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71.
The effects of pinealectomy and administration of melatonin, the major secretory product of the pineal gland, which is a direct free radical scavenger and an indirect antioxidant, were studied in rat hearts on the basis of cardiac morphology and biochemical findings. Three groups of Wistar rats were used: one group was the sham-operated control, one group consisted of pinealectomized rats and one group consisted of pinealectomized rats that were treated with melatonin. Serum cholesterol, tissue levels of malondialdehyde (MDA) and reduced glutathione (GSH), and heart weight were determined. Histochemical staining with the Van Gieson, PAS/Alcian blue at pH 2.5 and Masson's trichrome methods were performed in addition to hematoxylin-eosin staining. Levels of serum cholesterol and tissue MDA, and heart weight were increased in pinealectomized rats whereas GSH levels did not change. Melatonin administration reversed these effects. Microscopically, myocardial fibrosis and myxomatous degeneration of cardiac valves were detected in all pinealectomized rats. It can be concluded that pinealectomy of rats causes morphological changes in rat hearts, and short-term application of melatonin does not reverse these changes. 相似文献
72.
Age related macular degeneration (AMD) is the leading cause of visual impairment in the elderly and a major cause of blindness in the developed world. The disease can take two forms, geographic atrophy and choroidal neovascularisation. The pathogenesis of AMD is poorly understood. There are undoubtedly environmental and other risk factors involved and the adverse effect of smoking is well established. Several studies have shown that genetic factors are important but leave uncertainty about the magnitude and nature of the genetic component and whether it varies with the type of AMD. Several hereditary retinal dystrophies show similarities to AMD and these genes are potential candidate susceptibility genes. Particular interest has focused on the ABCR gene which is responsible for autosomal recessive Stargardt macular dystrophy. It has been claimed that heterozygotes for ABCR mutations are predisposed to AMD but the data are conflicting. Studies of the genes responsible for autosomal dominant Sorsby fundus dystrophy, Doyne honeycomb retinal dystrophy, and Best disease have given negative results. In one large AMD family, linkage has been reported to markers in 1q25-q31. Recent data suggest that the ApoE epsilon4 allele may be associated with reduced risk of AMD. A better understanding of the genetic factors in AMD would contribute to understanding the pathogenesis. If those at risk could be identified it may be possible to modify lifestyle or develop novel therapies in the presymptomatic stage to prevent disease or decrease its severity. 相似文献
73.
B. A. Sabel G. E. Schneider 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1988,71(2):365-376
Summary The effects of exogenous gangliosides on sprouting of optic tract axons was studied in hamsters which, after a right tectal lesion on the day after birth (P1), had an abnormal retinotectal projection from the left eye to the left superior colliculus (SC). Sprouting of these axons was induced by removing the competing input by right eye removal on postnatal day 9 (P9). Intraperitoneal GM1, given daily and started on P9, significantly stimulated the sprouting response. This was demonstrated by Fink-Heimer silver staining of anterograde axonal degeneration three days after the left eye was removed on P36. Terminal fields in the left SC were, in average, twice as large compared to controls. An estimate of the total number of terminals (silver stained particles) revealed a value of 7.9×106 for GM1 and 3.2×106 for control hamsters, respectively. Diencephalic structures which also receive collateral input from the sprouting optic tract did not show any alterations in the size of the terminal field due to GM1-treatment, suggesting that, in vivo, gangliosides fail to initiate sprouting in areas that have not previously been denervated. Unexpectedly, GM1-treated hamsters also had significantly smaller right SC damage and less left damage near the midline. Subsequent reanalysis of the data based on a lesion-matching procedure indicates that effects on reducing atrophy were independent of the GM1-enhanced sprouting of retinofugal axons. These findings provide the first direct evidence that exogenous GM1 stimulates lesion-induced axon sprouting in the mammalian brain. 相似文献
74.
