesis.

Animals↗
PubMed1993

Temporal expression of the gastrin (CCK-B) receptor during azaserine-induced pancreatic carcinogenesis.

Cholecystokinin (CCK-A) and gastrin (CCK-B) receptors have been demonstrated in the azaserine-induced rat pancreatic carcinoma DSL-6. In order to determine at what stage in azaserine-induced pancreatic carcinogenesis gastrin (CCK-B) receptors are first expressed, we examined the binding of [125I]gastrin-I to normal rat pancreas, azaserine-induced premalignant pancreatic nodules, grossly normal internodular pancreas, and DSL-6 carcinoma. We observed that specific gastrin binding was absent in normal pancreas, premalignant nodules, and internodular pancreas, and also reconfirmed our previous report of marked overexpression of gastrin (CCK-B) receptors in the DSL-6 carcinoma. Specific cholecystokinin (CCK) binding was present in all pancreatic tissue types tested. Therefore, we conclude that the presence of gastrin (CCK-B) receptors in the azaserine-induced pancreatic carcinoma DSL-6, in contrast to their absence in premalignant nodules, suggests that the expression of the gastrin (CCK-B) receptor may be important in the transformation from premalignant nodules to pancreatic cancer.

Animals↗
PubMed1993

Induction of diabetes mellitus in Syrian golden hamsters using stored equilibrium solutions of streptozotocin.

Streptozotocin (STZ), a compound composed of a mixture of alpha and beta anomers, is used experimentally for the chemical induction of diabetes mellitus in numerous animal species. It is routinely recommended that STZ be administered rapidly following dissolution because of its alleged instability in solution. In the present study, we examined the effect of varying the length of time from dissolution to administration on the ability of STZ to induce diabetes mellitus in male Syrian golden hamsters and examined STZ stability and state of equilibrium by high-pressure liquid chromatography. Effective diabetes induction was determined by monitoring plasma glucose concentrations 2 and 9 days after STZ treatment. Diabetes was successfully induced with solutions of STZ (50 mg/kg body weight given intraperitoneally on three consecutive days) used either immediately (24 degrees C), 2 hours (24 degrees C), or 5 to 7 days (6 degrees C) after dissolution in 0.1 M acetate buffer at pH 4.4 (storage temperature indicated in parentheses). Mean plasma glucose concentration was significantly higher in all STZ treatment groups at both time points when compared with acetate buffer-treated controls. There was no significant difference in plasma glucose concentration between STZ treatment groups. High-pressure liquid chromatography analysis demonstrated that the alpha- to beta-anomeric ratio of STZ had reached equilibrium in 84 minutes at 24 degrees C and by 26 hours at 6 degrees C following dissolution. Recovery of STZ was greater in solutions stored at 6 degrees C than at room temperature (24 degrees C).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Derivation of ductlike cell lines from a transplantable acinar cell carcinoma of the rat pancreas.

Two cell lines were derived from a transplantable acinar cell carcinoma that had been established from a primary carcinoma of the pancreas in an azaserine-treated Lewis rat. The cultured tumor cells initially produced amylase, but production of exocrine enzymes ceased after 1-2 weeks in culture. The cultured cells were tumorigenic in Lewis rats, and one line produced solid tumors composed of ductlike structures surrounded by dense fibrous tissue. The second cell line produced partially solid and partially cystic tumors with a mixed phenotype of squamous, mucinous, and glandular areas when it grew in vivo following regrafting. Both cell lines lost structural and immunohistochemical acinar cell markers while acquiring duct cell markers during culture and regrafting. These studies provide strong support for the hypothesis that ductlike carcinomas can arise from neoplastic pancreatic acinar cells in rats.

Animals↗
PubMed1992

Novel expression of gastrin (cholecystokinin-B) receptors in azaserine-induced rat pancreatic carcinoma: receptor determination and characterization.

Many reports have emphasized the role of gastrin as a growth factor for normal gastrointestinal mucosa and gastrointestinal cancers. Recent studies have pointed out that this peptide acts also as a growth factor for the pancreatic cancer cell line AR42J. This effect is mediated by gastrin [cholecystokinin (CCK)-B] receptors. In the present study, we investigated gastrin (CCK-B) receptor expression in the azaserine-induced rat pancreatic carcinoma DSL-6, comparing it to normal rat pancreas, and we also characterized CCK receptor subtypes in this tumor. The results showed that there is extensive gastrin binding to the DSL-6 pancreatic carcinoma. No evidence of specific gastrin binding to normal pancreas was found. Analysis of the ability of gastrin-17-I to inhibit 125I-gastrin-I binding demonstrated that gastrin bound to a single class of receptors with a Kd of 0.21 +/- 0.04 nM and a binding capacity of 184 +/- 29 fmol/mg protein. 125I-Gastrin-I binding was inhibited by the specific CCK-B receptor antagonist L365,260 approximately 40 times more effectively than by the specific CCK-A receptor antagonist L364,718. Analysis of the ability of cholecystokinin octapeptide (CCK-8) to inhibit 125I-Bolton-Hunter-CCK-8 binding revealed two CCK binding sites, i.e., a high affinity site and a low affinity site. The observed binding affinities of CCK-8 were then introduced into the computer analysis of the dose-inhibition curve of the ability of gastrin-17-I to inhibit binding of 125I-Bolton-Hunter-CCK-8, which was significantly better fit by a three-site model than by a two-site model. The three sites meet the criteria for CCK-B, high affinity CCK-A, and low affinity CCK-A receptors. The binding capacity of CCK-B receptors constitutes 34% of the total high affinity CCK binding sites. This study demonstrated that DSL-6 pancreatic carcinoma expresses three subtypes of CCK receptors. Gastrin (CCK-B) receptors, which were not detected in normal rat pancreas, constitute about one third of the total high affinity CCK receptors. We suggest that novel expression of gastrin (CCK-B) receptors may be generated by gene mutation or amplification during carcinogenesis and may play an important role in promoting tumor growth.

