bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dyspepsia and Helicobacter pylori in Japanese employees with and without ulcer history
Authors: SCHLEMPER RONALD J , VAN DER WERF SJOERD DJ , BIEMOND IZÄK , LAMERS CORNELIS BHW 
Published: March 2008

AbstractIn a Dutch working population, the apparent association between dyspeptic symptoms and Helicobacter pylori infection was found to be entirely due to subjects with an ulcer history. In general populations with a much higher prevalence of H. pylori infection and peptic ulcer disease, such as in Japan, the relationship between dyspepsia and H. pylori has yet to be clarified. A questionnaire on ulcer history and dyspeptic symptoms during the preceding 3 month period was obtained from apparently healthy Japanese employees who underwent a periodic medical examination. In addition, serum samples were analysed for anti‐H. pylori IgG antibodies. A total of 196 men and 35 women, aged 23–71 years, participated in the study. Seven women (20%) and 49 men (25%) had a diagnosis of peptic ulcer disease. Among 41 subjects with verified duodenal (26) and/or gastric (17) ulcer, 95% were H. pylori positive while 32% had had frequent dyspeptic symptoms in the 3 months prior to the study (29% of the 35 men and 50% of the 6 women). Among the 147 men and 28 women without an ulcer history, the 3 month period prevalence of frequent dyspepsia was 14 and 32%, respectively. The rate of H. pylori positivity was 80% in non‐ulcer dyspeptics and 68% in all other non‐ulcer subjects (95% confidence intervals: 61–92 and 61–76%, respectively). Significant differences in symptoms between H. pylori positive and negative subjects could not be detected, neither in the whole population nor in the non‐ulcer group. In conclusion, in this Japanese working population, no association was found between dyspeptic symptoms and H. pylori infection, irrespective of the inclusion of subjects with a peptic ulcer history.
Ultrasound‐guided fine needle aspiration biopsy of portal vein thrombosis in liver cirrhosis: Results in 15 patients
Authors: DE SIO ILARIO , CASTELLANO LUIGI , CALANDRA MARIA , ROMANO MARCO , PERSICO MARCELLO , DEL VECCHIO‐BLANCO CAMILLO 
Published: March 2008

AbstractBetween 1988 and 1992 ultrasound‐guided fine needle aspiration biopsies of thromboses in the main branches of the portal vein were carried out in 15 patients with liver cirrhosis. The aims of the study were to evaluate the usefulness, feasibility and diagnostic accuracy of this procedure in cirrhotics with known or suspected hepatocellular carcinoma. The procedure was carried out only in patients with a platelet count ≥40 000/μL and prothrombin activity ≥40%. A single pass, with a 22 gauge spinal needle, was performed in the portal vein lumen. Diagnosis of the aetiology of the portal vein thrombosis was obtained in all 15 cases. In 12 cases, a cytological diagnosis of hepatocellular carcinoma was made. In one case, the neoplastic cells aspirated were compatible with adenocarcinoma, and a subsequent colonoscopy confirmed the presence of colonic cancer. The material aspirated was compatible with chemically‐induced thrombosis in one patient who had undergone several percutaneous ethanol injection sessions for treatment of hepatocellular carcinoma, and in the last case only blood was aspirated, thus ruling out the coexistence of hepatic cancer. We conclude that fine needle aspiration biopsy of portal vein thrombosis is a feasible, low risk procedure that facilitates the diagnosis of hepatocellular carcinoma when fine needle biopsy of focal liver lesions fails. Fine needle aspiration biopsy of portal vein thrombosis is also useful in excluding neoplastic aetiology of portal vein thrombosis.
Secondary prevention of hepatocellular carcinoma
Authors: TANG ZHAO‐YOU , YANG BING‐HUI 
Published: March 2008

AbstractTwo decades have gone by since the earlier trials of alpha‐fetoprotein (AFP) screening for hepatocellular carcinoma (HCC) were conducted in Africa and China. It is accepted that early detection, diagnosis and treatment of HCC remains an important target to be achieved before a breakthrough appears on the primary prevention of HCC. In the present study, screening investigations were performed in a high risk population of HCC, defined as persons who had hepatitis, blood transfusions, a family history of HCC, and were hepatitis B virus carriers. Ultrasonography combined with AFP serosurvey was accepted as an effective screening procedure to detect small HCC. Early diagnosis of HCC was not difficult if tumour markers and medical imaging were combined. Early resection has been proven to prolong survival of patients with small HCC. Repeated intralesional ethanol injection is an alternative treatment to surgery, while transcatheter arterial embolization is a less effective alternative. Re‐resection of subclinical recurrence after curative resection has proven of merit in prolonging survival even further. Resection of small HCC remains an important approach in getting long‐term HCC survival and to improving 5‐year survival rates. It is more effective than treatment of large HCC. Studies on the secondary prevention of HCC have stimulated research into tumour markers, the natural history and cellular origin of HCC and oncogenes. However, the issue of ‘cost‐effectiveness’ remains to be evaluated.
Gastric microcirculatory disturbance and behaviour of leucocytes after thermal injury: Intravital observation of arteriovenous shunting channels in the gastric submucosal layer
Authors: YOSHIDA MASASHI , FUKUMURA DAI , WAKABAYASHI GO , OTANI YOSHIHIDE , OSHIMA ATSUSHI , SHIMAZU MOTOHIDE , KUBOTA TETSURO , KUMAI KOICHIRO , KUROSE IWAO , MIURA SOICHIRO , KITAJIMA MASAKI 
Published: March 2008

