Chemotherapeutic Effectiveness of Combining Cetuximab for Metastatic Colorectal Cancer Treatment: A System Review and Meta-Analysis.

This meta-analysis used the database including PubMed, Medline, Cochrane Library, CNKI, Chinese-Cqvip, and Wanfang for randomized controlled trials (RCTs) to investigate the clinical effectiveness for combining cetuximab treatment with chemotherapy for treating metastatic colorectal cancer (mCRC). A total of 12 RCTs involved 7,108 patients with mCRC were included. The patients received chemotherapy with (3,521 cases) or without cetuximab (3,587 cases). Outcomes were overall survival (OS), progression-free survival (PFS), disease control rate (DCR), overall response rate (ORR), odd ratio (OR), and risk ratio (HR). Our results showed that the chemotherapy alone group has shorter OS, PFS, and ORR than the chemotherapy plus cetuximab group, with significant differences (PFS:HR = 0.77, 95% CI = 0.72-0.82, P < 0.00001; OS:HR = 0.88, 95% CI = 0.79-0.99, P = 0.03; ORR:OR = 1.79, 95% CI = 1.30-2.47; P = 0.0003). Results of subgroup analysis showed that cetuximab treatment prolonged PFS and OS in KRAS wild-type patients, with statistically significant differences (PFS:HR = 0.79, 95% CI = 0.65-0.95, P = 0.01; OS:HR = 0.85, 95% CI = 0.74-0.98, P = 0.02). Combining cetuximab with chemotherapy, the PFS and OS of wild-type KRAS patients and the ORR of all patients were significantly improved.

Effect of acute exposure to PFOA on mouse liver cells in vivo and in vitro.

Increasingly, epidemiological evidences indicate chemosynthetic perfluorooctanoic acid (PFOA), an environmental pollutant, induces potential adverse effect on human health after long-term exposure. However, less study has been performed for assessment of acute effect of PFOA exposure on metabolic homeostasis. In experimental designs, PFOA-exposed liver cells in vivo and in vitro were used to discuss underlying mechanism related to PFOA-induced metabolic dysfunction. In serological tests, PFOA-exposed mice showed increased treads of liver functional enzymes in alanine transaminase (ALT), aspartate transaminase (AST), and total bilirubin (T-BIL), trypsinase, low density lipoprotein-cholesterol (LDL-C), and insulin, while blood glucose, high density lipoprotein-cholesterol (HDL-C), and glucagon levels were reduced. In histocytological observations, PFOA-exposed liver showed visible cytoplasmic vesicles, and intact pancreatic islets were observed in PFOA-exposed pancreas. Additionally, increased insulin-positive cells and reduced glucagon-positive cells were detected in PFOA-exposed islets. As shown in immunoassays, PFOA-exposed liver resulted in elevations of cluster of differentiation 36 (CD36)-labeled cells and CD36 protein. In mouse liver cell study, PFOA-exposed cells showed increased cell apoptotic count, and increased phosphorylated levels of Bcl-2 and Bad in the cells. Furthermore, PFOA-exposed liver cells exhibited elevations of CD36-labeled cells and CD36 protein. Taken together, the present data demonstrate that acute exposure to PFOA-impaired liver function is associated with inducting CD36 expression and apoptosis, as well as disrupting key hormones in the pancreas.

Endoscopic characteristics of multidrug-resistant tuberculosis combined with tracheobronchial tuberculosis / 中国内镜杂志

Objective To explore the endoscopic characteristics of multidrug-resistant tuberculosis (MDR-TB) combined with tracheobronchial tuberculosis (TBTB). Methods 248 MDR-TB as study group, they hospitalized from October 1st 2008 to June 31st, 2016. 274 cases of non MDR-TB with bacteria positive as control group over 2015, all of them received bronchoscopy, sputum cultured and drug sensitivity tested of Isoniazid and Rifampicin. We analyzed the results of bronchoscopy and demographic data. Results 248 cases of MDR-TB patients, of 175 (70.56%) were diagnosed TBTB by bronchoscopy, of 73 (29.44%) without TBTB. 274 cases of non MDR-TB with bacteria positive patients, of 146 (53.28%) were diagnosed TBTB, of 128 (46.72%) non TBTB, the difference of comparisons was statistically significant (χ2 = 16.42, P = 0.000). MDR-TB combined with TBTB median age was 32 years, non MDR-TB combined with TBTB median age 42 years, the difference was statistically significant (U = 9932.00, P = 0.001). Among the MDR-TB patients, of 75 (42.86%) TBTB in the upper right bronchial, of71 (40.57%) upper left bronchus, while non MDR-TB patients, of 70 (47.95%) and 60 (41.10%), there was no statistically significant difference (χ2 = 2.44, P = 0.786). Among the MDR-TB, of 76 (43.43%) were inflammation infiltration type, of 11 (6.29%) were necrosis type, of 13 cases (7.43%) granulation proliferative type, of 72 (41.14%) were scar stricture type, of 3 (1.71%) tube wall softening type. Among the non MDR-TB, in turn, TBTB type were 50 (34.25%), 41 (28.08%), 9 (6.16%), 40 (27.40%), 5 (3.43%), the difference were statistically significant (χ2 = 30.50, P = 0.000). Conclusions The detection rate of TBTB was higher in MDR-TB patients, that common occur in younger patients. TBTB common infringe on upper right bronchial and upper left bronchus, TBTB type most are inflammatory infiltration type and scar stricture type. More attention should be paid to bronchoscopy among MDR-TB patients.

Anticytoproliferative effect of Vitamin C on rat hepatic stellate cell.

This study was conducted to investigate the potential therapeutical benefit of Vitamin (VC), a potent antioxidant, on suppressing proliferation of immortalized rat liver stellate cell line (HSC-T6) in vitro, and to discuss the underlying mechanism. HSC-T6 was co-treated with different concentrations of VC (50, 100, 200 µmol/L) on designed time points. Then, cell viability was assessed by using MTT analysis, and the changes of cytomorphology was observed with apoptosis-specific TUNEL and immunohistochemical stains, as well as the intracellular target genes was determined by using RT-PCR, respectively. As the outcomes, VC-treated HSC-T6 showed significantly inhibited cell growth in a dose-dependent manner when compared to the vehicle control. Cytologically, VC increased TUNEL-labeled positive cells in cultured HSC-T6, which the cell count was greater than vehicle control. Meanwhile, VC-treated HSC-T6 showed elevated immunoreactive for TGF-ß1-labeled cells. Moreover, VC contributed to down-regulated expressions of intracellular c-myc, cyclin D1, mTOR mRNAs in HSC-T6. Collectively, these preliminary findings have demonstrated that VC-mediated anti-proliferative effect on HSCs is involved in molecular mechanisms of promoting apoptosis and blocking endogenous collagenation.