Adult ; Bone Neoplasms ; pathology ; surgery ; Female ; Giant Cell Tumor of Bone ; pathology ; surgery ; Humans ; Patella

OBJECTIVETo search for a simple and effective surgical approach to the management of moderate to severe pediatric concealed penis in children.

METHODSWe used Devine's technique via incision between the penis and scrotum in the treatment of 68 cases of moderate to severe pediatric concealed penis. The patients were aged 3 -13 (mean 6.5) years, 30 with moderate and 38 with severe pediatric concealed penis.

RESULTSThis strategy achieved good near- and long-term effects and satisfactory appearance of the penis, which was similar to that of circumcision. At 3 months after surgery, the penile length was 3 - 5.2 cm, averaging (2.35 +/- 0.35) cm.

CONCLUSIONDevine's technique via incision between the penis and scrotum is a simple and effective surgical option for moderate to severe pediatric concealed penis in children.

Adolescent ; Child ; Child, Preschool ; Humans ; Male ; Penis ; abnormalities ; surgery ; Scrotum ; surgery ; Urologic Surgical Procedures, Male ; methods

During oral glucose tolerance test(OGTT),endothelium-dependent vasodilation(EDD)at different time points in impaired glucose tolerance(IGT)group was lower than that in normal control group.EDD at 60 and 120 min in IGT + vitamin C group was higher than that in IGT group(all P＜0.05).There was a negative relationship between blood glucose level and EDD during OGTT in IGT patients.

OBJECTIVETo identify the anatomical variability of the left spermatic vein (LSV) and determine its effect on the induction of experimental left varicocele (ELV) in adolescent rats.

METHODSWe equally randomized 30 adolescent male SD rats to groups A (LSV collaterals fully ligated and the left renal vein constricted), B (only the left renal vein constricted), and C (sham operation), observed the courses of the LSVs and measured their diameters. At 30 days after operation, we analyzed the changes in the left kidneys and the diameters of the LSVs.

RESULTSIrregular collaterals were observed in 90% of the LSVs and no abnormal changes were found in the left kidneys after surgery. The postoperative LSV diameter was remarkably increased in group A as compared with the baseline ([1.47 +/- 0.15 ] vs [0.16 +/- 0.08] mm, P < 0.01), but showed no significant difference in group B ([0.31 +/- 0.49] vs [0.15 +/- 0.07] mm, P > 0.05) and C ([0.17 +/- 0.07] vs [0.16 +/- 0.06] mm, P > 0.05), and it was significantly longer in A than in B (P < 0.01). The success rate of ELV induction was 100% in group A and 10% in group B, but no varicocele was observed in group C.

CONCLUSIONCorrect identification of the anatomical course of the LSV and ligation of its irregular collaterals are essential for the establishment of a stable and consistent ELV model.

Animals ; Disease Models, Animal ; Kidney ; pathology ; Ligation ; Male ; Rats ; Rats, Sprague-Dawley ; Spermatic Cord ; blood supply ; Varicocele ; Veins ; abnormalities

Abstract: Due to the continued emergence of multiple variants of SARS-CoV-2, the ongoing pandemic has resulted in severe mortality over the past two years. After the Alpha, Beta, Gamma and Delta variants, the most recent new variant of concern (VOC) strain to emerge is Omicron (B.1.1.529), which evolved as a result of the accumulation of a large number of mutations. The Omicron variant, which has a much higher transmission rate than the Delta variant, soon replaced the Delta variant and others, is now the dominant variant worldwide. The emergence of Omicron poses new challenges for the prevention and control of COVID-19 and has raised a number of concerns worldwide. Recently, cases of Omicron infection have been reported in several parts of China, and therefore this paper provides a comprehensive analysis and summary of the epidemiology and immune escape mechanisms of the Omicron variant. We also suggest some therapeutic strategies against the Omicron variant, including rapid diagnosis, genome analysis of emerging variants, ramping up of vaccination drives and receiving booster doses, updating the available vaccines, designing of multivalent vaccines able to generate hybrid immunity, up-gradation of medical facilities and strict implementation of adequate prevention and control measures need to be given high priority to handle the on-going COVID-19 pandemic successfully.

