Search PubMed⌕ Search

Biomedical subjects

T Bamba

Publications and source records attributed to T Bamba.

At least 127 records · Page 7Linked to original sources
PubMed1996

Effectiveness of combined anticoagulant therapy for extending portal vein thrombosis in Crohn's disease. Report of a case.

PURPOSE: Portal vein thrombosis is a rare complication of Crohn's disease, and its precise cause and appropriate treatment are not known. We describe a patient with extending portal vein thrombosis in Crohn's disease who was successfully treated with combined anticoagulant therapy. METHOD: Urokinase and tissue plasminogen activator were administered from a catheter inserted into the superior mesenteric artery, and heparin and a serine protease inhibitor also were given intravenously. RESULTS: On admission, thromboembolic occlusion was observed throughout the entire portal venous system in association with massive ascites and remarkable intestinal edema. After administration of combined anticoagulant therapy, thrombus rapidly decreased in size, and color Doppler ultrasonography showed a gradual increase in portal venous flow. The patient had no recurrence of symptoms while receiving warfarin after resolution of thrombus. CONCLUSION: This case report suggests that combined anticoagulant therapy is effective for patients with severe portal vein thrombosis in Crohn's disease and that color Doppler ultrasonography is useful for evaluation of portal venous flow.

Adult↗
PubMed1996

Regulation of complement C3 synthesis by interleukin-1 and transforming growth factor-beta in rat non-transformed intestinal epithelial cell line, IEC-6.

Intestinal epithelial cells are an important source of many biologically active molecules that modulate immune responses in the mucosa. The purpose of this study was to demonstrate the synthesis of complement C3 component in the rat non-transformed crypt-like intestinal epithelial cell line, IEC-6. Unstimulated IEC-6 cells secreted a low level of C3 protein and showed weak expression of C3 mRNA. The addition of interleukin (IL)-1 beta induced a dose- and time-dependent increase in C3 production. These effects of IL-1 beta were observed at a concentration as low as 0.01 ng/ml and reached a plateau at a concentration of 5 ng/ml. The effects were observed at the mRNA level as early as 6 h after the beginning of incubation. Transforming growth factor (TGF)-beta alone had no effect. However, TGF-beta at low concentrations (0.001-1 ng/ml) enhanced the effect of IL-1 beta in increasing C3 production; this enhancement was not observed at high concentrations (5-10 ng/ml). These effects of TGF-beta were also observed at the mRNA level. The present findings indicate that intestinal epithelial cells are indeed capable of synthesizing complement C3 in response to IL-1 beta and TGF-beta.

Animals↗
PubMed1996

Altered polyamine biosynthesis with aging after massive proximal small bowel resection in rat.

We examined the effect of aging on polyamine biosynthesis in the small intestine. Two groups of male Wistar rats (young; 10-week-old, n = 40; old; 24-month-old, n = 40) underwent either a jejunal transection and reanastomosis or 90% proximal small bowel resection. The rats were sacrificed on the 1st, 2nd, 4th, and 7th postoperative day (POD). The mucosa was submitted for histological examination, weighed, and assayed for protein, DNA, RNA, and polyamine content. Ornithine decarboxylase (ODC) activity was measured and ODC mRNA in the mucosa was determined by Northern blot analysis. Compared with the values for wet weight and protein content in old rats, young rats showed significantly higher values for wet weight on the 1st and 2nd POD, and for protein content on the 1st POD, but there were no differences between young and old rats after the 4th POD. The values for ODC activity and ODC mRNA were significantly lower in old rats than in young rats on the 1st POD, but there were no differences between young and old rats after the 2nd POD. The value for putrescine in old rats was significantly lower on the 2nd POD, but was significantly higher on the 4th POD than that in young rats. The present study showed that, in old rats, the residual intestine after small bowel resection preserved sufficient adaptive capacity, but that the adaptive response was decreased. The findings in this study also suggest that a decrease in ODC mRNA expression is involved in the decreased adaptive response that occurs with aging.

Adaptation, Physiological↗
PubMed1996

Morphological identification of and collagen synthesis by periacinar fibroblastoid cells cultured from isolated rat pancreatic acini.

