Objective To investigate the proportion and function of CD_4~+ CD_(25)~+ regulatory T cells (CD_4~+ CD_(25)~+ Tr)in unexplained recurrent spontaneous abortion(URSA).Methods(1)Proportion measurement:the proportion of CD_4~+ CD_(25)~+ Tr cells in peripheral blood was measured by double-label flow cytometric analysis.The samples were taken from 15 URSA women,15 normal non-pregnancy women and 13 normal pregnancy women.(2)Function measurement:CD_4~+ CD_(25)~+ Tr ceils and CD_4~+ CD_(25)~+ T ce]ls were extracted from peripheral blood lymphocytes by the microbeads separation.The purity of CD_4~+ CD_(25)~+ Tr cells and CD_4~+ CD_(25)~+ T cells was measured by flow cytometry.The growth inhibitory effect of CD_4~+ CD_(25)~+ Tr cells on CD_4~+ CD_(25)~+ T cells was assessed in vitro.Results The proportion of CD_4~+ CD_(25)~+ Tr cells was decreased significantly in URSA women(6.9?1.8)% than that in normal non-pregnancy women[(10.8?1.1)%] (P0.05).Conclusion The results suggest that decrease in proportion and function of CD_4~+ CD_(25)~+ Tr cells may be associated with URSA.

The epidemiological survey of prevalence of NIDDM (non-insulin dependent diabetes mellitus) and IGT(impaired glucose tolerance)was conducted among 9450 residents aged 25～70 in some areas of Hubei Province, China. The results show that NIDDM and IGT prevalences are 2.62% and 4.48%, respectively. There is no significant difference between male and female (P>0.05). The NIDDM prevalence in cities is slightly higher than that in countryside, but the difference is not significant (P>0.05). However, the IGT prevalence in city is significantly higher than that in countryside (P<0.01). The prevalence of both NIDDM and IGT is increasing along with the age of the population. It is also significantly related to the family history of NIDDM, hypertension, and high body mass index (BMI). By using stepwise logistic regression to analyse the risk factors of NIDDM, age (OR=1.86),BMI(OR=2.69), family history (OR=2.84) and hypertension (OR=2.23) entered the model (significance level is α=0.05).

Objective To evaluate the diagnostic value of interferon-γ release assay of blood and pleural effusion for tuberculous pleurisy.Methods Fifty-six adult patients with suspected tuberculous pleurisy were enrolled in our study.The blood and pleural effusion interferon-γ release assay were measured by T-SPOT.TB test in 38 pleural tuberculosis patients and 18 nontuberculous pleurisy controls.The diagnostic sensitivity,specificity,predictive value of T-SPOT.TB in pleural effusion mononuclear cells (PE-MC) and peripheral mononuclear cells (PBMC) were analyzed.Results The sensitivities and specificities,positive predictive values and negative predictive values,respectively,of the PE-MC and PBMC for diagnosing were as follows:86.5％(95％ confidence interval[CI] 71.2％-95.5％) and 100％(95％CI 90.5％-100％);52.9％(95％CI 27.8％-77.0％) and 35.3％(95％CI 14.2％-61.7％);80.0％(95％CI 64.4％-90.9％) and 77.1％(95％CI 62.7％-88.0％);64.3％(95％CI 35.1％-87.2％) and 100％(95％CI 54.1％-100％).By ROC curve analysis,a cut-off value of 47SFC/2.5 × 105 cells in PE-MC showed a sensitivity of 89.2％ and a specificity of 88.2％.Conclusion T-SPOT.TB in PE-MC could be an accurate diagnostic method for tuberculous pleurisy in TB endemic settings.Moreover,47SFC/2.5 × 105 cells might be the optimal cut-off value for diagnosing tuberculous pleurisy.

Transcription factor EB(TFEB)is a member of the MiTF/TFE family and plays an important role in cell stress,metabolism,cancer and so on.There are relatively few studies on the role of TFEB in renal diseases.TFEB was initially found to be highly expressed in TFEB-fusion renal cell carcinoma and plays a key role in the development of re-nal cell carcinoma.Blocking the downstream signaling pathway activated by TFEB would be a promising treatment for TFEB-fusion renal cell carcinoma.On the contrary,the expression of TFEB in renal intrinsic cells is decreased in diabetic kidney disease,leading to a blockage in the autophagy-lysosome pathway.TFEB enhances the ability of cell stress and self-repair,and then delays the progress of diabetic kidney disease.In cystine nephropathy,TFEB expression is reduced in re-nal tubular epithelial cells and compensatory activation is insufficient as well.TFEB over-expression effectively eliminates intracellular cystine and repairs damaged lysosome,which is expected to alleviate or cure the Fanconi syndrome.In summa-ry,TFEB plays a key role in different kidney diseases,and targeted regulation of TFEB provides new hope for the treatment of kidney diseases.

