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981.
J Mayet KP O'Kane R Elton HA Johnstone M Shahi MA Ozkor AV Stanton NR Poulter PS Sever RA Foale DJ Webb SA Thom 《Canadian Metallurgical Quarterly》1997,11(9):595-597
It has been suggested that the deletion polymorphism of the angiotensin-converting enzyme (ACE) genotype may be important in the development of left ventricular hypertrophy (LVH). In order to test this hypothesis we investigated the interaction between blood pressure (BP), LVH and ACE genotype in 86 previously untreated hypertensive patients. Each underwent two-dimensional and Doppler echocardiography and ACE genotyping. There were no significant differences in BP, the parameters of left ventricular structure (including left ventricular mass index) or diastolic function between the three genotype groups. Additionally, there were no significant differences in the relationship between systolic BP and left ventricular mass index among the three genotype groups (II genotype, r = 0.46, P = 0.02; ID genotype, r = 0.42, P = 0.01; DD genotype, r = 0.34, P = 0.10; F = 0.38). In contrast to some previous studies, we have found in this group of previously untreated hypertensive subjects no evidence to suggest that the deletion polymorphism of the ACE genotype is important in the development of LVH. 相似文献
982.
Recent evidence describing a suboptimal clinical outcome in women with hydrosalpinges who undergo in-vitro fertilization (IVF) and embryo transfer suggests a potential deleterious effect of this fluid on in-utero embryo development. Consequently, we evaluated in-vitro mouse embryo development in the presence of hydrosalpingeal fluid (HF) collected from 10 infertile women of reproductive age. Chemical analyses showed both similarities and differences of these fluids to reported values for fluids collected from non-diseased Fallopian tubes. The HF had a significant deleterious effect upon mouse embryo cleavage and development to the expanded and hatched blastocyst stage, although the effect was variable among patients. Dilution of HF to 30% concentration with culture medium failed to negate this effect. This argues against the effect resulting from a relative lack of critical, supportive component(s) in the HF. Additionally, further experiments performed with cultures under an oil overlay significantly reduced the embryotoxicity of the HF. This evidence suggests there may be a lipophilic factor that can impair embryo development. The relatively poor IVF-embryo transfer success in women with proximally patent hydrosalpinges may be explained, at least in part, by reflux of a lipophilic embryotoxic factor(s) into the uterine cavity. 相似文献
983.
GE McClearn B Johansson S Berg NL Pedersen F Ahern SA Petrill R Plomin 《Canadian Metallurgical Quarterly》1997,276(5318):1560-1563
General and specific cognitive abilities were studied in intact Swedish same-sex twin pairs 80 or more years old for whom neither twin had major cognitive, sensory, or motor impairment. Resemblance for 110 identical twin pairs significantly exceeded resemblance for 130 fraternal same-sex twin pairs for all abilities. Maximum-likelihood model-fitting estimates of heritability were 62 percent for general cognitive ability, 55 percent for verbal ability, 32 percent for spatial ability, 62 percent for speed of processing, and 52 percent for memory. There was also evidence for the significant influence of idiosyncratic experience as the environmental component that most determines individual differences in cognitive abilities late in life. 相似文献
984.
F Duclos V Straub SA Moore DP Venzke RF Hrstka RH Crosbie M Durbeej CS Lebakken AJ Ettinger J van der Meulen KH Holt LE Lim JR Sanes BL Davidson JA Faulkner R Williamson KP Campbell 《Canadian Metallurgical Quarterly》1998,142(6):1461-1471
Limb-girdle muscular dystrophy type 2D (LGMD 2D) is an autosomal recessive disorder caused by mutations in the alpha-sarcoglycan gene. To determine how alpha-sarcoglycan deficiency leads to muscle fiber degeneration, we generated and analyzed alpha-sarcoglycan- deficient mice. Sgca-null mice developed progressive muscular dystrophy and, in contrast to other animal models for muscular dystrophy, showed ongoing muscle necrosis with age, a hallmark of the human disease. Sgca-null mice also revealed loss of sarcolemmal integrity, elevated serum levels of muscle enzymes, increased muscle masses, and changes in the generation of absolute force. Molecular analysis of Sgca-null mice demonstrated that the absence of alpha-sarcoglycan resulted in the complete loss of the sarcoglycan complex, sarcospan, and a disruption of alpha-dystroglycan association with membranes. In contrast, no change in the expression of epsilon-sarcoglycan (alpha-sarcoglycan homologue) was observed. Recombinant alpha-sarcoglycan adenovirus injection into Sgca-deficient muscles restored the sarcoglycan complex and sarcospan to the membrane. We propose that the sarcoglycan-sarcospan complex is requisite for stable association of alpha-dystroglycan with the sarcolemma. The Sgca-deficient mice will be a valuable model for elucidating the pathogenesis of sarcoglycan deficient limb-girdle muscular dystrophies and for the development of therapeutic strategies for this disease. 相似文献
985.
