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31.
Refocused insensitive nucleus enhancement by polarization transfer (RINEPT) from protons (1H) to a J-coupled phosphorus (31P) has been incorporated into three-dimensional (3D) chemical-shift-imaging (CSI) sequence on a clinical imager. The technique is demonstrated on a phantom and in in vivo human brain. The polarization-transfer efficiency (~1.2) is lower than the theoretical maximum of γ1H/γ31P≈ 2.4 resulting from 1H-1H homonuclear J couplings of similar magnitude competing with the 1H →31P transfer. Nevertheless, compared with direct 31P Ernst-angle excitation, signal gains of up to × 1.8 were obtained mainly as a result of T1 differences between 31P and the 1H. Spectral interpretation is simplified by editing out all non-proton-coupled 31P signals. The duration, ~50 min, and power deposition, ~1 W · kg?1, make the application suitable for human studies.  相似文献   
32.
Phosphorus was imaged in vivo in human cortical and trabecular bone and the T(1) and T(2) (*) were measured. An ultrashort TE (UTE) pulse sequence (TE = 70 microm) was used with half pulse excitation and radial mapping of k-space from the center out. T(2) (*) was measured using multiple echo times and T(1) was measured both by saturation recovery and by a method using different RF pulse amplitudes. Seven normal subjects (32-85 years) were examined. Phosphorus was imaged, with a true in-plane resolution of 2.9 x 2.9 mm and a signal-to-noise ratio (SNR) of 19:1, in both cortical and trabecular bone. The mean T(2) (*) value was 207 +/- 12 micros, and the mean T(1) value was 8.6 +/- 3.0 sec. Images and measurements were obtained in realistic times on a clinical MR system. This may provide a new approach to characterizing disease of bone.  相似文献   
33.
急性有机磷中毒患者的血钾变化及临床意义的探讨   总被引:1,自引:0,他引:1  
目的:探讨急性有机磷中毒患的血清钾变化及其临床意义。方法:对68例发病6小时内的急性有机磷中毒的患入院后测定血清钾,并根据不同的中毒程度、中毒方式、发病时间分组在比较,并设正常对照组对照。结果:中毒各组均有明显的低钾血症,与对照组比较均有显性意义(P<0.01),且重度中毒组与中、轻度组比较亦有显性意义(P>0.05),但两种不同的中毒途径与不同的中毒时间的组间血清钾的比较无显性意义(P>0.05)。结论:急性有机磷中毒可致明显的低钾血症,中毒越重,低钾血症越明显。在发病早期应注意监测血清钾的变化,及时纠正低血钾,预防或减轻中毒后严重合并症的产生。  相似文献   
34.
FOREWORDPeritonealdialysisrepresentssoluteandfluidexchangemainlybetweenperitonealcapillarybloodanddialysissolutionintheperitonealcavity'CombinedwithhemodialySisandrenaltransplantation,peritonealdialysisisusedmainlyforthetreatmentofrenalfailure,particularlyforchronicfailure'In1976,Prof'Popovichdevelopedcontinuousambulatoryperitonealdialysis(CAPD)basingontheconceptofcontinuousequilibrationdialysis('1'Fromthenon,peritonealdialysisfounditsclinicaluse'Continuouscyclicperitonealdialysis(CCPD…  相似文献   
35.
In view of the increasing evidence that a pathological glial activation plays a significant role in the development of neurodegenerative diseases, we investigated the underlying molecular signaling as a possible target for a pharmacological therapy. Here, we are particularly focusing on the endogenous modulation of the Ca2+ and cyclic nucleotide-dependent signaling by the nucleoside adenosine and its reinforcement by the xanthine derivative propentofylline (PPF). As an experimental model, we used cultured rat microglial cells and astrocytes that are immature, show a high proliferation rate, and resemble in several aspects pathologically activated glial cells. A prolonged increase of the cellular cAMP level favored the differentiation of cultured astrocytes and associated properties required for the physiological nerve cell function. On the other hand, a strengthening of the cyclic nucleotide-dependent signaling inhibited potentially neurotoxic properties of cultured microglial cells. Similar effects were obtained by treatment with propentofylline, which mimicked modulatory adenosine effects and increased the intracellular level of cAMP and cGMP. Such a pharmacological glial cell conditioning, obtained by modifying the strength and the timing of these second messengers, may provide a therapy of neurodegenerative diseases in which a pathological activation of microglial cells and astrocytes is discussed to play a pathogenic role.  相似文献   
36.
目的 探讨糖尿病肾病(DN)患者血清瞬时受体电位通道7(TRPM7)、沉默调节蛋白-1(Sirtuin-1)与钙磷代谢、颈动脉钙化的相关性。方法 选取2020年12月—2022年11月成都大学附属医院收治的97例DN患者作为DN组,另取同期在该院就诊的120例2型糖尿病患者作为对照组。采用实时荧光定量聚合酶链反应检测血清TRPM7的表达,酶联免疫吸附试验检测血清Sirtuin-1水平。采用Pearson法分析DN患者血清TRPM7、Sirtuin-1水平与钙磷代谢的相关性,并通过多因素Logistic逐步回归模型分析DN患者颈动脉钙化的危险因素。结果 DN组血肌酐、尿素氮、血清TRPM7、血磷、颈动脉钙化率高于对照组(P <0.05)。DN组Sirtuin-1、血钙低于对照组(P <0.05)。Pearson相关性分析结果显示,DN患者血清TRPM7与血钙呈负相关(r=-0.247,P=0.000),与血磷呈正相关(r=0.415,P=0.000);DN患者血清Sirtuin-1与血钙呈正相关(r=0.367,P=0.000),与血磷呈负相关(r=-0.505,P=0.00...  相似文献   
37.
