Endocrine effects of ovarian electrocautery in patients with polycystic ovarian disease

Summary. The mechanism by which ovarian electrocautery induces regular ovulatory cycles was studied in 16 women with polycystic ovarian disease (PCO) and compared with 25 normal fertile women who were undergoing sterilization by tubal electrocautery. Gonadotrophins (LH and FSH), prolactin, androgens, oestrogens, 17-hydroxy-progesterone and progesterone were determined immediately before operation and 24 h later. Following the sampling of blood for these tests, 100 μg of gonadotrophin releasing hormone (GnRH) was given intravenously and the LH and FSH responses were measured at 30 min. In the PCO-group, these tests were repeated after the first induced ovulatory cycle. After operation, LH increased only in the patients with PCO and this increase was associated with an enhanced response to GnRH, FSH showed a similar response to GnRH, also confined to the PCO-group. These pituitary responses are best explained by a change in ovarian feedback induced by the direct electrocautery of the glands in the PCO-group. There was little change in serum oestrogen. Prolactin showed an increment in all cases and serum androgens were reduced in all groups, most pronounced in the PCO patients, possibly as a result of the stress of operation. An ovarian factor—released or reduced by the electrocautery—seems to be responsible for the changes.     

Induction of spermatogenesis in isolated hypogonadotrophic hypogonadism with gonadotrophins and early intervention with intracytoplasmic sperm injection

Idiopathic hypogonadotrophic hypogonadism (IHH) is a potentially correctable cause of male infertility. However hormonal treatment is usually a slow process and artificial reproductive techniques such as intracytoplasmic sperm injection (ICSI) might be resorted to before full testicular response has been achieved. We report here an unusual variant of IHH of post-pubertal onset in which early intervention with ICSI was attempted. Our patient was 37 years old and presented with male infertility due to azoospermia and undetectable serum gonadotrophin concentrations. He had an apparently normal pubertal development, a testicular volume of 8 ml, normal pituitary-thyroid and pituitary-adrenal function, as well as normal computerized tomographic appearance of the sella region. A combination of human chorionic gonadotrophin (HCG) and menopausal gonadotrophins (HMG) was administered. Spermatozoa were first detected in the semen after 3 months and reached a concentration of approximately 2x10(6)/ml after 9 months. ICSI was attempted at this point; the spermatozoa had good fertilizing ability and three embryos were obtained and replaced. Unfortunately no pregnancy resulted. Treatment with 5000 IU HCG and 150 IU HMG three times per week was continued and sperm counts rose rapidly thereafter to reach 28.3x10(6)/ml after 16 months of injections. His wife conceived naturally during this period and the pregnancy is now in the second trimester. This case illustrates the good prognosis of the rare patient with IHH of post-pubertal onset when treated with gonadotrophins, and suggests that ICSI procedures should be delayed until final testicular maturation is attained.      

High-intensity focused ultrasound extracorporeal ablation of liver tissues in rabbits

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The molecular basis of beta-thalassemia in Lebanon: application to prenatal diagnosis

A study of the molecular lesions of beta-thalassemia in Lebanon revealed the presence of eight different mutations in 25 patients with Cooley's anemia. The IVS1 position 110 mutation predominated with a frequency of 62% and was almost invariably associated with Mediterranean chromosome haplotype I. Five other mutations commonly found in the Mediterranean area occurred with frequencies of 2% to 8%. In addition a G----C substitution in IVS1 position 5 (a lesion previously found in Chinese and Asian Indians) was demonstrated in a patient with Mediterranean haplotype IX. A new mutation at codon 29 was found in two other patients with haplotype II. The characterization of these beta-thalassemia mutations should allow the implementation of a prenatal diagnosis program in that country.     

B cell growth factor-induced proliferation of hairy cell lymphocytes and inhibition by type I interferon in vitro

Malignant B cells from hairy cell leukemia (HCL) patients are unable to proliferate when stimulated with standard B cell mitogens. Using chromatographically purified B cell growth factor (BCGF), HCL can be stimulated to proliferate as assessed by incorporation of tritiated thymidine [3HTdR] into DNA. Proliferation was found to be time dependent, with no detectable 3H-TdR incorporation in up to three days of culture, and significant stimulation evident at days 6 and 10. The presence of 10% BCGF in culture was an absolute requirement for HCL proliferation; however, this BCGF-induced DNA synthesis could be further augmented by the addition of anti-immunoglobulin heavy chain antibodies. BCGF-induced proliferation was abrogated in six of six patients by addition of 1,000 U/mL of recombinant alpha 2-interferon (IFN) at day 0, although 1,000 U/mL of recombinant gamma-IFN had no inhibitory effect in five of six patients studied. Specific cellular receptors for type I IFN were demonstrated in HCL by inhibition of binding of 125I-alpha 2-IFN by a 40-fold excess of unlabeled alpha 2 or beta IFN with no inhibition by unlabeled gamma-IFN. These data demonstrate that malignant HCL lymphoblasts express specific type I IFN receptors and that type I, but not type II IFN, can inhibit growth factor-induced DNA synthesis by hairy cells in vitro. They further suggest a direct antiproliferative mechanism of action for IFN in HCL and predict equivalent clinical activity by either alpha or beta, but not gamma IFN in this malignancy.     

热休克蛋白70、90基因在糖皮质激素抵抗型哮喘患者血单个核细胞中的表达

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Factor VIII gene inversions in severe hemophilia A: results of an international consortium study

Twenty-two molecular diagnostic laboratories from 14 countries participated in a consortium study to estimate the impact of Factor VIII gene inversions in severe hemophilia A. A total of 2,093 patients with severe hemophilia A were studied; of those, 740 (35%) had a type 1 (distal) factor VIII inversion, and 140 (7%) showed a type 2 (proximal) inversion. In 25 cases, the molecular analysis showed additional abnormal or polymorphic patterns. Ninety-eight percent of 532 mothers of patients with inversions were carriers of the abnormal factor VIII gene; when only mothers of nonfamilial cases were studied, 9 de novo inversions in maternal germ cells were observed among 225 cases (approximately 1 de novo maternal origin of the inversion in 25 mothers of sporadic cases). When the maternal grandparental origin was examined, the inversions occurred de novo in male germ cells in 69 cases and female germ cells in 1 case. The presence of factor VIII inversions is not a major predisposing factor for the development of factor VIII inhibitors; however, slightly more patients with severe hemophilia A and factor VIII inversions develop inhibitors (130 of 642 [20%]) than patients with severe hemophilia A without inversions (131 of 821 [16%]).