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Biomedical subjects

M Hatano

Publications and source records attributed to M Hatano.

At least 253 records · Page 14Linked to original sources
PubMed1987

Defective T-lymphocyte colony formation in patients with lupus nephritis.

To determine whether patients with systemic lupus erythematosus (SLE) and active nephritis have more profound defects in cell-mediated immunity (CMI), we studied T-colony-forming cells (TCFC) in 12 patients with lupus nephritis (LN) and 14 patients with chronic mesangial proliferative glomerulonephritis (CGN) without renal insufficiency. We also examined the activity of T-colony-stimulating factor (TCSF) in media conditioned by phytohaemagglutinin (PHA) stimulated peripheral blood lymphocytes (PHA-LCM). The levels of TCFC and TCSF were decreased in patients with LN compared with those in normal controls and lower in LN patients with the nephrotic syndrome (NS) than in those without NS. In contrast, these CMI parameters in CGN patients with or without NS did not differ from normal subjects. TCSF activity for TCFC in both normal individuals and LN patients was removed from PHA-LCM with interleukin 2 (IL 2) receptor bearing cultured T cells. These in vitro findings suggest that IL 2 is the essential factor contained in PHA-LCM. Our observations may lend further insight into the understanding of the immunoregulatory defect in LN.

Adolescent↗
PubMed1986

Expression of cytochrome P-450d by Saccharomyces cerevisiae.

Rat liver microsomal cytochrome P-450d was abundantly expressed in the yeast Saccharomyces cerevisiae by using a yeast-Escherichia coli shuttle vector consisting of rat liver P-450d cDNA and yeast acid phosphatase promoter. The expressed cytochrome P-450d was immunologically crossed with rat liver P-450d. The hydroxylase activity of estra-1,3,5(10)-triene-3, 17 beta-diol was 11 nmol/min per nmol P-450d, which is comparable to that reported previously for rat liver P-450d. The expressed P-450d content was nearlyt 1% of total yeast protein as estimated from immunoblotting, hydroxylase activity and optical absorpton of the reduced CO form.

Animals↗
PubMed1986

Rabbit kidney cells abortively infected with human cytomegalovirus are arrested in mitotic phase.

In rabbit kidney epithelial cells (RK13) abortively infected with human cytomegalovirus (HCMV), DNA synthesis at 1 or 2 days post-infection was enhanced 4 to 5 fold, compared to mock-infected cells. DNA analysis by isopycnic centrifugation revealed that the DNA newly synthesized in the virus infected RK13 cells was of cellular origin. HCMV infection also caused a marked increase in the mitotic activity of RK13 cells. When semi-confluent RK13 cells were infected more than 20 per cent of cells demonstrated mitosis at 72 hours post-infection although the rate of cell growth was considerably reduced compared to that of uninfected cells. The most frequent chromosomal change observed was fragmentation although other aberrations, gap, break, deletion etc. occurred also. Two immediate-early viral polypeptides with apparent molecular weights 72,000 (72K) and 76,000 (76K) daltons were produced in both RK13 cells and human embryonic lung cells (HEL) by 3 hours post-infection. Synthesis of the 76K polypeptide was greater than that of the 72K polypeptide in non-permissive RK13 cells whereas the reverse occurred in permissive HEL cells. Furthermore, of three early polypeptides which were expressed in productively infected HEL cells two, 88K and 80K, were not detected in abortively infected RK13 cells. These results suggest that the arrest in mitosis of the abortively infected RK13 cells and the subsequent chromosomal changes are associated with the altered expression of immediate-early or early virus functions in these cells.

Animals↗
PubMed1986

Latent infection of human ovarian teratocarcinoma cells with human cytomegalovirus. Brief report.

Persistent infection with human cytomegalovirus (HCMV) can be established in cultures of human ovarian teratocarcinoma (PA1) cells, and maintained for more than 200 days. Infected cultures maintained at 34 degrees C (PA1CMV34) and 37 degrees C (PA1CMV37) entered crisis and subsequently displayed massive cytopathic effects (CPE), whereas infected cultures maintained at 32 degrees C (PA1CMV32) and 39 degrees C (PA1CMV39) continued to release small amounts of infectious virus until 240 or 151 days post-infection (p.i.) respectively. PA1CMV32 cultures shifted to 37 degrees C at 258 days p.i. resumed synthesis of infectious virus which resulted in cell destruction, indicating that latent infection with HCMV was maintained in PA1 cells at 32 degrees C. In contrast, PA1CMV39 cells did not produce infectious virus even when cultured at 37 degrees C for more than 100 days after the temperature shift.

