佐金平木治疗经期病三则

笔者近十余年来,运用佐金平木法治疗由木火刑金所致的经行目赤、经行鼻齿衄、经行便血证,颇获效验.兹报告如下.

月经前后急重症治验三则

一、经行大汗淋漓张某,45岁,1986年3月5日初诊。素昔经来量多,近一年来月经来潮,量少色淡,全身大汗淋漓,面潮红,烘热,倦乏无力、脉虚数、舌质淡红,苔薄白。辨证:阴虚阳亢。治法:滋阴潜阳固汗。处方:生熟地各15克,当归身10克,炒白芍12克,生枣仁12克,玄参10克,乌梅1枚,炙龟版15克(先煎),煅牡蛎30克(先煎)。三剂后汗出已止,余症如前,继进滋阴益气之品,原方加入芋肉6克,太子参30克,淮牛膝10克,生黄芪20克。连服14剂,体复如常人。随访1年,月经正常,经行也不出汗。

Osteoporosis in celiac disease and in endocrine and reproductive disorders

As the increase in lifespan brings to light diseases that were previously not clinically detectable,osteoporosis has become an issue of worldwide significance. The disease is marked by a loss of bone mass; the bones become less dense,fragile and more prone to fracturing. Because it is regulated by endocrine and environmental factors,osteoporosis presents a multifactorial etiopathogenesis,with the genetic component accounting for 70% of an individual variation in bone mass density (BMD),the principal determinant,with age,of fracture risk. Pathological conditions such as celiac disease (CD) exacerbate the process of bone loss,so that the occurrence of osteoporosis in celiac subjects is of particular note: indeed,the screening of osteoporosis patients for this disease is advisable,since it may be the only sign of undiagnosed CD. An increase in interleukin IL-1β,of the IL-1 system,in the relatives of celiac patients confirms the genetic predisposition to osteoporosis and its presence is evidence of an association between the two conditions. The direct effect on the bones of CD is secondary to poor absorption of calcium and vitamin D. In women osteoporosis is indirectly associated with early menopause and amenorrhea,and it may follow prolonged breast-feeding and frequent pregnancies,while in men it is associated with hypogonadism and GH deficit. These endocrine and non-endocrine factors exert their effects on bones by modulating the RANK/RANK-L/OPG system. An appropriate lifestyle from adolescence onwards,together with early diagnosis of and treatment for CD and primary and secondary endocrine pathologies are important for the prevention of damage to the bones.

Evaluation of the best follow-up period and curative effect for acoustic neuroma treated with a gamma knife

Objective: To determine the best follow-up period with regard to curative effect for acoustic neuroma treated with a gamma knife. Methods: Sixty cases of acoustic neuroma were treated with a gamma knife. The follow-up period was from 3 to 102 months. Changes in the lesions and peripheral tissues and clinical symptoms were compared and the curative effectiveness of gamma knife treatment was evaluated. Results: The highest total effective rate (92.3%) was in the third period. There was a significant difference in the tumor size postoperatively. There was no edema in the peripheral tissues surrounding the tumor. It was not obvious that clinical symptoms changed. Conclusion: In this report, the best follow-up period was 24-36 months. Gamma knife treatment was still effective after 60 months post-operation.

Early calcium dysregulation in Alzheimer's disease:setting the stage for synaptic dysfunction

Alzheimer's disease(AD) is an irreversible and progressive neurodegenerative disorder with no known cure or clear understanding of the mechanisms involved in the disease process.Amyloid plaques,neurofibrillary tangles and neuronal loss,though characteristic of AD,are late stage markers whose impact on the most devastating aspect of AD,namely memory loss and cognitive deficits,are still unclear.Recent studies demonstrate that structural and functional breakdown of synapses may be the underlying factor in AD-linked cognitive decline.One common element that presents with several features of AD is disrupted neuronal calcium signaling.Increased intracellular calcium levels are functionally linked to presenilin mutations,ApoE4 expression,amyloid plaques,tau tangles and synaptic dysfunction.In this review,we discuss the role of AD-linked calcium signaling alterations in neurons and how this may be linked to synaptic dysfunctions at both early and late stages of the disease.

Cell cycle reactivation in mature neurons: a link with brain plasticity, neuronal injury and neurodegenerative diseases?

Although the cell cycle machinery is essentially linked to cellular proliferation, recent findings suggest that neuronal cell death is frequently concurrent with the aberrant expression of cell cycle proteins in post-mitotic neurons. The present work reviews the evidence of cell cycle reentry and expression of cell cycle-associated proteins as a complex response of neurons to insults in the adult brain but also as a mechanism underlying brain plasticity. The basic aspects of cell cycle mechanisms, as well as the evidence showing cell cycle protein expression in the injured brain, are reviewed. The discussion includes recent experimental work attempting to establish a correlation between altered brain plasticity and neuronal death, and an analysis of recent evidence on how neural cell cycle dysregulation is related to neurodegenerative diseases especially the Alzheimer＇s disease. Understanding the mechanisms that control reexpression of proteins required for cell cycle progression which is involved in brain remodeling, may shed new light into the mechanisms involved in neuronal demise under diverse pathological circumstances. This would provide valuable clues about the possible therapeu tic targets, leading to potential treatment of presently challenging neurodegenerative diseases.

Rabies virus co-localizes with early(Rab5) and late(Rab7) endosomal proteins in neuronal and SH-SY5Y cells

Rabies virus(RABV) is a highly neurotropic virus that follows clathrin-mediated endocytosis and p H-dependent pathway for trafficking and invasion into endothelial cells. Early(Rab5, EEA1) and late(Rab7, LAMP1) endosomal proteins play critical roles in endosomal sorting, maturity and targeting various molecular cargoes, but their precise functions in the early stage of RABV neuronal infection remain elusive. In this study, the relationship between enigmatic entry of RABV with these endosomal proteins into neuronal and SH-SY5 Y cells was investigated.Immunofluorescence, TCID_(50) titers, electron microscopy and western blotting were carried out to determine the molecular interaction of the nucleoprotein(N) of RABV with early or late endosomal proteins in these cell lines. The expression of N was also determined by down-regulating Rab5 and Rab7 in both cell lines through RNA interference. The results were indicative that N proficiently colocalized with Rab5/EEA1 and Rab7/LAMP1 in both cell lines at 24 and 48 h post-infection, while N titers significantly decreased in early infection of RABV. Down-regulation of Rab5 and Rab7 did not inhibit N expression, but it prevented productive infection via blocking the normal trafficking of RABV in a low pH environment. Ultrathin sections of cells studied by electron microscope also verified the close association of RABV with Rab5 and Rab7 in neurons. From the data it was concluded that primary entry of RABV strongly correlates with the kinetics of Rab-proteins present on early and late vesicles, which provides helpful clues to explain the early events of RABV in nerve cells.