Liver cirrhosis is characterized by the hyper-accumulation Liver fibrosis/cirrhosis is characterized by hyper-accumulaof connective tissue components in the liver and is often tion of fibrous tissue components and is commonly observed accompanied by hypo-albuminemia, ascites, and esophageal in later or terminal states of chronic hepatic diseases. In ongovarices. In a prolonged stage, severe hepatic failure, or hepaing work, we found that the administration of human recombitocellular carcinoma, can occur. Chronic hepatic injuries nant hepatocyte growth factor (hrHGF) suppressed the onset caused by drugs, chemicals, alcohol abuse, or viral infections of liver fibrosis/cirrhosis in several distinct models and accelare predominant pathogenic causes for cirrhosis. Although erated the recovery from liver fibrosis/cirrhosis in rats. Rethe pathogenic mechanisms of cirrhosis are not fully underpeated administration of porcine serum for 10 weeks to rats stood, the over-production of extracellular matrices in the induced liver fibrosis without any accompanying hepatocelluliver, as well as of chronic parenchymal hepatocellular injury, lar injuries; in addition, the intravenous (i.v.) administration are likely to initiate the onset of cirrhosis. Therefore, preferof hepatocyte growth factor (HGF) to these rats suppressed ential hepatocellular replication and cytoprotection against increases in fibrous components and hydroxyproline contents hepatic injuries, as well as the stimulation of degradation in the liver, thus preventing the onset of liver fibrosis. Reand remodeling of extracellular fibrous components, seems peated administration of dimethylnitrosamine (DMN) for four to inhibit the onset or progress of hepatic fibrosis/cirrhosis. weeks induced liver cirrhosis, as characterized by the hyperSeveral lines of studies have shown that hepatocyte growth accumulation of fibrous components, infiltration of mononufactor (HGF), originally purified as a potent mitogen for rat clear leukocytes, and hepatic dysfunction. When HGF was hepatocytes, 1-3 is the long-sought hepatotrophic factor for injected daily for four weeks along with DMN-treatment, the liver regeneration. [4][5][6][7] Following the onset of various types of onset of DMN-induced hepatic fibrosis/cirrhosis was suphepatic injuries, HGF messenger RNA expression is rapidly pressed; the numbers of infiltrating mononuclear cells, fibrous tissue components, and hydroxyproline content in the liver up-regulated in the livers of experimental animals. 8,9 Serum were decreased. When HGF was injected for two weeks fol-HGF levels are elevated in patients with various hepatic dislowing four weeks of DMN-treatment, HGF accelerated the orders. 10,11 Extensive in vivo studies on the efficacy of recomrecovery from liver cirrhosis and prevented death due to he-binant HGF on hepatic regeneration revealed that HGF elicits patic dysfunction. Likewise, HGF-injection suppressed the on-a potent hepatotrophic action. HGF strongly stimulates DNA set of liver fibrosis, when liver fibrosis had be...

No abstract

The relationship between blood vessels and amyloid beta (A beta)-protein deposits in the cortex of the Alzheimer's disease (AD) brain is still controversial. It is difficult to distinguish whether the A beta deposits are associated with blood vessels or neurons because of their widespread and complicated distribution. In this study, we investigated the distribution of A beta deposits in the cerebral white matter of the AD brain as a means of removing the bias of neuronal distribution. An immunohistochemical study of 100 serial sections, after pretreatment with formic acid for 24 h, revealed the presence of A beta deposits in the cerebral white matter of the AD brain. There are various morphological types of plaques containing A beta deposits in the white matter, the same as in the gray matter. While the majority of A beta deposits was of a circumscribed type such as "classic" and "primitive" plaques, "compact" and "diffuse" plaques were also observed in the white matter. The location of the A beta deposits was, for the most part, immediately beneath the gray matter. The distribution of A beta deposits in the white matter was found to correspond to the orientation of the blood vessels. Serial sections also revealed that these A beta deposits were distributed along a single blood vessel. These findings suggest that the deposition of A beta in the cerebral white matter is primarily related to the blood vessels.

Liver cirrhosis is characterized by the hyper-accumulation Liver fibrosis/cirrhosis is characterized by hyper-accumulaof connective tissue components in the liver and is often tion of fibrous tissue components and is commonly observed accompanied by hypo-albuminemia, ascites, and esophageal in later or terminal states of chronic hepatic diseases. In ongovarices. In a prolonged stage, severe hepatic failure, or hepaing work, we found that the administration of human recombitocellular carcinoma, can occur. Chronic hepatic injuries nant hepatocyte growth factor (hrHGF) suppressed the onset caused by drugs, chemicals, alcohol abuse, or viral infections of liver fibrosis/cirrhosis in several distinct models and accelare predominant pathogenic causes for cirrhosis. Although erated the recovery from liver fibrosis/cirrhosis in rats. Rethe pathogenic mechanisms of cirrhosis are not fully underpeated administration of porcine serum for 10 weeks to rats stood, the over-production of extracellular matrices in the induced liver fibrosis without any accompanying hepatocelluliver, as well as of chronic parenchymal hepatocellular injury, lar injuries; in addition, the intravenous (i.v.) administration are likely to initiate the onset of cirrhosis. Therefore, preferof hepatocyte growth factor (HGF) to these rats suppressed ential hepatocellular replication and cytoprotection against increases in fibrous components and hydroxyproline contents hepatic injuries, as well as the stimulation of degradation in the liver, thus preventing the onset of liver fibrosis. Reand remodeling of extracellular fibrous components, seems peated administration of dimethylnitrosamine (DMN) for four to inhibit the onset or progress of hepatic fibrosis/cirrhosis. weeks induced liver cirrhosis, as characterized by the hyperSeveral lines of studies have shown that hepatocyte growth accumulation of fibrous components, infiltration of mononufactor (HGF), originally purified as a potent mitogen for rat clear leukocytes, and hepatic dysfunction. When HGF was hepatocytes, 1-3 is the long-sought hepatotrophic factor for injected daily for four weeks along with DMN-treatment, the liver regeneration. [4][5][6][7] Following the onset of various types of onset of DMN-induced hepatic fibrosis/cirrhosis was suphepatic injuries, HGF messenger RNA expression is rapidly pressed; the numbers of infiltrating mononuclear cells, fibrous tissue components, and hydroxyproline content in the liver up-regulated in the livers of experimental animals. 8,9 Serum were decreased. When HGF was injected for two weeks fol-HGF levels are elevated in patients with various hepatic dislowing four weeks of DMN-treatment, HGF accelerated the orders. 10,11 Extensive in vivo studies on the efficacy of recomrecovery from liver cirrhosis and prevented death due to he-binant HGF on hepatic regeneration revealed that HGF elicits patic dysfunction. Likewise, HGF-injection suppressed the on-a potent hepatotrophic action. HGF strongly stimulates DNA set of liver fibrosis, when liver fibrosis had be...

Serum amyloid P component (AP) is a normal plasma constituent that is observed in senile plaques and neurofibrillary tangles in brains of Alzheimer''s disease (AD) patients. In this study we have evaluated the AP levels in sera of 16 patients with AD and in 16 control subjects by enzyme-linked immunosorbent assay. The AP level was 22.4 ± (SD) 7.0 µg/ml in the AD group and 34.4 ± (SD) 6.6 µg/ml in the control group. The AP level in the AD group was significantly lower than that of the control group (p < 0.01). In the control group, there was no correlation between AP levels and age. Our results suggest that the production of AP by the liver (hepatocytes), thought to be the only source, may be suppressed in AD patients and that the deposition of AP in senile plaques and neurofibrillary tangles is not due to its overproduction.