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Biomedical subjects

Y Ohta

Publications and source records attributed to Y Ohta.

At least 865 records · Page 48Linked to original sources
PubMed1988

Immunologic effects on peripheral lymphoid cells from patients with chronic hepatitis type B during administration of recombinant interleukin 2.

Nine patients with chronic hepatitis type B were treated with recombinant interleukin 2 (rIL-2). Side effects were limited to low-grade fever and headache, which were transient and tolerable for the patients. Seven normal volunteers and nine patients with chronic active hepatitis were administered by one bolus of 500 units of rIL-2. Acute effects of rIL-2 administration on lymphoid cells included a rapid decrease in lymphocytes, especially in cytotoxic T cells and natural killer cells. These acute effects resolved within 24 hours. There was no difference in the changes of immunological parameters between normal volunteers and patients. The same effects were seen during 28 days of rIL-2 administration. The number of lymphocytes and CD4 positive cells was increased after rIL-2 administration for 28 days (P less than 0.01). Natural killer cell activity, especially that of CD16+ and Leu-7- cells was also increased (P less than 0.05). These effects may favour the elimination of virus-infected hepatocytes.

Adult↗
PubMed1988

Increased serum soluble interleukin 2 receptor levels in patients with viral liver diseases.

Soluble interleukin 2 receptors (sIL 2R) in the sera of patients with viral liver diseases were quantified with a solid-phase enzyme immunoassay using two monoclonal antibodies against the receptors. The sIL 2R levels in patients with acute hepatitis, chronic hepatitis, liver cirrhosis and hepatocellular carcinoma were significantly higher than those in control subjects. In acute hepatitis patients, the high levels of sIL 2R observed during the florid stage returned to normal during remission. Levels in patients with chronic active hepatitis were significantly higher than in those with chronic persistent and lobular hepatitis, and levels observed during the exacerbation phase of chronic hepatitis were higher than they were during remission. Thus, in chronic hepatitis, sIL 2R levels increased in proportion to the inflammatory activity, and correlated well with serum transaminase (glutamic oxaloacetic transaminase: SGOT, glutamic pyruvic transaminase: SGPT) activities, but not with blood urea nitrogen or creatinine concentrations. In patients with a high degree of focal and piecemeal necrosis, serum sIL 2R levels increased further during recombinant interleukin 2 therapy. In post-hepatitic liver cirrhosis and hepatocellular carcinoma, sIL 2R levels correlated with serum cholinesterase and creatinine concentrations, but not with transaminase activities. Measurement of serum sIL 2R levels in patients with liver disease but without renal injury, may help in the diagnosis of inflammation in hepatitis, a process in which interleukin 2 may participate.

Hepatitis B Surface Antigens↗
PubMed1988

Serial observation of lymphocyte subpopulations and interleukin 2 production of T cells from patients with acute viral hepatitis and chronic active hepatitis.

T cell subpopulations and interleukin 2 (IL-2) production of T cells in peripheral blood from patients with acute viral hepatitis (AVH) and chronic active hepatitis (CAH) were studied to elucidate the change of T cells functions during the exacerbation of viral hepatitis. The ratio of the number of CD4-positive cells to CD8-positive cells (CD:CD8 ratio) was increased in many patients with AVH. During exacerbation of CAH, the CD4:CD8 ratio was higher than that during remission (p less than 0.01), due to a decrease in the number of CD8-positive cells. IL2 production of T cells in AVH and CAH with bridging necrosis was higher than that of T cells in normal controls (p less than 0.01, p less than 0.05, respectively). T cells from patients with CAH produced more IL2 during exacerbation than during remission (p less than 0.01). IL2 production of T cells and the CD4:CD8 ratio (p less than 0.005, p less than 0.01). The change in T cell subpopulations in AVH and during exacerbation of CAH was found to induce an immunological condition, in which T cells easily produce IL2, which induces a proliferation of cytotoxic T cells.

Hepatitis A↗
PubMed1988

Evidence for potentiation of lipid peroxidation in the rat liver after chronic ethanol feeding.

Hepatic steatosis was induced in rats by feeding nutritionally adequate liquid diet containing ethanol as 36% of energy for 4-5 weeks. After 24 h fasting and withdrawal from ethanol, liver ischaemia for 30 min followed by 2 h reperfusion resulted in a significant increase in microsomal lipid peroxide content and a decrease in reduced glutathione content as well as in protein synthesis with a rapid accumulation of triglyceride in the liver. In rats fed a non-ethanol diet or those fed a high-cholesterol diet with hepatic steatosis, however, similar phenomena were not found. These findings suggest that chronic ethanol feeding potentiates hepatic lipid peroxidation.

Animals↗
PubMed1988

Intrahepatic lymphocyte subpopulations in acute hepatitis in an adult with rubella.

Rubella accompanied by serum aminotransferase elevations occurred in a 24-yr-old man. Liver biopsy showed ballooning degeneration and focal necrosis of liver cells, clumped Kupffer cells, and infiltration of inflammatory cells, mainly of the mononuclear type. Most mononuclear cells in the liver were CD8-positive and CD16-negative cells (cytotoxic T cells) which were in broad contact with the surface of liver cells. Leu 7 (natural killer) cells were few and sporadic. HLA class I antigens were expressed on liver cell membrane. Although hepatic involvement in adult rubella is not generally recognized, it may have been the cause of this patient's liver injury. Thus, cytotoxic T cells may play a role in liver injury in acute rubella infections in adults.

Adult↗
PubMed1988

Contribution of hepatic reticuloendothelial system to glomerular IgA deposition in rat liver injury.

Liver damage was induced in rats by a single dose of dimethylnitrosamine or D-galactosamine. In the dimethylnitrosamine model, marked glomerular IgA deposition occurred between Days 4 and 28, with its peak at Day 14. Serum IgA levels were significantly increased at Days 2 and 4, then gradually decreased, and normalized at Day 14. In the D-galactosamine model, however, no such deposition was observed, though serum IgA levels similarly increased on Days 2 and 4. IgA content in high molecular weight fraction from serum increased at Day 3 in both models. This increment remained at Day 7 only in the dimethylnitrosamine model, in which carbon clearance from the circulation was significantly decreased at Day 3. These data suggest that dysfunction of the hepatic reticuloendothelial system is a factor contributing to glomerular IgA deposition occurring in liver injury.

Alanine Transaminase↗