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Biomedical subjects

M Berman

Publications and source records attributed to M Berman.

At least 109 records · Page 6Linked to original sources
PubMed1978

Metabolsim of apoB and apoC lipoproteins in man: kinetic studies in normal and hyperlipoproteininemic subjects.

The kinetics of apolipoproteins B and C were studied in 14 normal and hyperlipoproteinemic subjects after injection of exogenously (125)I-labeled very low density lipoprotein (VLDL) particles. Plasma radioactivities of apoB and apoC were determined over a period of 4 days in VLDL (d < 1.006) and total radioactivity in intermediate (IDL) (1.006 < d < 1.019), low (LDL) (1.019 < d < 1.063), and high (HDL) (1.063 < d < 1.21) density lipoproteins. The data were analyzed by the use of a model, developed mostly from these data, with the following results. The VLDL particle undergoes a series of incremental density changes, most likely due to a number of delipidation steps, during which apoB stays with the particle until the density reaches the IDL range. There is, however, a loss of apoC associated with these delipidation steps. In our normal subjects, all IDL apoB eventually becomes LDL. In our hyperlipemic subjects some of the apoB on IDL is also degraded directly. The apoC lost by VLDL and IDL recycles to HDL, and most of it is picked up again by newly synthesized VLDL. There is a slowdown of the stepwise delipidation process in all hyperlipemic individuals studied. Three additional features became apparent in the type III subjects. First, there is a significant increase (a factor of 2 compared to normal) in the apoB synthesis rate by way of VLDL; second, there is an induced direct apoB synthesis pathway by way of IDL (and/or LDL); third, a bypass of the regular stepwise VLDL delipidation pathway is induced by which VLDL particles lose apoC but none of their apoB, thereby forming a new particle with metabolic properties similar to LDL, but with a density still in the VLDL density range. Two type III patients treated with nicotinic acid and clofibrate showed a sharp decrease in their VLDL apoB synthesis rates. This was somewhat compensated by an increased IDL apoB synthesis rate. A type I patient on a medium chain triglyceride diet also showed a number of metabolic changes, including reduced VLDL apoB synthesis and the induction of considerable IDL and/or LDL apoB synthesis.

Adult↗
PubMed1978

Endogenously labeled low density lipoprotein triglyceride and apoprotein B kinetics.

The kinetics of endogenously labeled low density lipoprotein (LDL) triglycerides (TG) and apoprotein B (apoB) have been studied in four normal and in four hyperlipemic subjects using double tracers. Analysis of the data suggests that most LDL triglycerides turn over about 10 times faster than apoB (0.003/min vs. 0.0003/min) and that about 10% of the LDL particles contain most of the TG found with LDL. It is not possible to determine from the analysis whether each new LDL particle arrives with the excess TG or whether only a subpopulation of particles contains most of the TG. The kinetic analysis further suggests that triglyceride-rich LDL particles do not exchange with an extraplasma compartment as most LDL particles do, and thus, they behave more like very low density lipoprotein particles. A compartmental model accounting for both the LDL-TG and LDL-apoB kinetics is proposed.

Apolipoproteins↗
PubMed1978

Regulation of collagenase. Therapeutic considerations.

Why the cornea ulcerates, in the sense of what goes awry, may be related to the trapping of wound healing in a phase of proteolytic debridement related to a persistent epithelial defect. The initial avascularity of the cornea makes it particularly vulnerable to proteolytic damage. Studies on the biochemistry and cell biology of corneal ulceration have indicated that sequential interactions occur which result in the generation of collagenase activity and the development of ulceration. It is likely that the interactions are susceptible to intervention; and it is thought that eventual, successful treatment of corneal ulceration will require a complex therapy, with interventions at multiple sites of regulation.

Animals↗
PubMed1977

Activation of hepatic adenylate cyclase by guanyl nucleotides. Modeling of the transient kinetics suggests an "excited" state of GTPase is a control component of the system.

A three-state model developed originally from analysis of the steady state kinetics of hepatic adenylate cyclase has been extended to account for the transient kinetics of activation by guanyl-5'-yl imidodiphosphate (Gpp(NH)p). In contrast to activation by Gpp(NH)p, activation of the enzyme by GTP proceeds not only without a lag phase but is of considerably lower magnitude. These differences between Gpp(NH)p and GTP can be explained by the hypothesis that GTP is hydrolyzed at the nucleotide regulatory site(s) associated with adenylate cyclase and that GTPase activity is revealed uniquely when the enzyme system is in its state of highest adenylate cyclase activity. With this hypothesis, the characteristics of activation by GTP could be simulated. The implications of this model are discussed with respect to the actions of hormones and cholera toxin on adenylate cyclase activity.

Adenylyl Cyclases↗
PubMed1977

Lens correction of infantile myopia in identical twins: a case report.

