It has been reported that metastasis-associated gene 1 (Mta1) is overexpressed in many malignant tumors with high metastatic potential. In addition, some studies indicated that MTA1 participated in invasion, metastasis, and survival of cancer cells by regulating cell migration, adhesion and proliferation. But the role of MTA1 is unclear in vitro in the development of cervical cancer cells. This study investigated whether and how MTA1 mediated cell proliferation, migration, invasion and adhesion in cervical cancer. MTA1 expression level was detected by Western blot in two cervical cancer cell lines of different invasion potentials. The effects of MTA1 expression on SiHa cell apoptosis, cycle, proliferation, migration, invasion and adhesion were tested by flow cytometry, MTT, wound-healing assay, Transwell assay and adhesion assay, respectively. The expression levels of p53, E-cadherin, and β-catenin activity were evaluated in untreated and treated cells. The results showed that MTA1 protein expression was significantly higher in SiHa than in HeLa, which was correlated well with the potential of migration and invasion in both cell lines. Furthermore, the cell invasion, migration and adhesion capabilities were decreased after inhibition of MTA1 expression mediated by Mta1-siRNA transfection in SiHa. However, no significant differences were found in cell apoptosis, cycle, and proliferation. In addition, E-cadherin and p53 protein levels were significantly up-regulated, while β-catenin was significantly down-regulated in SiHa transfected with the siRNA. These results demonstrated that MTA1 played an important role in the migration and invasion of cervical cancer cells. It was speculated that the decreased migration and invasion capability by inhibiting the MTA1 expression in the SiHa cell line may be mediated through the altered expression of p53, and E-cadherin/β-catenin complex. MTA1 could serve as a potential therapeutic target in cervical cancer.
The effects of epigenetic modification on the differentiation of islet cells and the expression of associated genes (Pdx-1, Pax4, MafA, and Nkx6.1, etc) were investigated. The promoter methylation status of islet differentiation-associated genes (Pdx-1, Pax4, MafA and Nkx6.1), Oct4 and MLH1 genes of mouse embryonic stem cells, NIH3T3 cells and NIT-1 cells were profiled by methylated DNA immunoprecipitation, real-time quantitative PCR (MeDIP-qPCR) techniques. The histone modification status of these genes promoter region in different cell types was also measured by using chromatin immunoprecipitation real-time quantitative PCR methods. The expression of these genes in these cells was detected by using real-time quantitative PCR. The relationship between the epigenetic modification (DNA methylation, H3 acetylation, H3K4m3 and H3K9m3) of these genes and their expression was analyzed. The results showed that: (1) the transcription-initiation-sites of Pdx-1, MafA and Nkx6.1 were highly methylated in NIH3T3 cells; (2) NIH3T3 cells showed a significantly higher level of DNA methylation modification in the transcription-initiation-site of Pdx-1, Pax4, MafA and Nkx6.1 genes than that in mES cells and NIT-1 cells (P<0.05); (3) NIT-1 cells had a significantly higher level of H3K4m3 modification in the transcription-initiation-site of Pdx-1, Pax4, MafA and Nkx6.1 genes than that in mES cells and NIH3T3 cells (P<0.05), with significantly increased level of gene expression; (4) NIH3T3 cell had a significantly higher level of H3K9m3 modification in the transcription-initiation-site of Pdx-1, Pax4, MafA and Nkx6.1 genes than that in mES cells and with NIT-1 cell (P<0.05), with no detectable mRNA expression of these genes. It was concluded that histone modification (H3K4m3 and H3K9m3) and DNA methylation might have an intimate communication between each other in the differentiation process from embryonic stem cells into islet cells.
The mechanism of injury on the human glomerular endothelial cells (ciGENC) induced by preeclampsia serum was investigated. Concentration of maternal serum sFlt-1 protein was detected by ELISA. Fluorescently-labeled bovine serum albumin infiltrating through lower chamber of Transwell was measured by multifunction microplate reader. Morphologic change of ciGENC was observed under inverted phase contrast microscope. The concentration of sflt-1 in preeclampsia groups was significantly increased as compared with control group (P<0.01). Permeability in preeclampsia groups was significantly increased as compared with control group (P<0.01). By contrast with severe preeclampsia group, the permeability of ciGENC monolayer in mild preeclampsia group was decreased significantly (P<0.05). Intervention of exogenous VEGF significantly decreased permeability of ciGENC in preeclampsia groups. It was concluded that sFlt-1 increased ciGENC permeability by damaging integrity of endothelial barrier function.
