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31.
M. El Majdoubi D. A. Poulain D. T. Theodosis 《The European journal of neuroscience》1996,8(7):1377-1389
The present ultrastructural study analysed the distribution of glutamatergic synapses on oxytocin- and vasopressin-secreting neurons in the rat supraoptic nucleus (SON) after post-embedding immunogold labelling for glutamate and GABA, oxytocin or vasopressin. About 20% of SON axo—somatic synapses were enriched in glutamate immunoreactivity, visible over synaptic-like vesicles, mitochondria and synaptic densities. Double labelling for glutamate and GABA showed that putative glutamatergic terminals were distinct from GABAergic terminals. In ultrathin sections stained for glutamate and either oxytocin or vasopressin, the proportion of glutamatergic synapses was similar on oxytocinergic and vasopressinergic somata in virgin rats under basal conditions of peptide release as well as in lactating rats, in which oxytocin secretion is enhanced. Cross-sectional soma areas were significantly increased in lactating rats: oxytocinergic profiles were, on average, ˜40% larger than in virgin rats. However, the incidence of axo—somatic glutamatergic synapses (assessed as mean number of synapses per 100 μm of plasmalemma or proportion of somatic surface apposed to synaptic active zones) did not diminish, indicating that there was a compensatory increase of synapses during lactation. Also, we found an increase in the number of glutamatergic terminals making synaptic contact simultaneously onto two or more oxytocinergic elements in the same plane of section. Our observations therefore indicate that SON oxytocinergic and vasopressinergic neurons are innervated to a similar extent by a relatively large proportion of glutamatergic synapses. They reveal, moreover, that glutamatergic afferents participate in the lactation-induced synaptic plasticity of the oxytocinergic system. 相似文献
32.
33.
J. M. Porcher C. Lafuma R. El Nabout M. P. Jacob P. Sébastien P. A. Borm S. Honnons G. Auburtin 《International archives of occupational and environmental health》1993,65(Z1):S209-S213
This research is designed to evaluate a number of biological markers to estimate harmful exposure on coal miners from different mining regions in France and to relate the outcome to differences in prevalence of coal worker pneumoconiosis (CWP) between these regions. Eight epidemiological groups of active and ex-miners (smokers and non-smokers) have been selected in the French collieries (North, Lorraine and Provence) according to their occupational and pneumoconiotic status. The following biomarkers have been evaluated: cellularity of sputum, elementary analysis of particles in TEM/EDAX, plasma neutral metalloendo peptidase elastase type (NMEP), leucocyte elastase (HLE), fibronectin (FN) and elastin peptides. Pulmonary alveolitis, expressed by sputum cellularity, is different between active workers groups but not related to the general background of pneumoconiosis prevalence in the French collieries. In the plasma parameters, fibronectin, HLE and NMEP significantly increased in all groups of coal mine workers as compared to the control group, except for fibronectin parameter in Lorraine collierie. The degree of increase of these parameters allow us to discriminate the different groups and suggest that plasma FN, HLE and NMEP may be considered as biological markers of chronic inhalation of coal mine dust particles. The decrease of elastin peptides level in the Lorraine group alone suggests a specific alteration of elastin metabolism. These parameters were not related to the development of pneumoconiosis and its degree of severity. 相似文献
34.
Myofibroblasts and the progression of diabetic nephropathy 总被引:23,自引:3,他引:20
Essawy M; Soylemezoglu O; Muchaneta-Kubara E; Shortland J; Brown C; El Nahas A 《Nephrology, dialysis, transplantation》1997,12(1):43-50
Background. The cellular mediators of progressive
renal fibrosis in diabetic nephropathy remain unknown. Myofibroblasts have
been implicated in the pathogenesis of experimental and clinical renal
fibrosis. Their role in the progression of diabetic nephropathy is the
subject of this study.Subjects and methods. We have
studied by immunohistochemistry the expression of cytoskeletal proteins
associated with the activation of myofibroblasts; &agr;-smooth-muscle
actin (&agr;-SMA), vimentin (Vi) and desmin (D), in the kidneys of 25
patients with diabetic nephropathy (5 patients with diabetic nephropathy (5
patients had a superimposed glomerulonephritis). Comparisons were made with
normal tissue for three kidneys removed for renal-cell carcinoma.
