摘要:

AbstractIn order to investigate the pathogenesis of acute gastric mucosal lesion after thermal injury, microcirculatory disturbance was assessed and observation of the behaviour of leucocytes was performed. Gastric blood flow decreased at 15 min post‐thermal injury, and partially improved at 2 h; however, it decreased again at 5 h post‐thermal injury. Mucosal microcirculatory disturbance was observed by using vascular labelling with monastral blue B. Deposits of monastral blue B were observed centring mainly on collecting venules but were also observed in the capillaries. Submucosal microcirculatory disturbance was observed through an intravital microscope. The irregularity of the wall and segmental constriction in the venules and presence of an arteriovenous shunting channel was observed in the submucosal layer at 5 h post‐thermal injury. The percentage of rolling or sticking leucocytes that passed the confluence of a prevenule and a venule were significantly increased at 5 h after thermal injury. The present study revealed depression of gastric blood flow, mucosal and submucosal microcirculatory disturbance, and a significant increase of rolling and sticking leucocytes in the peripheral part of venules after thermal injury. Leucocyte‐endothelial interactions may occur under such conditions and this interaction may play an important role in inducing the microcirculatory disturbance that results in an acute gastric mucosal lesion after thermal injury. The present study also demonstrated the possibility of intravital study of gastric submucosal arteriovenous shunting c

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1995.tb01585.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractTo evaluate the pathophysiology underlying gastric mucosal lesions induced by lateral hypothalamic (LH) lesions, we investigated the changes in acid secretion, gastric mucosal blood flow, gastric mucus and mucosal integrity in the corpus during the 4 h period and 48 h after the production of bilateral electrolytic LH lesions in male Sprague‐Dawley rats. Gastric mucosal lesions were macroscopically produced 24 h (63%) and 48 h (83%) after LH lesions, although there were no visible lesions at 7 h. Gastric acid secretion was significantly increased 48 h after LH lesions, compared with that in the control group. Gastric mucosal blood flow and transmucosal potential difference (PD) in the LH lesion group immediately decreased after LH lesions and did not recover during 4 h and at 48 h. On the contrary, in the control group, gastric mucosal blood flow decreased after the brain surgery but soon recovered, and there was no significant change in PD. LH lesions resulted in the reduction of intramucosal mucus to 50% 3 h after LH lesions. Moreover, we exposed the stomach to 10 mmol/L taurocholic acid (TCA) 3 h after LH lesions to examine the disruption in gastric mucosal defensive function in rats with LH lesions. The recovery of the reduced PD by TCA was slow and gastric mucosal lesions were easily formed in the LH lesion group. These results suggest that gastric mucosal ischaemia after lesioning of LH immediately results in the disruption of mucosal defensive function before the formation of visible gastric lesions, and predisposes to the formation of gastric mucosal lesions by a delayed increase in acid secretio

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1995.tb01586.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractRoxatidine acetate, a new H2receptor antagonist, was compared with ranitidine in the treatment of duodenal ulcers in a double‐blind multicentre study. Eighty‐four patients with endoscopically proven duodenal ulcer were randomized to receive 150 mg roxatidine acetate or 300 mg ranitidine at bedtime. Repeat endoscopy was performed after 4 weeks (25–33 days) and if the ulcer had not healed, another endoscopy was performed after a further 4 weeks of treatment. Using per protocol analysis 73.6% of ulcers treated with roxatidine healed at 4 weeks compared to 72.2% of ulcers treated with ranitidine (P=NS). The healing rates at 8 weeks were 92% with roxatidine and 83.3% with ranitidine (P=NS). Using equivalence tests, the healing rate of roxatidine was found to be equivalent to that of ranitidine within a 20% region. Roxatidine users took significantly less antacids than ranitidine users (P<0.05). There were no significant adverse effects due to roxatidine or ranitidine. Roxatidine is a safe effective drug in the treatment of duodenal ulcers with a healing rate comparable to that of ranit

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1995.tb01587.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractThe absorption of lithocholate and its sulfate and glucuronide in rat jejunum and terminal ileum was studied. Tracer amounts of radiolabelled bile acids were administered to the ligated intestinal segments, and their absorption was monitored by biliary excretion through a bile duct catheter. Absorption of lithocholate was faster in the terminal ileum than in the jejunum. Although the sulfation reduced lithocholate absorption in the jejunum, it did not affect lithocholate absorption in the terminal ileum. This was due to the Na+‐dependency of ileal absorption of lithocholate‐sulfate assessed by perfusion studies. In contrast, the glucuronidation markedly reduced lithocholate absorption both in the jejunum and the terminal ileum. These findings indicate that the glucuronidation is more effective than sulfation in detoxifying lithocholate as far as the prevention of its intestinal absorption is concer

