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Biomedical subjects

A Moses

Publications and source records attributed to A Moses.

31 records · Page 2Linked to original sources

An acupuncture-associated outbreak of hepatitis B in Jerusalem.

Two clusters of between five and eleven cases of hepatitis B associated with acupuncture treatment by a physician occurred in Jerusalem in late 1986. The origin of the outbreak is believed to have been an Ethiopian immigrant surgical patient, a known HBsAg carrier, who infected an operating room nurse during a surgical procedure. This is the first recorded instance of transmission of HBV from an Ethiopian immigrant to the local Israeli population. We reiterate the need for the enforcement of correct sterilization techniques in all skin-piercing settings, a step which in many countries will require the licensing of a variety of occupations not presently covered by health regulations.

Acupuncture Therapy↗

Tibial epiphyseal development: a cross-sectional histologic and histomorphometric study in the New Zealand white rabbit.

Sequential histomorphometric studies on the developing rabbit tibia from birth to skeletal maturity demonstrate that growth plate height lessens as longitudinal growth diminishes. Differing rates of development proximally and distally are documented. Distally, growth plate height, width, and area and total epiphyseal area peak or reach near maximum values by 3 weeks, whereas proximally, they do so by 8 weeks (except for height, which also peaks at 3 weeks). The distal growth plate is being obliterated by 16 weeks, at which time the proximal growth plate remains well structured and open. The distal tibia and fibula develop as one tissue mass. The articular cartilage and epiphyseal cartilage are continuous from birth, whereas a single ossification center and a single growth plate are present by 8 weeks. The data point to the presence of intrinsic growth plate, as well as systemic, control mechanisms affecting skeletal growth. Knowledge of temporal and quantitative features of epiphyseal and growth plate development will greatly aid in the elucidation of the underlying controls.

Aging↗

A longitudinal study of the growth of the New Zealand white rabbit: cumulative and biweekly incremental growth rates for body length, body weight, femoral length, and tibial length.

This longitudinal study documents cumulative and incremental growth in the New Zealand white rabbit from 2 to 34 weeks of age at biweekly intervals. Body weight, body length, femoral length, and tibial length have been assessed in 17 male and 12 female rabbits, with the data tabulated separately. A specially designed restrainer was used that allowed the sequential clinical measurements and femoral and tibial radiographs to be performed without the use of anesthesia. Skeletal growth was complete at 28 weeks, with the 34-week values thus representing mature adult lengths. The mean body weight at 2 weeks of age was 6% that at 34 weeks, and by 16 weeks, 72% of the weight at 34 weeks was achieved. Weight continued to increase in the adult. The mean body length at 2 weeks was 40% that at 34 weeks, and by 16 weeks, 91% of mature adult length was achieved. The mean femoral length at 2 weeks was 38% of the adult length, and at 16 weeks, it reached 95% of adult length. The mean tibial length at 2 weeks was 38% of the adult length, and 94% of the adult value was achieved by 16 weeks. The longitudinal data document the rate and extent of growth of the New Zealand white rabbit, and allow for more accurate timing and quantitation of physical and systemic interventions on the developing skeleton of the commonly investigated New Zealand white rabbit.

Animals↗

Selective resistance to parathyroid hormone in cultured skin fibroblasts from patients with pseudohypoparathyroidism type Ib.

We measured cAMP production in response to agonists in cultured skin fibroblasts from subjects with pseudohypoparathyroidism type Ib (PHP Ib; normal phenotype, resistance to PTH only, normal guanine nucleotide stimulatory coupling protein activity) and skin fibroblasts from normal subjects. There were no significant differences in basal or prostaglandin E1- and forskolin-stimulated cAMP production in PHP Ib vs. normal fibroblasts. Fibroblasts from 7 of 10 subjects with PHP Ib had significantly reduced peak cAMP responses to PTH [3.95 +/- 0.88 vs. 15.9 +/- 4.2 pmol/100 micrograms protein (mean +/- SD); n = 7 for both groups; P less than 0.001]. PTH-stimulated cAMP production was significantly reduced in the 7 subjects with PHP Ib at all concentrations of PTH tested [3-1000 ng/ml human PTH-(1-34)]. In the other 3 subjects with PHP Ib, the cAMP response to PTH was either normal (2 subjects) or above the normal range (1 subject). Thus, skin fibroblasts from many, but not all, subjects with PHP Ib have selective resistance to PTH in terms of cAMP response. Since the defect is hormone specific and persists in culture, we suggest that an intrinsic defect in the PTH receptor may cause PTH resistance in certain subjects with PHP Ib. The cause of PTH resistance in the subjects with a normal cAMP response to PTH is not known, but the data suggest heterogeneity even within the PHP Ib subgroup.

