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排序方式: 共有1313条查询结果,搜索用时 15 毫秒
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R A Zager E J Teubner S Adler 《Laboratory investigation; a journal of technical methods and pathology》1987,56(2):180-188
To determine whether tubular reabsorption of low molecular weight proteins (LMWPs) alters ischemic tubular injury, rats were infused with 25 mg of lysozyme (isoelectric point (pI) 11.3), cytochrome C (pI 10.6), ribonuclease (pI 8.7), or myoglobin (pI 7.0), and during this time 25 minutes of bilateral renal artery occlusion (RAO) was induced. RAO control rats received either saline or 25 mg of albumin. Renal injury was assessed 24 hours later by blood urea nitrogen, creatinine, and histology. Lysozyme, ribonuclease, and myoglobin each exacerbated ischemic damage (increased tubular necrosis, cast formation, azotemia), but to comparable degrees (e.g., blood urea nitrogen range 75 +/- 8 to 100 +/- 5 mg/dl versus controls, 29 +/- 2 to 36 +/- 7; p less than 0.01). Rendering lysozyme anionic (pI 4.5) by succinylation did not diminish its acute renal failure-potentiating effect. Cytochrome C which is freely filtered but poorly reabsorbed had a minimal impact on the ischemic process. Infusion of LMWPs did not alter blood pressure, renal blood flow, or induce renal injury in the absence of RAO. During a sublethal ischemic event (10 minutes of RAO) LMWP infusion exacerbated proximal tubular luminal membrane damage before an adverse effect on other critical determinants of cell integrity were apparent (adenine nucleotide pools, oxidant stress). We conclude that endocytic LMWP reabsorption by proximal tubules can exacerbate superimposed ischemic tubular necrosis independent of any direct nephrotoxic protein effect. This action is not influenced by protein isoelectric point and appears to be mediated by a primary intensification of ischemic luminal membrane damage. 相似文献
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Neurofibromatosis 2 (NF2) is an inherited cancer syndrome resulting from
mutations in the NF2 tumor suppressor gene. Analysis of NF2 mutations has
revealed some general genotype-phenotype correlations. Severe disease has
been associated with mutations that produce a premature termination while
more mild disease has been associated with missense mutations. Here, we
provide experimental proof for these genotype-phenotype correlations by
demonstrating that nonsense mutations fail to produce stable merlin protein
while missense mutations result in the generation of merlin proteins
defective in negative growth regulation. This inability to suppress cell
growth may result from defects in the function of merlin at several levels,
including failure to form an intramolecular complex. Based on these
findings, we propose a model for merlin growth suppression that provides a
framework for analyzing NF2 patient mutations and merlin function.
相似文献
26.
JS Pooni Dr DWL Hukins PF Harris RC Hilton KE Davies 《Surgical and radiologic anatomy : SRA》1986,8(3):175-182
Posterior and anterior heights, cross-sectional area and shape were measured for all the intervertebral discs in four spines from elderly human cadavers. Disc height was a minimum at the T4-5 level; thoracic discs were less wedge-shaped than those in the cervical and lumbar regions. Cross-sectional area increased from the cranial to caudal extremity; at the L5-S1 level the nucleus pulposus occupied a high proportion of this area. Cervical discs tended to have an elliptical cross-sectional shape, thoracic discs were more circular and lumbar discs tended to have an elliptical cross-section which was flattened or re-entrant posteriorly. This shape distribution was quantified by defining a shape index which had a maximum value of 1 for a circular cross-section. Orientations of the reinforcing fibres in the outer lamellae of the anterior annulus fibrosus were measured from 27 discs by X-ray diffraction. For these measurements, C3-4, T7-8 and L2-3 were chosen as representative of cervical, thoracic and lumbar discs. The fibre tilt, with respect to the axis of the spine, was significantly less in the cervical discs (at 65 degrees) than in the thoracic and lumbar discs (about 70 degrees). These findings are interpreted in relation to differing functional requirements and possible mechanisms of failure in the cervical, thoracic and lumbar regions of the spine in the light of current knowledge on the biomechanics of the intervertebral disc. 相似文献
27.
Experimental glomerulopathy alters renal cortical cholesterol,SR-B1, ABCA1, and HMG CoA reductase expression 下载免费PDF全文
Previous studies indicate that acute tubular injury causes free cholesterol (FC) and cholesteryl ester (CE) accumulation within renal cortex/proximal tubules. This study assessed whether similar changes occur with glomerulopathy/nephrotic syndrome, in which high-circulating/filtered lipoprotein levels increase renal cholesterol supply. Potential adaptive changes in cholesterol synthetic/transport proteins were also assessed. Nephrotoxic serum (NTS) or passive Heymann nephritis (PHN) was induced in Sprague-Dawley rats. Renal injury (blood urea nitrogen, proteinuria) was assessed 2 and 7 days (NTS), or 10 and 30 days (PHN) later. FC and CE levels in renal cortex, isolated glomeruli, and proximal tubule segments were determined. SR-B1 (a CE influx protein), ABCA1 (a FC exporter), and HMG CoA reductase protein/mRNA levels were also assessed. FC was minimally elevated in renal cortex (0 to 15%), the majority apparently localizing to proximal tubules. More dramatic CE elevations were found ( approximately 5 to 15x), correlating with the severity of proteinuria at any single time point (r >/= 0.85). Cholesterol increments were associated with decreased SR-B1, increased ABCA1, and increased HMG CoA reductase (HMGCR) protein and its mRNA. Tubule (HK-2) cell culture data indicated that SR-B1 and ABCA1 levels are responsive to cholesterol supply. Experimental nephropathy can increase renal FC, and particularly CE, levels, most notably in proximal tubules. These changes are associated with adaptations in SR-B1 and ABCA1 expression, which are physiologically appropriate changes for a cholesterol overload state. However, HMGCR protein/mRNA increments can also result. These seem to reflect a maladaptive response, potentially contributing to a cell cholesterol overload state. 相似文献
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Detecting pre-ovulatory luteinizing hormone surges in urine 总被引:2,自引:1,他引:2
Kesner JS; Knecht EA; Krieg EF Jr; Wilcox AJ; O'Connor JF 《Human reproduction (Oxford, England)》1998,13(1):15-21
The study objectives were to determine (i) if pre-ovulatory luteinizing
hormone (LH) surges, undetected in urine by two immunoradiometric assays
(IRMA), were detectable by an ultrasensitive immunofluorometric assay
(IFMA) and (ii) the influence of creatinine adjustment on the detection and
timing of the urinary LH surges. Daily urine specimens were contributed by
healthy 25-36 year old volunteers during 14 ovulatory menstrual cycles for
an epidemiological study conducted in 1983-1985. Specimens were selected as
having been previously assayed by two IRMA without consistently detecting
LH surges. These urine specimens were remeasured using an IFMA and adjusted
for creatinine concentration. IFMA measurements revealed unambiguous LH
surges in all cycles. Adjusting IRMA urinary LH values for creatinine
concentrations revealed previously undetected LH surges in four of eight
cycles. Creatinine adjustment also altered the timing of IRMA and IFMA LH
surges by 1-5 days. These results demonstrate an IFMA that detects pre-
ovulatory LH surges in unpreserved, frozen urine from cycles where such
surges were previously undetectable. Further, creatinine adjustment can
markedly affect detection and timing of the onset and peak of the urinary
LH surge. While our analysis suggests that this adjustment improves the
validity of the LH measure, this requires further investigation.
相似文献
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