Correlations were studied between clinical and biochemical parameters with
the expression renal cytoskeletal proteins. Results.
In normal kidneys, cells expressing &agr;-SMA were confined to the
vascular media and adventia while immunoreactive Vi was detected in
glomerular epithelial cells. In diabetic kidneys, cells expressing
&agr;-SMA were detected primarily in the renal interstitium and to a
lesser extent in some glomeruli in association with mesangial
proliferation. Vimentin immunostain decreased in glomeruli displaying
diabetic hyalinosis and sclerosis. By contrast, strong Vi immunoreactivity
was noted in atrophic diabetic tubules and to a lesser extent in the
interstitium. Desmin was not detected in either normal or diabetic kidneys.
Close correlations were observed between the expression of renal
cytoskeletal proteins and the progression of renal insufficiency.
Interstitial &agr;-SMA proved to be a predictor of progressive diabetic
nephropathy (R2 for 1/serum Cr slope=0.608,
P=0.00001). This predictive parameters; tubular atrophy
(R2=0.477, P=0.00004) and interstitial fibrosis
(R2=0.28, P=0.001). Conclusion.
We have demonstrated in this study the neoexpression of cytoskeletal
proteins within diabetic kidneys. This has allowed the identification of
new predicting histological markers for the progression of diabetic
nephropathy. 相似文献
35.
36.
The purpose of this study was to determine the nature and amounts of prostaglandins (PGs) produced by squamous carcinoma cells (SCC) and the sensitivity of these cells to non-steroidal anti-inflammatory drugs. SCC of four lines of the tongue and one line of facial epidermis of humans were incubated in phosphate buffer solution with 14 C-arachidonic acid (AA). Radioactive metabolites in aqueous methanol were chromatographed on Sep-Pack CIS cartridges, separated and quantitated by means of TLC, autoradiography, and liquid scintillation counting. The results showed that cyclooxygenase products, PGs, were the major products formed by all cell lines, and PGE2 was predominant among the PGs detected. Two radioactive bands corresponding to PGF2α and three unseparated standards of PGA2 , 15-keto-PGE2 , and 13,14-dihydro-15-keto-PGE2 were detected in lesser amounts. Very small amounts of the lipoxygenase products 12-and 15-HETE were found. The concentrations of indomethacin, ibuprofen and aspirin required to inhibit 50% of PGE2 synthesis (IC50 ) by SCC lines were .008- .080, .080–6.4 and 32–88 μM, respectively. 相似文献
37.
Transforming growth factor-beta(1) in the kidney and urine of patients with glomerular disease and proteinuria. 总被引:6,自引:2,他引:4
Dimitrios S Goumenos Sotiris Tsakas Abdel Meguid El Nahas Sotiria Alexandri Simon Oldroyd Pantelitsa Kalliakmani John G Vlachojannis 《Nephrology, dialysis, transplantation》2002,17(12):2145-2152
BACKGROUND: Transforming growth factor-beta(1) (TGF-beta(1)) is the major fibrogenic growth factor implicated in the pathogenesis of renal scarring. Proteinuria is a poor prognostic feature for various types of glomerular disease and its toxic action may be related to the activation of tubular epithelial cells towards increased production of cytokines and chemoattractant peptides. In this work we studied the site of synthesis and expression profile of TGF-beta(1) in the renal tissue of patients with heavy proteinuria and examined the relation of this expression with the urinary excretion of TGF-beta(1). METHODS: Twenty-five patients with heavy proteinuria (8.4+/-3.0 g/24 h) were included in the study. All patients underwent a diagnostic kidney biopsy and were commenced on immunosuppressive therapy with corticosteroids and cyclosporin. The sites of synthesis and expression profile of TGF-beta(1) mRNA and protein in the kidney were examined by in situ hybridization and immunohistochemistry. Urinary and plasma TGF-beta(1) levels were determined by ELISA before the initiation of treatment and 6 months later and compared with those of normal subjects and of patients with IgA nephropathy and normal urinary protein excretion. RESULTS: The site of synthesis and expression of TGF-beta(1) in the renal tissue of patients with heavy proteinuria was mainly localized within the cytoplasm of tubular epithelial cells. Interstitial expression was also present but glomerular TGF-beta(1) expression was found only in patients with mesangial proliferation. Urinary TGF-beta(1) excretion was significantly higher in nephrotic patients compared with normal subjects and with patients with IgA nephropathy and normal urinary protein excretion (783+/-280 vs 310+/-140 and 375+/-90 ng/24 h, respectively; P<0.01). In patients with remission of proteinuria after immunosuppressive therapy, urinary TGF-beta(1) excretion was significantly reduced (from 749+/-290 to 495+/-130 ng/24 h; P<0.01), while in patients with persistent nephrotic syndrome, it remained elevated. CONCLUSIONS: The localization of TGF-beta(1) mRNA and protein within tubular epithelial cells, along with its increased urinary excretion in patients with nephrotic syndrome, suggest the activation of these cells by filtered protein towards increased TGF-beta(1) production. 相似文献
38.