Spectacles were prescribed for 5-year-old identical twins with similar high, uncorrected, isometropic myopia. One received the full correction, and the other was undercorrected by 4 D. The fully corrected subject was a constant esotrope at distance and near; the undercorrected subject exhibited exotropia at near only. Evaluations over a 5-month period indicated that the full correction was the treatment of choice.

Child, Preschool↗
PubMed1977

High density lipoprotein metabolism in man.

The turnover of (125)I-high density lipoprotein (HDL) was examined in a total of 14 studies in eight normal volunteers in an attempt to determine the metabolic relationship between apolipoproteins A-I (apoA-I) and A-II (apoA-II) of HDL and to define further some of the determinants of HDL metabolism. All subjects were first studied under conditions of an isocaloric balanced diet (40% fat, 40% carbohydrate). Four were then studied with an 80% carbohydrate diet, and two were studied while receiving nicotinic acid (1 g three times daily) and ingesting the same isocaloric balanced diet. The decay of autologous (125)I-HDL and the appearance of urinary radioactivity were followed for at least 2 wk in each study. ApoA-I and apoA-II were isolated by Sephadex G-200 chromatography from serial plasma samples in each study. The specific activities of these peptides were then measured directly. It was found that the decay of specific activity of apoA-I and apoA-II were parallel to one another in all studies. The mean half-life of the terminal portion of decay was 5.8 days during the studies with a balanced diet.Mathematical modeling of the decay of plasma radioactivity and appearance of urinary radioactivity was most consistent with a two-compartment model. One compartment is within the plasma and exchanges with a nonplasma component. Catabolism occurs from both of these compartments. With a balanced isocaloric diet, the mean synthetic rate for HDL protein was 8.51 mg/kg per day. HDL synthesis was not altered by the high carbohydrate diet and was only slightly decreased by nicotinic acid treatment. These perturbations had effects on HDL catabolic pathways that were reciprocal in many respects. With an 80% carbohydrate diet, the rate of catabolism from the plasma compartment rose by a mean of 39.1%; with nicotinic acid treatment, it fell by 42.2%. Changes in the rate of catabolism from the second compartment were generally opposite those in the rate of catabolism from the plasma compartment, suggesting that these two catabolic pathways may be reciprocally regulated.

Adolescent↗
PubMed1977

Effects of estrogen on thyroxine-binding globulin metabolism in rhesus monkeys.

To investigate the effects of estrogen on thyroxine-binding globulin (TBG) metabolism, 4 female Rhesus monkeys were studied before and 3-4 weeks after implantation of beta-estradiol (E2)-containing capsules. In addition, 2 of the animals were also studied for the first 7 days after the start of E2. Serum E2 increased 10-fold from 20 +/- 7 to 212 +/- 41 pg/ml. Serum TBG, initially 20.2 +/- 6 mug/ml, was elevated by 24 h after E2 implantation, and reached a steady level of 46.8 +/- 5.0 mug/ml by 7-10 days. For the turnover studies, highly purified [125I]iodo-TBG was injected iv and serum [125I]PBI and urinary 125I excretion were measured daily. TBG kinetics were evaluated by use of a compartmental model. Although a 2-compartment model was sufficient to fit the control and late E2 data, a 3-compartment model was developed in order to account for the modifications observed during the early E2 period. The final decay rate (k) of TBG was 0.26 +/- 0.01/day during the control period and was slightly lower after E2 (0.23 +/- 0.01/day). In the 2 monkeys studied during the early E2 period, the major effect of E2 was a stimulation of the TBG production rate. This was simulated in the model by a stepwise increase occurring in the last quarter of the first day after E2. There was also an abrupt redistribution of TBG in the compartments defined by the model. The total distribution or serum equivalent volume of TBG after 3-4 weeks of E2 increased 1.4-fold, from 338 +/- 37 ml to 458 +/- 22 ml, and the metabolic clearance rate increased 1.3-fold, from 90 +/- 10 ml/d to 113 +/- 12 ml/d. The increase in the final TBG production rate (2.9-fold) was only slightly greater than the rate calculated for the early E2 period, and was similar to the increase we have recently found in monkey hepatocytes studied in vitro after isolation from E2-treated animals. It appears that stimulation of hepatic synthesis of TBG accounts for the elevated serum levels of TBG observed after estrogen.

Animals↗
PubMed1977

The turnover and conversion to glucose of alanine in newborn and grown dogs.

The extent of transfer of carbon atoms from alanine to glucose was examined in pups and grown dogs. [U-14C]Alanine and [2-3H]glucose were injected intravenously and by using the SAAM-26 program a compartmental model was formulated from the tracer data to quantify the kinetics of the alanine- and glucose-carbon system. A 3-compartment model was necessary to describe the alanine-carbon kinetics. Strict identification of these compartments with physiological counterparts was not possible. The overall transport (turnover) rate of alanine-C was found not to change significantly with age when calculated on the basis of body weight. Carbon atoms from alanine reach glucose by three identifiable pathways of different speed. The kinetics suggest that the different pathways are at least in part due to differences in the metabolism of the three carbon atoms of alanine. In pups less than 11 days of age 45-49% of the carbon atoms leaving the alanine subsystem enter glucose; in adults it was 70%. In young pups 18-19% of glucose-C utilized was derived from alanine-C, whereas in adults, 62%. Accordingly a smaller percentage of carbon atoms utilized as alanine appears in glucose and a smaller percentage of glucose-C is derived from alanine in pups than in grown dogs.