Pigment epithelium-derived factor (PEDF) is an antiangiogenic factor which is effective in tumour inhibition in a variety of tumours and has not yet been studied in bladder tumour before. In this study the expression of PEDF, interleukin-1α (IL-1α) and -8 (IL-8) in bladder tumours was investigated. Immunohistochemistry was performed on 64 bladder tumour and 23 normal uroepithelium samples. Expression change of the factors was compared with clinicopathological parameters. Correlations between PEDF, IL-1α and IL-8 were analyzed. None of the factors was in relation to gender, tumour occurrence, and size or onset pattern. PEDF (P=0.014) and IL-1α (P=0.049) expression was down-regulated with grade progression. PEDF expression was lower in normal uroepithelium than in papillary urothelial neoplasm of low malignant potential (PUNLMP) (P=0.000) and carcinoma (P=0.009) whilst IL-1α (P=0.000 and P=0.000 respectively) and IL-8 (P=0.000 and P=0.023 respectively) expression was higher in the same grouping. PEDF expression had a negative correlation with IL-8 in PUNLMP (P=0.049, r=−0.578) as well as in tumour grouping (P=0.033, r=−0.276). Deranged expressional change of PEDF, IL-1α and IL-8 could be in relation to loss of differentiation from normal uroepithelium to papillary lesion and eventually to carcinoma.
This study investigated the tight junction (TJ) protein expression of the intestinal mucosa in a rat tail-suspension model under simulated weightlessness. Twenty-four Wistar rats were randomly divided into three groups: CON group (n=8), control; SUS-14 d group (n=8), tail-suspension for 14 days; SUS-21 d group (n=8), tail-suspension for 21 days. Occludin and Zonula Occluden-1 (ZO-1) expression levels were determined by immunohistochemical analysis and mRNA fluorescent quantitative PCR. Plasma levels of diamine oxidase (DAO) and d-lactate were determined using enzymatic spectrophotometry. Immunohistochemical results for occludin and ZO-1 showed disruption of the TJs in the intestinal mucosa in SUS-14 d and SUS-21 d groups. The expression levels of occludin and ZO-1 in SUS-21 d group were lower than those in SUS-14 d group, and significantly lower than those in CON group (Occldin: 0.86±0.02 vs 1.01±0.03 vs 1.63±0.03 and ZO-1: 0.82±0.01 vs 1.00±0.02 vs 1.55±0.01, P<0.01). Moreover, the levels of plasma DAO and d-lactate in SUS-21 d group were higher than those in SUS-14 d group, and significantly higher than those in CON group (DAO: 27.58±0.49 vs 20.74±0.49 vs 12.94±0.21 and d-lactate: 37.86±0.74 vs 28.26±1.01 vs 17.76±0.91, P<0.01). There were significant negative correlations between occludin or ZO-1 expression levels and DAO (r2=0.9014, r2=0.9355, P<0.01) or d-lactate levels (r2=0.8989, r2=0.9331, P<0.01). Occludin and Zo-1 were reduced in intestinal mucosa both in mRNA and protein levels in the rat tail-suspension model. The significant negative correlations between expression levels of TJs and plasma levels of DAO or d-lactate support the hypothesis that intestinal permeability is increased due to a decrease in TJ protein expression during tail-suspension from 14 days to 21 days.
Antitumor effects of erythromycin and the related mechanism were investigated in the present study. Neuroblastoma cells (SH-SY5Y) were exposed to erythromycin at different concentrations for different durations. Cell proliferation was measured by cell counting, and cell viability was examined by MTT assay. Cell cycle phase distribution and the cytosolic calcium level were detected by flow cytometry. Mitochondrial membrane potential was measured by the JC-1 probe staining and fluorescent microscopy. The expression of an oncogene (c-Myc) and a tumor suppressor [p21 (WAF1/Cip1)] proteins was analyzed by using Western blotting. Erythromycin could inhibit the proliferation of SH-SY5Y cells in a concentration- and time-dependent manner. The cell cycle was arrested at S phase. Mitochondrial membrane potential collapsed and the cytosolic calcium was overloaded in SH-SY5Y cells when treated with erythromycin. The expression of c-Myc protein was down-regulated, while that of p21 (WAF1/Cip1) protein was up-regulated. It was concluded that erythromycin could restrain the proliferation of SH-SY5Y cells. The antitumor mechanism of erythromycin might involve regulating the expression of c-Myc and p21 (WAF1/Cip1) proteins.