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 channels.
Role of mucosal microcirculation in gastric lesions induced by lateral hypothalamic lesions in rats
Authors: SAITA HIROSHI , MURAKAMI MOTONOBU , KITA TORU 
Published: March 2008

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 secretion.
Intestinal absorption of lithocholate and its sulfate and glucuronide in rats
Authors: TAKIKAWA HAJIME , YOKOTE MICHIKO , SANO NAOYO , NAKAKI MOTOE , YAMANAKA MASAMI 
Published: March 2008

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 concerned.
Serum pepsinogen I and pepsinogen II, and the ratio of pepsinogen I pepsinogen II in peptic ulcer diseases: With special emphasis on the influence of the location of the ulcer crater
Authors: WU MING‐SHIANG , WANG HSIU‐PO , WANG JIN‐TOWN , WANG TEH‐HONG , LIN JAW‐TOWN 
Published: March 2008

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 different locations of the ulcer crater.
Secretory and biosynthetic responses of gastrin and somatostatin to acute changes in gastric acidity
Authors: KAPUSCINSKI MIREK , SHULKES ARTHUR 
Published: March 2008

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 studies.
Detection of hepatitis B virus precore stop codon mutants by selective amplification method: Frequent detection of precore mutants in hepatitis B e antigen positive healthy carriers
Authors: NAKAHORI SUSUMU , YOKOSUKA OSAMU , EHATA TOSHIKI , CHUANG WANG‐LONG , IMAZEKI FUMIO , ITO YOSHIMI , OHTO MASAO 
Published: March 2008

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 site Sty I for wild‐type viruses and Dde I for the mutants. The amplification products with these primers were digested with Sty I 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 with Dde I 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 106 copies 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 HBV carriers.
Cytokines, nitric oxide synthesis and liver regeneration
Authors: DECKER KARL F , OBOLENSKAYA MARIA Y 
Published: March 2008

AbstractDuring the prereplicative period of liver regeneration the changes in the levels of mRNA for tumour necrosis factor‐α (TNF‐α) and its receptors were nearly synchronous. The mRNA levels reached their maximum 1 – 3 h after operation and exceeded the values for intact animals about tenfold. Lipopolysaccharide stimulation induced an increase in TNF‐α and TNF receptor production comparable with that occurring during regeneration.Nitric oxide (NO) production in the regenerating liver was determined by electron paramagnetic resonance (EPR) spectroscopy. The first increase in NO production occurred approximately 1 h after partial hepatectomy (PHE). The second and more pronounced peak of NO production was observed about 6 h after PHE when the hepatocytes entered the first cell cycle; it originated mainly from these cells. The consequent minimum of NO synthesis coincided with the maximal rate of DNA synthesis. The third gradual rise of NO production was seen at the transit from the first to the second cell cycle of the hepatocytes and the entrance of the non‐parenchymal cells into proliferation.Hepatocytes, Kupffer and endothelial cells were isolated from livers after PHE. They were found to start their main NO production in the described sequence at the times corresponding to their respective entrance into the cell cycle. The maxima of NO synthesis were inversely correlated to the DNA‐synthesizing activity of the individual cell type.
Role of sinusoidal endothelial cells in liver disease
Authors: OKANOUE TAKESHI , MORI TAKASHI , SAKAMOTO SHINICHI , ITOH YOSHITO 
Published: March 2008

AbstractWe characterized the structural changes of sinusoidal endothelial cells in chronic ethanolfed rats and rats with cirrhosis induced by thioacetamide. The phenotypic changes of sinusoidal endothelial cells in fibrotic rats induced by thioacetamide and the reversibility of these changes were also investigated under transmission and scanning electron microscopy, regular microscopy and by immunohistochemistry with laminin and von Willebrand factor antibodies. The diameter and porosity of sinusoidal endothelial fenestrations were increased in chronic ethanol‐fed rats without liver fibrosis, however, they decreased within 4 weeks of the cessation of thioacetamide treatment. A basement membrane‐like structure in Disse's space was noted 6 weeks after thioacetamide treatment. Laminin was detected in Disse's space after 4 weeks and von Willebrand factor was detected in the cytoplasm as granular fluorescence after 6 weeks of thioacetamide treatment. Reversibility of the phenotypic changes of the sinusoidal endothelial cells was demonstrated in fibrotic liver of rats that received thioacetamide for 6 weeks after long‐term discontinuation of thioacetamide administration. These results indicate that the structural and immunohistochemical characteristics of sinusoidal endothelial cells change in chronic ethanol‐fed rats and fibrotic rats and these changes are reversible.
Role of adhesion between activated macrophages and endothelial cells in the development of two types of massive hepatic necrosis in rats
Authors: MOCHIDA SATOSHI , OHNO AKIHIKO , ARAI MASAHIRO , FUJIWARA KENJI 
Published: March 2008

