Acquired Immunodeficiency Syndrome ; immunology ; Adolescent ; Chemokines ; immunology ; Child ; Child, Preschool ; Female ; Humans ; Male

Antibodies, Antineutrophil Cytoplasmic ; blood ; Child ; Female ; Hematuria ; etiology ; Humans ; Kidney ; pathology ; physiopathology ; Kidney Function Tests ; Proteinuria ; etiology ; Renal Insufficiency ; etiology ; Vasculitis ; blood ; complications ; pathology

Purpose To explore the expression of Aurora kinase A (Aurora-A), minichromosome maintenance protein 7 (MCM7) and human papillomavirus type 16 E7 protein (HPV 16 E7) in uterine cervical squamous cell carcinoma (CSCC) and to investigate their relationship with clinicopathological factors. Methods Immunohistochemical method was employed on 20 cases of low-grade cervical intraepithelial neoplasia (CIN1) , 30 cases of high-grade cervical intraepithelial neoplasia (CIN2+3), 40 cases of CSCC, and 20 ca-ses of chronic cervicitis. Results (1) Aurora-A localized in the cytoplasm and nucleus. MCM7 protein positive staining localized in the nucleus. In the nucleus, and (or) the cytoplasm appeared brown particles positive for HPV 16 E7. (2) The expression of Aurora-A, MCM7 and HPV 16 E7 were higher in the group of CIN2+3 and CSCC than that in the group of chronic cervicitis or CIN1 ( P<0. 0083). (3) In cervical cancer, the expression of Aurora-A, HPV 16 E7 showed positive correlation (P<0. 001, rs =0. 657). The expression of MCM7, HPV 16 E7 showed positive correlation (P<0. 001, rs =0. 616). The expression of Aurora-A, MCM7 showed positive correlation (P<0. 001, rs =0. 597). (4) Aurora-A expression levels was associated with tumor cell differentiation, clinical stage and lymph node metastasis (P<0. 05). MCM7 expression levels was associated with tumor cell differentiation and clinical stage (P<0. 05). HPV 16 E7 expression had no correlation with patient age, tumor size, tumor differentiation, clinical stage and lymph node metastasis (P>0. 05). Conclusion Aurora-A, MCM7 and HPV 16 E7 expression are gradually increased with disease progres-sion, and closely related to the occurrence and development of cervical cancer, they are expected to be early diagnosis, early treatment of biological indicators of cervical cancer.

BACKGROUND:Keloid is a very chalenging problem in plastic surgery. Its pathogenesis is very complex, resulting from the combined action of many factors, such as various cytokines, signal transduction pathways, extracelular matrix,etc. At present, a critical role for mechanical force and mechanotransduction in the pathogenesis of keloids has been broadly concerned and becomes the focus of studying the pathogenesis of keloids.
OBJECTIVE:To summarize the progress of the mechanosignaling pathway involved in the pathogenesis of keloids in order to further understand the pathogenesis of keloids and provide new ideas for the prevention of keloids.
METHODS: The PubMed database and Elsevier database were retrieved for articles published from January 2000 to July 2014 by computer with key words of “keloid, molecular mechanism, mechanical stress, cutaneous scar, mechanobiology, mechanosignaling pathway” in English. A total of 23 articles were included which related to the molecular signal transduction mechanism and mechanosignaling pathway about keloids.
RESULTS AND CONCLUSION:The mechanosignaling transduction pathways, such as transforming growth factor-β/Smad, MAPK, integrin, Wnt/β-catenin, RhoA/ROCK and tumor necrosis factor-α/nuclear factor-κB signaling pathway, play an important role in the formation and development of keloids. A number of clinical trials have also shown the effectiveness of a part of mechanosignaling transduction pathway inhibitors in wound healing and reducing scar hyperplasia. The research about mechanosignaling transduction pathways involved in keloids has made some progress, but most stil remain in animal experimental stage. Secondly, various mechanosignaling transduction pathways about correlation and intersectionality stil need further studies to achieve a breakthrough in the prevention of keloids.

Objective This paper is mainly to discuss accuracy and clinical application value of MDCT double-period enhanced scanning with low -tension water enteroclysis for colon cancer preoperative TNM stag-ing.Methods Sixty-two colon cancer patients with complete images and pathological data were selected in our hospital from January 2012 to May 2013 .We retrospectively analyzed CT image changes of the tumor location ,the extent of tumor invasion,the surrounding fat space,lymph node metastasis and distant metastasis.We compared them with postoperative pathology to prove the accuracy of MDCT double -period enhanced scanning with low -tension water enteroclysis.Results The results showed that its accuracy rate reached to 90.32%(56/62)in co-lon cancer preoperative Stage T,80.64%(50/62)in Stage N,and 100%(62/62)in Stage M respectively.Con-clusions MDCT double-period enhanced scanning with low -tension water enteroclysis can accurately display the site of colon cancer and determine the scope of tumor invasion ,lymph node metastasis and distant metastasis , and give more precise diagnosis of colon cancer and preoperative staging assessments .In conclusion , it can be used as the preferable method of preoperative examination in the colon cancer .