This study aimed to examine the preparation of cationic lipid microbubble (CLM), and evaluate its physical and chemical properties and toxicity, measure the gene transfection efficiency by ultrasound triggered microbobble destruction (UTMD) in combination with CLM. The CLM was prepared by the method of the thin film hydration, and its morphology was observed under the electron microscopy at 1st, 3rd, 7th, 10th, and 14th day after preparation, respectively. The size, Zeta potential and stability of CLM were tested. The acute toxicity of CLM was assessed. The green fluorescent protein gene (EGFP) transfection efficiency was evaluated. The experiment grouping was as follows: naked plasmid group (P group), ultrasonic irradiation plus naked plasmid group (P-US group), naked plasmid plus CLM group (P-CLM group), naked plasmid plus ultrasound and CLM group (UTMD group). The expression of EGFP was detected by fluorescent microscopy and flow cytometry. The results showed that CLMs were spherical in shape, with the similar size and good distribution degree under the light and electron microscopies. The size of CLMs was varied from 250.4±88.3 to 399.0±99.8 nm and the Zeta potential of CLMs from 18.80±4.97 to 20.1±3.1 mV. The EGFP expression was the strongest in the UTMD group, followed by the P-CLM group, P-US group and P group. Flow cytometry results were consistent with those of fluorescent microscopy. The transfection efficiency was substantially increased in the P-US group, P-CLM group and UTMD group as compared with that in the P group, almost 7 times, 10 times and 30 times higher than that in the P group respectively. It is suggested that CLMs prepared by the method of thin film hydration are uniform in diameter, and proved non-toxic. UTMD combined with CLM can significantly increase the transfection efficiency of EGFP to targeted cells.
Our previous studies demonstrated that CD151 gene promoted neovascularization in ischemic heart model. To improve the delivery efficacy and target specificity of CD151 gene to ischemic heart, we generated an adeno-associated virus (AAV) vector in which CD151 expression was controlled by the myosin light chain (MLC-2v) promoter to achieve the cardiac-specific expression of CD151 gene in ischemic myocardium and to limit unwanted CD151 expression in extracardiac organs. The function of this vector was examined in rat ischemic myocardium model. The protein expression of CD151 in the ischemic myocardium areas, liver and kidney was confirmed by using Western blot, while the microvessels within ischemic myocardium areas were detected by using immunohistochemistry. The results showed that MLC-2v significantly enhanced the expression of CD151 in ischemic myocardium, but attenuated its expression in other organs. The forced CD151 expression could increase the number of microvessels in the ischemic myocardium. This study demonstrates the AAV-mediated and MLC-2v regulated CD151 gene is highly expressed in the ischemic myocardium and cardiac-specific delivery that is more efficiently targets CD151 to the ischemia myocardium after myocardial infarction.
The chronic-hypoxia-resistant gastric cancer cell line was established, and its biological characteristics were explored and compared with the parental cell line. Gastric cancer cell lines were cultured under the degressive oxygen concentration. Cell doubling time was calculated by cell counting method. Chemo-resistance ability of cells was tested by MTT assay. Irradiation tolerance of cells was evaluated by colony forming method. Cell cycle distribution was tested with flow cytometry. Invasive ability was tested by Transwell method. The expression levels of GLUT-1 and HIF-1α were detected by using Western blot. MNK45/HYP cells successfully survived under the 1% concentration of oxygen and its cell doubling time was 35.01±1.02 h, while that of MNK45 was 27.35±0.83 h (P<0.01). The percentage of MNK45/HYP cells in G0/G1 stage was (58.3±6.1)%, and that of MNK45 cells was (42.2±6.0)% (P<0.05). Comparing with the parental cells MNK45, drug resistance indexes of 5-Fu, PTX, OXA, Sn38, GEM and VP16 in MNK45/HYP cells were respectively 5.3, 1.3, 3.6, 2.2, 4.8 and 4.4. Colony forming ability of MNK45/HYP cells after irradiation was also significantly higher than MNK45 cells. The invasive number of MNK45/HYP cells was 107.7±17.5, while that of MNK45 cells was 59.0±9.9. The expression levels of GLUT-1 and HIF-1α in MNK45/HYP cells were significantly higher than those in MNK45 cells. MNK45/HYP cells hold biological characteristics of hypoxia tumor with good tolerance to chronic hypoxia, and can be used for the research of solid tumor under chronic hypoxia condition.
