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Biomedical subjects

M Berman

Publications and source records attributed to M Berman.

At least 145 records · Page 8Linked to original sources
PubMed1981

Acute transverse myelitis: incidence and etiologic considerations.

There have been few population-based studies of acute transverse myelitis (ATM). Therefore, incidence and population selectivity of this disorder in different regions is not well known. Data on all Jewish patients with ATM throughout Israel were collected for the period 1955 through 1975. Based on 62 patients who satisfied rigid diagnostic criteria, the average annual incidence rate was 1.34 per million population. No significant difference in incidence was noted between European/American-born and Afro/Asian-born populations. There was no significant seasonal or annual fluctuation in frequency. In 37% of the patients, a history of infection prior to ATM was reported, more commonly among younger patients. ATM rarely evolved into multiple sclerosis. More than one-third of the patients with ATM made a good recovery; in another one-third recovery was only fair; 14 patients failed to improve and 3 died. If other population-based studies of ATM were undertaken, comparison with our results might shed further light on the causes of this disorder.

Acute Disease↗
PubMed1981

Glucose disposal and gluconeogenesis from alanine in tumor-bearing Fischer 344 rats.

For the study of glucose carbon recycling and incorporation of carbon atoms from plasma glucose, [3-3H]glucose and [U-14C]alanine were injected into inbred non-tumor-bearing (NTB) and tumor-bearing (TB) male F344 rats. The glucose and alanine kinetics were determined in relation to antecedent food intake and carcass weight loss. Whereas fed NTB and TB rats appropriately experienced reduced glucose disposal with decreased food intake (0.99 vs. 0.29 mg/min -100 g(-1) compared wtih observations in starved NTB rats), starved TB rats exhibited increased glucose utilization. Both fully fed and cachectic TB groups exhibited increased isotopic carbon recycling compared to the carbon recycling of NTB control groups, whereas starved TB rats did not demonstrate increased recycling compared to the carbon recycling (27% of C-atoms recycled). These findings suggest that alterations of glucose turnover, carbon recycling, and gluconeogenesis in the fed host parallel hypophagia and weight loss, regardless of TB status.

Alanine↗
PubMed1981

Influence of nicotinic acid on metabolism of cholesterol and triglycerides in man.

The mechanisms for the hypolipidemic action of nicotinic acid were examined in 12 patients with hyperlipidemia. Most patients were studied in the hospital on a metabolic ward. The first month was a control period followed by 1 month on nicotinic acid. During treatment with nicotinic acid, the triglycerides (TG) decreased in total plasma by an average of 52% and in very low density lipoproteins (VLDL) by 36%. Transport rates of VLDL-TG were determined by multicompartmental analysis following injection of [3H]glycerol as a precursor. Nicotinic acid decreased transport (synthesis) of VLDL-TG by an average of 21%. Kinetic modeling of the VLDL-TG data suggested that the TG reduction was due to a decrease in TG content of VLDL and hence a reduction in lipoprotein size more than number. For the whole group, plasma cholesterol fell during nicotinic acid therapy by a mean of 22%. The drug produced no detectable changes in fecal excretions of cholesterol (neutral steroids) or bile acids. However, it induced a small but significant increment in hepatic secretion of biliary cholesterol that might have led to a net loss of cholesterol from the body even though this loss could not be detected by sterol balance. Despite this increase in outputs of biliary cholesterol, there was not a significant increase in molar % cholesterol or in % saturation of gallbladder bile. Therefore, it is doubtful that nicotinic acid enhances the risk for cholesterol gallstones.

Absorption↗
PubMed1981

Hydrolysis of rat chylomicron acylglycerols: a kinetic model.

A quantitative model describing the kinetics of hydrolysis of rat chylomicron acylglycerols by bovine milk lipoprotein lipase has been developed using data from studies on rat lymph chylomicrons containing doubly labeled acylglycerols. The detailed analysis indicates that, in addition to hydrolysis from tri- to di-, di- to mono-, and monoacylglycerol to glycerol, and apparently direct hydrolysis pathway of tri- to monoacylglycerol is also present. This accounts for the transient accumulation of monoacylglycerol seen in some of the experiments. For most hydrolysis steps, a Michaelis-Menten mechanism adequately describes the rate of hydrolysis as a function of lipoprotein lipase concentration. A higher order, more complex mechanism, however, is necessary for the apparent tri- to monoacylglycerol hydrolysis pathway. A mathematical function that describes the way free fatty acid released can control the rates of hydrolysis, and how the presence of the binding sites for free fatty acid on albumin in the incubation medium can modulate this, in included. The model simultaneously satisfies the kinetics of hydrolysis for tri-, di-, and monoacylglycerol together with the kinetics of the glycerol and fatty acid moieties for a wide range of albumin and lipoprotein lipase concentrations.

