Disease relevance of Cecum

• METHODS: Ileus was induced by abdominal surgery (laparotomy and cecum palpation) or peritonitis (acetic acid, intraperitoneally) [1].
• Lb. plantarum + arginine administration significantly reduced the level of the released liver enzymes, hepatocellular necrosis and inflammatory cell infiltration, bacterial translocation, and the number of Enterobacteriaceae in the cecum and colon [2].
• In contrast, the time required for a lactulose load to reach the cecum was significantly greater in the patients with hepatic encephalopathy (p < 0.01) and increased as a function of the hepatic encephalopathy grade.(ABSTRACT TRUNCATED AT 250 WORDS)[3]
• (On the other hand, the expression of EG-VEGF mRNA was not detected in colorectal normal mucosae.) Stable EG-VEGF infectors of colorectal cancer cell line SW620 were produced, EG-VEGF transfectants were implanted into cecum and s.c., and cell proliferation was evaluated [4].
• IL-10-deficient mice kept in SPF conditions developed colitis in all segments of the colon (cecum and proximal and distal colon) [5].

High impact information on Cecum

• These results show that Casp-1, which is both proapoptotic and proinflammatory, is essential for S. typhimurium to efficiently colonize the cecum and PP and subsequently cause systemic typhoid-like disease in mice [6].
• In vitro under short-circuit conditions, cecum actively absorbed Na and Cl (JnetNa = 5.6 +/- 0.3, JnetCl = 1.5 +/- 0.3 mu eq.cm-2.h-1) with a short-circuit current (Isc) of 6.29 +/- 0.2 mu eq.cm-2.h-1.Cl substitution with sulfate decreased both JnetNa and Isc by 1.3 mu eq/cm2.h-1.HCO3 removal decreased both JnetNa and Isc 3.3 mu eq.cm-2.h-1 [7].
• Thus, cecum exhibits a distinct type of electrogenic Na electrogenic Na absorption which is partially dependent on the presence of Cl and HCO3, not blocked by amiloride but by phenamil [7].
• The cecum is exteriorized through a midline incision, and 1.5 X 10(5) MCA-38 liver-derived (LD) tumor cells in 0.1 ml was injected into the ileocolic vein (ICV) [8].
• In the cecum, areas under the concentration curves decreased from day 1 to day 8 for lactulose, galactose, and fructose (P less than 0.01), while an increase was found for lactic acid (P less than 0.001), acetic acid (P less than 0.0001), and total VFA (P less than 0.001) [9].

Chemical compound and disease context of Cecum

• Expression of Ostalpha-Ostbeta mRNA was increased in cecum and proximal colon of cholic acid-fed mice and in chenodeoxycholate-treated mouse CT26 colon adenocarcinoma cells [10].
• Chlorpromazine, administered at a dose of 30 mg/kg/day, IP for 7 days, produced marked pathologic changes in the guinea pig cecum, consisting of inflammation, edema and hemorrhage [11].
• Rabbits were then killed, and colonization of jejunum and ileum by anaerobic bacteria and luminal colonization of jejunum, ileum, and cecum by RDEC-1 was quantitated [12].
• In the laparoscopic-assisted resection group, under CO2 pneumoperitoneum (4-6 mmHg), the cecum was identified, dissected free, and exteriorized through a 4 mm port [13].
• All of the effective mice (17) which were given 0.2% chrysazin diet and which survived more than 500 days developed adenomatous hyperplasia with cystic glands of the cecum [14].

Biological context of Cecum

• Analysis of the phenotypes revealed that the soluble IGF2R affects the size of some organs (colon and cecum) exclusively by reducing the biological activity of IGF-II, whereas in other organs (stomach and skin) the biological activity of the receptor is at least in part independent of IGF-II and must involve an interaction with other factor(s) [15].
• Gastric emptying of 99mTc and mouth to cecum transit time, as measured by the breath hydrogen technique, after a mixed meal containing lactulose and 99mTc-diethylenetriaminepentaacetate, were assessed once before, twice during, and once after the period of study medication [16].
• In addition, choleragen increased cecal mucosal content of adenosine 3':5'-cyclic phosphate but did not alter the histology of the cecum [17].
• Quantitative measurements of apoptosis, Bax and Bcl-xL protein expression in the ApcMin mice revealed the ratio of Bax/Bcl-xL expression and apoptosis increased in the small intestine but decreased in the cecum, consistent with the regional tumorigenesis observed after sulindac [18].
• The aim of the study was to evaluate the influence of oligofructose on putrescine, spermidine and spermine concentrations in the cecum, the portal vein and the liver of rats and to assess their involvement in cecal enlargement and the modulation of hepatic lipid metabolism [19].