The benefit achieved by concurrent chemoradiotherapy (CCR) and sequential chemoradiotherapy (SCR) vs radiotherapy (RT) alone for patients with stage II–IVa nasopharyngeal carcinoma (NPC) was compared. A total of 113 patients with stage II–IV a NPC were allotted into CCR group (n=38), SCR group (n=36) and RT alone group (n=39). All patients were irradiated with the same RT technique to ≥66 Gy at 2 Gy per fraction, conventional 5 fractions/week in all groups. The CCR group received concurrent chemotherapy of weekly cisplatin for 7 weeks, and the SCR group received neoadjuvant and (or) adjuvant chemotherapy. The results showed that the 3- and 5-year overall survival rate was significantly higher in CCR group than in RT alone group (92.16% vs 61.54%, 81.58% vs 51.28%, P<0.005). The median survival time was significantly longer in CCR group than in RT alone group (67.8 months vs 52.7 months, P<0.005). It was concluded that CCR could significantly improve overall survival rate, progression-free survival rate, and median survival time when compared with RT alone.
The inhibitory effects of Endostar in combination with radiotherapy in BALB/c nude mice model of human CNE2 nasopharyngeal carcinoma and the mechanism were investigated. In nude mice model of CNE2 nasopharyngeal carcinoma, the inhibitory rate and the sensitizing enhancement ratio (E/O) were calculated according to the tumor volumes in different groups. The expression of microvascular density (MVD) in tumor tissues was examined by using immunohistochemistry staining. The transcription of VEGF gene was detected by using RT-PCR. The inhibitory rate in Endostar+ radiotherapy group was higher than in other groups. In Endostar+radiotherapy group, the tumor volume was significantly decreased and the E/O ratio was 2.335, suggesting that Endostar could be a radiosensitizer. The expression of MVD of tumor tissues in Endostar+radiotherapy group was reduced significantly. The expression of the MVD in treatment groups was significantly different from that in control group (P<0.05). Compared to other groups, VEGF mRNA expression in Endostar+radiotherapy group was decreased remarkably. Endostar in combination with radiotherapy significantly inhibited the growth of CNE2 tumor. The combination therapy decreased the expression of VEGF, and inhibited tumor angiogenesis and proliferation. When combined with radiotherapy, Endostar acted as a radiosensitizer.
The curative efficacy of percutaneous transluminal angioplasty and stenting (PTAS) in the treatment of patients with ischemia cerebrovascular disease caused by artery stenosis was explored. The clinical data of 111 patients with ischemia cerebrovascular disease receiving PTAS in Guangdong Province General Hospital from Aug. 2007 to Nov. 2009 were retrospectively analyzed. In total 132 stents were implanted in the 111 patients. The mortality and rate of neural and non-neural complications were assessed perioperatively. Outcomes [including the frequency of transient ischemic attack (TIA), stroke, or death from vascular diseases) were assessed after operation. NIHSS rating was performed in all cases before and at first week, 6th month and 12th month after the operation. The PTAS success rate was 100%. The degree of stenosis was reduced after PTAS. The total complication rate during perioperative period was 15.3% (the rate of neural complications was 3.6%). Sixty-seven patients were followed up. Three patients (4.48%) developed cerebrovascular events within 1 month, containing one case of TIA, one case of ipsilateral mild stroke and one case of contralateral mild stroke. No severe stroke or death was observed. During a follow-up period of 12 months 7 patients had cerebrovascular events (10.44%), including 2 cases of ipsilateral TIA (2.99%), 2 cases of ipsilateral mild stroke and 2 cases of contralateral mild stroke (2.99%), one case of severe stroke (1.49%). In 13 patients receiving DSA re-examination one year after PTAS, 2 patients (15.38%) had in-stent restenosis. NIHSS scores were obviously decreased during a follow-up period as compared with those pre-operation (P<0.05). It was concluded that PTAS could significantly alleviate the neural function deficit of the patients with ischemia cerebrovascular disease. The success rate of PTAS was high, and the rate of complications was lower and the clinical outcomes were satisfactory. PTAS is a safe and effective therapeutic method, though the long-term outcomes need further study.