We studied the actions of D1 and D2 dopamine agonists and antagonists on the coupling of horizontal cell axons in the turtle retina by a combination of pharmacological and electrophysiological methods. Both D1 and D2 receptors were identified in membrane fractions by radioligand binding using [3H]-SCH 23390 and [3H]-spiperone, respectively. The KD of both receptor classes were identical (0.21 nM) but D1 receptor density exceeded that of D2 receptors by more than four-fold. D1 agonists increased the activity of adenylate cyclase in a dose-dependent manner, whereas D2 agonists were without significant effect by themselves, nor did D2 antagonists block the D1-mediated increase in adenylate cyclase activity. Intracellular recordings and Lucifer Yellow dye injections were used to characterize the modifications of the receptive field profile of horizontal cell axons (H1AT) exposed to different pharmacological agents. Dopamine or D1 agonists (0.05 - 10 microM) induced a marked constriction of the H1AT receptive field, whereas D2 agonists elicited a small expansion of the receptive field. However, in the presence of a D1 antagonist, as well as IBMX to inhibit phosphodiesterase, D2 agonists (10 - 70 microM) induced a marked increase in the receptive field profile. These results indicate that both D1 and D2 dopamine receptors play a role in shaping the receptive field profile of the horizontal cell axon terminal in the turtle retina.  相似文献   
38.
Cyclic peptide disulfides of the general formula were synthesized from the corresponding peptide derivatives [Boc-Cys(Trt)(Gly)-n-Cys(Trt)-OBut] by oxidation with iodine in methanol and by subsequent removal of the terminal groups with trifluoroacetic acid. Acid ionization constants of the obtained peptides were determined by potentiometric titration in aqueous KCl (0.1 mol/L) medium. All compounds have two dissociable hydrogens, corresponding to carboxyl (pK1= 2.35–2.84) and to terminal amino group (pK2= 5.61–6.93); pK1, values show first an upward and then a downward trend with the increase in ring size; the opposite is true for pK2, values. These trends could be tentatively attributed to the intramolecular salt bridge (-COO——-NH+3-) formation.  相似文献   
39.
Decreased response of beta-adrenergic receptor has been considered to he one of the causes of increased responsiveness of the bronchi in asthma. Since beta-adrenergic receptor has two subtypes, beta1 and beta2, and the bronchodilating effect of beta stimulants is mediated by beta2-receptor, responsiveness of the bronchi is expected to correlate to the cyclic AMP response of lymphocytes to a beta2-stimulant. Responsiveness of the bronchi was expressed as respiratory threshold to acetylcholine (RT-Ach), which was the minimal concentration of acetylcholine solution to cause an initial decrease of FEV1 of more than 20% of the baseline value. Beta1 and heta2-responses were expressed as the increments of cyclic AMP content of 106 lymphocytes incubated with norepinephrine (beta1-stimulant) and salbutamol (beta2-stimulant).
RT-Ach showed a significant correlation with the beta2-cyclic AMP response of lymphocytes, but not with the beta1 -response among patients with asthma. Sixteen symptomatic patients on continuous beta-stimulants showed lower RT-Ach value and diminished beta2-receptor activity of lymphocytes compared with 14 patients in remission. These results suggest that selective beta2-adrenergic blockade may he one of the causes of bronchial hypersensitivity in asthma, though it should be noted that in this study beta-adrenergic responses were examined in lymphocytes and were compared with the responsiveneness of the bronchi. Possible beta-receptor subsensitivity induced by administration of beta-stimulants is discussed.  相似文献   
40.
This study was undertaken to investigate the presence of messengerRNA (mRNA) for prepro-endothelin-I (ET-1) and the known receptorsubtypes (ETA and ETB) in human endometrium at different stagesof the menstrual cycle obtained at hysterectomy. Northern blotanalysis revealed expression of ET-1 mRNA in human endometriumduring the normal menstrual cycle. The concentration of ET-1mRNA in endometrial tissue was greater during the menstrualand proliferative phases than during the ovulatory and secretoryphases. Immunoreactive ET-1 was secreted into the medium ofisolated endometrial stromal cells. Oestradiol and progesteronesignificantly attenuated ET-1 release in endometrial stromalcells cultured for 6 days. ETA and ETB mRNA were also presentin endometrial tissue of the normal cycle. The concentrationof ETA receptor mRNA was greater in the proliferative phasethan in the secretory phase, whereas expression of ETB mRNAincreased in menstrual phase. ET-1 significantly increased extracellularaccumulation of cyclic AMP (cAMP), intracellular generationof inositol phosphates and significantly enhanced DNA synthesisin cultured endometrial stromal cells from the proliferativephase. Our results showed that human endometrial cells synthesizedand released ET-1, and contained ETA and ETB receptors whichwere functionally coupled to phosphoinositide breakdown andto adenylate cyclase with the increase of cAMP by ET-1 stimulation.Our findings suggest that ET-1 may have a potential autocrineand/or paracrine function in human endometrial stromal cells.  相似文献   
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