Diffuse well differentiated papillary mesothelioma is a rare neoplasms of the peritoneal cavity which has generally been regarded as a tumor with low-grade malignant potential [1-4]. The well differentiated papillary mesotheliomas reported in recent literature are considered as border line lesions with a long term benign clinical course. There are however, only few studies with small numbers of diffuse well differentiated mesotheliomas [1, 2, 5, 6]. The synchronous appearance of such a lesion with a second malignancy therefore is a very rare event. Such a clinical scenario would suggest diffuse tumor spread to the peritoneum resulting in an inappropriate palliative procedure alone-being undertaken. To our knowledge this is the first report of the simultaneous occurrence of a rectal carcinoma in combination with a diffuse well differentiated papillary mesothelioma of the peritoneum. 相似文献
986.
Transgenic NOD backcross mice expressing pancreatic interleukin 10 (IL-10) were crossed and backcrossed to NOD.B6 Idd3 Idd10 mice, which have diabetes-resistance alleles at Idd3 and Idd10 on chromosome 3 and have a very low frequency diabetes and insulitis. Insulitis and diabetes developed in almost all IL-10 transgenic backcross 1 (BC1) mice of the H2g(7/g7) haplotype regardless of the allelic status at Idd3 and Idd10. Furthermore, diabetes occurred in 23% of IL-10 transgenic H2g(7/d) BC1 mice. These results indicate that pancreatic IL-10 is able to overcome the diabetes protection afforded by C57BL/6 (B6)-derived alleles at Idd3 and Idd10 as well as the absence of NOD MHC homozygosity, if other non-MHC NOD-derived Idd alleles are provided. 相似文献
987.
988.
HS Chen JW Pellegrini SK Aggarwal SZ Lei S Warach FE Jensen SA Lipton 《Canadian Metallurgical Quarterly》1992,12(11):4427-4436
Excessive activation of NMDA receptors is thought to mediate the calcium-dependent neurotoxicity associated with hypoxic-ischemic brain injury, trauma, epilepsy, and several neurodegenerative diseases. For this reason, various NMDA antagonists have been investigated for their therapeutic potential in these diseases, but heretofore none have proven to be both effective and safe. In the present study, memantine, an adamantane derivative similar to the antiviral drug amantadine, is shown to block the channels activated by NMDA receptor stimulation. From whole-cell and single-channel recording experiments, the mechanism of action of memantine is deduced to be open-channel block, similar to MK-801; however, unlike MK-801, memantine is well tolerated clinically. Compared to MK-801, memantine's safety may be related to its faster kinetics of action with rapid blocking and unblocking rates at low micromolar concentrations. Furthermore, at these levels memantine is an uncompetitive antagonist and should theoretically allow near-normal physiological NMDA activity throughout the brain even in the face of pathologically high focal concentrations of glutamate. These pharmacological properties confer upon memantine a therapeutic advantage against NMDA receptor-mediated neurotoxicity with few side effects compared with other organic NMDA open-channel blockers. Moreover, memantine is increasingly effective against escalating levels of glutamate, such as those observed during a stroke. Low micromolar concentrations of memantine, levels known to be tolerated by patients receiving the drug for the treatment of Parkinson's disease, prevent NMDA receptor-mediated neurotoxicity in cultures of rat cortical and retinal ganglion cell neurons; memantine also appears to be both safe and effective in a rat stroke model. These results suggest that memantine has considerable therapeutic potential for the myriad of clinical entities associated with NMDA receptor-mediated neurotoxicity. 相似文献
989.
990.