Biomedical subjects

I Berman

Publications and source records attributed to I Berman.

32 records · Page 2Linked to original sources

PubMed1985

Localization of collagenase in the growth plate of rachitic rats.

In the transition from proliferation to hypertrophic cell zones in the growth plate, there is an increase in chondrocyte volume and a corresponding decrease in collagen content to accommodate the enlarging cells. It is postulated that collagenase accounts for this collagen loss. To test this hypothesis, tibial growth plates were obtained from normal rats, rachitic rats deficient in vitamin D and phosphate, and rats after 48 and 72 h of healing from rickets. Collagenase was quantitated by a pellet assay based on the release of solubilized collagen from the endogenous insoluble collagen in the tissue homogenates. A fourfold greater collagen release and a concomitant sixfold greater hypertrophic cell volume were measured in rachitic growth plates compared with normal age-matched controls. During healing of rickets, collagenase activity and hypertrophic cell volume returned almost to control levels. Rachitic growth plates were dissected into the juxtaepiphyseal 1/3 and the juxtametaphyseal 2/3. The latter portion contained greater than 95% of the hypertrophic cells and 86% of the collagenase. The collagen-degrading activity was extracted from this region and was shown to be a true collagenase by its production of typical A fragments of tropocollagen produced by collagenase action. The enzyme was activated by aminophenylmercuric acetate and trypsin and was inhibited by EDTA, 1,10-phenanthroline, and a tissue inhibitor of metalloproteinases from human articular cartilage. Inhibitors of aspartic, cysteine, and serine proteases had no effect. Micropuncture fluids aspirated from rachitic cartilage contained latent collagenase activity, indicating an extracellular localization. Negative tests for hemoglobin in the rachitic cartilage samples indicated that there was no contamination by capillaries and that this was not a source of collagenase. It is concluded that extracellular collagenase accounts for the loss of cartilage matrix in the hypertrophic zone, and that this process may be distinct from that of capillary invasion.

Animals↗

PubMed1983

Proteoglycans from rabbit articular and growth plate cartilage. Ultracentrifugation, gel chromatography, and electron microscopy.

Proteoglycans are considered to be important for the mechanical properties of articular cartilage and growth plate and for the regulation of calcification of growth plate. We have used ultracentrifugation, gel chromatography, and electron microscopy to characterize and compare proteoglycans isolated from rabbit articular cartilage, uncalcified growth plate, and calcified cartilage. We found that proteoglycans from articular cartilage were more resistant to extraction than were proteoglycans from uncalcified growth plate and calcified cartilage. Long term neutral decalcification of calcified cartilage resulted in degraded proteoglycans. The chondroitin sulfate chains from all three tissues had similar size distribution. Gel chromatography and electron microscopy of proteoglycan monomers suggested that those from uncalcified growth plate were largest, those from articular cartilage intermediate, and those from calcified cartilage smallest. Proteoglycan aggregates from articular cartilage were longer than those from uncalcified growth plate. Both biochemical and quantitative electron microscopic data suggested the existence in mineralizing cartilage of at least two different sized populations of proteoglycan aggregates.

Animals↗

PubMed1981

Role of kidney in the catabolic clearance of human platelet antiheparin proteins from rat circulation.

UNLABELLED: Stimulated platelets release at least two antiheparin proteins: platelet factor 4 (PF4) and low affinity platelet factor 4 (LA-PF4) from which beta-thromboglobulin (beta TG) is derived. We have found previously marked elevation of LA-PF4/beta TG antigen in platelet poor plasma of patients with chronic renal failure, whereas levels of PF4 remained normal. Therefore, we examined the role of the kidneys in the metabolic clearance of LA-PF4/beta TG and PF4. The supernates of aggregates of thrombin-stimulated human platelets were injected into sham operated control rats, nephrectomized rats, and into rats with acute ureteral ligation. The disappearance of human LA-PF4/beta TG antigen and PF4 in rat plasma determined by specific radioimmunoassays followed biphasic exponential curves. The half-lives (t1/2) for the fast and slow components of LA-PF4 in control rats were 6.4 and 68.4 min. Nephrectomy significantly increased these times to 9.7 and 144 min, while ureteral ligation resulted in no significant change. Comparison of the level of LA-PF4/beta TG antigen and of creatinine in aorta and in renal vein showed 25%-30% extraction of these compounds by the kidney. Less than 0.1% of the total LA-PF4 antigen injected was recovered in the urine of control rats. In contrast to these results, the clearance of PF4 was not affected by nephrectomy. IN CONCLUSION: (1) functional renal tissue is necessary for normal clearance of LA-PF4/beta TG, but renal excretion does not play a major role in its elimination suggesting that the protein is catabolized by the kidney; and (2) catabolic clearance of PF4 does not depend on functioning kidney tissue.

Animals↗

PubMed1980

Characterization of intracellular viral RNA in interferon-treated cells chronically infected with murine leukemia virus.

