巻号一覧
47 巻, 1 号
選択された号の論文の6件中1～6を表示しています
- |<
- <
- 1
- >
- >|
-
Karl Decker1998 年 47 巻 1 号 p. 1-9
発行日: 1998年
公開日: 2009/03/27
ジャーナル フリーThe gut is the major source of inflammatory agents that affect the liver. Of these com-pounds, the endotoxins are the most frequent and best studied intruders. The resident macrophages of the liver, the Kupffer cells, are among the first to respond to this complex. Following contact with the cluster of differentiation (CD) 14 protein, the complex triggers a signal cascade involving the nuclear factor KB. This factor enhances the expression of inflammation-related genes, e.g. those encoding cytokines. Tumor necrosis factor-a is responsible for nearly all of the effects ascribed to endotoxins (lipopolysaccharides). Interleukin (IL)-6, also a product of lipopolysaccharide-activated Kupffer cells, may be instrumental in eliciting the acute-phase response of hepatocytes, while transforming growth factor-β promotes conversion of quiescent hepatic stellate cells into a collagen-producing myofibroblast-like form. A different signal pathway triggered by bound endotoxin involves a mitogen-activated protein kinase and leads to the activation of phospholipase A2 and the synthesis of the eico-sanoids. Endotoxin also induces a nitric oxide synthase in Kupffer cells. This inorganic mediator may participate in the relaxation of the hepatic sinusoid, but may also, together with macrophage-derived superoxide, produce strong oxidants. Tumor necrosis factor-a and nitric oxide play a significant role during liver regeneration after partial hepatectomy. Of the various effects of eicosanoids, their regu-latory role in cytokine production by Kupffer cells may be the most important. The regulation of Kupffer cell functions by cell volume change has very recently become apparent.抄録全体を表示PDF形式でダウンロード (6090K) -
Young S. Kim1998 年 47 巻 1 号 p. 10-18
発行日: 1998年
公開日: 2009/03/27
ジャーナル フリーMucins are high molecular weight glycoproteins which are heavily glycosylated with many carbohydrate side chains. In epithelial cancers such as colorectal cancer, both qualitative and quanti-tative alterations in carbohydrate and polypeptide moieties of mucin glycoproteins occur. These changes in mucin glycoproteins are one of the most common phenotypic markers of colorectal carcino-genesis and may play an important pathobiological role. The expression of some of the sialylated carbohydrate antigens appears to correlate with a poor prognosis and increased metastatic potential in colorectal cancer. The increased exposure of peptide epitopes of mucin glycoproteins in colorectal cancer appears to be due to either abnormal glycosylation and/or altered levels of mucin gene tran-scription. In addition, dysregulation of tissue specific mucin genes occurs in colorectal cancers. This information is currently being exploited for further elucidation of the molecular mechanisms involved in carcinogenesis, tumor progression and metastasis, and the development of novel methods of colo-rectal cancer diagnosis and therapy.抄録全体を表示PDF形式でダウンロード (1568K) -
浅山 圭世, 相川 直樹1998 年 47 巻 1 号 p. 19-27
発行日: 1998年
公開日: 2009/03/27
ジャーナル フリーBased on the concept of the systemic inflammatory response syndrome (SIRS), a one year retrospective study was carried out to examine SIRS criteria as a simple and rapid predictor of outcome for emergency patients. Among a total of 2, 180 patients transported to the emergency room by ambu-lance, 318 (14.8%) had primary SIRS and 389 (17.8%) met SIRS criteria at some point during the entire treatment period. The admission rate for primary SIRS increased sequentially as more SIRS criteria were met, rising from 15.4% in non-SIRS to 100% when all four criteria were met. The mor-tality of primary SIRS also increased sequentially as more SIRS criteria were met, rising from 1.4% in non-SIRS to 35.3% when all four criteria were met. Furthermore, heart rate, C-reactive protein and platelet count were considered to be potentially useful new criteria for a group of SIRS patients with a high risk of mortality (high-risk SIRS), based on a comparison of variables between SIRS patients who died and SIRS patients who survived. The mortality associated with primary SIRS increased sequen-tially as more high-risk SIRS criteria were met, rising from 7.6% when none were met to 50.0% when two criteria were met. Considering the high specificity of primary SIRS for admission (89.5%) and mortality (86.8%), SIRS criteria have clinical and prognostic importance in the management of emer-gency patients. Given the high mortality (29.9%), the new high-risk SIRS criteria may also be useful as entry criteria for clinical trials of innovative therapies for patients with SIRS.抄録全体を表示PDF形式でダウンロード (2667K) -