Bromodeoxyuridine↗
PubMed1986

Guinea pig complement fixation by tissues from hypocomplementaemic renal diseases.

Recently many studies have been done to identify complement pathway activation in renal tissue from patients with renal disease. We examined whether tissues obtained by renal biopsy from such patients would fix guinea pig complement. Nine out of 15 patients with systemic lupus erythematosus (SLE), 4 out of 7 patients with mesangiocapillary glomerulonephritis (MCGN), and 2 out of 7 cases with acute glomerulonephritis (AGN) fixed guinea pig C3. We found that tissues from 5 out of 9 guinea pig C3-positive SLE cases fixed guinea pig C4, while none of the guinea pig C3-positive tissues from patients with MCGN or AGN fixed guinea pig C4. These guinea pig C3-positive renal tissues were further studied for interaction with C4-deficient guinea pig serum, EDTA guinea pig serum, heated guinea pig serum, and EGTA Mg2+ guinea pig serum. The results indicated that activation of both the alternate and classical complement pathways occurred with tissues from patients with SLE, while activation of the alternate pathway occurred with MCGN and AGN. Results for tissues from AGN and MCGN patients indicated the presence of C3 convertase and protease which interacted with guinea pig C3.

Biopsy↗
PubMed1986

Effects of intravenous administration of a calcium antagonist on prostaglandins and thromboxane in plasma and urine in humans.

The effects of a calcium antagonist [Nicardipine hydrochloride (NH)] on the prostaglandin [prostaglandin E2 (PGE2), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha)] and thromboxane B2 levels in the blood and urine were examined in 6 patients with essential hypertension following intravenous infusion of NH for 120 minutes. At the same time, the plasma renin activity (PRA), plasma aldosterone concentration (PAC), and plasma and urinary electrolyte levels were also determined. During NH administration, the blood pressure was significantly decreased (p less than 0.05) with an increased pulse rate (p less than 0.05). PRA was significantly increased after NH loading (p less than 0.05) but PAC showed no change. The plasma PGE2 and 6-keto-PGF1 alpha levels tended to increase slightly, while the blood thromboxane B2 level showed a decreasing tendency. The 6-keto-PGF1 alpha to thromboxane B2 ratio was significantly increased after NH loading as compared to the preloading ratio (p less than 0.05), and then returned to the preloading value at about 30 minutes after discontinuation of NH loading. The urinary excretions of PGE2, 6-keto-PGF1 alpha and thromboxane B2, PGE2 and 6-keto-PGF1 alpha tended to decrease after NH loading. In particular, the decrease in PGE2 was statistically significant (p less than 0.05). No change occurred in the urinary excretion of thromboxane B2. The above findings indicate that NH increased the plasma 6-keto-PGF1 alpha to thromboxane B2 ratio but decreased the urinary excretion of prostaglandins. In addition, the possible involvement of an enhanced 6-keto-PGF1 alpha/thromboxane B2 ratio in part of the hypotensive mechanism of NH is suggested.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Human cytomegalovirus persistent infection in a human central nervous system cell line: production of a variant virus with different growth characteristics.

The susceptibility of human central nervous system cell lines to human cytomegalovirus (HCMV) and the fate of infected cultures were studied. Significant amounts of infectious progeny virus were produced in 118MGC glioma and IMR-32 neuroblastoma, but not in KGC oligodendroglioma cells when the cultures were infected with wild-type virus (HCMVwt) at an m.o.i. of 10 p.f.u. per cell. Further passage of infected 118MGC cells resulted in the establishment of a long-term persistent infection. This infection, designated 118MGC/Towne, continuously produced infectious virus (HCMVpi) with titres ranging from 10(2) to 10(5) p.f.u./10(6) cells up to 360 days post-infection (corresponding to 50 subcultures). Since no temperature-sensitive mutants, defective interfering particles or interferon-like activity were found in the 118MGC/Towne cultures, maintenance of the persistent infection seemed to be due to a balance between the release of infectious virus and the growth of uninfected cells. The HCMVpi produced in long-term persistently infected cultures was shown to be different from the HCMVwt originally used to infect by the following characteristics: HCMVpi replicated slowly and yielded lower amounts of progeny virus than HCMVwt; HCMVpi induced a 73,000 mol. wt. immediate early protein that was not synthesized in HCMVwt-infected cells; HCMVpi had a different DNA structure from that of HCMVwt. These results suggest that HCMVpi is a slower growing variant of HCMVwt and probably plays an important role in the maintenance of the persistent infection.

Cell Division↗