B.C Figueiredo L Hu A.M Bedard W Tetzlaff A.Claudio Cuello 《Journal of chemical neuroanatomy》1996,12(1):15-27
We have tested the hypotheses that nerve growth factor treatment in adult post-hypothyroid rats can: (1) restore cross-sectional area of cholinergic cells of the nucleus basalis and (2) prevent further atrophy of these neurons following cortical infaction. In addition, we assessed the expression of p75NGFR and p140trkA mRNAs in the nucleus basalis cells of post-hypothyroid rats. Rats were rendered hypothyroid by the addition of propylthiouracil to their diet beginning on embryonic day 19 until the age of 1 month. At this time both the pups and their dams continued to receive 0.05% propylthiouracil in their diet and the pups were thyroidectomized. At 60 days, propylthiouracil treatment was interrupted and thyroxine levels were restored to normal by daily subcutaneous administration of physiological levels of thyroxine. Morphometric analysis identified atrophied nucleus basalis magnocellularis cholinergic cells at two ages, days 75 and 105, identified by in situ hybridization for p75NGFR and p140trkA mRNAs in methylene blue stained cells (day 75) and choline acetyltransferase immunostaining (day 105). The mean number of silver grains (pixels) per μm2 (mean±S.E.M.) of cell body cross-sectional area for p75NGFR mRNA in the nucleus basalis magnocellularis of euthyroid rats was 3.43±0.89, which was not statistically different from post-hypothyroid animals (4.02±1.07). A similar finding was noted for p140trkA mRNA: mean number of grains in the euthyroid group was 5.54±0.96 and was not statistically different from the post-hypothyroid group (6.32±1.45). Nerve growth factor treatment in adulthood (between days 75 and 82) did not restore cross-sectional area from early thyroid deprivation. However, it prevented further atrophy of nucleus basalis magnocellularis neurons following cortical devascularization inflicted in adulthood (day 75). 相似文献
75.
Salahuddin Saira; Ookutsu Shoji; Goto Kazufumi; Nakanishi Yoshihiko; Nagata Yukihiro 《Human reproduction (Oxford, England)》1995,10(9):2382-2385
We have evaluated the effects of embryo density and the co-cultureof unfertilized (degenerating) oocytes on the development ofin-vitro fertilized (IVF) mouse embryos. In experiment 1, groupsof one, five, 10 or 20 zygotes were cultured in 20 µldrops of modified human tubal fluid (HTF) medium for 168 h at38.7°C in 5% CO2 and 95% air. As the embryo density increased,significantly (P < 0.05) higher rates of embryos reachedhatched blastocyst stage. In addition, the time required forhatching after IVF was significantly (P < 0.05) shortenedby the increase in embryo density. In experiment 2, 10 IVF zygoteswere cultured with or without 10 unfertilized (degenerating)oocytes in 20 µl drops of HTF medium. The rates of IVFembryos that developed to morula, blastocyst, expanded blastocystand hatched blastocyst stages were decreased significantly (P< 0.01) by culturing embryos with unfertilized oocytes comparedwith culturing embryos alone. In experiment 3, groups of oneor 10 IVF zygotes or 10 IVF zygotes plus 10 unfertilized oocyteswere cultured in 20 µl drops of HTF medium and the numberof cells per blastocyst was examined at 120 h after IVF. Increasingembryo density resulted in a significant (P < 0.05) increasein the number of cells per blastocyst. In contrast, the cellnumber of IVF embryos that developed to blastocyst decreasedsignificantly (P < 0.05) when they were cultured with unfertilizedoocytes. The results suggest that in-vitro development of IVFmouse embryos is enhanced by increasing embryo density and isimpaired by co-culture with unfertilized (degenerating) oocytes. 相似文献
76.
Gabrielle J. Halpern Dov Inbar Joseph Attias Mordechai Shohat 《American journal of medical genetics. Part A》2001,101(3):195-197
We report a brother and sister with ectodermal dysplasia, ectrodactyly, and macular dystrophy (the EEM syndrome). Both children had abnormalities of the hands and the hair, and bilateral macular degeneration. The clinical picture in both is similar to, but less severe than, that described in the previously reported cases of this rare syndrome. Even though the parents are not related, they are both of Jewish Yemenite origin, and the possibility of a common ancestor cannot be ruled out. This would suggest autosomal recessive inheritance. The clinical picture in these patients suggests either variable expression or genetic heterogeneity in the EEM syndrome and further delineates the clinical and genetic spectrum of this condition. © 2001 Wiley‐Liss, Inc. 相似文献
77.