1. A New Method for Quantifying Insulin Resistance and Secretion伊東 克彦, 和田 孝雄, 槇村 博之, 松岡 瑛1998 年 47 巻 1 号 p. 28-36
発行日: 1998年
公開日: 2009/03/27
ジャーナル フリーTo elucidate abnormalities in the feedback relationships between plasma glucose and plasma insulin levels in diabetic patients, we have introduced the vector autoregressive modeling method as a new for tool feedback analysis. This technique was applied to plasma glucose and insulin level data from a series of 977 frequently-sampled oral glucose tolerance tests (FS-OGTT). Neither special instruments nor medications were used in FS-OGTT. We were able to predict the degree of the plasma glucose response occurring after an impulse-like increase in plasma insulin at 1 mU/mL, as well as the plasma insulin response triggered by an impulse-like increase in plasma glucose at 1 mg/dL, in the form of “impulse response curves”. The predicted impulse response curve of glucose to insulin gradually changed from negative to positive with incremental changes in the fasting plasma glucose level, reflecting increased insulin resistance. Furthermore, the response of insulin to glucose decreased in a stepwise fashion with the incremental changes in the fasting plasma glucose level. Our findings confirm the usefulness of impulse response curves as clinical indicators. In addition, analytical data point to a possible contribution of excessive hepatic glucose production to the pathogenesis of the insulin resistance in non-insulin-dependent diabetes mellitus.抄録全体を表示PDF形式でダウンロード (616K) -
伊藤 義彰, 植松 大輔, 荒木 信夫, 村松 和浩, 渡辺 茂, 福内 靖男1998 年 47 巻 1 号 p. 37-41
発行日: 1998年
公開日: 2009/03/27
ジャーナル フリーIntracellular acidosis has been considered to play a pivotal role in the progression of neu-ronal damage after cerebral ischemia. However, continuous measurement of the intracellular potential of hydrogen (pH) has not been done during and after ischemia. We measured temporal changes in intracellular pH in the feline cerebral cortex in vivo during and after ischemia using a novel fluorescent pH probe, 2', 7'-biscarboxyethyl carboxyfluorescein (BCECF). A closed cranial window was installed in the left temporal skull. BCECF acetoxymethyl ester was superfused over the cortex, hydrolyzed and trapped in cortical cells. Intracellular pH was measured utilizing excitation light at 507nm and fluo-rescent light at 550.5nm. Focal cerebral ischemia for 60 minutes was induced by means of middle cere-bral artery occlusion. Intracellular pH in the severely ischemic group became significantly acidic (p<0.01) during ischemia and the acidosis persisted for at least 30 minutes after recirculation. The pH change was not significant in the mildly ischemic group. The severity of ischemia was determined based on the mean transit time, which was calculated from the hemodilution curve obtained by bolus injec-tion of saline. The extent of ischemia was further confirmed pathologically (p<0.01). The above results suggest that intracellular acidosis resulting from severe ischemia persists even after recircula-tion.抄録全体を表示PDF形式でダウンロード (363K) -
Tetsuya Otsuki, Johnson M. Liu1998 年 47 巻 1 号 p. 42-44
発行日: 1998年
公開日: 2009/03/27
ジャーナル フリーFanconi anemia (FA) is an autosomal recessive disorder that leads to aplastic anemia. Cells from FA patients are abnormally sensitive to DNA cross-linking agents such as mitomycin C. FA con-sists of at least five subgroups (FA-A through -E). The genes defective in the FA-C and FA-A groups have recently been cloned. Transfection of the normal FA gene into mutant cells corrects the hyper-sensitivity to DNA cross-linking agents and improves cell viability in vitro. The function of the FA gene products is still unclear, however. For patients lacking a compatible bone marrow transplantation donor, an experimental trial of gene therapy for group C FA is ongoing at the National Institutes of Health.抄録全体を表示PDF形式でダウンロード (270K)
- |<
- <
- 1
- >
- >|