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1995.tb01588.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractAlterations in phenotype and function of intestinal macrophages occur in inflammatory bowel disease (IBD) but it is unclear whether these changes result from the recruitment of circulating monocytes to the intestine or from proliferation of resident intestinal macrophages. We sought to demonstrate the arrival of blood monocytes, the precursors of macrophages, in IBD mucosa. Peripheral blood mononuclear cells were isolated from 23 patients with clinically active intestinal inflammation (13 Crohn's disease, eight ulcerative colitis, two infective colitis), then radiolabelled with99mtechnetium (Tc)‐stannous colloid (n=13) or111indium (In)‐oxine (n=10) before re‐injection and abdominal scanning. Four patients had demonstrable intestinal monocyte uptake using [99mTc]‐stannous colloid, while six [111In]‐oxine‐labelled monocyte scans were positive. Uptake sites correlated with actively inflamed regions. Patients demonstrating monocyte uptake had been treated with corticosteroids for a significantly (P<0.02) shorter duration (median 3vs20 days) than those with negative scans. There was no significant difference between positive and negative scans for disease category, clinical or histological disease activity, or radioisotope used. Biopsies of inflamed mucosa from two patients suffering ulcerative colitis who had positive scans showed a high proportion of CD14‐positive macrophages, 4–9% of which contained autoradiographic grains. These results demonstrate that blood monocytes are recruited to the mucosa of actively inflamed bowel, and suggest that this process may be inhibited by corticosteroids. Moreover, the phenotype of the recently‐arrived monocytes indicates their susceptibility to stimulation by lipopolysaccharide, and suggests a mechanism for the continuing inflammation in the bacterial product

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1995.tb01589.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractpS2 is a 60 amino acid secretory polypeptide which belongs to a newly described family of trefoil‐shaped growth factors. It is widely distributed throughout the gastrointestinal tract, particularly adjacent to damaged mucosa, and is also expressed by some epithelial tumours such as breast carcinoma. The aim of this study was to examine the expression of pS2 in pancreatic cancer. The presence of pS2 was analysed immunohistochemically using two antibodies, a polyclonal (pNR‐2) and a monoclonal (pS2TM) in 42 cases of pancreatic adenocarcinoma and 10 cases of ampullary carcinoma. The findings were compared with chronic pancreatitis and normal pancreas.No immunostaining was seen in normal pancreas, with the exception of one area of ductular proliferation, and although 8/10 cases of chronic pancreatitis expressed pS2, it was focal and confined to the occasional duct. In contrast, a significant proportion of malignant cells in 23/42 (55%) of pancreatic adenocarcinoma and 8/10 (80%) of ampullary tumours expressed immunoreactive pS2.The finding of pS2 expression in more than 50% of pancreatic and ampullary carcinomas in contrast to the findings seen in chronic pancreatitis and normal pancreas suggests that pS2 may play an important role in the growth of these highly malignant tumo

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1995.tb01590.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractTo investigate the effect of the location of the ulcer crater on the serum levels of pepsinogen I (PGI), pepsinogen II (PGII) and the ratio of PGI/PGII, these parameters were determined in 161 healthy controls, 29 patients with gastric ulcer in the gastric body (GU‐I), 65 with coexistent gastroduodenal ulcer (GU‐II), 104 with gastric ulcer in the prepyloric region (GU‐III), and 116 with duodenal ulcer (DU). Serum PGI levels were significantly higher (P<0.01) in patients with GU‐III (110.6 ± 65.1 ng/mL), GU‐II (100.0 ± 46.6 ng/mL), and DU (92.2 ± 35.2 ng/mL) than in the controls (77.4 ± 31.4 ng/mL), while there were no significant differencs between GU‐I (82.5 ± 36.3 ng/mL) and the controls. Patients with gastric ulcer in any region had significantly higher (P<0.01) serum PGII levels (GU‐I, 20.0 ± 15.7 ng/mL; GU‐II, 15.5 ± 10.9 ng/mL; GU‐III, 14.3 ± 10.0 ng/mL) than the controls (10.6 ± 6.0 ng/mL) and the patients with DU (10.0 ± 5.5 ng/mL), whereas no significant differences existed between the latter two. The ratio of PGI/PGII in GU‐I (5.86 ± 3.90) was significantly lower (P<0.01) than any other group (controls, 8.83 ± 4.70; GU‐II, 8.33 ± 4.99; GU‐III; 9.64 ± 6.13; DU, 10.45 ± 4.49), while patients with DU it was significantly higher (P<0.01) than any other groups. These findings indicate that peptic ulcer is comprised of a heterogeneous group of diseases. A normal level of serum PGI, an increased level of PGII, and a decreased ratio of PGI/PGII in GU‐I patients reflected extensive atrophic gastritis, while an elevated level of PGI, a normal level of PGII, and an increased ratio of PGI/PGII in DU patients implicated hypersecretory status coexistent with superficial fundic gastritis. These findings suggest functional heterogeneity of the gastric mucosa according to the

