Role of quit supporters and other factors associated with smoking abstinence in adolescent smokers: a prospective study on Quitline users in the Republic of Korea

The aim of this study elucidated the effectiveness of Quitline among adolescent smokers, as well as other factors associated with adolescent smoking cessation in the Republic of Korea. For 642 adolescent Quitline users aged 13-19 years, the information on demographic characteristics, smoking and cessation related factors, and cessation outcome was collected. Cox proportional hazard models were applied. 13.4% of boys and 6.6% of girls maintained smoking cessation for 1 year. Having a high level of self-efficacy had a preventive effect on relapse in both genders. Boys with parents or other family members as quit supporters, and boys with a higher number of past cessation attempts, were more likely to relapse. It was even more pronounced among boys who reported low self-efficacy. Relapse was increased with marginal significance among girls with parents or other family members as quit supporters. It is evident that Quitline is an effective way to encourage adolescent smoking cessation in Korea. Reinforcing self-efficacy and enhancing the cooperative behaviors of parents or other family member quit supporters could be additional contributors for maintaining cessation among adolescent smokers who want to quit.     

Apigenin Sensitizes Huh-7 Human Hepatocellular Carcinoma Cells to TRAIL-induced Apoptosis

TNF-related apoptosis-inducing ligand (TRAIL) is a promising agent for management of cancer because of its selective cytotoxicity to cancer cells. However, some cancer cells have resistance to TRAIL. Accordingly, novel treatment strategies are required to overcome TRAIL resistance. Here, we examined the synergistic apoptotic effect of apigenin in combination with TRAIL in Huh-7 cells. We found that combined treatment of TRAIL and apigenin markedly inhibited Huh-7 cell growth compared to either agent alone by inducing apoptosis. Combined treatment with apigenin and TRAIL induced chromatin condensation and the cleavage of poly (ADP-ribose) polymerase (PARP). In addition, enhanced apoptosis by TRAIL/apigenin combination was quantified by annexin V/PI flow cytometry analysis. Western blot analysis suggested that apigenin sensitizes cells to TRAIL-induced apoptosis by activating both intrinsic and extrinsic apoptotic pathway-related caspases. The augmented apoptotic effect by TRAIL/apigenin combination was accompanied by triggering mitochondria-dependent signaling pathway, as indicated by Bax/Bcl-2 ratio up-regulation. Our results demonstrate that combination of TRAIL and apigenin facilitates apoptosis in Huh-7 cells.     

A quantitative comparison of basal ganglia neuronal activities of normal and Parkinson's disease model rats

The purpose of this study was to identify consistent characteristic changes of neuronal activity in basal ganglia (BG) nuclei associated with Parkinson's disease (PD) so that a reliable index of PD can be derived. A simple algorithm for automatic identification of firing patterns was devised as an essential tool to achieve this goal. A detailed quantitative analysis of firing patterns as well as firing rate was performed in three BG nuclei: the subthalamic nucleus (STN), the substantia nigra pars reticulate (SNpr), and the globus pallidus (GP). The results showed that the firing rate of STN neurons was not significantly altered in PD model rats. We also did not find a significant alteration in firing rates in the SNpr and GP between normal and PD model rats. In contrast, consistent changes of firing patterns were observed in all three BG nuclei in that the percentage of neurons with a regular firing pattern decreased whereas those with irregular, mixed, or burst patterns increased. This enables a simple algorithm based on burst detection and the shape of the interspike interval histogram to identify whether the neuronal activity is from normal or PD model rats.     

Proteomic analysis of phosphotyrosyl proteins in human embryonic stem cell-derived neural stem cells

Phosphorylation can reveal essential cell functions, such as cell differentiation, signal transduction, metabolic maintenance and cell division. The aim of this study was to investigate phosphorylated protein expression changes during neuronal lineage differentiation from hESCs. To measure the phosphorylated protein expression change during neuronal differentiation, we performed a comparative phosphoproteome analysis using 2-DE after MALDI-TOF MS and an MS/MS protein identification method, making a comparison between neural lineage differentiating cells and normal embryoid bodies (EBs) differentiated from human embryonic stem cells (hESCs) and profiling constituent phosphorylated proteins. Of 36 differentially expressed protein spots, 12 spots were shown to be up-regulated in differentiating neural cells. Specifically, the 7 up-regulated proteins of the 12 have potential roles in neuronal differentiation or neuronal damage recovery, including ACTB, heterogeneous nuclear ribonucleoprotein A2B1 (hnRNP A2B1), heterogeneous nuclear ribonucleoprotein L (hnRNP L), SET, chaperonin-containing TCP-1, vimentin and voltage-dependent anion channel protein 1 (VDAC1). These proteins are discussed further below.     

Somatic mutations of caspase-2 gene in gastric and colorectal cancers

There is mounting evidence that evasion of apoptosis is a hallmark of cancer. Caspase-2, which plays roles in both extrinsic and intrinsic apoptosis pathways, is considered a candidate tumor suppressor. The aim of this study was to explore the possibility that genetic alterations of caspase-2 gene are present in human cancers. In this study, we analyzed the entire coding sequences of human caspase-2 gene for the detection of somatic point mutations in 90 gastric carcinomas and 100 colorectal carcinomas by polymerase chain reaction (PCR)-single strand conformation polymorphism (SSCP). Of the cancers analyzed, two gastric cancers (2/90; 2.2%) and two colorectal cancers (2/100; 2.0%) harbored somatic missense mutations of caspase-2. The mutations consisted of p.V46M (at prodomain), p.S157L (at prodomain), p.R357K (at p13 subunit), and p.R397L (at p13 subunit). We expressed these tumor-derived mutants in 293 T cells and found that three of the mutants decreased cell death activity of caspase-2. Our data indicate that somatic mutation of caspase-2 is rare in gastric and colorectal carcinomas. However, functional data of the caspase-2 mutations also suggest that caspase-2 gene mutation might affect the pathogenesis of some gastric and colorectal cancers by inactivating cell death function of caspase-2.     