Iliac and sacral articular cartilage of 25 human sacroiliac joints (1–93 years) are examined by light microscopy and immunohistochemistry
in order to gain further insight into the nature and progress of degenerative changes appearing during aging. These changes
can already be seen in younger adults as compared to cartilage degeneration known in other diarthrodial joints. Structural
differences between sacral and iliac cartilage can already be observed in the infant: the sacral auricular facet is covered
with a hyaline articular cartilage, reaching 4 mm in thickness in the adult and staining intensely blue with alcian blue at
pH1. Iliac cartilage of the newborn is composed of a dense fibrillar network of thick collagen bundles, crossing each other
at approximately right angles. A faint staining with alcian blue suggests a low content of acidic glycosaminoglycans. In the
adult, iliac cartilage becomes hyaline and its maximal thickness reaches 1–2 mm. Both articular facets exhibit morphological
changes during aging that are more pronounced in the iliac cartilage and resemble osteoarthritic degeneration; the staining
pattern of the extracellular matrix becomes inhomogenous, chondrocytes are arranged in clusters and the articular surface
develops superficial irregularities and fissures. Sometimes fibrous tissue fills up these defects. Nevertheless, large areas
of iliac cartilage remain hyaline in nature. Sacral articular cartilage often remains largely unaltered until old age. The
sacral subchondral bone plate is usually thin and shows spongiosa trabeculae inserted at right angles, suggesting a perpendicular
load on the articular facet. Iliac subchondral spongiosa shows no definite alignment and joins the thickened subchondral bone
plate in an oblique direction. The iliac cartilage therefore seems to be stressed predominantly by shearing forces, arising
from the changing monopodal support of the pelvis during locomotion. The subchondral bone plate on both the iliac and sacral
auricular facet is penetrated by blood vessels that come into close contact with the overlying articular cartilage. These
vessels may contribute to the high incidence of rheumatoid and inflammatory diseases in the human sacroiliac joint. Immunolabelling
with an antibody against type II collagen reveals a diminished immunoreactivity in the upper half of adult sacral cartilage
and only a faint and irregular labelling in the iliac cartilage. Type I collagen can be detected in a superficial layer on
the sacral articular surface and around chondrocyte clusters in iliac cartilage, as in dedifferentiating chondrocytes during
the development of osteoarthritis.
Accepted: 22 April 1998 相似文献
78.
M. F. Humphrey S. A. Dunlop A. Shimada L. D. Beazley 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1992,90(3):630-634
Summary In this study, we crushed one optic nerve in the frog Litoria (Hyla) moorei and at intervals thereafter anterogradely labelled optic axons with horseradish peroxidase (HRP). For one series, HRP was applied between the eye and the crush site and in a second series between the crush site and the chiasm. A tectal projection of regenerating axons was seen in both series but, in addition, up to 12 weeks post-crush, the second series displayed an additional projection. Its appearance matched that of the disconnected, but persisting, optic axon terminals which are found after enucleation or optic nerve ligation. We conclude that, in the frog, many disconnected optic axons persist throughout the period of optic nerve regeneration and of restoration of an orderly retino-tectal map.Abbreviation HRP
horseradish peroxidase 相似文献
79.
扬子鳄胚胎中肾发生及退化 总被引:2,自引:1,他引:2
目的:在11个不同发育时期扬子鳄胚胎中观察中肾的发生及退化过程。方法:采用电镜、细胞化学及免疫组织化学方法。结果:孵育第6期在中肾管前端附近出现一些中肾小泡。第8期形成“S”形中肾小管。第13—17期鳄胚体前部部分中肾小管盲端内陷,形成原始的肾小囊和肾血管球,中肾小管显著伸长并迂回曲折。第20一22期,体前后部中肾组织均已形成完整的肾单位。中肾小管颈段由纤毛柱状上皮细胞组成,近球小管上皮细胞含丰富的PAS阳性物质并呈表皮生长因子(EGF)、转化生长因子(TGFβ1)和生长抑素(SS)免疫阳性反应。第24—28期,体前部至后部的中肾组织依次退化。结论:(1)扬子鳄中肾除重吸收作用外还具有内分泌功能;(2)中肾退化时,细胞凋亡依次表现为核固缩,出现大量凋亡小体,线粒体数目剧增并膨胀,线粒体等细胞器自溶及核消失;(3)中肾退化可能与小管细胞中TGFβ1及SS大量表达有关。 相似文献
80.
The neurodegeneration in the CA1 subfield of hippocampus exhibited a dorsal-ventral gradient of susceptibility in global ischemia (82% dorsoseptally and only 16% ventrotemporally). Scopolamine (SCOP) did not improve the neuronal damage caused by the global ischemic challenge in rats and did not reduce the infarct area after the focal MCA-occlusion in mice. No differences were observed between saline and SCOP-treated animals in the physiologic parameters, except for a slight increase in rectal temperature. In contrast, treatment of hippocampal cultures with increasing concentrations of SCOP (1 nM to 1 mM) under glutamate incubation had a beneficial effect on neuronal viability. These data show that (1) there is substantial gradient of vulnerability of the hippocampus from dorsal to ventral in global ischemia and (2) that interactions between the NMDA, muscarinic receptors and their corresponding neurotransmitter inputs to hippocampal neurons are evident in vitro and may play a crucial role in neuronal neurodegeneration. However, the mechanisms underlying the high vulnerability of dorsal hippocampus still remain enigmatic. 相似文献