The neurodegenerative polyglutamine diseases are caused various disease proteins. Although these mutant proteins are by an expansion of unstable polyglutamine repeats in expressed ubiquitously in neuronal and non-neur...The neurodegenerative polyglutamine diseases are caused various disease proteins. Although these mutant proteins are by an expansion of unstable polyglutamine repeats in expressed ubiquitously in neuronal and non-neuronal cells, they cause selective degeneration of specific neuronal populations. Recently, increasing evidence shows that polyglutamine disease proteins also affect non-neuronal cells. However, it remains unclear how the expression of polyglutamine proteins in non-neuronal cells contributes to the course of the polyglutamine diseases. Here, we discuss recent findings about the expression of mutant polyglutamine proteins in non-neuronal cells and their influence on neurological symptoms. Understanding the contribution of non-neuronal polyglutamine proteins to disease progres- sion will help elucidate disease mechanisms and also help in the development of new treatment options.展开更多
In the present paper, 70 cases of retrograde affection of the lumbar vertebrae are randomly and evenly divided into treatment group and control group. Shenshu (BL 23), Qihaishu (BL 24), Dachangshu (BL 25), Weizhong (B...In the present paper, 70 cases of retrograde affection of the lumbar vertebrae are randomly and evenly divided into treatment group and control group. Shenshu (BL 23), Qihaishu (BL 24), Dachangshu (BL 25), Weizhong (BL 40), Jiaji (EX B 2), etc. are used. In treatment group, acupuncture, TDP irradiation and cupping are performed, and in control group, only acupuncture is given. After 30 sessions (3 therapeutic courses) of treatment, in treatment and control groups, the total effective rates are 91.43% and 71.43% respectively. The therapeutic effect of comprehensive treatment is significantly superior to that of simple acupuncture therapy (P<0.05).展开更多
Objective:To study gene expression of collagen types IX and X in human lumbar intervertebral discs during aging and degeneratio n and to explore the role of collagen types IX and X in disc degeneration. Methods:Fetal,...Objective:To study gene expression of collagen types IX and X in human lumbar intervertebral discs during aging and degeneratio n and to explore the role of collagen types IX and X in disc degeneration. Methods:Fetal, adult and pathologic specimens were subjected t o in situ hybridization with cDNA probes to investigate mRNA-expressions of typ es IX and X collagen gene. Results:In fetal intervertebral discs, positive mRNA hybridiza tion signals of type IX collagen were concentrated in the nucleus pulposus and t he inner layer of anulus fibrosus. Interstitial matrix of the nucleus pulposus a lso showed positive type X collagen staining. Positive mRNA hybridization signal s of types IX and X were not detected in the middle and outer layers of anulus f ibrosus. In adult specimens, expression of type IX collagen mRNA was markedly de creased. No hybridization signals of type X collagen was observed. As for pathol ogical specimens, there was no gene expression of type IX collagen. In severe de generated discs from adults, there were focal positive expressions of type X col lagen. Conclusions:Obvious changes of collagen gene expression occur with aging. Expression of type IX collagen decreases in adult and pathological d iscs. Results of type X collagen expression suggest that type X collagen is expr essed only in older adult and senile discs (i.e., when disc degeneration has alr eady reached a terminal stage), indicating the terminal stage of degeneration.展开更多
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-...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.展开更多
文摘The neurodegenerative polyglutamine diseases are caused various disease proteins. Although these mutant proteins are by an expansion of unstable polyglutamine repeats in expressed ubiquitously in neuronal and non-neuronal cells, they cause selective degeneration of specific neuronal populations. Recently, increasing evidence shows that polyglutamine disease proteins also affect non-neuronal cells. However, it remains unclear how the expression of polyglutamine proteins in non-neuronal cells contributes to the course of the polyglutamine diseases. Here, we discuss recent findings about the expression of mutant polyglutamine proteins in non-neuronal cells and their influence on neurological symptoms. Understanding the contribution of non-neuronal polyglutamine proteins to disease progres- sion will help elucidate disease mechanisms and also help in the development of new treatment options.
文摘In the present paper, 70 cases of retrograde affection of the lumbar vertebrae are randomly and evenly divided into treatment group and control group. Shenshu (BL 23), Qihaishu (BL 24), Dachangshu (BL 25), Weizhong (BL 40), Jiaji (EX B 2), etc. are used. In treatment group, acupuncture, TDP irradiation and cupping are performed, and in control group, only acupuncture is given. After 30 sessions (3 therapeutic courses) of treatment, in treatment and control groups, the total effective rates are 91.43% and 71.43% respectively. The therapeutic effect of comprehensive treatment is significantly superior to that of simple acupuncture therapy (P<0.05).
文摘Objective:To study gene expression of collagen types IX and X in human lumbar intervertebral discs during aging and degeneratio n and to explore the role of collagen types IX and X in disc degeneration. Methods:Fetal, adult and pathologic specimens were subjected t o in situ hybridization with cDNA probes to investigate mRNA-expressions of typ es IX and X collagen gene. Results:In fetal intervertebral discs, positive mRNA hybridiza tion signals of type IX collagen were concentrated in the nucleus pulposus and t he inner layer of anulus fibrosus. Interstitial matrix of the nucleus pulposus a lso showed positive type X collagen staining. Positive mRNA hybridization signal s of types IX and X were not detected in the middle and outer layers of anulus f ibrosus. In adult specimens, expression of type IX collagen mRNA was markedly de creased. No hybridization signals of type X collagen was observed. As for pathol ogical specimens, there was no gene expression of type IX collagen. In severe de generated discs from adults, there were focal positive expressions of type X col lagen. Conclusions:Obvious changes of collagen gene expression occur with aging. Expression of type IX collagen decreases in adult and pathological d iscs. Results of type X collagen expression suggest that type X collagen is expr essed only in older adult and senile discs (i.e., when disc degeneration has alr eady reached a terminal stage), indicating the terminal stage of degeneration.
基金supported by a fellowship from CONACyT (No. 203355)supported by grants from UNAM (No. PAPIIT IN219509)CONACyT (No. 48663)
文摘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.