We have recently found that Moloney murine leukemia virus assembles within cytoplasmic vacuoles of chronically infected NIH/3T3 cells rather than at their surface (submitted for publication). In the present study we found that if these cells were treated with interferon (IF) for 24 to 48 h the intracellular virus particles accumulated at a two- to threefold-higher level than that observed in untreated cells. Nevertheless, despite this accumulation, no difference between IF-treated and untreated cells was observed in the amount of the total cytoplasmic viral RNA or in its 35S or 21S species. When cellular virions were sedimented from the cytoplasmic fraction, a markedly higher amount of viral RNA was detected in the viral pellet of IF-treated cells than was detected in untreated cells, whereas the amount of viral RNA left in the virus-free cytoplasm of IF-treated cells was much lower than that in the untreated cells. Furthermore, the amount of the cytoplasmic polyriboadenylic acid-containing viral RNA was also remarkably higher in the IF-treated cells. Viral polyribosomes appeared to be fully functional in IF-treated cells, since no effect of IF on viral protein synthesis could be detected. Analysis of the nuclear viral RNA showed no difference between IF-treated and untreated cells after 24 h of IF treatment. Both contained a comparable amount of 35S viral RNA. However, at 48 h a significant accumulation of viral RNA was observed in the nucleus of the IF-treated cells as compared with the untreated cells, although in both cases only 35S species were evident. This accumulation appeared to activate a degradation process which destroyed nuclear viral RNA, since a dramatic shift toward smaller-sized molecules of viral RNA and a remarkable reduction in its amount were observed after 72 h of IF treatment.

Animals↗

PubMed1980

Secreted platelet proteins with antiheparin and mitogenic activities in chronic renal failure.

The levels of secreted platelet antigen (LA-PF4/beta TG) were measured by radioimmunoassay in samples of PPP obtained from human blood collected on EDTA and inhibitors of platelet release reaction. These levels in plasma of 17 normal individuals, 18 nondialyzed patients with chronic renal failure, and nine patients on hemodialysis were 31.9 +/- 2.8 ng/ml, 135.1 +/- 21.4, and 291.8 +/- 26.3, respectively. No significant differences were observed in platelet counts and in the levels of this antigen in PRP of these three groups of individuals. The levels of PF4 in PPP of eight normal individuals and in plasma of seven patients with chronic renal failure were 7.41 +/- 0.67 and 7.53 +/- 1.11 ng/ml, respectively. During processing of blood samples in the absence of platelet release inhibitors, platelets of patients with chronic renal failure released less LA-PF4/beta TG antigen than did normal platelets. The mean levels of LA-PF4/beta TG antigen excreted in urine of six normal individuals and 10 patients with chronic renal failure were 57.75 and 1461.5 ng/100 mg of creatinine per day, respectively. After 3 hr hemodialysis, LA-PF4/beta TG antigen levels in PPP increased from 291.8 +/- 26.3 ng/ml to 505.3 +/- 87.3. By contrast, this antigen in three patients with successful kidney transplants rapidly returned to levels close to normal following graft function. Immunoreactive material from pooled urine of patients with chronic renal failure was isolated by isoelectric focusing. This material focused at pH 10.0 to 10.8 and induced DNA biosynthesis in 3(3 swiss cells, indicating its similarity to PBP. It is proposed that elevation of LA-PF4/beta TG antigen observed in plasma of patients with chronic renal failure resulted from the impaired handling of this protein by the kidney.

Adult↗

PubMed1977

Biosynthetic and structural studies of hemoglobin in a patient with congenital dyserythropoietic anemia type I.

A 25 year old woman with congenital dyserythropoietic anemia (CDA) Type I is described. Typical morphologic abnormalities of the erythroid precursors in the bone marrow by light and electron microscopy, marked ineffective erythropoiesis and iron loading were present, Globin chain synthetic ratios as well as functional and structural studies on the patients hemoglobin were normal, ruling out the presence of thalassemia or a mutant hemoglobin which can both give rise to morphologic and clinical features similar to CDA. The laboratory findings on this patient and family members and a brief review of the literature are presented.

Adult↗

PubMed1975

An autoradiographic and morphological study of mouse bone marrow littoral cells during and after treatment with urethane.

This study demonstrates that the labeling index of mouse marrow littoral cells can be markedly altered as a result of treatment with ethyl carbamate (urethane). Young C57/BL mice were given daily intraperitoneal urethane injections for periods up to 6 days. Following treatment each day, as well as daily over a 10 day recovery period, a group of animals was administered tritiated thymidine every 3 hr over a 24 hr period and sacrificed 1/2 hr after the last injection. Marrow was embedded in epon and 0-5 mum sections cut for autoradiographic and light microscopic analysis. A thirty-five-fold increase in the percentage labeled littoral cells was observed after three injections of urethane. The labeling index of littoral cells fluctuated during the treatment period and during the 10 day recovery period. The albeling data are discussed in relation to the possible effects of urethane on the cell cycle of mouse marrow littoral cells; the morphological sequela to urethane treatment and the possibility that littoral cells may act as stem cells.

Animals↗

PubMed1974