Acrylic Resins ; adverse effects ; Adult ; Breast Implantation ; adverse effects ; Female ; Humans ; Magnetic Resonance Imaging ; methods ; Middle Aged

OBJECTIVETo study the effects of specific small interfering RNA (siRNA) on Smoothened (Smo) gene expression and the proliferation and apoptosis of colorectal cancer LoVo cells.

METHODSThree different siRNAs (siRNA-1, siRNA-2, and siRNA-3, respectively) were transfected into LoVo cells via cationic liposome, and the changes of Smo mRNA level were determined using semi-quantitative RT-PCR 48 h after transfection. Flow cytometry and MTT assay were performed to assess the effect of the siRNAs on the proliferation and apoptosis of LoVo cells.

RESULTSForty-eight hours after Smo siRNA-1 transfection, Smo mRNA expression in LoVo cells decreased by about 63.56%, a reduction significantly greater than that in cells transfected with the other two siRNAs. The cell proliferation decreased significantly after Smo siRNA-1 transfection in comparison with the control cells, and 48 h after transfection, significantly higher apoptosis rate was observed in Smo siRNA-1-transfected cells than in the control cells.

CONCLUSIONSpecific siRNA can significantly decrease Smo mRNA expression and inhibit the proliferation while inducing apoptosis of LoVo cells.

Apoptosis ; genetics ; Cell Line, Tumor ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; genetics ; Humans ; RNA, Small Interfering ; genetics ; Receptors, G-Protein-Coupled ; deficiency ; genetics ; Smoothened Receptor ; Time Factors ; Transfection

BACKGROUNDIncreasing evidence suggests that many neurons may die through apoptosis in Alzheimer's disease (AD). Mitochondrial dysfunction has been implicated in this process of neuronal cell death. One promising approach for preventing AD is based upon anti-apoptosis to decrease death of nerve cells. In this study, we observed the memory improving properties of curcumin in mice and investigated the neuroprotective effect of curcumin in vitro and in vivo.

METHODSThe mice were given AlCl(3) orally and injections of D-galactose intraperitoneally for 90 days to establish the AD animal model. From day 45, the curcumin group was treated with curcumin for 45 days. Subsequently, the step-through test, neuropathological changes in the hippocampus and the expression of Bax and Bcl-2 were carried out to evaluate the effect of curcumin on the AD model mice. In cultured PC12 cells, AlCl(3) exposure induced apoptosis. The MTT assay was used to measure cell viabilities; flow cytometric analysis to survey the rate of cell apoptosis; DNA-binding fluorochrome Hoechst 33258 to observe nuclei changes in apoptotic cells and Western blot analysis of Bax, Bcl-2 to investigate the mechanisms by which curcumin protects cells from toxicity.

RESULTSCurcumin significantly improved the memory ability of AD mice in the step-through test, as indicated by the reduced number of step-through errors (P < 0.05) and prolonged step-through latency (P < 0.05). Curcumin also attenuated the neuropathological changes in the hippocampus and inhibited apoptosis accompanied by an increase in Bcl-2 level (P < 0.05), but the activity of Bax did not change (P > 0.05). AlCl(3) significantly reduced the viability of PC12 cells (P < 0.01). Curcumin increased cell viability in the presence of AlCl(3) (P < 0.01). The rate of apoptosis decreased significantly in the curcumin group (P < 0.05) when measured by flow cytometric analysis. Curcumin protected cells by increasing Bcl-2 level (P < 0.05), but the level of Bax did not change (P > 0.05).

CONCLUSIONSThis study demonstrates that curcumin improves the memory ability of AD mice and inhibits apoptosis in cultured PC12 cells induced by AlCl(3). Its mechanism may involve enhancing the level of Bcl-2.

Aluminum Compounds ; toxicity ; Alzheimer Disease ; drug therapy ; psychology ; Animals ; Apoptosis ; drug effects ; Cells, Cultured ; Chlorides ; toxicity ; Curcumin ; pharmacology ; therapeutic use ; Disease Models, Animal ; Female ; Learning ; drug effects ; Memory ; drug effects ; Mice ; Neuroprotective Agents ; pharmacology ; PC12 Cells ; Rats

BACKGROUNDExposure to cigarette smoke stimulates the proliferation of human pulmonary artery smooth muscle cells (HPASMCs) in vivo and in vitro. However, the molecular mechanism remains unclear. This study aimed at investigating the role of signaling pathways involving protein kinase C alpha (PKCα) and cyclin D1 in the cigarette smoke extract (CSE)-induced HPASMCs proliferation.