To investigate the effects of VitalStim therapy coupled with conventional swallowing training on recovery of post-stroke dysphagia, a total of 120 patients with post-stroke dysphagia were randomly and evenly divided into three groups: conventional swallowing therapy group, VitalStim therapy group, and VitalStim therapy plus conventional swallowing therapy group. Prior to and after the treatment, signals of surface electromyography (sEMG) of swallowing muscles were detected, swallowing function was evaluated by using the Standardized Swallowing Assessment (SSA) and Videofluoroscopic Swallowing Study (VFSS) tests, and swallowing-related quality of life (SWAL-QOL) was evaluated using the SWAL-QOL questionnaire. There were significant differences in sEMG value, SSA, VFSS, and SWAL-QOL scores in each group between prior to and after treatment. After 4-week treatment, sEMG value, SSA, VFSS and SWAL-QOL scores were significantly greater in the VitalStim therapy plus conventional swallowing training group than in the conventional swallowing training group and VitalStim therapy group, but no significant difference existed between conventional swallowing therapy group and VitalStim therapy group. It was concluded that VitalStim therapy coupled with conventional swallowing training was conducive to recovery of post-stroke dysphagia.
In order to investigate the biological function of transforming growth factor-β1 (TGF-β1) during fibrosis in denervated skeletal muscle, we recruited sciatic nerve injury model of SD rats in which denervated gastrocnemius was isolated for analysis. At different time points after operation, denervated muscle was examined by several methods. Masson trichrome staining showed morphological changes of denervated skeletal muscle. Quantitative RT-PCR detected the rapid increase of TGF-β1 expression at mRNA level after nerve injury. It was found that a peak of TGF-β1 mRNA expression appeared one week post-operation. The expression of collagen I (COL I) mRNA was up-regulated in the nerve injury model as well, and reached highest level two weeks post-injury. Immunoblot revealed similar expression pattern of TGF-β1 and COL I in denervated muscles at protein level. In addition, we found that the area of the gastrocnemius muscle fiber was decreased gradually along with increased interstitital fibrosis. Interestingly, this pathological change could be prevented, at least partly, by local injection of TGF-β1 antibodies, which could be contributed to the reduced production of COL I by inhibiting function of TGF-β1. Taken together, in this study, we demonstrated that the expression of TGF-β1 was increased significantly in denervated skeletal muscle, which might play a crucial role during muscle fibrosis after nerve transection.
Gas gangrene is an emergency condition, which usually develops after injuries or surgery. This study was designed to investigate clinical characteristics, appropriate therapy, and effective control of nosocomial cross-infection of gas gangrene in Wenchuan earthquake victims. Data on diagnosis, treatment, and prevention of confirmed, suspected, or highly suspected gas gangrene were collected. Sixty-seven (2.41%) cases of suspected gas gangrene were found, in which 32 cases were highly suspected of gas gangrene and 5 cases were confirmed by culture of Clostridium perfringens. Thereof, injury sites were mainly located on the limbs, and typical indications, including crepitation, severe localized pain, swelling, wound discoloration, dark red or black necrotic muscle, foul smell as well as different degrees of systemic toxic performance were common among them. After hospitalization, all patients were isolated and had surgery quickly to remove dead, damaged or infected tissue. The wounds were also exposed for drainage and washed or padded with 3% liquid hydrogen peroxide for disinfection before all diagnostic test results were available. Additionally, high doses of antibiotics (mainly penicillin) were given for the prevention of infection, and supportive therapy was applied for corresponding symptoms control. Among those cases, no fatality was reported. In summary, in post-disaster emergency relief, the diagnosis of gas gangrene should be primarily based on clinical manifestations; while patient isolation, wound debridement and disinfection, as well as antibiotics treatment, is the main measures for proper treatment and control of nosocomial infection for gas gangrene.
