- Email: [email protected]
Infection of cells and HIV
419 transfer a~lempt was 3X% (X/2 I ). with an implantation tale per transferred embryo of 19%. Of the eight clinical pregnancies. one spontaneous abortion occurred at seven weeks’ gestation. Three women have delivered. two at 35 weeks by emergency caesarean section for worsening preeclampsia and one at 37 weeks after a normal vaginal birth. Four pregnancies continue to progress normally beyond the second trimester. Women may become pregnant after the age of natural menopause hy means of in r,ifru> fertilization of donated oocytes. However. thorough medical screening before embryo transfer is essential to reduce to a minimum obstetric risks common in this older population. MV Saucr t I ) Women’s Hospital. Los Anecles, CA 90033. USA
Testicular 17-ketosternid reductase deficiency: gynecnmastia and hypogonadism in men.
Infection
of cells and HIV.
To determine how and where HIV hides. we used a powerful new single cell technology. PCR in si/u. to detect infected cells in which the only evidence in the cells of infection is a transcriptionally silent proviral gcnome. Even at relatively early stages of infection there are large numbers of these covertly infected cells. CD-I’T helper lymphocytes and monocytes in lymphoid tissues that can escape detection by the immune system and thus perpetuate infection. A small fraction (about 1%) of the cells in this reservoir continually undergo a transition to a state of active viral gene expression induced by an immune response. Elimination of these cells will eventually lead to the depletion of CD4’ lymphocytes that is the hallmark of AIDS. AT Haase (3) University ofMinnesota, Minneapolis. MN 55455-0312. USA
cause of
I7-Ketosteroid reductase deficiency results in male pseudohermaphroditism because conversion of the weak androgen androstenedione to the more potent androgen testosterone is impaired. If ;I he-onset form exists. hypogonadism and gynecomastia caused by decreased testosterone production and increased estrogen production. respectively, would be expected as the major clinical manifestations in men. We studied 48 male subjects. ranging from I4 to 26 years of age. who had idiopathic pubertal gynecomastia. Serum concentrations of gonadal and adrenal steroid hormones were measured before and after the administration of corticotropin and after the combined administration of chorionic gonadotropin and dexamethasone for three days. We identified three unrelated subjects (ages 16. I7 and 26 years) with results indicative of a partial deficiency of testicular l7-ketosteroid reductase. The three sub.jects had gynecomastia as well as decreased libido and impotence. Their mean t+ SD) base-line serum andostenedione and estrone concentrations were elevated as compared with the levels in the 45 subjects without this enzyme deficiency tandrostenedione. 380 ? 70 r~.r I IO ? 70 ng per deciliter (I3 + 2 I’S 4 f 2 nmol per liter); estrone I38 f I2 I’S 46 f 9 pg per milliliter (51 I + 44 I’S 170 + 33 pmol per liter). The concentration of androstenedione and estrone in spermatic venous serum were I9 times higher and 73 times higher, respectively, than in normal men. The serum concentrations of follicle-stimulating hormone and luteinizing hormone in these sub.jects were inappropriately low, suggesting the presence of hypogonadotropic hypogonadism. A late-onset form of testicular l7-ketosteroid reductase deficiency can cause gynecomastia and hypogonadism in men.
Endogenous tissue-type plasminogen cardial infarction.
341, 321 (1993) 328.
A recent analysis utilizing blood specimens provided by participants at the beginning of the Physicians’ Health Study has provided evidence that endogenous tissue-type plasminogen activator (tPA) is a strong marker for future risk of Ml. In the blood study. specimens from 231 participants who subsequently experienced myocardial infarction were analyzed, together with blood from 231 controls who remained free of Ml. Cases and controls were matched according to age and smoking status. Baseline levels of tPA were significantly higher in cases than controls (P = 0.03). There was a clear gradient effect, with relative risks of Ml from lowest to highest quintile of tPA of 1.00. I .27, 1.75. 1.88 and 2.81 (Ptrend = 0.0008). However, when the results were adjusted for risk factors that influence the progression of atherosclerosis, particularly HDL-cholesterol. the association of tPA and MI risk largely disappeared, suggesting that elevated tPA levels may be a result, rather than a cause. of atherosclerotic coronary disease. Since endogenous tPA levels may increase in response to important pre-clinical coronary disease, this variable may prove to be a valuable means of identifying those at increased risk for Ml. Brigham
(3) Nr//rrre (4) Lancer 1297
and myo-
The identification of biochemical markers that are reliable predictors of risk of myocardial infarction can be useful in determining patients in whom risk factor reduction measures should be most aggressively pursued.