METHODSSynchronized HPASMCs were treated with different concentrations of CSE. Cell proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and cell counting. Cell cycle was analyzed by flow cytometry with propidium iodide staining. Activation of PKCα was measured by detecting the expression of PKCα protein in the cytosolic and membrane fractions using Western blotting analysis. Small interfering RNA (siRNA) was used to knockdown PKCα and cyclin D1. The cyclin D1 mRNA was assessed by real-time RT-PCR. The PKCα and cyclin D1 protein levels were detected by Western blotting.

RESULTSLow concentrations of CSE (1% - 10%) stimulated proliferation of HPASMCs, with its maximal effect at 5%. CSE (5%) led to PKCα activation. Inhibition of PKCα activity using Gö 6976 or siRNA-mediated knockdown of PKCα significantly attenuated CSE-induced cell proliferation and G1/S transition. Cyclin D1, one of key regulators of G1/S transition, was found to be upregulated by 5% CSE at both the mRNA and protein levels. CSE-stimulated cell proliferation and G1/S transition was abolished by cyclin D1 siRNA. Moreover, Gö 6976 or PKCα siRNA significantly suppressed CSE-induced upregulation of cyclin D1 at both the mRNA and protein levels.

CONCLUSIONPKCα-cyclin D1 pathway at least partially mediates the CSE-induced proliferation in HPASMCs.

Cell Proliferation ; Cells, Cultured ; Cyclin D1 ; physiology ; G1 Phase ; Humans ; Muscle, Smooth, Vascular ; pathology ; Myocytes, Smooth Muscle ; pathology ; Protein Kinase C-alpha ; physiology ; Pulmonary Artery ; pathology ; S Phase ; Signal Transduction ; Smoke ; adverse effects ; Tobacco ; adverse effects

The present study was aimed to investigate the role of cyclin D1 in human pulmonary artery smooth muscle cells (HPASMCs) proliferation and migration induced by cigarette smoke extract (CSE). The eukaryotic expression vector of antisense cyclin D1 gene (pIRES2-EGFP-ascyclin D1) was recombinated. The recombinant and empty vector were separately transfected into normal HPASMCs using liposome. Then the cells were treated with or without 5% CSE. The cells were randomly divided into six groups: control group, vector group, antisense cyclin D1 group, 5% CSE group, vector+5% CSE group and antisense cyclin D1+5% CSE group. The expressions of cyclin D1 mRNA and protein were detected by real-time fluorescence RT-PCR and Western blot, respectively. The proliferation of HPASMCs was examined by cell cycle analysis, MTT assay and proliferation cell nuclear antigen (PCNA) immunocytochemical staining. The migration of HPASMCs was measured by Transwell cell test. The results showed that the eukaryotic expression vector of antisense cyclin D1 gene was constructed and transfected into HPASMCs successfully. The cyclin D1 mRNA and protein levels in antisense cyclin D1 group were significantly lower than those in control group (P<0.05). In 5% CSE group, the cyclin D1 mRNA and protein levels were elevated significantly compared with those in control group (P<0.05), and the indicators of cell and migration in antisense cyclin D1+5% CSE group were remarkably lower than those in 5% CSE group (P<0.05). These results suggest that CSE could promote HPASMCs proliferation and migration through up-regulation of cyclin D1 expression. PIRES2-EGFP-ascyclin D1 could attenuate CSE-induced proliferation and migration of HPASMCs by suppressing the expression of cyclin D1, which implicates that cyclin D1 might be involved in the process of HPASMCs proliferation and migration stimulated by CSE.
Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Cyclin D1 ; physiology ; Humans ; Muscle, Smooth, Vascular ; cytology ; pathology ; Myocytes, Smooth Muscle ; cytology ; pathology ; Pulmonary Artery ; cytology ; pathology ; Smoke ; adverse effects ; Tobacco ; adverse effects