Objective:To explore the MRI features of cerebral amyloid angiopathy-related inflammation (CAA-ri).Methods:The clinical and imaging data of 12 patients with CAA-ri diagnosed in Affiliated Guizhou Aviation Industry Cor Ltd No 300 Hospital of Zunyi Medical University (9 cases), Xingyi People′s Hospital (2 cases) and Anshun people′s Hospital (1 case) from June 2013 to June 2020 were analyzed retrospectively. There were 3 females and 9 males, aged from 57 to 89 years old, with an average age of 71±10 years. The twelve patients included 5 cases with probable CAA-ri and 7 cases with possible CAA-ri. The duration of the disease ranged from 30 minutes to 2 years. One patient has ApoE ε4/ε4 gene overexpressed. All the 12 patients underwent MRI, including susceptibility weighted imaging in 12 cases, DWI in 10 cases, contrast enhanced MRI (CE-MRI) in 9 cases, MRS in 3 cases, MRA in 7 cases, and perfusion-weighted imaging in 1 case.Results:Imaging features of CAA-ri included encephalopathic, tumoral, classical cerebral amyloid angiopathy(CAA) manifestations. Twelve cases of encephalopathic manifestations showed patchy white matter hyperintensity (WMH) involving U-shaped fibers on T 2 weighted fluid-attenuated inversion recovery sequence (FLAIR), usually asymmetric,with various degree of mass effect, no diffusion restriction on DWI and no enhancement on CE-MRI. One case showed a single tumoral lesion with irregular enhancement on CE-MRI. The classic CAA findings included hemorrhagic lesions (microhemorrhage in 8 cases, lobar hemorrhage in 6 cases, subarachnoid hemorrhage in 3 cases, iron deposition on the brain surface in 7 cases) and ischemic lesions (microinfarction in 1 case, enlarged perivascular space and interlobar space in 4 cases). Follow-up showed lesions absorption and/or new lesion formation in 5 cases. Conclusions:The MRI features of CAA-ri are mainly patchy WMH involving U-shaped fibers on T 2 FLAIR, usually asymmetric, with wandering and alternating features, and inconsistency with clinical manifestations.

Diagnosis, Differential ; Humans ; Parathyroid Glands

Over-expression of Fas ligand (FasL) on tumor cell surface can induce the apoptosis of specific activated tumor infiltrating lymphocytes (TILs) via the Fas/FasL pathway, leading to the formation of a site of immune privilege surrounding the tumor mass for escaping immune surveillance and promoting tumor proliferation, invasion and metastasis. The blocking effect of miR-21 on FasL-mediated apoptosis in breast cancers was investigated in this study. The expression levels of miR-21 and FasL in human breast carcinoma cell lines were detected by using RT-PCR and Western blotting. FasL as a target gene of miR-21 was identified by Luciferase assay. The apoptosis of Jurkat T lymphocytes induced by MCF-7 cells was determined by flow cytometry. It was found that in four human breast cancer cell lines, FasL expression level in MCF-7 cells was the highest, while miR-21 was down-regulated the most notably. After miR-21 expression in MCF-7 cells was up-regulated, FasL was identified as a target gene of miR-21. When the effector/target (E/T) ratio of MCF-7 cells and Jurkat cells was 10:1, 5:1 and 1:1, the inhibitory rate of apoptosis of Jurkat T lymphocytes induced by MCF-7 cells was 95.81%, 93.16% and 91.94%, respectively. It is suggested that in breast cancers miR-21 expression is negatively associated with FasL expression, and FasL is a target gene of miR-21. miR-21 targeting and regulating FasL-mediated apoptosis will bring us the possibility of a new tumor immunotherapy via breaking tumor immune privilege.

To explore the changes in metabolites in the greasy tongue coating in patients with chronic gastritis.

Objective By detecting the expression levels of Foxp3 in CD4+CD25+ regulatory T cells of peripheral blood mononuclear cells (PBMCs) in rheumatoid arthritis (RA),and the Foxp3 gene promoter region methylation to explore its role in the pathogenesis of RA.Methods Twenty-five RA patients and 10 healthy controls were selected,and the PBMCs were extracted by density gradient centrifugation.Foxp3 expression levels of CD4+CD25+ regulatory T cells were detected by flow cytometry.The real-time fluorescence quantitative PCR assay was used to detect the Foxp3 mRNA expression in PBMCs; and bisulfate processing gene sequencing was used to determinethe differences in Foxp3 gene promoter sequence methylation level of PBMCs.The comparison between groups was analyzed using one-way ANOVA; two sets of qualitative data were compared using Fisher's exact test.Results The expression levels of Foxp3 mRNA in the CD4+CD25+regulatory T cells of active RA patients (2.31±0.25) was significantly lower than inactive RA group (3.68±0.26) and healthy controls (5.67±0.34),the difference was statistically significant (P＜0.05).The Foxp3 mRNA expression level in inactive RA group was lower than that of the healthy controls (P＜0.05).Foxp3 promoter region-67,-74 sites of methylation level in PBMCs of RA patients (46％) was significantly higher than that of the healthy controls (6％).Conclusion Reduction in the number of CD4+CD25+ regulatory T cells may be involved in the pathogenesis of RA and Foxp3 gene promoter methylation levels plays a key role in this process.