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21.
The subcellular distribution in rat liver and the topography in intracellular and plasma membranes of connexin 32, a major protein component of gap junctions, was studied using sequence-specific anti-peptide antibodies generated to extracellular and intracellular domains of the protein. The distribution of connexin 32 in liver analyzed using SDS-polyacrylamide gel electrophoresis and Western blotting showed the relative protein levels in the subcellular fractions to be: lateral plasma membranes > Golgi membranes > sinusoidal plasma membranes > lysosomes. Low amounts of connexin 32 were detected in microsomes, endosomes, and bile canalicular plasma membranes. Six highly conserved cysteine residues are located in the amino acid sequences comprising the two extracellular loops of all connexins thus far isolated, and these loops are positioned to extend the channel in the lipid bilayers across the intercellular region of the gap junction. In the present work, the intramolecular disulfide bonds linking the extracellular loops in gap junctions were shown to be present in connexins located in plasma membranes, Golgi, and a microsomal fraction, and it was concluded that the disulfide linkages were formed in the endoplasmic reticulum. In addition, immature configurations of connexin 32, probably occurring during membrane insertion, were detected in liver microsomal fractions. The results contribute to charting of the biogenetic routes followed by connexins in hepatocytes and the general mechanisms of gap junction assembly. 相似文献
22.
HM Chaung CH Hong CP Chiang SK Lin YS Kuo WH Lan CC Hsieh 《Canadian Metallurgical Quarterly》1996,95(7):545-550
This review reports the different genetic factors that have been identified either as risk factor for Alzheimer's disease (AD) or directly causing the disease. First are reviewed epidemiological data and biological mechanisms about the apoplipoprotein E gene allele epsilon 4 that is a major risk factor for Alzheimer's disease. The second part describes the mutations responsible for early-onset autosomal dominant AD found in three different genes. The gene located on chromosome 21 encodes the amyloid precusor protein (APP). The presenilin 1 and presenilin 2 genes, located on chromosome 14 and 1 respectively, encode not yet known membrane proteins. 相似文献
23.
We provide a unified framework for the investigation of convergence properties of the iterative algorithms for photon attenuation correction in SPECT, including the iterative Chang method--a commonly used approach in which an average attenuation factor calculated over all projection angles is employed in a pointwise correction scheme. A new average attenuation factor calculated along the projection line is introduced, which can compensate exactly for the attenuation effect in the case of a uniform activity distribution. We propose a new hybrid approach in which we use this new average attenuation factor initially and then shift to the iterative Chang method in later iterations. This hybrid approach was evaluated in a simulation study by use of a computer-generated phantom with both non-uniform activity and non-uniform attenuation distributions. The results demonstrate that this hybrid approach improves the convergence speed of the iterative Chang method and produces reconstructed images of high quality. 相似文献
24.
In an attempt to validate the use of topographical mapping of EEG as a method of localising cerebral function, EEG was recorded during a simple motor task. A minimum of 20 sec artifact-free EEG was recorded from 24 healthy right handed subjects in each of 4 conditions: eyes open 1, motor task (left/right, order randomized), eyes open 2. EEG amplitude maps were computed in delta, theta, alpha, and beta (1 and 2). Differences were seen between the eyes open and the motor conditions in alpha, beta 1 and beta 2 localised to the motor and supplementary motor areas. It is argued that topographical mapping of EEG is a valid method of localising cognitive function in healthy individuals for the Luria task. 相似文献
25.
We report a case of homozygous alpha-thalassaemia with hydrops fetalis presenting at 22 weeks of gestation. In utero exchange transfusion was performed with maternal blood at 23 weeks. 25 weeks and 29 weeks of gestation. The fetus was delivered at 29 weeks of gestation without significant neonatal complication. Post-transfusion haemoglobin pattern after transfusion suggested that a total haematocrit of 0.52 may be the desired post-exchange transfusion haematocrit to aim for and the total haematocrit of haemoglobin A and haemoglobin Portland dropped approximately one percent per day. 相似文献
26.