Adolescent↗

Longitudinal roentgencephalometric study of the growth of the New Zealand white rabbit: cumulative and biweekly incremental growth rates for skull and mandible.

A longitudinal roentgencephalometric study of the New Zealand white rabbit has documented postnatal skull and mandible growth from 2 to 34 weeks of age. Dorsoventral and lateral radiographs were performed using a specially constructed restrainer that allowed for standardized films and did not require the use of anesthesia. Assessments from 17 male and 12 female rabbits at biweekly intervals documented cumulative growth as well as biweekly incremental growth. Indices reported here include skull length, interzygomatic width, intercondylar width, and mandibular length. Mean skull length at 2 weeks was 54% of that at 34 weeks, and by 16 weeks 91% of adult skull length was achieved. Mean interzygomatic width at 2 weeks was 60% of that at 34 weeks, and by 16 weeks 91% of adult male and 94% of adult female widths were achieved. Mean mandibular length at 2 weeks was 47% of that at 34 weeks, and by age 16 weeks 90% of adult length was achieved. Mean intercondylar width at 2 weeks was 57% of that at 34 weeks, and by 16 weeks 89% of adult male and 93% of adult female widths were achieved. Biweekly increments decreased continually from 2 weeks of age on for all indices.

Aging↗

Receptors and growth-promoting effects of insulin and insulinlike growth factors on cells from bovine retinal capillaries and aorta.

It has been suggested that elevated levels of insulin or insulin-like growth factors (IGFs) play a role in the development of diabetic vascular complications. Previously, we have shown a differential response to insulin between vascular cells from retinal capillaries and large arteries with the former being much more insulin responsive. In the present study, we have characterized the receptors and the growth-promoting effect of insulinlike growth factor I (IGF-I) and multiplication-stimulating activity (MSA, an IGF-II) on endothelial cells and pericytes from calf retinal capillaries and on endothelial and smooth muscle cells from calf aorta. We found single and separate populations of high affinity receptors for IGF-I and MSA with respective affinity constants of 1 X 10(-9) M-1 and 10(-8) M-1 in all four cell types studied. Specific binding of IGF-I was between 7.2 and 7.9% per milligram of protein in endothelial cells and 9.1 and 10.4% in the vascular supporting cells. For 125I-MSA, retinal endothelial cells bound only 1.7-2.5%, whereas the aortic endothelial cells and the vascular supporting cells bound between 5.6 and 8.5% per milligram of protein. The specificity of the receptors for IGF-I and MSA differed, as insulin and MSA was able to compete with 125I-IGF-I for binding to the IGF-I receptors with 0.01-0.1, the potency of unlabeled IGF-I, whereas even 1 X 10(-6) M, insulin did not significantly compete with 125I-MSA for binding to the receptors for MSA. For growth-promoting effects, as measured by the incorporation of [3H]thymidine into DNA, confluent retinal endothelial cells responded to IGF-I and MSA by up to threefold increase in the rate of DNA synthesis, whereas confluent aortic endothelial cells did not respond at all. A similar differential of response to insulin between micro- and macrovascular endothelial cells was reported by us previously. In the retinal endothelium, insulin was more potent than IGF-I and IGF-I was more potent that MSA. In the retinal and aortic supporting cells, no differential response to insulin or the IGFs was observed. In the retinal pericytes, IGF-I, which stimulated significant DNA synthesis beginning at 1 X 10(-9) M, and had a maximal effect at 5 X 10(-8) M, was 10-fold more potent than MSA and equally potent to insulin. In the aortic smooth muscle cells, IGF-I was 10-100 times more potent than insulin or MSA. In the retinal and aortic supporting cells, no differential response to insulin or the IGFs was observed. In the retinal pericytes, IGF-I, which stimulated significant DNA synthesis beginning at 1 X 10(-9) M, and had a maximal effect at 5 X 10(-8) M, was 10-fold more potent than MSA and equally potent to insulin. In the aortic smooth muscle cells, IGF-I was 10-100 times more potent than insulin or MSA. In addition, insulin and IGF-I at 1 X 10(-6) and 1 X 10(-8) M, respectively, stimulated these cells to grow by doubling the number of cells as well. In all responsive tissues, the combination of insulin and IGFs were added together, no further increase in effect was seen. These data showed that vascular cells have insulin and IGF receptors, but have a differential response to these hormones. These differences in biological response between cells from retinal capillaries and large arteries could provide clues to understanding the pathogenesis of diabetic micro- and macroangiopathy.

