[RUPTURE OF THE GALLBLADDER, LESIONS OF THE LIVER, SMALL AND LARGE INTESTINE, IN CLOSED INJURY].
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The effect of exercise on large intestinal function has been determined in 14 healthy but normally sedentary men and women, aged 22-34 yr while on a constant diet. For an initial 3-5-wk period (control) no activity was allowed. Six subjects then undertook a 9-wk training schedule by the end of which they were capable of jogging for 1 h per day, 5 days a week. A further 6 subjects undertook a similar training schedule that lasted for only 7 wk, at the end of which they were jogging for 45 min per day. Finally, 2 subjects were studied continuously while taking light exercise for 6 wk and then jogging for a further 3 wk. Physical fitness was monitored and showed significant changes with maximum aerobic capacity increasing from 2.4 +/- 0.5 to 3.1 +/- 0.4 L/min, maximum heart rate after a step test falling from 152 +/- 8 to 129 +/- 5 beats per minute, and resting pulse rate also falling from 56 +/- 4 to 50 +/- 5 beats per minute. High-density lipoprotein cholesterol also increased significantly. Colonic function was assessed by measurement of stool weight and transit time, using the continuous radiopaque marker technique, fecal pH, nitrogen excretion, and ammonia concentration. No change was observed overall in mean daily fecal weight [124 +/- 39 (control) and 129 +/- 49 g/day (exercise)], transit time [55 +/- 20 (control), 54 +/- 23 h (exercise)], nor in fecal frequency, dry stool weight, pH, ammonia, or total nitrogen excretion. Significant changes did occur in 5 individuals with significant slowing of transit time in 2 and speeding up in 3. Overall transit time increased in 9 subjects and decreased in 5; hence, when diet is constant, exercise has marked effects on physical fitness but no consistent effect on large bowel function.
We studied the distribution of main frequencies of spontaneous activity (in the range of 2-4 cycles/min) of the stomach and large intestine in healthy individuals and patients with stomach and colon cancer before and after gastrectomy and resection or total colectomy. The rhythm was recorded noninvasively (from body surface) with Ag/AgCl electrodes connected to a 3-channel portable electrogastrograph. We determined general peculiarities of rhythm formation in the stomach and large intestine in healthy individuals on an empty stomach and after mixed feeding and evaluated changes in spontaneous activity in patients with stomach and colon cancer before and after gastrectomy, resection, or total colectomy. Rhythmic activity of the stomach was coordinated with that of the large intestine in healthy individuals, but not in patients with tumors before the start of specific therapy. Multichannel cutaneous electrogastroenterography and recording of spontaneous electrical activity in the epigastric and perianal regions reflect functional relationships between the stomach and large intestine.
Study of blood group A- and B-active glycosphingolipid content of the epithelium of the large intestine of 16 strains of inbred rats led to the discovery of two related strains, SHR and WKY, devoid of A-active glycolipids, whereas all strains expressed B-active glycolipids. This finding evidenced a new A/non-A genetic polymorphism in the rat. Blood group A-active glycolipids were isolated from the large intestine of F344 rats and purified by affinity chromatography on immobilized Helix pomatia lectin. Three glycolipid fractions were separated by preparative thin-layer chromatography and characterized by electron-impact mass spectrometry of their permethylated and permethylated-LiAlH4-reduced derivatives. They were identified as a tetraglycosylceramide (A-4), a hexaglycosylceramide (A-6), and a difucosylated heptaglycosylceramide (A-7) with small amounts of monofucosylated octaglycosylceramide (A-8). Methylation analysis and fragmentation indicated that A6 and A-8 had a lacto- and A-7 a neolactotetraosylceramide core, respectively, identical to the core structures of B-6 and B-7 previously characterized in the large intestine of WF rats (Angström et al. (1987) Biochim. Biophys. Acta 926, 79-86). Upon methylation analysis, B-6 and B-7 purified from SHR (A-deficient) and F344 (A-expressing) were found identical to those of WF rats. This result indicated that precursor substrates for the synthesis of A-active glycolipids were available in SHR rats and thus the genetic deficiency of A-active glycolipid expression probably originated in a defect of the termination of the blood group A determinant by the alpha-3-N-acetylgalactosaminyltransferase.
From our experience of malignant lymphoma in the large intestine and reviewing the Japanese literature, it might be concluded that this particular lesion was extremely rare, and was found predominantly in the right side of the colon. In contrast to the other malignant neoplasms in the large intestine, malignant lymphoma was found fairly often in children, which was accompanied by intussusception not infrequently.
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The ability of Escherichia coli to survive stress during growth in different environments is, in large part, dependent on rpoS and the genes that comprise the rpoS regulon. E. coli BJ4 and an isogenic BJ4 rpoS mutant were used to examine the influence of the rpoS gene on E. coli colonization of the streptomycin-treated mouse large intestine. Colonization experiments in which the wild-type E. coli BJ4 and its rpoS mutant were fed individually as well as simultaneously to mice suggested that E. coli BJ4 does not face prolonged periods of nutrient starvation in the mouse large intestine and that the rpoS regulon is not expressed during long-term colonization after adaptation of the bacteria to the gut environment.
