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Objective The traditional round incision or cross incision brain harvesting method can not meet the requirements of protecting the donor's remains. In this study, the method of brain removal through a posterior incision on the scalp of both ears was proposed, which effectively protected the donor's remains. Methods Adopting the incision 2. 0 cm above the external occipital protuberance to the most front edge of the auricle to obtain a complete brain. Results The incision did not involve the head and face skin, which was small and conducive to suture repair and reduce exudation. Conclusion The incision effectively protects the donor' s remains, and it will be conducive to the establishment and development of the brain bank.
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[Abstract] Objective To elucidate the important role of Nogo-A in climacteric neurodegeneration such as memory impairment by observing memory function and the expression of Nogo-A in hippocampus and striatum of rats under low estrogen condition. Methods Fouthy-five female SD rats were divided into sham operation group, ovariectomized group and ovariectomized estrogen treatment group with 15 rats in each group. Medication was given 2 weeks after ovariectomized. Estrogen treatment group was subcutaneously injected in groin with estrogen [25 μg/ (kg.d)] dissolved in sterile sesame oil. The sham operation group and the ovariectomized group were given the same amount of aseptic sesame oil. Samples were collected after 6 weeks of drug treatment. The difference of memory function of rats in three groups was observed by conditioned fear training experiment, and the expression of Nogo-A in hippocampus and striatum was observed by immunohistochemistry and Western blotting. Results Compared with the sham and estrogen treatment group, memory function in ovariectomized group decreased significantly and the number of Nogo-A positive neurons in hippocampus and striatum of ovariectomized rats was significantly higher than that of sham operation group (P 0. 05). The result of immunoblotting was consistent with the above-mentioned immunohistochemical result. Conclusion The increased expression of Nogo-A in hippocampus and striatum under low estrogen condition may be one of the key reasons for memory impairment in climacteric women.
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Nogo protein is the fourth member of reticulin famity. Nogo mRNA produced by encoding gene transcription, forms three different RNA transcripts due to different promoter and splicing modes, namely Nogo-A, Nogo-B and Nogo-C protein. Nogo protein was first found in the central nervous system, and then proved to be widely expressed in peripheral tissues such as heart, liver and vascular endothelium. Studies have shown that Nogo protein can participate in the regulation of myocardial fibrosis through RhoA/Rho-associated kinase(ROCK) pathway, endoplasmic reticulum stress, Sce61 a and other signaling pathways. In this paper, the relationship between Nogo-A, Nogo-B, Nogo-C and myocardial fibrosis is briefly introduced.
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As bioactive lipids, sphingolipids participate in the signal transduction of many important physiological processes such as growth and apoptosis. Besides, abnormal levels of sphingolipids were detected in a variety of clinical conditions including hypertension and coronary heart disease, suggesting that sphingolipid metabolism is involved in the occurrence and development of cardiovascular diseases. This paper reviewed the relationship between sphingolipid metabolism with four common cardiovascular diseases, coronary heart disease, hypertension, arrhythmia and heart failure, and the mechanisms involved. What's more, the prospect of sphingolipid pathway as a potential target for the diagnosis and treatment of cardiovascular diseases is put forward.
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As a member of the reticulin family, Nogo is mainly involved in processes such as tissue regeneration, apoptosis and tumor growth after tissue injury. Cardiovascular disease is one of the main diseases that threaten human health at present. In recent years, research on Nogo in the cardiovascular system has become increasingly extensive. Changes in the expression of Nogo during myocardial fibrosis, myocardial cell apoptosis and vascular remodeling suggest that it may play a certain role. This article reviews the distribution of Nogo in the heart and its role in cardiovascular disease, in order to reveal its possible role and mechanism in cardiovascular diseases.
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Hot flashes are the most common specific symptom of perimenopausal women, which seriously endangers their physical and mental health and quality of life. Because the pathogenesis of hot flashes is not yet clear, and existing estrogen replacement therapy has many limitations and contraindications, it is particularly urgent and important to explore the pathogenesis of hot flashes and find new therapeutic targets. Recent studies suggest that abnormalities of KNDy neurons in the arcuate nucleus of hypothalamus when estrogen decreases during perimenopause are the key factors that trigger hot flashes. Some scholars believe that KNDy neurons in the arcuate nucleus are involved in the occurrence of hot flashes by regulating the pulse release of gonadotropin-releasing hormone and its downstream luteinizing hormone, while some other scholars believe that KNDy neurons in the arcuate nucleus play a key role in the process of hot flashes by regulating the median preoptic nucleus of the hypothalamic preoptic area. Therefore, this review intends to summarize the above two types of current relationship between the KNDy neurons in the arcuate nucleus and the occurrence of hot flashes and the possible mechanisms by which KNDy neurons participate in hot flashes, and lay a theoretical foundation for the exploring of new targets and method for the treatment of perimenopausal hot flashes.
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Hot flashes are the most common symptoms of menopausal women, and their symptoms are closely related to the occurrence of cardiovascular disease, which seriously affects the physical and mental health of menopausal women. Therefore, avoiding and alleviating the occurrence of hot flashes during menopause has become a topic of great concern today. It is generally believed that the hot flashes are caused by the dysfunction of hypothalamic thermoregulatory center, but its exact pathogenesis has not been elucidated. Recent studies have shown that menopausal hot flashes are the result of the interaction of estrogen with a variety of neurotransmitters, and monoamine neurotransmitters like norepinephrine, 5-hydroxytryptamine and dopamine play a central role, which are summarized as follows.