AbstractSinusoidal endothelial cell damage is produced by activation of hepatic macrophages after endotoxin administration in rats pretreated with Cornyebacterium parvum or undergoing 70% hepatectomy. Such damage causes fibrin deposition in the hepatic sinusoids leading to massive hepatic necrosis. In the C. parvum model, cytotoxic mediators, such as tumour necrosis factor (TNF)α and superoxide anions released from activated hepatic macrophages directly destroy sinusoidal endothelial cells. In contrast, in the partial hepatectomy model, endothelial cell damage occurs as a result of fibrin deposition due to derangement of the coagulation equilibrium regulated by tissue factor and thrombomodulin expressed on hepatic macrophages and sinusoidal endothelial cells, respectively. Immunohistological examination revealed that the expression of ICAM‐1 in sinusoidal endothelial cells and LFA‐1 in hepatic macrophages was greater in both models than in normal rats preceding the development of hepatic necrosis. The extent of liver injury was significantly attenuated by treatment with monoclonal antibodies against both adhesion molecules in the C. parvum model, but aggravated in the partial hepatectomy model, compared to control rats. We conclude that adhesion of activated macrophages to endothelial cells via LFA‐1 and ICAM‐1 in the hepatic sinusoids is essential for endothelial cell destruction in the C. parvum model, but can act protectively against provocation of fibrin deposition in the hepatectomy model.
Roles of oxidative stress in activation of Kupffer and Ito cells in liver fibrogenesis
Authors: TSUKAMOTO HIDEKAZU , RIPPE RICHARD , NIEMELÄ ONNI , LIN MIN 
Published: March 2008

AbstractAn increasing body of experimental evidence is emerging to incriminate oxidative stress as a pivotal signal for liver fibrogenesis. This paper reviews the results from our studies testing this hypothesis. In the rat model of alcoholic liver disease, the importance of oxidative stress was supported by marked accentuation of liver fibrosis by dietary supplementation of iron, a pro‐oxidant, and the significant correlation of the liver malondialdehyde (MDA) and 4‐hydroxynonenal (4HNE) levels with the hepatic collagen accumulation. Both MDA and 4HNE adduct epitopes were detected intensely and diffusely in close association with collagen deposition. The direct cause and effect relationship between MDA/4HNE and Ito cell stimulation was indicated by the demonstration of Ito cell collagen gene induction by these aldehydes in culture. In primary cultures of rat Kupffer cells (KC), addition of antioxidants such as α‐tocopherol acetate and succinate suppressed mRNA expression and the release of interleukin (IL)‐6 and tumour necrosis factor alpha (TNFα). In rats with biliary fibrosis, an increase in the liver MDA level was accompanied by enhanced mRNA expression of procollagen α 1 (I) and transforming growth factor β 1 in Ito cells; and that of TNFα and IL‐6 in KC. Furthermore, the gel shift assay of KC nuclear extracts showed enhanced NF‐kB DNA binding activity. These results support the proposal that enhanced oxidative stress constitutes an important signal for activation of Kupffer and Ito cells in experimental liver fibrogenesis.
Integrity of myosin light chain kinase is essential for Ito cell contraction
Authors: WATANABE SUMIO , WANG XIAN‐EN , HIROSE MIYOKO , OIDE HIROSUMI , SHIMIZU HIDETAKE , KITAMURA TSUNEO , YUMOTO ATUKO , SUZUKI SATOKO , MIYAZAKI AKIHISA , SATO NOBUHIRO 
Published: March 2008

AbstractHepatic sinusoidal Ito cells (fat storing cells) are believed to play a regulatory role on hepatic sinusoidal blood flow through their contraction. The detailed mechanism of contraction of Ito cells, however, is still unknown. The present study was undertaken to clarify the effect of new myosin light chain kinase inhibitor, wortmannin, on Ito cell contraction. Ito cells prepared from rat liver were cultured for 4 days before the study. The contraction of Ito cells, which was monitored and analysed by time‐lapse video tape recording, was triggered by addition of endothelin‐1. Wortmannin pretreatment for 1 h inhibited endothelin‐induced Ito cell contraction dose‐dependently. Therefore, the integrity of the actomyosin system is essential for Ito cell contraction and normal sinusoidal blood flow.