Animals↗
PubMed1992

Overexpression of cholecystokinin receptors in azaserine-induced neoplasms of the rat pancreas.

Cholecystokinin (CCK) is a growth factor for normal pancreas. Numerous studies also suggest that CCK promotes pancreatic carcinogenesis in the rat. Our previous studies suggested that growth of preneoplastic pancreatic foci was stimulated by CCK more than that of normal pancreas. We hypothesized that such differential growth might be due to increased numbers of CCK receptors in neoplastic tissue. Azaserine-induced pancreatic carcinoma (DSL6) had an increased high-affinity CCK receptor binding capacity of 122 +/- 23 (SD) fmol/mg protein compared to 12 +/- 2 fmol/mg protein in normal pancreas (P less than 0.001). The Kd of the high-affinity site was 0.33 +/- 0.04 nM for carcinoma and 0.46 +/- 0.08 nM for normal pancreas (P less than 0.01). The amount of cholecystokinin octapeptide (CCK-8) bound to high-affinity receptor was 8.6 +/- 1.9 fmol/mg protein for DSL6 compared to 0.6 +/- 0.2 fmol/mg protein in normal pancreas (P less than 0.001). Azaserine-induced premalignant nodules were compared to remaining internodular pancreas. Nodules demonstrated a mean high-affinity CCK receptor binding capacity of 38 +/- 9 fmol/mg protein compared to 6 +/- 3 fmol/mg protein in internodular pancreas (P less than 0.001). The amount of CCK-8 bound to high-affinity receptor was 3.1 +/- 0.8 fmol/mg protein in nodules compared to 0.6 +/- 0.3 fmol/mg protein in internodular pancreas (P less than 0.001). Overexpression of high-affinity CCK-8 receptor in premalignant and malignant azaserine-induced tumors may result in a growth advantage relative to normal pancreas.

Animals↗
PubMed1992

Mechanism of prevention of development of N-nitrosobis(2-oxopropyl)amine induced pancreatic carcinoma by a protein-free diet in hamsters.

It has been shown that feeding a protein-free diet prior to injection of N-nitrosobis(2-oxopropyl)amine (BOP) can inhibit the development of pancreatic carcinoma in the hamster. The purpose of this study was to determine whether this inhibition is due to a direct effect on the pancreas or to a systemic mechanism. Pancreas transplantation was used to create four groups of two-pancreas hamsters (Group 1: protein-containing diet donor/protein-containing diet host; Group 2: protein-containing diet donor/protein-free diet host; Group 3: protein-free diet donor/protein-containing diet host; Group 4: protein-free diet donor/protein-free diet host). Animals were fed either a protein-containing diet or a protein-free diet for four weeks preoperatively. One day after transplantation, the two-pancreas animals received a 40 mg/kg body weight, subcutaneous, single dose of BOP. Animals in all groups were maintained on a regular protein-containing diet postoperatively, and were then sacrificed 42 weeks after BOP injection. The results showed that a) the incidence of carcinoma in groups 2, 3, and 4 was significantly lower than that in group 1; b) there was no significant difference in group 2 between donor and host pancreas; c) the incidence of carcinoma in the donor pancreas was lower than that in the host pancreas in groups 3 and 4. These results confirm that the protein-free diet significantly inhibits the development of BOP induced pancreatic carcinoma in the hamster. The inhibitory effect appears to act both directly on the pancreas and through an indirect systemic mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1991

Anthrax in wildlife in the Luangwa Valley, Zambia.

An abnormally high mortality among hippos (Hippopotamus amphibius) in the Luangwa River valley between June and November 1987 and estimated to number more than 4000 deaths was attributed to anthrax. Several other species, particularly Cape buffalo (Syncerus caffer) and elephant (Loxodonta africana), appear to have been affected. A smaller outbreak of anthrax in hippos occurred between August and September 1988, approximately 100 km up-river. A field study was arranged in August 1989 to assess the extent of environmental contamination by Bacillus anthracis and the risks to people in the area, to study possible methods of control and to equip local laboratory staff for continued monitoring of the disease. The study confirmed the enzootic status of the region. The characteristics of the outbreaks of anthrax in 1987 and 1988, and the results of the field study are described.

Animals↗