Animals↗

Prolactin and thyroid-stimulating hormone responses to thyrotropin-releasing hormone in cases of hyperprolactinemia with normal and abnormal sella tomograms.

An intravenous bolus of 500 micrograms of thyrotropin-releasing hormone (TRH) was used to test prolactin and thyroid-stimulating hormone (TSH) responses in normoprolactinemic patients and in hyperprolactinemic patients with normal and abnormal sella turcica. The prolactin response showed a mean increment of 64.1 +/- 46.3 ng/ml in normoprolactinemic women. In patients with hyperprolactinemia, the mean increment was 14.1 +/- 22.4 ng/ml and 13.8 +/- 33.1 ng/ml for patients with normal and abnormal sella, respectively. The difference in the prolactin response between the normoprolactinemic patients and either group of hyperprolactinemic patients is significant (P less than 0.005). The mean baseline TSH in normoprolactinemic patients is significantly higher than in patients with hyperprolactinemia with normal and abnormal sella. The mean increment of TSH after TRH stimulation is significantly higher in normoprolactinemic patients than in either group of patients with hyperprolactinemia (P less than 0.005). These results suggest an inhibitory action of hypothalamic dopamine on the response of both prolactin and TSH to TRH in patients with hyperprolactinemia. The hypothalamic dopamine mechanism might also be the factor leading to suppression of baseline TSH levels in hyperprolactinemic patients. In addition, these results suggest that patients with hyperprolactinemia, with or without changes in the sella turcica, might have various degrees of the same pathology affecting the lactotropes.

Adult↗

The relation between oral contraceptive use and subsequent development of hyperprolactinemia.

Serum prolactin levels were determined in 123 patients who presented with menstrual irregularities and/or infertility of more than 1 year's duration. Sixty-three patients had hyperprolactinemia with serum prolactin levels of 26 to 843 ng/ml (normal 5 to 22 ng/ml); 44.4% of this group of patients received oral contraceptive for a period of 2 months to 7 years. Sixty patients were normoprolactinemic, with serum prolactin levels of 3 to 22 ng/ml; 33.4% of this group received oral contraceptives for a period of 6 months to 7 years. The age of presentation, onset of symptoms, age at which they started on oral contraceptives, and duration of use were tabulated. The data were analyzed using chi 2 test corrected for continuity. There was no significant difference in age at the time of evaluation between oral contraceptive users and nonusers with hyperprolactinemia. The relative odds developing hyperprolactinemia were 2.64 times greater among women who has used oral contraceptives for more than 1 year and 6.25 times greater if this use started before the age of 25.

Adolescent↗

Metabolic effects of a fat- and carbohydrate-rich meal in rats.

To investigate meal-induced changes in hepatic fat and carbohydrate metabolism in rats, hepatic venous, portal venous, and aortal plasma levels of several metabolites as well as changes in hepatic glycogen and lactate content were measured during and after the first nocturnal meal following a 12-h fast. The rats were fed a diet with about 46%, 41%, and 13% of the total energy (approximately 16.5 kJ/g) derived from carbohydrates, fats, and protein, respectively. During the later part of the meal and thereafter, plasma triglyceride level increased in all blood vessels. After a transient initial decrease, portal venous and aortal nonesterified fatty acid (NEFA) levels, net hepatic NEFA uptake, and hepatic beta-hydroxybutyrate (BHB) production increased and reached fasting (meal onset) values by 30 min after the meal. Although liver glycogen did not change significantly, the liver released glucose continuously. The liver initially accumulated lactate and maintained a high lactate concentration despite switching from lactate uptake to net release of lactate around 10 min into the meal. Taken together, these data indicate that hepatic glycolysis, gluconeogenesis, and considerable fatty acid oxidation occur concurrently in rat liver during and after a fat- and carbohydrate-rich meal. The findings are relevant to contemporary hypotheses of the metabolic control of eating and, in particular, to hypotheses linking hepatic fatty acid oxidation to postprandial satiety.

3-Hydroxybutyric Acid↗