Anatomical context of Cecum

• Less than 20% of 14C instilled into the cecum as glucose was recovered in feces and only about 15% of this fecal 14C was in a dialyzable form [20].
• On the fourth day, the cecum was intubated and a suspension of raw wheat starch (50 g, in 500 ml of 154 mM NaCl and containing 10 g of polyethylene glycol 4000) was infused into the distal ileum at 2 ml/min [21].
• Salicylazosulfapyridine transit times from duodenum to cecum were also very similar to simultaneous measurements of transit by scintigraphic monitoring of technetium 99m [22].
• Neural stimulation caused chloride secretion in cecum, reduced chloride absorption in sigmoid colon, but caused no change in transverse colon; sodium absorption decreased in cecum [23].
• CONCLUSIONS: The results show a direct contractile effect of ETs on circular smooth muscle of guinea pig cecum and the presence of both ETA- and ETB-receptor subtypes [24].

Associations of Cecum with chemical compounds

• The fate of glucose in the colon of rats and man was investigated by measuring breath 14CO2 and fecal 14C after direct instillation of 14C-labeled glucose, acetate, and lactate into the cecum [20].
• DSS produced water, sodium and chloride secretion into the in vivo rat cecum [25].
• After direct instillation of SASP and lactulose into the cecum, the appearances of their metabolites (sulfapyridine in plasma and hydrogen in breath) were rapid (1-10 min) and simultaneous [22].
• The mucosal concentration of acetaldehyde was significantly higher in the rectum compared with the cecum (198 +/- 23 vs. 120 +/- 23 nmoles.g colon-1, p less than 0.05), but was not affected by chronic ethanol feeding [26].
• A similar increment of serum bilirubin levels was observed after injection of bilirubin into the cecum of Wistar rats [27].

Gene context of Cecum

• Fgf9 null (Fgf9(-/-)) mouse embryos have agenesis of the embryonic cecum, lacking both mesenchymal expansion and an epithelial bud [28].
• From E11.5 onwards, Fgf10 expression is found throughout the cecum mesenchyme [29].
• IL-10-deficient mice with active colitis exhibited a four- to fivefold greater expression of MAdCAM-1 in the cecum and colon compared with their healthy controls or to IL-10 k/o mice with no evidence of colitis [30].
• COX-1 mRNA was constitutively expressed in the intact cecum, and its expression level was not altered after the mechanical stimulus [31].
• In conclusion, COX-2, but not COX-1, plays a significant role in mechanical stimulus-induced peritoneal formation in the mouse cecum [31].

Analytical, diagnostic and therapeutic context of Cecum

• In both the bile duct ligation model and the cecum ligation and puncture model, mRNA expression levels of rlst-1 were down-regulated [32].
• The appearance of sulfapyridine in plasma after oral administration of salicylazosulfapyridine (SASP) was evaluated as a method for defining arrival time in the cecum, an index of small bowel transit [22].
• Surgical procedures to improve cecal stool flow (cecostomy, ileocecostomy) elicited a significant decrease in constitutive ICAM-1 expression in both cecum and distal colon [33].
• P. aeruginosa or the combination of PA-I and exotoxin A was lethal to mice when injected into the cecum after partial hepatectomy [34].
• At 7 days after infection the proximal jejunum, distal ileum, cecum, and proximal colon were removed from each rabbit and examined for the presence of adherent organisms under light microscopy, after Giemsa staining of Formalin-fixed secretions, and by transmission electron microscopy [35].

References