Rat pancreatic periacinar fibroblastoid cells (PFCs) appear to be involved in intralobular fibrosis and acinar cell regeneration. We isolated pancreatic acini of the rat, cultured the fibroblastoid cells, and characterized the cells morphologically and immunohistochemically. Isolated acini were seeded on culture dishes, and spindle-shaped cells migrated and proliferated. On Electronmicroscopic examination, microfilament bundles were seen, and the intracellular localization of vimentin, alpha-smooth muscle actin, and non-muscle myosin was identified immunohistochemically. These findings strongly suggest that the cells were myofibroblast-like. The PFCs were also demonstrated, immunohistochemically, to contain prolyl hydroxylase, type-I procollagen, type-III procollagen, type-IV collagen, fibronectin, and laminin. Stimulation by transforming growth factor beta 1 (TGF beta 1) increased intracellular immunoreactive prolyl hydroxylase and collagen synthesis in the PFCs. These findings indicate that PFCs proliferate in culture as myofibroblast-like cells and synthesize extracellular matrix components. It is possible that PFCs are involved in intralobular fibrosis in response to stimulation with TGF beta 1.

Animals↗
PubMed1996

Ulcerative colitis complicated by gastroduodenal lesions.

A case of ulcerative colitis complicated with gastric and duodenal lesions is reported. The patient was a 17-year-old male who was admitted with bloody diarrhea and abdominal pain. Based on the endoscopic and histological findings of the colon, a diagnosis of ulcerative colitis was made. Upper gastrointestinal endoscopy showed multiple erosions and granular changes in the antral greater curvature of the stomach and descending portion of the duodenum. Histological examination of the stomach and duodenum revealed marked inflammatory cell infiltration and crypt abscesses. Clinically, the gastric and duodenal lesions did not respond to antiulcer drugs, but were alleviated by steroid. It was concluded that the pathogenesis of the gastric and duodenal lesions in this patient was similar to that of the colonic lesions of ulcerative colitis.

Adolescent↗
PubMed1996

Interleukin 4 acts as an inducer of decay-accelerating factor gene expression in human intestinal epithelial cells.

BACKGROUND & AIMS: Decay-accelerating factor (DAF) protects host tissues from the attack of autologous complement activation. In this study, we attempted to define the cytokine regulation of DAF messenger RNA (mRNA) expression in human intestinal epithelial cells. METHODS: The effects of cytokines on DAF mRNA accumulation were evaluated by Northern blot analysis. The DAF protein expression was analyzed by both immunoprecipitation and immunoblotting. RESULTS: Interleukin (IL)-4 induced a marked increase in DAF mRNA accumulation in HT-29 cells. In this line, IL-1 beta evoked only weak induction, and IL-6, IL-8, IL-10, and interferon gamma had no effect. The effect of IL-4 was observed in a dose-dependent manner and confirmed at the protein level. The increase in DAF mRNA accumulation reached a maximum at 3-6 hours and then gradually decreased. These effects of IL-4 on DAF mRNA and protein expression were also observed in T84 cells. The mRNA stability studies suggested that IL-4 regulates DAF gene expression mainly at the transcriptional level. CONCLUSIONS: In human intestinal epithelial cells, IL-4 acts as a potent inducer of DAF mRNA expression, suggesting a cytoprotective role for IL-4 against autologous complement activation.

CD55 Antigens↗
PubMed1996

Local secretion of complement C3 in the exocrine pancreas: ductal epithelial cells as a possible biosynthetic site.

BACKGROUND & AIMS: The complement system participates in the local immune system in various tissues. In this study, we investigated the local secretion of complement C3 into the pancreatic fluid and attempted to determine a possible biosynthetic site. METHODS: C3 protein in human pancreatic fluid was analyzed by, immunoblotting. The C3 messenger RNA (mRNA) expression in several pancreatic carcinoma cell lines was analyzed by the polymerase chain reaction and/or Northern blotting. The secretion of C3 by these pancreatic carcinoma cells was assessed by metabolic labeling and immunoprecipitation experiments. RESULTS: In five samples of human pancreatic fluid, C3 was detected as a molecule composed of alpha and beta chains. C3 mRNA expression was observed in the ductal cell carcinoma lines (PANC-1 and MIA PaCa-2) but not in the acinar cell line (HPC-YO and AR-42J). C3 production in these cells was enhanced by interleukin 1 beta and tumor necrosis factor alpha at both the protein and the mRNA levels. CONCLUSIONS: (1) Complement C3 is secreted into the exocrine fluids of the pancreas. (2) Ductal epithelial cells are possible biosynthetic sites for C3. (3) The proinflammatory cytokines, interleukin 1 beta and tumor necrosis factor alpha are effective stimulators of local C3 production in the pancreas.

Adult↗
PubMed1996

Increase in mucosal and connective tissue-type mast cells in the stomach with acetic acid-induced ulcer in rat.

