A ketogenic diet(KD)refers to an eating pattern designed to achieve a low-calorie content,minimum carbohydrate intake,high-fat consumption,and standard protein levels.A ketogenic diet is used in clinical practice to treat conditions including heart disease,diabetes,obesity,autism,glioblastoma,and other cancers.Although a ketogenic diet has not been recommended for any neurological disorders except epilepsy,extensive recent research suggests that such a diet may have a neuroprotective effect and may thus represent a new dietary therapy for the treatment of Parkinson's disease(PD).In this review,we discuss in detail the mechanisms responsible for the neuroprotective effects of a ketogenic diet in Parkinson's disease,with the aim of providing references for future clinical and experimental studies.

Parkinson's disease(PD)is a common progressive neurodegenerative disease mainly affecting the motor system.Various genetic factors and cellular mechanisms underlying PD have recently been discovered.Emerging evidence suggests that epigenetic modifications play a very important role in the pathogenesis,prevention,and treatment of PD.Epigenetic modification mediates genetic and environmental interactions mainly through complex interactions of DNA methylation,histone modification,and non-coding RNA,thereby affecting expression in the absence of changes in DNA sequence.In this review,we summarize the epigenetic modification mechanisms involved in the pathogenesis of Parkinson's disease.In this review,we summarize the epigenetic modification mechanisms involved in the pathogenesis of Parkinson's disease.Recent studies have found that traditional Chinese medicine can participate in the regulation of abnormal epigenetic modifications in the treatment of PD.Traditional Chinese medicine benefits from its multi-level and multi-target regulatory effects,and various traditional Chinese medicine monomers,compound prescriptions,and techniques have been evaluated,confirming that this is a promising approach for improving symptoms in PD.This review summarizes the mechanisms by which epigenetic modifications contribute to P D,explores the role of traditional Chinese medicine,and provides new ideas for clinical treatment and drug development in PD through epigenetic intervention.

Parkinson's disease(PD)is a common progressive neurodegenerative disease mainly affecting the motor system.Various genetic factors and cellular mechanisms underlying PD have recently been discovered.Emerging evidence suggests that epigenetic modifications play a very important role in the pathogenesis,prevention,and treatment of PD.Epigenetic modification mediates genetic and environmental interactions mainly through complex interactions of DNA methylation,histone modification,and non-coding RNA,thereby affecting expression in the absence of changes in DNA sequence.In this review,we summarize the epigenetic modification mechanisms involved in the pathogenesis of Parkinson's disease.In this review,we summarize the epigenetic modification mechanisms involved in the pathogenesis of Parkinson's disease.Recent studies have found that traditional Chinese medicine can participate in the regulation of abnormal epigenetic modifications in the treatment of PD.Traditional Chinese medicine benefits from its multi-level and multi-target regulatory effects,and various traditional Chinese medicine monomers,compound prescriptions,and techniques have been evaluated,confirming that this is a promising approach for improving symptoms in PD.This review summarizes the mechanisms by which epigenetic modifications contribute to P D,explores the role of traditional Chinese medicine,and provides new ideas for clinical treatment and drug development in PD through epigenetic intervention.

A ketogenic diet(KD)refers to an eating pattern designed to achieve a low-calorie content,minimum carbohydrate intake,high-fat consumption,and standard protein levels.A ketogenic diet is used in clinical practice to treat conditions including heart disease,diabetes,obesity,autism,glioblastoma,and other cancers.Although a ketogenic diet has not been recommended for any neurological disorders except epilepsy,extensive recent research suggests that such a diet may have a neuroprotective effect and may thus represent a new dietary therapy for the treatment of Parkinson's disease(PD).In this review,we discuss in detail the mechanisms responsible for the neuroprotective effects of a ketogenic diet in Parkinson's disease,with the aim of providing references for future clinical and experimental studies.