The purpose of this study was to fabricate decelluarized valve scaffold modified with polyethylene glycol nanoparticles loaded with transforming growth factor-β1 (TGF-β1), by which to improve the extracellular matrix microenvironment for heart valve tissue engineering in vitro. Polyethylene glycol nanoparticles were obtained by an emulsion-crosslinking method, and their morphology was observed under a scanning electron microscope. Decelluarized valve scaffolds, prepared by using trypsinase and TritonX-100, were modified with nanoparticles by carbodiimide, and then TGF-β1 was loaded into them by adsorption. The TGF-β1 delivery of the fabricated scaffold was measured by asing enzyme-linked immunosorbent assay. Whether unseeded or reseeded with myofibroblast from rats, the morphologic, biochemical and biomechanical characteristics of hybrid scaffolds were tested and compared with decelluarized scaffolds under the same conditions. The enzyme-linked immunosorbent assay revealed a typical delivery of nanoparticles. The morphologic observations and biological data analysis indicated that fabricated scaffolds possessed advantageous biocompatibility and biomechanical property beyond decelluarized scaffolds. Altogether this study proved that it was feasible to fabricate the hybrid scaffold and effective to improve extracellular matrix microenvironment, which is beneficial for an application in heart valve tissue engineering.
To construct a lentiviral shRNA vector targeting human protein phosphatase 1D magnesium-dependent (PPM1D) gene and detect its effectiveness of gene silencing in human gliomas, specific siRNA targets with short hairpin frame were designed and synthesized. DNA oligo was cloned into the pFU-GW-iRNA lentiviral expression vector, and then PCR and sequencing analyses were conducted to verify the constructs. After the verified plasmids were transfected into 293T cells, the lentivirus was produced and the titer of virus was determined. Real-time quantitative PCR and Western blot were performed to detect the PPM1D expression level in the infected glioma cells. PCR and Western blot analyses revealed the optimal interfering target, and the virus with a titer of 6×108 TU/mL was successfully packaged. The PPM1D expression in human glioma cells was knocked down at both mRNA and protein levels by virus infection. The expression of PPM1D mRNA and protein was decreased by 76.3% and 87.0% respectively as compared with control group. The multiple functions of human glioma cells after PPM1D RNA interference were detected by flow cytometry and cell counting kit-8 (CCK-8). Efficient down-regulation of PPM1D resulted in significantly increased cell apoptosis and reduced cell proliferation and invasion potential in U87-MG cells. We have successfully constructed the lentiviral shRNA expression vector capable of stable PPM1D gene silencing at both mRNA and protein levels in glioma cells. And our data gave evidence that the reduced cell growth observed after PPM1D silencing in glioma cells was at least partly due to increased apoptotic cell death.
Retroperitoneal laparoscopic live donor nephrectomy offers an intrinsic advantage over conventional transperitoneal laparoscopic nephrectomy because of the potentially lower risk for early and late donor intraperitoneal complications. Herein we presented our experience performing retroperitoneal laparoscopic live donor nephrectomy in 105 donors. All donor nephrectomy was successful. There were no donor deaths and no conversion to open surgery. Mean operation time was 112 min (range, 70–200 min). Intraoperative blood loss was 10–150 mL with an average of 30 mL. Warm ischemia time was 1.3 to 6 min with an average of 3.1 min. Postoperative retroperitoneal hematoma occurred in only one case and there were no other surgical complications. Donors were discharged from the hospital 5 to 10 days postoperation. Average postoperative hospital stay was 6.4 days. One graft was removed due to acute rejection. Delayed graft function occurred in two recipients but renal function returned to normal within four weeks. The other recipients had normal renal function in two weeks except three recipients in four weeks. We believe that retroperitoneal laparoscopic live donor nephrectomy is safe, reliable, and less invasive.
This study examined the effect of nicotine on the expression of mutant p53 (mt-p53) in bladder cancer rats. The rat models of bladder cancer were established by infusing N-methyl-nitroso-urea (MNU, 10 mg/kg every 2 weeks for 8 weeks) into the bladder. Pathological examination on the bladder was conducted to confirm the establishment of the model. All the bladder cancer rats were randomly divided into an MNU group and 3 nicotine groups. In the nicotine groups, the rats were intragastrically administered nicotine at different concentrations (25, 15, 5 mg/kg respectively) 3 times per week for 8 weeks. The mt-p53 expression was detected by the immunohistochemical method. The results showed that rat bladder cancer models developed histopathological changes of bladder transitional cell carcinoma. The positive rate of mt-p53 expression in the 3 nicotine groups (25, 15, 5 mg/kg) was 75.00%, 58.33% and 41.67% by the 14th week, respectively, significantly higher than that in the MNU group (33.33%) (all P<0.05). The mt-p53 expression rate was positively correlated with the medication dose and time (P<0.05). It is concluded that nicotine may play an important role in the development of bladder cancer partially by increasing the expression of mt-p53.