Age Factors↗
PubMed1977

Pertechnetate distribution in man after intravenous infusion: a compartmental model.

Using a primed infusion technique, distribution of pertechnetate was monitored in normal volunteer subjects over an 8-hr period. Two groups of subjects were studied, during hours 0-4 (n = 8) and hours 4-8 (n = 7), respectively, of the infusion. At 6.5 hr a large dose of NaI (1000 mg) was administered intravenously to the second group. Plasma, salivary, and urinary radioactivities were assayed, and external counts were made of radioactivities over the neck, thigh, and right upper abdomen. A kinetic model was developed for pertechnetate based upon the distribution data, the iodide perturbation, and known physiology for pertechnetate and iodide. The model has three major subsystems: (1) the thyroid trap; (2) a whole-body distribution, containing plasma and two extravascular compartments; and (3) the gastrointestinal tract, including the salivary, stomach (including upper small intestine), and two lower intestinal compartments. One of the latter, which turns over very slowly, is believed to represent bowel wall. The large NaI dose markedly reduced transport into compartments of the thyroid trap, the saliva, and the stomach and small intestine. This study shows that, in most respects, pertechnetate is distributed qualitatively but not quantitatively like iodide but that, unlike iodide, large bowel distribution plays an important role, especially in long-term studies.

Adult↗
PubMed1976

Evidence for a new intermediate state in the mechanism of (Na+ + K+)-adenosine triphosphatase.

A rapid mixing technique was used to follow the intermediate formation of phosphorylated enzyme and liberation of inorganic phosphate by a microsomal preparation of (Na+ + K+)-ATPase. In the presence of 100 mM Na+,but without added K+, phosphorylation reaches a constant level at a rate which is dependent on ATP concentration. Inorganic phosphate production lags during the inital phase of phosphorylation and then accumulates at a constant rate. These observations favor a scheme in which Pi is liberated as the result of turnover of the phosphorylated enzyme. In the presence of 100 mM Na+ and 2.5 mM K+ phosphate production was resolved into two phases consisting of an initial 'burst' and late steady state phase...

Adenosine Triphosphatases↗
PubMed1976

Cerebral dominance for consciousness.

In a prospective study we evaluated the relationship of level of consciousness to hemispheric side of lesion following acute cerebrovascular injury. Fifty-seven percent of patients with left hemispheric lesions had initial impairment of consciousness, in contrast to 25% with right-sided damage.

Cerebrovascular Disorders↗
PubMed1976

Effects of age and fasting on gluconeogenesis from glycerol in dogs.

The extent of gluconeogenesis from glycerol was examined in pups and adult dogs. With use of the SAAM-26 program, a four compartment model was formulated from tracer data to calculate the kinetics of the glycerol:glucose system. In the postabsorptive state gluconeogenesis from glycerol declines with age: 13.8% of glucose carbon originated from glycerol in 0- to 4-day-old pups, 6% in adults. Approximately 50% of glycerol carbon is converted to glucose carbon independent of age. During fasting, a) the percentage of glucose carbon arising from glycerol carbon increased to 13.3% and 10.3% in adult dogs and pups 5-19 days old, respectively, in younger pups it declined to 3.4%; b) glycerol production increased in adults, but decreased in the youngest pups; c) glucose production and utilization decreased at all ages, and a smaller percentage of glycerol carbon was converted to glucose carbon, especially in the youngest pups. Thus in neonates fasting decreases gluconeogenesis from glycerol.

Aging↗
PubMed1976

Effects of arterial versus venous sampling on analysis of glucose kinetics in man.

A compartmental model is presented to account for transient and steady-state changes in blood glucose concentration which result from transit through the forearm and hand in man. This model permits the inter-conversion of arterial and venous data and the derivation of arterial equivalent total body glucose models from venous data. Data were obtained from subjects in the basal state following a pulse injection of [1-14C]glucose tracer. An artery, an antecubital vein, and a dorsal vein of a heated hand (68 degrees C environment) were sampled. Blood transit time is shorter 0.3 vs. 1.0 min) and irreversible glucose loss is reduced (1.9 vs. 2.9%) in the heated hand preparation when compared to the antecubital vein preparation. Because of the smaller correction required and the smaller variation among individuals when heated hand rather than antecubital vein data are obtained, we suggest that for analysis of whole-body kinetics such data should be used along with the compartmental model correction when arterial data cannot be obtained.

Adult↗
PubMed1976

Directional forces.

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Extraoral Traction Appliances↗