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1995.tb01591.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractThe activity of gastric parietal cells in terms of hydrochloric acid (HCl) secretion is regulated by the interaction of stimulatory substances (e.g. gastrin) and inhibitors (e.g. somatostatin) acting in an endocrine and paracrine mode, as well as luminal factors. In the present study the following parameters were measured: the synthesis (mRNA), storage (tissue peptide concentration) and secretion (plasma peptide concentration) of somatostatin and gastrin following short‐term treatment of rats with pentagastrin (acid stimulant), secretin, omeprazole (reduces gastric acidity by inactivating gastric H/K ATPase) and the somatostatin analogue octreotide (reduces gastric acidity by inhibiting both the parietal cell and gastrin). The mRNA coding for H/K ATPase and carbonic anhydrase II (CA II), the two enzymes responsible for the generation of hydrogen ions from the parietal cell, were also quantitated. In response to octreotide, somatostatin peptide and mRNA levels in the fundus rose to 180 ± 16% (P<0.001) and 1073 ± 356% (P<0.05) of control, respectively. In contrast, octreotide caused a decrease in antral somatostatin peptide and its mRNA did not change significantly. No significant changes in synthesis, secretion or storage of gastrin were observed except for omeprazole induced hypergastrinaemia (580 ± 76%,P<0.001). H/K ATPase and CA II mRNA were largely unaffected except for an increase in CA II mRNA following octreotide and a decrease in H/K ATPase mRNA after pentagastrin. These data support the concept of the differential control of antral and fundic somatostatin synthesis and provide evidence for a regulatory loop by which somatostatin can influence its own synthesis. H/K ATPase and CA II mRNA were not regulated in concert, as reported to occur in isolated canine parietal cells, a result that reiterates the need for these type of whole animal stu

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1995.tb01592.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractHepatocellular carcinoma (HCC) with extrahepatic spreading is not uncommon. In order to delineate the clinical and radiological pictures of HCC with intracranial metastasis, 33 documented cases were analysed. Eighteen had brain parenchymal metastasis without skull involvement; the other 15 cases disclosed skull metastasis with brain invasion. The underlying HCC are mainly of expanding (13/33, 39.4%) and multifocal (13/33, 39.4%) types. Eighteen cases (18/33, 54.5%) had mental changes not related to hypoglycaemia or hepatic encephalopathy. Eighteen cases (18/20, 90%) disclosed hyperdense mass lesions by non‐contrast computed tomography (CT) scans and 17 cases showed homogeneous enhancement (17/22, 77.3%) by post‐contrast CT images. In the non‐skull involved group, five cases (5/12, 41.7%) disclosed ring‐shape enhancement and 14 cases (14/16, 87.5%) had perifocal oedema, which were not seen in the skull involved group. Eight cases (8/33, 24.2%) presented as intracerebral haemorrhage. Twelve (12/33, 36.4%) died of brain herniation. Most (14/18, 77.8%) non‐skull involved cases had simultaneous lung metastasis without bony metastasis, while the skull involved group often (10/15, 66.7%) disclosed extracranial bony metastasis without lung metastasis. The difference in extracranial metastasis was statistically significant (P<0.05). The multivariate survival analysis disclosed that lower lactate dehydrogenase level (≤316 U/L,P= 0.029) and treatments (surgery or radiation,P= 0.001) were positively associated with longer survival.In conclusion, HCC with intracranial metastasis is symptomatic and life‐threatening. Half the cases may come from pulmonary metastasis and the other half may be from bony metastasis. Brain irradiation or surgery can prolong t

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1995.tb01593.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractThe precore region of hepatitis B virus (HBV) is indispensable for secretion of e antigen protein. Therefore, the precore stop codon mutants may play an important role in the process of e antigen seroconversion. However, the presence of the mutants in hepatitis B e antigen positive carriers has not been fully studied because of difficulties in detecting the mutants in the presence of large amounts of wild‐type viruses. To overcome this, a sensitive method has been developed to detect the presence of G to A stop codon mutants at codon 28 of precore region. Primers for polymerase chain reaction (PCR) were devised to introduce restriction enzyme siteStyI for wild‐type viruses andDdeI for the mutants. The amplification products with these primers were digested withStyI to exclude the products from wild‐type viruses. The remaining amplicon from precore mutants were re‐amplified, and the presence of precore mutant was confirmed withDdeI digestion. The presence of precore mutants was examined in 61 HBV carriers by the method combining PCR and restriction enzyme digestion. Approximately 0.1% of precore mutant DNA among 106copies of wild‐type virus DNA was detectable by this method. The presence of the precore mutants was detected in seven of 10 (70%) e antigen positive asymptomatic carriers, and in 29 of 36 (81%) e antigen positive patients with chronic liver diseases, and in all 15 (100%) anti‐e antibody positive patients with chronic liver diseases.This study revealed that a small amount of the precore mutants was present in the majority of H

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1995.tb01594.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY