Int J Clin Exp Patho
-
Int J Clin Exp Patho · Jan 2017
Associations of SRD5A2/CYP17/CYP19/VDR gene polymorphisms with the development and clinical progression of benign prostatic hyperplasia: a case-control study in northern Chinese population.
This study aims to explore the effect of gene polymorphisms of 5a-reduction enzyme (SRD5A2), steroidogenic cytochrome P-450 17alpha-hydroxylase (CYP17), aromatase cytochrome P450 family 19 (CYP19) and vita-min D receptor (VDR) on benign prostatic hyperplasia (BPH) susceptibility and clinical progress. A total of 452 BHP patients and 501 healthy individuals were selected in Harbin Medical University Daqing School from October 2014 and December 2015 as the case and control groups. All BPH patients received drug treatment and were subsequently divided into the progression and non-progression groups based on their therapeutic efficacy. ⋯ Compared with individuals carrying FF genotype and F allele at VDRVDR Fok I, those with ff genotype and f allele at VDRVDR Fok I may have increased susceptibility to BPH (all P < 0.05). Logistic regression analysis showed that SRD5A2 V89L and CYP17 -34T>C polymorphisms and CYP17 -34T>C (TC + CC)/SRD5A2 V89L (VV) combined genotypes were significantly related with the clinical progression of BHP. These results revealed that SRD5A2 V89L and CYP17 -34T>C polymorphisms were associated with the risk of BPH and its clinical progression.
-
Int J Clin Exp Patho · Jan 2017
The regulatory role of Mcl-1 in apoptosis of mouse peritoneal macrophage infected with M. tuberculosis strains that differ in virulence.
Myeloid cell leukaemia-1 (Mcl-1) is a valuable target in tumour treatments. However, several reports have suggested that Mcl-1 may play a role in tuberculosis infection. Therefore, we investigated the function of Mcl-1 in tuberculosis infection and the underlying regulatory mechanism. ⋯ Mcl-1-shRNA intervention effectively down-regulated Mcl-1 expression, significantly increased host macrophage apoptosis, and induced cytochrome-c expression in mouse peritoneal macrophages infected with MTB strains of different virulence, and these changes were influenced by the virulence of the MTB strains. The mitochondria-mediated intrinsic apoptotic pathway play an important role before Mcl-1-shRNA-trated, and then with the extrinsic apoptotic pathway co-regulate host macrophage apoptosis.
-
Int J Clin Exp Patho · Jan 2017
Mcl-1 signals pathway inhibitors in mouse peritoneal macrophage apoptosis infected with the Xinjiang strain of M. tuberculosis.
A present, myeloid cell leukemia-1 (Mcl-1) was suggested as a potential new target for controlling latent TB infection. Therefore, we investigated the role of the Mcl-1 signalling pathway in mouse peritoneal macrophages infected with XJ-MTB, aiming at finding a new strategy for TB management in Xinjiang. We using TUNEL, Immunohistochemical analysis, ELISA, HE, RT-PCR and Western blot detected macrophages apoptosis, the damage of mice tissues and the expression of apoptosis genes and proteins. ⋯ In conclusion, the MAPK signalling pathway inhibitor PD98059 down-regulated Mcl-1 expression and effectively increased macrophage apoptosis in mice infected with XJ-MTB. Furthermore, it also relief pathological organ damage and promote the elimination of inflammation. The intrinsic apoptotic pathway plays a predominant role in the regulatory role.
-
Int J Clin Exp Patho · Jan 2015
Silencing of SIAH1 in SH-SY5Y affects α-synuclein degradation pathway.
Seven in absentia homolog (SIAH) is a ubiquitin ligase that monoubiquitinates α-synuclein. Lewy bodies are characteristically rich in monoubiquitinated α-synuclein. We aimed to determine the effect of siRNA-SIAH1 on α-synuclein autophagy and UPS degradation in SH-SY5Y. ⋯ These data show silencing SIAH1 increased cell proliferation and inhibited apoptosis in SH-SY5Y neuroblastoma cells. SIAH1 knockdown enhanced the clearance of non-aggregated α-synuclein by UPS. SIAH1 is a potential target for treatment of Parkinson's disease.
-
Int J Clin Exp Patho · Jan 2015
Review Case ReportsBone formation following lenalidomide-dexamethasone combination therapy in cases of multiple myeloma refractory to high-dose chemotherapy with bortezomib and autologous peripheral blood stem cell transplantation: report of a case and review of the literature.
A 41-year-old man presented with the chief complaint of right hip pain that had persisted for 6 months. F18-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) imaging showed FDG accumulation in the right pubic bone. A bone biopsy specimen from the site revealed findings suggestive of a plasma cell tumor. ⋯ The patient was then administered eight cycles of combined lenalidomide-dexamethasone therapy, which resulted in a marked decrease of the FDG accumulation in the right pubic bone and disappearance of uptake in the right hip bone. There was radiographic evidence of bone formation at these sites. This is only the second reported case in which treatment with the immunomodulatory drug lenalidomide and concomitant dexamethasone has been found to induce bone formation.