39.
Quantitative SPECT leads to improved performance in discrimination tasks related to prodromal Alzheimer's disease. 总被引:5,自引:0,他引:5
Georges El Fakhri Marie Foley Kijewski Marilyn S Albert Keith A Johnson Stephen C Moore 《Journal of nuclear medicine》2004,45(12):2026-2031
We investigated the impact of the quantitation and reconstruction protocol on clinical tasks. The performance of standard clinical reconstruction procedures in discrimination tasks related to the diagnosis of prodromal Alzheimer's disease (AD) was compared with the performance of a quantitative approach incorporating improved corrections for scatter, attenuation, intrinsic spatial resolution, and distance-dependent spatial resolution. METHODS: Seventeen normal controls (normal group), 56 subjects who did not have dementia, who did have memory problems, but who did not develop AD within 5 y of follow-up (questionable group), and 27 subjects who did not have dementia, who did have memory problems, and who did develop AD over the follow-up period (converter group) were considered in this study. (99m)Tc-hexamethylpropyleneamine oxime SPECT and MRI studies were performed for each subject at baseline. The standard quantitation protocol (STD), routinely used in our clinic, consisted of Compton window scatter correction followed by filtered backprojection with attenuation correction using a uniform attenuation map. In the improved quantitative approach (QUAN), projections were corrected for scatter by use of a general spectral method and reconstructed by use of ordered-subset(s) expectation maximization, incorporating corrections for collimator response and attenuation using both a uniform attenuation map (QUANunif) and a nonuniform attenuation map (QUANnonunif). Mean SPECT activity concentration and MRI volume were estimated for 7 structures: rostral anterior cingulate gyrus, caudal anterior cingulate gyrus, posterior cingulate gyrus, hippocampus, basal forebrain, amygdala, and the banks of the superior temporal sulcus. Data were analyzed by pairwise discriminant analysis, and performance in binary group discrimination was measured by correlated receiver-operating-characteristic analysis. RESULTS: The use of QUANnonunif yielded a small but systematic improvement in discrimination accuracy for normal versus converter groups (accuracy or area under the receiver-operating-characteristic curve [Az], 0.965), normal versus questionable groups (Az, 0.973), and questionable versus converter groups (Az, 0.881) compared with the results obtained with QUANunif (Az, 0.955, 0.962, and 0.866, respectively). Discrimination performance was significantly lower (P < 0.05) with STD than with QUAN in all 3 tasks (Az with STD, 0.906, 0.878, and 0.768, respectively). MRI volume estimation led to a lower overall performance in all 3 tasks than did QUANnonunif (Az with MRI, 0.947, 0.917, and 0.872, respectively). CONCLUSION: Improved quantitative image reconstruction with accurate compensation for scatter, attenuation, and variable collimator response led to significantly better performance in discrimination tasks related to the diagnosis of prodromal AD than did standard clinical reconstruction procedures. The use of a nonuniform brain attenuation map yields a small improvement in discrimination accuracy. 相似文献
40.