Animals↗
PubMed1981

Induction of lymphomas in mice by busulfan and chloramphenicol.

Busulfan causes long-lasting defects in the hematopoietic stem cells and in the immune system of mice. We designed studies to determine whether chloramphenicol further damaged the already defective hematopoietic stem cells of mice that were pretreated with busulfan, and we unexpectedly observed that mice given injections of the combination of busulfan and chloramphenicol developed lymphomas in relatively high incidence. The disease is invariably associated with splenomegaly and enlargement of the thymus. Leukocytosis with lymphoblasts in the peripheral blood occurred in some affected mice. The malignant cell is a lymphoblast of thymic origin. Thirteen of 37 mice which received both busulfan and chloramphenicol developed lymphomas. An additional five of the remaining 24 mice without proven lymphoma died and were not autopsied. Twelve of the 13 proven lymphomas developed within 280 days from the start of the experiment. Four of the 35 mice treated with busulfan alone developed lymphomas, and an additional five of the remaining 31 died but were not autopsied. Two of 41 mice treated with only chloramphenicol developed lymphomas. Of the mice treated with either busulfan or chloramphenicol alone that developed lymphomas, all did so more than 280 days from the start of the experiment. None of the control mice developed lymphoma. We conclude that both busulfan and chloramphenicol may induced lymphomas in mice that are not known to develop them spontaneously. The combination of both busulfan and chloramphenicol increased the frequency and accelerated the onset of the disease.

Animals↗
PubMed1981

Detection of high erythropoietin titers in renal extracts of hypoxic rats.

Previous attempts to extract erythropoietin from the kidneys have not been uniformly successful and have yielded only small amounts. Attempts were therefore made to extract erythropoietin from renal extracts prepared from the supernatant obtained after homogenizing kidneys in various liquids and centrifuging at 2300 x g. Detectable amounts of erythropoietin were recovered from kidneys of nonhypoxic male but not female rats. After exposure to hypoxia, the amounts increased to levels greater than 6.0 U/kidney from males after 8 hr of hypoxia. Erythropoietin became detectable in extracts from kidneys obtained from females after 2 hr of hypoxia and rose to levels of 0.54 U/kidney after 4 hr of hypoxia. The amount of plasma trapped in the kidneys at the time of extraction was not sufficient to account for a significant amount of this erythropoietin, and erythropoietin was not detected in extracts made from livers or spleens. Severalfold larger titers of erythropoietin were detected in renal extracts, by a simple extraction procedure, than was the case in previous attempts. The reasons for this difference are discussed.

Animals↗
PubMed1980

Prostaglandin E1 binding and adenylate cyclase activation in normal and transformed fibroblasts.

The binding of [3H]prostaglandin E1 to membranes of clones of normal rat kidney fibroblasts (NRK cells) has been measured. Cell lines that responded to prostaglandin E1, such as NRK and NRK transformed with Schmitt-Ruppin strain of Rous sarcoma virus (SR-NRK cells), have a high affinity prostaglandin E1 binding site. Murine-sarcoma-virus-transformed lines of NRK cells are unresponsive to prostaglandin E1 and have reduced prostaglandin E1 binding Exposure of cells to prostaglandin E1 results both in decreased prostaglandin E1 responsiveness and reduced prostaglandin E1 binding. Activation of adenylate cyclase is correlated to binding of prostaglandin E1 to receptors in both NRK and SR-NRK cell membranes. Mathematical models suggest that GTP decreases the affinity of hormone for its receptor while increasing the catalytic efficiency of adenylate cyclase, and that aggregates of occupied receptors may play an important role in the activation of adenylate cyclase.

Adenylyl Cyclases↗
PubMed1980

Collagenase levels in a new model of experimental herpetic interstitial keratitis.

A reproducible model of severe herpetic interstitial keratitis was developed by injecting live herpes simplex virus type 2 intrastromally into the corneas of presensitized rabbits. Herpes-infected corneas showed significantly more stromal infiltration and vascularization, iritis, conjunctivitis, and epithelial disease than the control corneas injected with cell supernatant without virus. Levels of total collagenase detected in the culture media of the herpes-infected corneas were high and were similar to those observed previously in alkali-burned rabbit corneas. Unlike alkali-burned corneas, the herpes-infected corneas showed much more of the enzyme in the latent form during the first two days of culture.