Wnt/β-catenin is a signaling pathway associated with embryonic development, organ formation, cancer, and fibrosis. Its activation can repair kidney damage during acute kidney injury (AKI) and accelerate the occurrence of renal fibrosis after chronic kidney disease (CKD). Interestingly, p53 has also been found as a key modulator in AKI and CKD in recent years. Meantime, some studies have found crosstalk between Wnt/β-catenin signaling pathways and p53, but more evidence is required on whether they have synergistic effects in renal disease progression. This article reviews the role and therapeutic targets of Wnt/β-catenin and p53 in AKI and CKD and proposes for the first time that Wnt/β-catenin and p53 have a synergistic effect in the treatment of renal injury.

Wnt/β-catenin is a signaling pathway associated with embryonic development, organ formation, cancer, and fibrosis. Its activation can repair kidney damage during acute kidney injury (AKI) and accelerate the occurrence of renal fibrosis after chronic kidney disease (CKD). Interestingly, p53 has also been found as a key modulator in AKI and CKD in recent years. Meantime, some studies have found crosstalk between Wnt/β-catenin signaling pathways and p53, but more evidence is required on whether they have synergistic effects in renal disease progression. This article reviews the role and therapeutic targets of Wnt/β-catenin and p53 in AKI and CKD and proposes for the first time that Wnt/β-catenin and p53 have a synergistic effect in the treatment of renal injury.

Wnt/β-catenin is a signaling pathway associated with embryonic development, organ formation, cancer, and fibrosis. Its activation can repair kidney damage during acute kidney injury (AKI) and accelerate the occurrence of renal fibrosis after chronic kidney disease (CKD). Interestingly, p53 has also been found as a key modulator in AKI and CKD in recent years. Meantime, some studies have found crosstalk between Wnt/β-catenin signaling pathways and p53, but more evidence is required on whether they have synergistic effects in renal disease progression. This article reviews the role and therapeutic targets of Wnt/β-catenin and p53 in AKI and CKD and proposes for the first time that Wnt/β-catenin and p53 have a synergistic effect in the treatment of renal injury.

Wnt/β-catenin is a signaling pathway associated with embryonic development, organ formation, cancer, and fibrosis. Its activation can repair kidney damage during acute kidney injury (AKI) and accelerate the occurrence of renal fibrosis after chronic kidney disease (CKD). Interestingly, p53 has also been found as a key modulator in AKI and CKD in recent years. Meantime, some studies have found crosstalk between Wnt/β-catenin signaling pathways and p53, but more evidence is required on whether they have synergistic effects in renal disease progression. This article reviews the role and therapeutic targets of Wnt/β-catenin and p53 in AKI and CKD and proposes for the first time that Wnt/β-catenin and p53 have a synergistic effect in the treatment of renal injury.

Animals ; Chronic Disease ; Female ; Genetic Therapy ; Male ; Mesenchymal Stem Cell Transplantation ; Myocardial Infarction ; physiopathology ; therapy ; Swine ; Vascular Endothelial Growth Factor A ; genetics ; Ventricular Function, Left

As a major active component extracted from traditional Chinese herb Tripterygium wilfordii Hook F, triptolide exhibits multiple pharmacological effects. Autophagy is an evolutionary conserved intracellular catabolic process involved in cytoplasmic materials degradation. Autophagic dysfunction contributes to the pathologies of many human diseases, which makes it a promising therapeutic target. Recent studies have shown that triptolide exerts neuroprotection, anti-tumor activities, organ toxicity, and podocyte protection by modulating autophagy. This article highlights the current information on triptolide-modulated autophagy, analyzes the possible pathways involved, and describes the crosstalk between autophagy and apoptosis modulated by triptolide, in hope of providing implications for the roles of autophagy in pharmacological effects of triptolide and expanding its novel usage as an autophagy modulator.
Animals ; Apoptosis ; drug effects ; Autophagy ; drug effects ; Diterpenes ; pharmacology ; Epoxy Compounds ; pharmacology ; Humans ; Neoplasms ; drug therapy ; pathology ; Neuroprotective Agents ; pharmacology ; Phenanthrenes ; pharmacology ; Podocytes ; drug effects