Gastric ulcers were induced in rats by acetic acid treatment, and the mast cell kinetics in the lesions were studied. Within 24 h, mast cells had disappeared from the treated site and from the marginal zone, corresponding to the area of severe tissue injury. Regenerating epithelium appeared at day 10, and the lesion had healed by day 30. In this healing process, the number of mast cells was significantly increased, and their density in the regenerating mucosa, marginal mucosa, and marginal muscularis propria was 3.2 1.8, and 7.5-fold the control level, respectively. The increase in the number of mast cells was preceded by an increase in the percentage of S-phase mast cells. Mast cells in the mucosa were Alcian blue (AB)+/safranin (S)- and rat mast cell protease (RMCP) I-/II+, consistent with the features of mucosal mast cells throughout the observation period. On the other hand, most mast cells in the muscularis propria exhibited AB+/S+ and RMCP I+/II+ in the early period of ulcer healing. The latter feature was changed to RMCP I+/II- on day 30, indicating that immature CTMC appeared and then developed into mature CTMC during the ulcer healing. The significant change in the number of mast cells suggests that mast cells play an important role in the development and healing of gastric ulcers.

Acetates↗
PubMed1996

[Basic and clinical studies of pazufloxacin on infectious enteritis research group of T-3761 on infectious enteritis].

A clinical study was carried out on pazufloxacin (PZFX) in 137 patients including shigellosis, Salmonella enteritis, enteropathogenic Esherichia coli enteritis and cholera, and carriers of these pathogens. Antibacterial activity of PZFX against clinical isolates, fecal concentration of PZFX and effects of PZFX on fecal microflora were also investigated. The overall clinical efficacy rate was 97.2%. The bacteriological efficacy rates were 98.2% against Shigella spp., 81.8% against Salmonella spp., 50% against Vibrio cholerae O1, and 100% against E. coli, V. parahaemolyticus, Aeronomas spp., Plesionomas shigelloides and V. cholerae non-O1, respectively. Side effect (epigastralgia) was observed in 1 of 130 cases (0.8%). The rate of abnormal laboratory findings was 11.2% (11/98). These were mainly elevation of GOT and/or GPT and increased eosinophils. The clinical usefulness rate was 95.2%. The MIC90 values of PZFX against Shigella spp., Salmonella spp. and E. coli were 0.025, 0.025 and 0.025 micrograms/ml, respectively. The results of fecal drug concentration and the effects on fecal microflora in one patient were compatible with those obtained in healthy volunteers.

4-Quinolones↗
PubMed1996

[Biological properties of the colony-promoting activity in extracts prepared from murine kidney].

Aqueous extracts prepared from the murine kidney (MKE) promoted colony formation derived from murine hematopoietic progenitor cells in serum-free cultures stimulated by interleukin-3 (IL-3) and erythropoietin (Epo). MKE itself did not stimulate any colony formation. MKE preferentially enhanced granulocyte-macrophage colony forming units (CFU-GM), but did not promote any erythroid colony formation. The CFU-GM colony promotion by MKE was observed at day 6 after the culture started, and the colony-promoting activity (CPA) was maintained at the same level until day 16. MKE showed no CPA in the cultures using cells obtained from 5-FU-injected mice and from c-kit(+)-enriched treatment. Furthermore, MKE acted synergistically with granulocyte-colony-stimulating factor (CSF), macrophage-CSF, IL-6 and IL-11 on colony formation, but did not act with GM-CSF, stem cell factor and Epo. From the results of various experiments and gel-filtration chromatography, it is estimated that the colony-promoting factor detected in MKE is a heat stable protein with about 20 KDa molecular weight. These results suggest that MKE promotes colony formation by murine myeloid progenitor cells, and that the target cell populations of MKE are relatively mature in the hematopoietic differentiation pathway.

Animals↗
PubMed1996

Severe anemia in a patient with isolated adrenocorticotropin deficiency.

A 64-year-old man was referred to our hospital for evaluation of progressive anemia. On admission, he had a severe normocytic normochromic anemia [hemoglobin 7.5 g/dl] requiring a blood transfusion. Endocrinological studies demonstrated an isolated ACTH deficiency. After receiving glucocorticoid replacement therapy, his anemia was rapidly corrected, his hematocrit and hemoglobin remained elevated for approximately 4 months. We present evidence that glucocorticoid plays an important role in the physiological regulation of human erythropoiesis.

Adrenocorticotropic Hormone↗
PubMed1996

[Malabsorption syndrome due to membrane transporter abnormality in absorptive epithelial cells].

Pathogenesis, clinical features and diagnosis of malabsorption syndrome caused by membrane transporter abnormality of absorptive epithelial cells, such as glucose-galactose malabsorption or inherited amino acid transporter abnormality, are reviewed in this paper. It is rare for us to examine the patients with these diseases, but they are important for study of mechanisms of membrane digestion and membrane transporter in absorptive epithelial cells. Recent advances in molecular biology or genetics have made us details for the etiology of these diseases and may result in the development for new therapy.