Bowel perforation after erlotinib treatment in a patient with non-small cell lung cancer

Erlotinib is accepted as a standard second-line chemotherapeutic agent in patients with non-small cell lung cancer who are refractory or resistant to first-line platinum- based chemotherapy. There has been no previous report of bowel perforation with or without gastrointestinal metastases related to erlotinib in patients with non-small cell lung cancer. The exact mechanism of bowel perforation in patients who received erlotinib remains unclear. In this report, we report the first case of enterocutaneous fistula in a female patient with metastatic non-small cell lung cancer 9 months, following medication with erlotinib as second-line chemotherapy.     

Maca (Lepidium meyenii) for treatment of menopausal symptoms: A systematic review

Maca (Lepidium meyenii), an Andean plant of the brassica (mustard) family has been used for centuries in the Andes as an adaptogenic plant to manage anemia, infertility and female hormone balance. The aim of this review was to assess the evidence for and against the effectiveness of the maca plant as a treatment for menopausal symptoms. We searched 17 databases from their inception up to June 2011 and included all randomized clinical trials (RCTs) that compared any type of maca-based intervention to a placebo for the treatment of menopausal symptoms. All studies were assessed for methodological quality using the Cochrane ‘risk of bias’ assessment tool. Four RCTs met all inclusion criteria. These RCTs tested the effects of maca on menopausal symptoms in healthy perimenopausal, early postmenopausal, and late postmenopausal women. Using the Kupperman Menopausal Index and the Greene Climacteric Score, all RCTs demonstrated favorable effects of maca. There have been very few rigorous trials of maca for menopausal symptoms. The results of our systematic review provide limited evidence for the effectiveness of maca as a treatment for menopausal symptoms. However, the total number of trials, the total sample size, and the average methodological quality of the primary studies, were too limited to draw firm conclusions. Furthermore, the safety has not been proved yet. Therefore, the efficacy and safety should be tested in larger studies.     

Impact of acute kidney injury on clinical outcomes after ST elevation acute myocardial infarction

Purpose

This study aimed to compare the incidence and clinical significance of transient versus persistent acute kidney injury (AKI) on acute ST elevation myocardial infarction (STEMI).

Materials and Methods

The study was a retrospective cohort of 855 patients with STEMI. AKI was defined as an increase of ≥0.3 mg/dL in creatinine level at any point during hospital stay. The study population was classified into 5 groups: 1) patients without AKI; 2) patients with mild AKI that was resolved by discharge (creatinine change less than 0.5mg/dL compared with admission creatinine during hospital stay, transient mild AKI); 3) patients with mild AKI that did not resolve by discharge (persistent mild AKI); 4) patients with moderate/severe AKI that was resolved by discharge (creatinine change more than 0.5 mg/dL compared with admission creatinine, transient moderate/severe AKI); 5) patients with moderate/severe AKI that did not resolve by discharge (persistent moderate/severe AKI). We investigated 1-year all-cause mortality after hospital discharge for the primary outcome of the study. The relation between AKI and 1-year mortality after STEMI was analyzed.

Results

AKI occurred in 74 (8.7%) patients during hospital stay. Adjusted hazard ratio for mortality was 3.139 (95% CI 0.764 to 12.897, p=0.113) in patients with transient, mild AKI, and 8.885 (95% CI 2.710 to 29.128, p<0.001) in patients with transient, moderate/severe AKI compared to patients without AKI. Persistent moderate/severe AKI was also independent predictor of 1 year mortality (hazard ratio, 5.885; 95% CI 1.079 to 32.101, p=0.041).

Conclusion

Transient and persistent moderate/severe AKI during acute myocardial infarction is strongly related to 1-year all cause mortality after STEMI.     

Effect of intravitreal bevacizumab on vascular endothelial growth factor expression in patients with proliferative diabetic retinopathy

Purpose

To investigate the effect of bevacizumab (Avastin; Genentech, San Francisco, CA, USA) on vascular endothelial growth factor (VEGF) expression and inflammation in fibrovascular membranes in patients with proliferative diabetic retinopathy (PDR).

Materials and Methods

Fibrovascular membranes from 19 eyes of 18 patients with PDR were studied using immunohistochemistry and analyzed in the following 3 groups; group 1: 4 inactive PDR eyes, group 2: 10 active PDR eyes treated preoperatively with adjunctive intravitreal bevacizumab, group 3: five active PDR eyes not treated preoperatively with bevacizumab. Immunohistochemical staining for VEGF, CD31 and CD68 were done.

Results

The immunoreactivity to VEGF and CD 31-positive blood vessels was significantly higher in membranes from group 3 than group 1 (p = 0.007 for VEGF, 0.013 for CD 31-positive vessels). Intravitreal bevacizumab caused a reduction in VEGF expression and vascular densities in 4 out of 10 (40%) excised membranes from eyes with PDR. However, six membranes (60%) in group 2 still demonstrated relatively strong VEGF expression and high vascular density. Infiltration of macrophages was observed in 16 out of the 19 membranes, and the density of macrophages was increased in group 2 compared with group 1 (p = 0.043).

Conclusion

Intravitreal bevacizumab injections caused some reduction in VEGF expression and vascular densities in a limited number of active PDR patients. A single intravitreal bevacizumab injection may not be enough to induce complete blockage of VEGF and pathologic neovascularization in active PDR patients. Repeated injections, panretinal photocoagulation and/or PPV may be necessary following intravitreal bevacizumab to reinforce the anti-VEGF effect of the drug.