M Castro-Magana (2) Winthrop-University Hospital. Mineola, NY I I SO I, USA (I) Lt//tce/ (1993) (2) Iv En,q/ J Md
activator
(1993) (1993)
362. 341.
359 116.5
PIM Ridker (4) and women’s Hospital Boston. MA 022 15, USA
Testicular 17-ketosternid reductase deficiency: gynecnmastia and hypogonadism in men.
Infection
of cells and HIV.
To determine how and where HIV hides. we used a powerful new single cell technology. PCR in si/u. to detect infected cells in which the only evidence in the cells of infection is a transcriptionally silent proviral gcnome. Even at relatively early stages of infection there are large numbers of these covertly infected cells. CD-I’T helper lymphocytes and monocytes in lymphoid tissues that can escape detection by the immune system and thus perpetuate infection. A small fraction (about 1%) of the cells in this reservoir continually undergo a transition to a state of active viral gene expression induced by an immune response. Elimination of these cells will eventually lead to the depletion of CD4’ lymphocytes that is the hallmark of AIDS. AT Haase (3) University ofMinnesota, Minneapolis. MN 55455-0312. USA
cause of
I7-Ketosteroid reductase deficiency results in male pseudohermaphroditism because conversion of the weak androgen androstenedione to the more potent androgen testosterone is impaired. If ;I he-onset form exists. hypogonadism and gynecomastia caused by decreased testosterone production and increased estrogen production. respectively, would be expected as the major clinical manifestations in men. We studied 48 male subjects. ranging from I4 to 26 years of age. who had idiopathic pubertal gynecomastia. Serum concentrations of gonadal and adrenal steroid hormones were measured before and after the administration of corticotropin and after the combined administration of chorionic gonadotropin and dexamethasone for three days. We identified three unrelated subjects (ages 16. I7 and 26 years) with results indicative of a partial deficiency of testicular l7-ketosteroid reductase. The three sub.jects had gynecomastia as well as decreased libido and impotence. Their mean t+ SD) base-line serum andostenedione and estrone concentrations were elevated as compared with the levels in the 45 subjects without this enzyme deficiency tandrostenedione. 380 ? 70 r~.r I IO ? 70 ng per deciliter (I3 + 2 I’S 4 f 2 nmol per liter); estrone I38 f I2 I’S 46 f 9 pg per milliliter (51 I + 44 I’S 170 + 33 pmol per liter). The concentration of androstenedione and estrone in spermatic venous serum were I9 times higher and 73 times higher, respectively, than in normal men. The serum concentrations of follicle-stimulating hormone and luteinizing hormone in these sub.jects were inappropriately low, suggesting the presence of hypogonadotropic hypogonadism. A late-onset form of testicular l7-ketosteroid reductase deficiency can cause gynecomastia and hypogonadism in men.
Endogenous tissue-type plasminogen cardial infarction.
341, 321 (1993) 328.
A recent analysis utilizing blood specimens provided by participants at the beginning of the Physicians’ Health Study has provided evidence that endogenous tissue-type plasminogen activator (tPA) is a strong marker for future risk of Ml. In the blood study. specimens from 231 participants who subsequently experienced myocardial infarction were analyzed, together with blood from 231 controls who remained free of Ml. Cases and controls were matched according to age and smoking status. Baseline levels of tPA were significantly higher in cases than controls (P = 0.03). There was a clear gradient effect, with relative risks of Ml from lowest to highest quintile of tPA of 1.00. I .27, 1.75. 1.88 and 2.81 (Ptrend = 0.0008). However, when the results were adjusted for risk factors that influence the progression of atherosclerosis, particularly HDL-cholesterol. the association of tPA and MI risk largely disappeared, suggesting that elevated tPA levels may be a result, rather than a cause. of atherosclerotic coronary disease. Since endogenous tPA levels may increase in response to important pre-clinical coronary disease, this variable may prove to be a valuable means of identifying those at increased risk for Ml. Brigham
(3) Nr//rrre (4) Lancer 1297
and myo-
The identification of biochemical markers that are reliable predictors of risk of myocardial infarction can be useful in determining patients in whom risk factor reduction measures should be most aggressively pursued.
M Castro-Magana (2) Winthrop-University Hospital. Mineola, NY I I SO I, USA (I) Lt//tce/ (1993) (2) Iv En,q/ J Md
activator
(1993) (1993)
362. 341.
359 116.5
PIM Ridker (4) and women’s Hospital Boston. MA 022 15, USA