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MG Astapenko W Otto TM Trofimowa H H?ntzschel B Tautenhahn D Reinelt H Treutler AI Speranskij NM Mylow WA Duljapin TA Tarasenkowa 《Canadian Metallurgical Quarterly》1976,31(16):641-646
On the basis of own observations of courses the author adopts a definite attitude to the early symptomatology of the rheumatoid arthritis. During the first weeks of the rheumatoid arthritis the following symptoms are found: articular syndromes, more frequently in form of obstinate polyarthralgias, mono-oligoarthritis, accompanied by morning rigidity and accelerated BSR as well as impairment of the general condition. In the majority of the patients only the tentative diagnosis rheumatoid arthritis may be made. After a one to three months' course of the disease the diagnosis becomes more probable. It is above all based on constancy and symmetry, characteristic localisation of the articular process, morning rigidity, radiologically paraarticular loosening of the structure and morphological symptoms of an acute and subacute synovialitis. 6 to 12 months after the beginning of the disease a clinical picture forms which allows to make the diagnosis of a certain or classical rheumatoid arthritis in accordance with the criteria of the ARA. The occurrence of a high activity of multiple affection of the joints (permanent symmetrical polyarthritis including the small joints of the hands and feet), distinctive morning rigidity, high fever and much accelerated BSR, beginning with the first weeks of the disease, speaks for the possibility of the development of an arthrovisceral form of the course of rheumatoid arthritis. 相似文献
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纳米羟基磷灰石(HAP)增强聚合物基复合材料是替换硬组织的最理想材料,是植入材料的研究重点之一。为了制备与天然骨结构非常相似的复合材料,必须首先制备出性能优良的的纳米HAP粉体。对水热法制备HAP纳米晶须的工艺进行了研究,研究了反应时间、温度、起始反应物的浓度、钙磷比以及反应体系的pH值对合成HAP纳米晶须形貌的影响。用X射线衍射(XRD)、扫描电镜(SEM)和红外光谱(FT-IR)法,对制备的羟基磷灰石进行了表征和分析。结果表明:生成的HAP晶须的长度及长径比随反应时间的延长而增大。温度〈150℃时,得到HAP晶须;温度〉180℃,则得到细小HAP晶体的聚集产物。当反应物的pH=9时,得到的是缺钙型的HAP;当反应物的pH〈4时,产物中出现新相磷酸氢钙;当pH=2时,得到纯的磷酸氢钙。 相似文献
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Cellular mechanisms for developmental toxicity of chlorpyrifos: targeting the adenylyl cyclase signaling cascade 总被引:8,自引:0,他引:8
X Song FJ Seidler JL Saleh J Zhang S Padilla TA Slotkin 《Canadian Metallurgical Quarterly》1997,145(1):158-174
Developmental neurotoxicity caused by chlorpyrifos exposure is generally thought to target cholinesterase but chlorpyrifos may also act on cellular intermediates, such as adenylyl cyclase, that serve global functions in the coordination of cell development. In the current study, neonatal rats were exposed to apparently subtoxic doses of chlorpyrifos (no weight loss, no mortality) either on Postnatal Days 1-4 or on Postnatal Days 11-14, and the effects on components of the adenylyl cyclase cascade were evaluated in brain regions that are enriched (forebrain) or sparse (cerebellum) in cholinergic innervation, as well as in a nonneural tissue (heart). In all three, chlorpyrifos evoked deficits in multiple components of the adenylyl cyclase cascade: expression and activity of adenylyl cyclase itself, functioning of G-proteins that link neurotransmitter and hormone receptors to cyclase activity, and expression of neurotransmitter receptors that act through this cascade. Disruption of signaling function was not restricted to transduction of cholinergic signals but rather extended to adrenergic signals as well. In most cases, the adverse effects were not evident during the immediate period of chlorpyrifos administration, but appeared after a delay of several days. These results suggest that chlorpyrifos can affect cell development by altering the activity and reactivity of the adenylyl cyclase signaling cascade, a major control point for trophic regulation of cell differentiation. The effects are not restricted to cholinergic targets, nor even to the central nervous system. Hence, disruption of cell development by chlorpyrifos is likely to be more widespread than previously thought. 相似文献
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Continuous intracameral infusions of a balanced salt solution (0.175 microliter min-1) have been reported to raise intraocular pressure (IOP) in anesthetized rats. Palm et al. (1995) previously reported that this effect was attenuated significantly by inclusion of arginine-vasopressin (AVP, 10 ng 0.175 microliter-1) in the infusate. This study used experimental and computer simulation methods to investigate factors underlying these changes in IOP. First, constant intracameral infusions of artificial cerebrospinal fluid (aCSF) at different fixed rates (0.049-0.35 microliter min-1) were used to estimate the outflow resistance. Secondly, IOP responses were measured during an 2 hr intracameral infusion of either aCSF or AVP that was the sum of a small constant component (0.05 microliter min-1) and a larger periodic component (0.25 microliter min-1, cycling for 4 min on, then 4 min off); the mean infusion rate was 0.175 microliter min-1. As shown previously for 0.175 microliter min-1 constant infusions, the periodic aCSF infusion induced a significant rise in IOP that was attenuated by AVP administration. Complex demodulation analysis and the estimated gain parameter of a second order transfer function fit to the periodic responses indicated that outflow resistance increased significantly during the infusions in both aCSF and AVP groups, but that the indices of resistance did not differ significantly between aCSF and AVP infused eyes. This finding implies that changes in outflow resistance do not explain the difference in IOP responses to intracameral aCSF and AVP. The two responses differed significantly, though, in damping factors, such that the aCSF responses were considerably more underdamped than the AVP responses. It is hypothesized that aCSF-induced increase in IOP reflects both (1) a small component reflecting increased outflow resistance and (2) a larger non-resistive component. Since the non-resistive component is insensitive to pretreatment with acetazolamide, it is suggested that the aCSF-induced elevation in IOP reflects primarily vascular perfusion changes that are reduced by local vasoconstrictor actions of AVP. The latter mechanism likely maintains vascular perfusion of the globe when intraocular hypertension develops. 相似文献