NADPH oxidase 1 (Nox1), a homolog of gp91(phox), is dominantly expressed in large intestinal epithelium, and reactive oxygen species derived from Nox1 are suggested to serve a role in host defense. We report that interferon (IFN)-gamma, a crucial transactivator of the gp91(phox) gene, also stimulates expression of Nox1 mRNA and protein in large intestinal epithelium (T84 cells), leading to fourfold upregulation of superoxide anion (O(2)(-)) generation. Introduction of small interfering Nox1 RNA completely blocked this priming. We cloned the region from -4,831 to +195 bp of the human Nox1 gene. To reveal IFN-gamma-responsive cis elements, we performed transient expression assays using a reporter gene driven by serially truncated Nox1 promoters in T84 cells. IFN-gamma-responsive elements were located between -4.3 and -2.6 kb, and one gamma-activated sequence (GAS) element present at -3,818 to -3,810 bp exhibited this IFN-gamma-dependent promoter activity. IFN-gamma caused tyrosine phosphorylation of signal transducer and activator of transcription 1 (STAT1) and produced a protein-GAS complex that was recognized by anti-STAT1 antibody. The introduction of three-point mutation of GAS, which did not interact with STAT1, completely canceled the IFN-gamma-dependent promoter activity of the region from -4,831 to +195 bp. A Janus protein tyrosine kinase 2 inhibitor (AG490) blocked the IFN-gamma-stimulated tyrosine phosphorylation of STAT1, promoter activity of the -4,831 to +195 bp region, Nox1 mRNA expression, and O(2)(-) production, also suggesting a crucial role of STAT1 and GAS in the IFN-gamma-stimulated transcription of the Nox1 gene. Our results support a potential contribution of Nox1 to mucosal host defense and inflammation in the colon.
Escherichia coli F-18, a normal human fecal isolate, is an excellent colonizer of the streptomycin-treated mouse large intestine. E. coli F-18 Col-, a derivative of E. coli F-18 which no longer makes the E. coli F-18 colicin, colonizes the large intestine as well as E. coli F-18 when fed to mice alone but is eliminated when fed together with E. coli F-18. Random sequences of E. coli F-18 DNA were cloned into pRLB2, a par-B-stabilized derivative of pHC79. The entire gene library was transformed into E. coli F-18 Col- and fed to streptomycin-treated mice. The mouse large intestine selected a predominant clone which contained a recombinant plasmid (pRLB7) that enhanced E. coli F-18 Col- colonizing ability 100-fold but did not stimulate colicin synthesis. Moreover, pRLB7 simultaneously improved the survival of E. coli F-18 Col- in stationary phase in vitro, utilizing nutrients derived from mouse cecal mucus, and stimulated synthesis of both type 1 fimbriae and three E. coli F-18 Col- outer membrane proteins (74, 71, and 69 kDa). The 6.5-kb E. coli F-18 DNA sequence in pRLB7 does not contain either the fim operon or pilG (hns), both known to be involved in type 1 fimbrial synthesis. The sequence encodes six proteins, all smaller than the three E. coli F-18 Col- outer membrane proteins whose synthesis it stimulates. Collectively, the results suggest that the cloned E. coli F-18 DNA sequence contains one or more regulators of E. coli F-18 Col- operons expressed in the mouse large intestine in vivo and in isolated mouse cecal mucus in vitro.
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It was found that repeated transplantation of ACATOL strain cells resulted in a loss of their sensitivity to growth-stimulating effect of pentagastrin. The effect of gastrin receptor antagonist proglumide, on ACATOL cells growth was inconstant. ACATOL tumor was sensitive to VIP and glucagon in vitro (as shown by adenylate cyclase activity assay), that makes the model promising for selecting potent hormone drugs against colorectal cancer.
The distribution of Chabertia (Ch.) ovina, Oesophagostomum (O.) venulosum and Trichuris spp. within the large intestine of naturally infected sheep in the dependence of worm counts and the presence of nematodes of other species or genera was evaluated. The large intestine was divided into 4 sections. More than 75% of Ch. ovina were found within the disk-like section of the colon independently from worm count and presence of nematodes of other species. O. venulosum and Trichuris spp. preferred the caecum and the first section of the colon up to the beginning of the disk-like section. In both, the share of worms recovered from the first section of the colon did increase with higher worm counts. The simultaneous presence of O. venulosum and Trichuris spp. had a significantly negative influence on the share of Trichuris spp. isolated from the caecum.
OBJECTIVE: To study the value of point mutant genes in the diagnosis of hepatic metastasis of large intestinal carcinoma. METHODS: Techniques of PCR-SSCP and DNA sequencing were used to detect point mutations of p53 and k-ras genes in primary focus, hepatic metastatic focus, and bile. RESULTS: 50 cases of large intestinal cancer were detected. 38 cases (76.0%) had p53 and k-ras gene mutations. p53 gene mutations were detected in 28 cases (56.0%) and k-ras gene mutations in 16 cases (32.0%). The same point mutant genes in bile with primary focus were detected in 10 out of 12 patients with hepatic metastasis (83.3%). CONCLUSIONS: The tumor cells of hepatic metastasis show the same clonal origin with primary focal cells that had same point mutant genes. Detection of the point mutant genes in bile is of value in the diagnosis of hepatic metastasis of large intestinal carcinoma.
The effects of intestinal resection on several intestinal parameters have been studied in the large intestine of rats one month after the surgical operation. The results show that both 50% and 80% distal small bowel resection increased net fluid absorption and mucosal permeability and caused expansion of the intercellular spaces of the large intestine. The increase in net fluid absorption was dependent upon the extent of the intestine removed. The cAMP and cGMP content of cecal and colonic mucosa were significantly reduced after jejunoilectomy. Changes in nucleotide levels were dependent on the length of the intestine resected. On the other hand, mucosa Na,K-ATPase specific activity was only increased in the cecum after 80% intestinal resection. The results are discussed in terms of adaptation to prevent diarrhea.
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