Animals↗
PubMed1980

Benign recurrent intrahepatic cholestasis: studies of bilirubin kinetics, bile acids, and cholangiography.

Three patients with benign recurrent intrahepatic cholestasis are described. They had had between five and 16 attacks of cholestasis. Between attacks the liver function tests, including serum bile acids, were normal. Serial serum bilirubin and bile acid estimations during the cholestasis in one patient revealed a consistent discrepancy between the serum bilirubin and bile acid concentrations during three consecutive attacks. In the other two patients the serum concentrations of bile acids and bilirubin varied in parallel. Analysis of the individual serum bile acids did not reveal high concentrations of any 'toxic' bile acid. In one patient, plasma bromsulphthalein (BSP) curves were obtained during both remission and cholestatic periods. The 45 minute retention was slightly increased (10.8%) during remission. During the cholestasis, the 45 minute retention (25%) and the fractional extraction coefficient (Ke=0.069 min-1) were markedly abnormal. The hepatic clearance of unconjugated radiobilirubin was normal at all times in this patient, although during cholestasis, conjugated bilirubin reflexed from the liver to the plasma and was then cleared slowly with a half life of approximately 12 hours. Treatment with corticosteroids, cholestyramine, and phenobarbitone was unsatisfactory.

Adult↗
PubMed1980

A model for carbon kinetics among plasma alanine, lactate, and glucose.

To account for the exchange of carbon atoms among alanine, lactate, and glucose in vivo, [2,3-3H]- and [U-14C]alanine or [3-3H]- and [U-14C]glucose were injected simultaneously to nonanesthetized normal dogs. The concentrations in plasma of 14C-labeled alanine, lactate, and glucose, and the injected 3H-labeled substrate were followed for 160 min after injection of the tracers. An integrated kinetic model describing the exchange of carbon atoms among substrates was developed from these data. The analysis suggests that there is a very rapid exchange of the carboxyl carbon of alanine with lactate in contrast to carbons 2 and 3. The model was used to calculate the fluxes of carbon atoms among the substrates in a steady state. In normal dogs plasma alanine and lactate contribute 14% of the carbon atoms released into the circulation as glucose.

Alanine↗
PubMed1980

Transfer of carbon atoms among circulating glucose, alanine, and lactate in pancreatectomized dogs.

The rates of transfer of carbon atoms (mg C . kg body wt-1 . min-1) among plasma glucose, alanine, and lactate have been calculated in pancreatectomized dogs from the tracer concentration versus time curves in the plasma after an intravenous injection of either [2,3-3H]- and [U-14C]alanine or [3-3H]- and [U-14C]glucose. The calculations were based on an integrated kinetic model derived earlier from experimental data. In comparison to normal dogs, in insulin-deprived pancreatectomized dogs, the rate of turnover of glucose (mg C . kg-1 . min-1) is increased about twofold, but the turnover rates of lactate and alanine are not changed significantly. About twice as much carbon is transferred from lactate to glucose, whereas the transfer of carbon from alanine is increased by 47%. Carbon transfer to glucose from unidentified sources is also doubled. In conclusion, in the pancreatectomized dog, gluconeogenesis is increased not by an increased production of alanine and lactate but by an increased diversion of their carbon atoms to glucose at the expense of other pathways.

Alanine↗
PubMed1980

Stromal vascularization prevents corneal ulceration.

Experiments were performed with a model of focal, thermal-induced ulceration to test the clinical impression that vascularization prevents ulceration of the corneal stroma. Slow-release polymers containing a vasoproliferase agent (tumor angiogenesis factor) were placed in corneal pockets 2 mm central to the limbus of albino rabbits. These polymers elicited blood vessel ingrowth up to the implant. Control eyes received empty polymers which caused minimal to no vessel growth. Polymers were removed, and each cornea received a focal, thermal burn placed just central to the polymer site. All control corneas ulcerated: most (79%) developed deep stromal or perforating ulcers. Only 25% of prevascularized corneas developed stromal ulcers, and none was deep or perforating. After thermal burns, vessels in both groups grew at the same linear rate toward the burned area. There was a direct relationship between the distance separating the nearest blood vessel and the burned area at the time of burning and the maximum depth of stromal ulceration. Thus prevention of or less severe stromal ulceration is correlated with the earlier presence of vessels in the burned area.

Angiogenesis Inducing Agents↗