The general characteristics, outcomes and risk factors of the patients with aortic dissection (AD) were evaluated in a single medical center. From January 2002 to December 2008, 284 patients with AD were treated and followed-up at our institution, including 105 cases of type A AD and 179 cases of type B AD. The patients in each type were divided into three groups according to management: medical treatment group (A or B), open surgery group (A or B), and stent-graft group (A or B). The characteristics and follow-up outcomes were compared between the groups or subgroups. The results showed that there was significant difference in the prognosis for type A AD between medical treatment group and open surgery group, but there was no significant difference in the prognosis for type B AD between medical treatment group and stent-graft group. Independent risk factors of follow-up mortality for patients with type A AD included a history of atherosclerosis (HR, 3.807; 95% confidence interval [CI], 1.489 to 7.611; P=0.003), in-hospital hypotension/shock (HR, 4.687; 95% CI, 1.846 to 11.900; P=0.001), in-hospital myocardial ischemia or infarction (HR, 3.734; 95% CI, 1.613 to 8.643; P=0.002), pleural effusion (HR, 2.210; 95% CI, 1.080 to 4.521; P=0.030), branch vessel involvement (HR, 2.747; 95% CI, 1.202 to 6.278; P=0.016) and surgical treatment (HR, 0.177; 95% CI, 0.063 to 0.502; P=0.001). And there were insignificant independent predictors for mortality of the patients with type B AD. It was concluded that there were significant differences in characteristics and one year mortality between type A AD and type B AD, but after one year, there was no significant difference in the mortality and complications of them. There were several discordant risk factors of AD, such as female gender, age, thrombus, abrupt onset of pain that were considered as the risk factors in some papers. And there was no definite risk factor of mortality in this study in the patients with type B AD.
The IL-8 and MMP-7 genes participate in the carcinogenesis of many malignancies, but the role of both genes in cervical cancer is not fully elucidated. The aim of this study was to determine the frequency of IL-8 and MMP-7 gene mutations and to assess their effects on the risk of early stage cervical cancer and lymph node metastasis. The clinical stage and histological grade of cervical cancer were also studied. The peripheral blood from the patients with early stage cervical cancers and normal controls was collected and the DNA was extracted. The incidence of IL-8 and MMP-7 gene mutations was assessed by using tetra-primer amplification refractory mutation system polymerase chain reaction (ARMS PCR) and restriction fragment length polymorphism (RFLP). The data were statistically analyzed by x2 test. The results showed that: (1) The genotype frequency of IL-8 -251AT and TT was significantly higher in the cervical cancer group than in the normal control group (OR=2.290 and 2.619 respectively, P=0.001), and it was also higher in the lymphatic metastasis group than that without metastasis (OR=2.917, P=0.035); (2) The frequency of MMP-7 -181G/G genotype was significantly higher in the cervical cancer group and in the lymphatic metastasis group (P<0.05); (3) The incidence of IL-8 mutation was two times higher in IIa cervical cancer group than in Ib1 and Ib2 cervical cancer group (P=0.006). For the MMP-7 gene, there was statistically significant difference in the incidence of mutation between the Ib1, Ib2 and the IIa (P=0.000); (4) Different histological types and different grades of cervical cancer had different incidence of mutations, statistically. It was suggested that there was significant difference in the genotype of IL-8 -251TT and MMP-7 -181GG polymorphism between the cervical cancer group and the lymph node metastasis group. Moreover, individuals with IL-8 T allele or MMP-7 G allele carriers were at significantly higher risk of cervical cancer, particularly the early (IIa) and medium, poorly differentiated cervical cancer (G2+G3).
Cognitive decline is a common complication after cardiac surgery with cardiopulmonary bypass (CPB), but as such no pharmacological therapy has been shown to be efficacious in preventing the decline. However, gastrodin has been shown to have multi-pharmacological effects on neurological functions. We undertook this study to test the hypothesis that gastrodin would potentially prevent CPB-associated neurocognitive decline. We randomly assigned 200 patients undergoing mitral valve replacement surgery to receive either gastrodin (40 mg/kg) or saline after the induction of anesthesia and subsequently evaluated cognitive function before surgery, at discharge, and at 3rd month after surgery by using a battery of five neurocognitive tests, or adverse effects of gastrodin postoperatively. Neurocognitive decline in postoperative function was defined as a drop of 1 SD or more in the scores on tests of any one of the four domains of cognitive function. Cognitive decline occurred in 9% of the patients in the gastrodin group in contrast to 42% in the control group (P<0.01) at discharge. Cognitive outcome could be determined at 3rd month in 87 patients in the gastrodin group and 89 in the control group. Cognitive decline was detected in 6% in the gastrodin group and 31% in the control group (P<0.01). The incidences of possible adverse effects were similar between two groups. These results indicate that gastrodin is an effective and a safe drug for the prevention of neurocognitive decline in patients undergoing mitral valve replacement surgery with CPB.