Objective:To study the expression and clinical significance of collagen type Ⅰ alpha 2 chain (COL1A2) in glioma , and its effect on the migration and invasion of glioma cell lines.Methods:Through in-depth mining of the data related to COL1A2 in the Oncomine database, meta-analysis of its expression in different types of tumors, different grades and different molecular types of glioma, and then through the Chinese glioma genome map project (Chinese Glioma Genome Atlas, CGGA) database to explore the relationship between its expression level and the prognosis of glioma patients. The COL1A2 gene was functionally annotated by gene ontology (GO) and Pathway analysis. The annotation content includes cell components, biological processes, molecular functions and related signal pathways.Results:A total of 426 research results on COL1A2 in different types of tumors were collected in the Oncomine database, 114 of which were statistically different, 103 studies with increased COL1A2 expression, and 11 studies with decreased expression; the analysis shows there were 22 studies on high expression of COL1A2 in tumors, and no studies on low expression. Analysis of different grades of glioma and different molecular types of glioma Compared with the control group, COL1A2 was highly expressed in various types of glioma. Through the analysis of the gene chip data of the CGGA database, it was found that in glioblastoma, low expression levels of COL1A2 were significantly associated with an improved prognosis in patients with glioma ( P<0.05). Next, through GO and Pathway annotations, it was found that COL1A2 was involved in the biological processes of NAD metabolic salvage pathway, cell and cell signal transduction, circadian rhythm regulation and so on. Finally, through the construction of overexpression and knockdown cell lines in glioblastoma cell lines U87 and T98, scratch experiments and transwell cell function experiments confirmed that COL1A2 can significantly promote the migration and invasion of glioblastoma cell lines. Conclusions:Low expression levels of COL1A2 were significantly associated with improved prognosis in patients with glioma. Knockdown and overexpression of COL1A2 on glioblastoma cell lines U87 and T98 manifested that COL1A2 can promote glioblastoma cell lines migration and invasion ability. Based on the above results, COL1A2 may be used as an indicator for judging the prognosis of glioblastoma and as a potential biological target for therapy.

America medical education system has more important effect on our long-education program.Based on the analysis of the characters in medical education between China and America,several suggestions about obstetric and gynecological teaching have been brought up to accommodate the new tendency,as well as the culture of specialists in the future.

BACKGROUND:Bone marrow mesenchymal stem cells(BM-MSCs)have been shown to possess the potential to differentiate into oocytes.However,immune rejection and a limited number of donors of BM-MSCs constrain the applications of BM-MSCs.Several studies have demonstrated that human umbilical cord matrix stem cells(UC-MSCs)also have an intrinsic ability to differentiate into oocyte-like cells in vitro.OBJECTIVE:To establish the method for UC-MSCs culture and to investigate the in vitro differentiation potential of UC-MSCs towards germ cells.METHODS:Umbilical cord from full-term normal deliveries was obtained in sterile condition.Collagenase I-digested cells were cultured in DMEM.The immunophenotype of cells was determined by flow cytometry.Lipoblasts,osteoblasts and chondroblasts were induced in different condition cultures.The expression of germ cells specific marker in UC-MSCs was determined by reverse transcdption-polymerase chain reaction.Follicular fluid was employed to induce UC-MSCs differentiation into germ cells.RESULTS AND CONCLUSION:Spindle-like umbilical cord cells were shown and cells in culture were extended to more than 10passages.BM-MSCs-like immunophenotypes were shown:CD29,CD44,CD73(SH3),CD90 and CD105(SH2)were positive;SSEA-4 was weakly positive;CD31,CD34,CD45 and HLA-DR were negative.After UC-MSCs were induced in different condition cultures,lipid droplet-,bone tubercle-,and cartilage tubercle-like structures emerged and the mRNA expressions of specific gene of fat,bone and cartilage were observed.Germ cells markers,OCT4,Stella,Ifitm3,were expressed in UC-MSCs.After induced by 5%,10% or 20% follicular fluid,cells aggregated and oocyte-like structures were observed.Human UC-MSCs could be cultured and amplificated in vitro.UC-MSCs showed immunophenotypes similar to BM-MSCs.UC-MSCs had the potential to differentiate into lipoblasts,osteoblasts,and chondroblasts.Oocyte-like structure was induced in vitro from UC-MSCs with germ cells specific marker.These findings suggest that UC-NSCs have the potential to differentiate into germ cells.

Objective To develop a mouse model of premature ovarian failure (POF) by chemical treatment or radiotreatment. Methods Eighty Kunming mice were divided into four groups, including chemical treatment group that were administered Cyclophosphamide and Busulfan, radiotreatment group receiving 60Co ? ray irradiation, control group and castrated group. To evaluate the animal model, vaginal smears were collected daily for estrous cycle determination, and serum hormone levels and histological changes in ovaries were examined. Results Estrous cycles became irregular after chemical treatment or radiotreatment (P0.05). Compared to control group, ovaries from chemical treatment and radiotreatment groups showed ovarian atrophy and interstitial fibrosis. The number of growing follicles and non-atretic primordial follicles was notably reduced (P