WH Newman LM Zhang MR Castresana MG Currie BF Becker 《Canadian Metallurgical Quarterly》1994,54(18):1351-1356
Atrial natriuretic peptide (ANP) and sodium nitroprusside (SNP) increase cGMP in vascular smooth muscle cells and act as vasodilators in some, but not all, blood vessels. In this present study, we attempted to correlate the ability of these two agents to dilate blood vessels with the ability to increase cGMP in cultured vascular smooth muscle cells. In the isolated guinea pig heart, SNP dose-dependently increased coronary flow while ANP was ineffective. In smooth muscle cells cultured from the coronary system, SNP increased intracellular cGMP in a dose-dependent manner while ANP had no effect on cGMP in these cells. In isolated guinea-pig thoracic aorta, precontracted with K+, both ANP and SNP produced relaxation and ANP was the more potent. In smooth muscle cells cultured from the aorta, ANP and SNP increased cGMP and the potency relationship was similar to the intact vessel. These results support the view that phenotypic properties of vascular smooth muscle cells can account for differences in the response of blood vessels to vasodilators. 相似文献
27.
28.
A new interest in replacing neurons lost to trauma or disease has been generated by findings that challenge the traditional view of the static (irreparable) adult brain. The discovery of stem cells and neurogenesis in the adult central nervous system is responsible for much of this interest. 相似文献
29.
The heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-beta]pyridine NPhIP) is a major dietary component in individuals eating cooked meats or fish. This heterocyclic amine requires biochemical activation, mainly through cytochrome P4501A2, and can be detoxified chiefly by 4'hydroxylation through other cytochromes, and be in turn converted through phase 2 enzymes to readily excreted conjugates. The active form of PhIP is mutagenic in Salmonella typhimurium TA98 and is a useful substrate to study the possible chemoprotective action of phytochemicals. We found that black and green tea depressed the mutagenicity of PhIP in dose-related fashion, and decaffeinated tea was less powerful an inhibitor. This led to the study of caffeine, that displayed effective dose-related inhibition of the mutagenicity of PhIP. Other antioxidants such as lycopene, the active antioxidant from tomatoes, and daidzein and genistein from soy products, also had a dose-related inhibition of the mutagenicity of PhIP. We conclude that PhIP is a good substrate found in several human foods to determine the protective effect of phytochemicals from vegetables, and beverages. 相似文献
30.
Vascular nephropathies are a steadily increasing cause of end-stage renal failure. Arterionephrosclerosis and arteriolonephrosclerosis are common features in the hypertensive patient. This is especially true for blacks of African descent, in whom hypertension and nephrovasculopathies are a major cause of renal insufficiency. That primary hypertension leads to renal vascular lesions, glomerular obsolescence and interstitial fibrosis has long been established. It should not, however, obscure the fact that renal vascular lesions can be observed in animal models as well as in some humans, especially young blacks, in the absence of, or anticipating the onset of hypertension. This leads to considering the hypothesis that nephroangiosclerosis might stem from a genetic defect in the renal vascular bed and that this defect is strongly associated with the hypertensive trait. Atherosclerotic renal disease is a major, potentially treatable cause of chronic renal disease is a major, potentially treatable cause of chronic renal failure, especially in whites. It leads to renal atrophy, but the ischemic kidney retains a vigorous potential for tubular cell regeneration, which pleads for early recognition and treatment. Recent data suggest that renal ischemia, be it due to renal artery stenosis or to cholesterol crystal embolism, ranks among the multiple causes of secondary focal segmental glomerulosclerosis. Irrespective of its initial mechanism, ischemia induces renal fibrosis, the pathophysiology of which is centered on increased generation of angiotensin II. Finally, renal vascular lesions are commonly observed in the course of various nephropathies, even in the absence of hypertension, and the relationship between these lesions and the unfavorable prognosis of glomerulopathies, especially primary focal-segmental glomerulosclerosis, membranous glomerulopathy and IgA glomerulonephritis, remains to be elucidated. Expanding knowledge of the spectrum of nephrovasculopathies opens perspectives for investigating, understanding and treating a major mechanism of progressive renal insufficiency. 相似文献