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Biomedical subjects

G Mor

Publications and source records attributed to G Mor.

70 records · Page 4Linked to original sources
PubMed1984

Risk in the vaginal delivery of the large fetus.

The problem of the excessively weighted fetus was studied. For this purpose, over a period of 2 years, each delivery with fetal weight of 4,500 g or more was included in the study. The history and examination findings of the present pregnancy were reviewed following delivery. The postpartum outcome and later complications in both mothers and infants were investigated prospectively. A total of 82 deliveries of large babies were included in the study and the outcome was compared with that of parallel deliveries of babies within the normal weight range (2,500-4,000 g). Factors frequently associated with excessive fetal weight were identified. A relatively high perinatal mortality and morbidity relating to vaginal delivery were observed among the large infants. In all those cases who developed delay in the second stage of labour, Caesarean section is proposed when macrosomia is clinically suspected and confirmed by ultrasonic assessment. Moreover elective Caesarean section should be considered before labour, when macrosomia is associated with hyperglycaemia or other pathology.

Adult↗
PubMedDate not supplied

Regulation of fas ligand expression in breast cancer cells by estrogen: functional differences between estradiol and tamoxifen.

During neoplastic growth and metastasis, the immune system responds to the tumor by developing both cellular and humoral immune responses. In spite of this active response, tumor cells escape immune surveillance. We previously showed that FasL expression by breast tumor plays a central role in the induction of apoptosis of infiltrating Fas-immune cells providing the mechanism for tumor immune privilege. In the present study, we showed that FasL in breast tissue is functionally active, and estrogen and tamoxifen regulate its expression. We identified an estrogen recognizing element like-motif in the promoter region of the FasL gene, suggesting direct estrogen effects on FasL expression. This was confirmed by an increase in FasL expression in both RNA and protein levels in hormone sensitive breast cancer cells treated with estradiol. This effect is receptor mediated since tamoxifen blocked the estrogenic effect. Interestingly, tamoxifen also inhibited FasL expression in estrogen-depleted conditions. Moreover, an increase in FasL in breast cancer cells induces apoptosis in Fas bearing T cells and, tamoxifen blocks the induction of apoptosis. These studies provide evidence that tamoxifen inhibits FasL expression, allowing the killing of cancer cells by activated lymphocytes. This partially explains the protective effect of tamoxifen against breast cancer.

Breast Neoplasms↗
PubMedDate not supplied

Changes in blood pressure in the lying and sitting positions in normotensive, borderline and hypertensive subjects.

Blood pressure of hypertensive subjects reacts differently from that of borderline or normal subjects at rest in either sitting or lying positions. In the hypertensive group the diastolic pressure tends to rise more on consecutive measurements and the systolic blood pressure tends to fall less than in the two other groups. Similarly, on going from the lying to the sitting position, diastolic blood pressure of hypertensives rises less than that of normotensive or borderline hypertensive individuals. Thus, people with 'casual' hypertension differ in their reaction to rest and changes in body position in their reaction to rest and changes in body position with respect to normotensives or borderline hypertensives. This behavior could lead to labelling of subjects as 'normal' or 'hypertensive' depending on position and timing of the blood pressure measurement.

Blood Pressure↗
PubMedDate not supplied

Estradiol regulates monocyte chemotactic protein-1 in human coronary artery smooth muscle cells: a mechanism for its antiatherogenic effect.

OBJECTIVE: The protective effect of estrogen against early atherosclerosis in animal models is well documented, but the mechanisms responsible for this effect are not well understood. The earliest recognizable event in the pathogenesis of atherosclerosis is an increased recruitment of macrophages into the arterial subendothelium. Macrophages first play a protective role by removing low-density lipoproteins, but when the cholesterol is in excess, macrophages are converted into foam cells and form atheromas. Recent human and animal data indicate that the recruitment of macrophages to the arterial wall is mediated by monocyte chemotactic protein-1 (MCP-1). We hypothesized that one of the mechanisms of estrogen's protective effect against atherosclerosis may be the down-regulation of MCP-1 expression in the arterial wall. DESIGN: Human coronary artery smooth muscle cells were replicated to confluence in smooth muscle cell basal medium supplemented with growth factors and 5% fetal bovine serum. Before each experiment, cells were incubated for 24 h with phenol red-free medium containing 5% charcoal-stripped calf serum, and then they were treated with various concentrations of 17beta-estradiol as well as selective estrogen receptor (ER) modulators, raloxifene and tamoxifen. MCP-1 messenger ribonucleic acid (mRNA) levels were quantified by Northern blots. MCP-1 protein was quantified using an enzyme-linked immunosorbent assay. ER expression was evaluated by reverse transcriptase-polymerase chain reaction. RESULTS: Human coronary artery smooth muscle cells expressed MCP-1 mRNA and produced MCP-1 protein. Estradiol induced up to 40% inhibition in mRNA expression at concentrations 10-9 M and higher. Raloxifene and tamoxifen also resulted in an inhibition, but the inhibition was less than when induced by estradiol. Estradiol also inhibited the MCP-1 protein production in a concentration-dependent manner (p < 0.05). Coronary smooth muscle cells expressed both ERalpha and ERbeta. CONCLUSION: Our findings suggest that one of the mechanisms by which estrogen prevents atherosclerosis is by down-regulating MCP-1 expression, thus decreasing macrophage recruitment to the arterial wall.

Animals↗
PubMedDate not supplied

Absence of neural responses following suppression of the immune response by cyclophosphamide.

Injection of sheep red blood cells (SRBC) as an antigenic stimulus, causes significant increases (up to 300%) in multiunit neural activity in the preoptic area/anterior hypothalamus of conscious rats. This increase occurs on the fifth or sixth day after immunization, at the time of first appearance of circulating antibodies at a serum titer of 1:32, increasing to 1:128 by day 10 following sensitization. Treatment with the immunosuppressive drug cyclophoshamide was able to prevent both antibody production and the expected increases in electrical activity in 5 of 6 rats; the one remaining animal showed a low level of circulating anti-SRBC antibodies on day 10 (1:32) and also, a small increase (36%) in neural activity at the expected time. These results provide further evidence that activation of the immune system is able to alter neuronal activity in an area of the brain important in the regulation of both neuroendocrine and neuroimmunomodulatory mechanisms, and that such activity is probably due to soluble secretory products released from components of the immune system.

Animals↗
PubMedDate not supplied

Aging of the population of a city and its implications for hospital-based services: the example of Tel Aviv-Yaffo.

The Tel Aviv (Israel) Medical Center serves an area with 270,000 residents, more than 20 percent of whom are over 65 years of age. This high proportion of elderly patients and increasing costs of hospitalization have prompted the center to develop alternative health care services that have made it possible for a number of aged patients to remain at home and ambulatory. Two such alternatives to hospitalization--the center's Day Care Clinic and Home Care Clinic--are described and estimates of savings in hospitalization costs are presented.

Adolescent↗