Carbohydrates↗
PubMed1995

Effects of serine protease inhibitors on accumulation of polymorphonuclear leukocytes in the lung induced by acute pancreatitis in rats.

The administration of a high-dose of a serine protease inhibitor is recommended in patients complicated by multiple organ failure (MOF), including adult respiratory distress syndrome (ARDS), induced by acute pancreatitis. The accumulation of polymorphonuclear leukocytes (PMN) in affected organs is considered to be one of the causative factors of MOF. Adhesion to endothelial cells (EC), via adhesion molecules, and the transendothelial migration of PMN is closely associated with the accumulation of PMN. We examined the effects of two serine protease inhibitors, ulinastatin (UT) and gabexate mesilate (GM), on EC-PMN adhesion and transendothelial migration in human umbilical vein EC and 51Cr-labeled PMN in vitro. EC-PMN adhesion, and the expression of intercellular adhesion molecule-1 (ICAM-1) and endothelial cell adhesion molecule-1 (ELAM-1) on EC induced by IL-1 beta and TNF alpha, were reduced by the pretreatment of EC with these inhibitors. The transendothelial migration of PMN stimulated by IL-8 was also inhibited by pretreating PMN with UT or GM. We also examined whether these inhibitors reduced PMN accumulation in the lung in rats with acute pancreatitis induced by a closed duodenal loop. The myeloperoxidase activity in and histological findings of the lung suggested that UT and GM reduced PMN accumulation. In conclusion, serine protease inhibitors may inhibit PMN accumulation in ARDS due to acute pancreatitis.

Acute Disease↗
PubMed1995

Effects of short-term administration of the CCK receptor antagonist, KSG-504, on regeneration of pancreatic acinar cells in acute pancreatitis in rats.

Cholecystokinin (CCK) receptor antagonists have been reported on have an inhibitory effect on acute experimental pancreatitis, but their long-term administration is also reported to block pancreatic regeneration. We examined whether the short-term administration of KSG-504 (KSG), a synthetic CCK-A receptor antagonist, inhibited the regeneration of pancreatic acinar cells after ethionine-induced acute pancreatitis in rats. KSG (50 mg/kg), given 12 times by subcutaneous injection at 6-h intervals, prevented the reduction of protein, amylase, and trypsinogen levels, and the DNA content of the pancreas and facilitated the recovery of these values. Ornithine decarboxylase activity in pancreatic tissue and a 5-bromo-2'-deoxyuridine labeling study indicated that DNA synthesis was accelerated in rats treated with KSG. These findings suggest that the short-term administration of KSG inhibits the development of ethionine-induced acute pancreatitis and facilitates the regeneration of acinar cells.

Acute Disease↗
PubMed1995

Band 4.2 Shiga: 317 CGC-->TGC in compound heterozygotes with 142 GCT-->ACT results in band 4.2 deficiency and microspherocytosis.

A novel compound heterozygous mutation of 317 CGC-->TGC with 142 GCT-->ACT in human red cell band 4.2 deficiency is described. A proband and his son suffered from compensated haemolysis with nearly complete deficiency of red cell band 4.2. Their red cell morphology exhibited microspherocytosis resembling classic hereditary spherocytosis (HS). Sodium dodecylsulphate-polyacrylamide gel electrophoresis (SDS-PAGE) showed band 4.2 to be nearly missing (< 1% of normal controls) with the presence of 74 kD and 72 kD isoforms in trace amounts. Other family members (daughters older and younger than the son) exhibited nearly normal amounts of 72kD as a wild form of band 4.2 on SDS-PAGE with the presence of the 74kD isoform in a trace amount. The proband and his son demonstrated two compound heterozygous mutations in trans: i.e. nucleotide (nt) 949 CGC-->TGC (codon 317 Arg-->Cys) in exon 7 and nt 424 GCT--ACT (codon 142 Ala-->Thr) in exon 3 of the band 4.2 gene. The two daughters demonstrated only the mutation of nt 949 CGC-->TGC in exon 7 in heterozygous states, but no 142 mutation. Therefore the proband and his son were compound heterozygotes of these two mutations in trans. It is interesting to note that the 74 kD isoform of band 4.2 protein existed in a trace amount in the two daughters in spite of the absence of the 142 Ala-->Thr mutation. In addition, even in the presence of the 142 mutation in one allele in the proband and his son, their red cell morphology demonstrated classic HS with microspherocytosis, although a homozygous state of the 142 mutation known as the Nippon type of band 4.2 deficiency exhibits ovalostomatocytosis.

Aged↗