In order to explore the difference of intraocular pressure (IOP) at different points of cornea before and after laser in situ keratomileusis (LASIK), IOP was measured by Tono-Pen Tonometer at central cornea, pericentral cornea and limbus respectively and analyzed statistically. After LASIK, IOP was dropped significantly at central cornea and pericentral cornea (P<0.05), while no statistically significant change occurred at limbus (P>0.05). There was no statistically significant difference in IOP at different points before LASIK (F=0.110, P=0.896), but statistically significant difference was found after LASIK (F=7.375, P=0.001). It was suggested that reliable IOP after LASIK could be obtained from the limbus by Tono-Pen tonometer.
Inhibitory ability of children with developmental dyscalculia (DD) was investigated to explore the cognitive mechanism underlying DD. According to the definition of developmental dyscalculia, 19 children with DD-only and 10 children with DD&RD (DD combined with reading disability) were selected step by step, children in two control groups were matched with children in case groups by gender and age, and the match ratio was 1:1. Psychological testing software named DMDX was used to measure inhibitory ability of the subjects. The differences of reaction time in number Stroop tasks and differences of accuracy in incongruent condition of color-word Stroop tasks and object inhibition tasks between DD-only children and their controls reached significant levels (P<0.05), and the differences of reaction time in number Stroop tasks between dyscalculic and normal children did not disappear after controlling the non-executive components. The difference of accuracy in color-word incongruent tasks between children with DD&RD and normal children reached significant levels (P<0.05). Children with DD-only confronted with general inhibitory deficits, while children with DD&RD confronted with word inhibitory deficits only.
It remains controversial whether tumor necrosis factor (TNF)-α antagonism is effective for asthma. This meta-analysis was performed to evaluate efficacy of TNF-α antagonism in treatment of patients with asthma. MEDLINE, EMBASE, LILACS, and CINAHL databases were searched for English-language studies published through January 3, 2010. Randomized-controlled trials comparing TNF-α antagonism with control therapy were selected. For each report, data were extracted in relation to the outcomes analyzed: asthma exacerbation, asthma quality of life questionnaire scores, and forced expiratory volume in 1 second. Four assessable trials were identified including 641 patients with asthma. TNF-α antagonism therapy was superior to control therapy in preventing exacerbations in asthmatics [pooled odds ratio 0.52 (95% confidence interval 0.29–0.88), P=0.02]; however, there was a nonsignificant reduction in asthma quality of life questionnaire scores [0.23 (0 to 0.47), P=0.05], forced expiratory volume in 1 second [0.03, (−0.14 to 0.10), P=0.74] when analyzed using standardized mean differences. TNF-α antagonism was superior to control chemotherapy in terms of asthma exacerbation, but not asthma quality of life questionnaire scores or forced expiratory volume in 1 second.
We described clinical process of two cases of intraocular lymphoma in aspects of early diagnosis by fine needle aspiration (FNA) and biopsy and treatment by intravitreal methotrexate (MTX). Two patients were suspected to have primary intraocular lymphoma (PIOL) with geographic yellow-white infiltrates and vitreous opacity. FNA confirmed malignant intraocular lymphoma in one patient and failed in the other patient due to complication of vitreous hemorrhage. Subsequent vitreous biopsy confirmed malignant intraocular lymphoma in the other patient. Both patients were treated by intravitreal methotrexate. In case 1 the tumor had complete remission and follow-up of 12 months had not found any signs of recurrence. In case 2 the patient died of brain metastasis 22 months after the ocular biopsy. Our findings demonstrate that although cytological examination of vitrectomy specimens remains the gold standard in diagnosis of PIOL, examination of FNA and biopsy increases the reliability of early diagnosing or excluding a PIOL. Individualized intravitreal methotrexate can be used to effectively treat PIOL. More effective integrated program treating primary central nervous system lymphoma/PIOL is worthy of looking forward to.