MicroRNAs (miRNA) mediate distinct gene regulatory pathways triggered by epidermal growth factor receptor (EGFR) activation, which occurs commonly in lung cancers with poor prognosis. In this study, we report the discovery and mechanistic characterization of the miRNA miR-7 as an oncogenic "oncomiR" and its role as a key mediator of EGFR signaling in lung cancer cells. EGFR activation or ectopic expression of Ras as well as c-Myc stimulated miR-7 expression in an extracellular signal-regulated kinase (ERK)-dependent manner, suggesting that EGFR induces miR-7 expression through a Ras/ERK/Myc pathway. In support of this likelihood, c-Myc bound to the miR-7 promoter and enhanced its activity. Ectopic miR-7 promoted cell growth and tumor formation in lung cancer cells, significantly increasing the mortality of nude mice hosts, which were orthotopically implanted with lung cancers. Quantitative proteomic analysis revealed that miR-7 decreased levels of the Ets2 transcriptional repression factor ERF, the coding sequence of which was found to contain a miR-7 complementary sequence. Indeed, ectopic miR-7 inhibited production of ERF messages with a wild-type but not a silently mutated coding sequence, and ectopic miR-7 rescued growth arrest produced by wild-type but not mutated ERF. Together, these results identified that ERF is a direct target of miR-7 in lung cancer. Our findings suggest that miR-7 may act as an important modulator of EGFRmediated oncogenesis, with potential applications as a novel prognostic biomarker and therapeutic target in lung cancer. Cancer Res; 70(21); 8822-31. ©2010 AACR.

Self-reported short sleep duration in obese individuals may be a surrogate marker of emotional stress and subjective sleep disturbances, whose detection and management should be the focus of our preventive and therapeutic strategies for obesity.

Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation. It is most likely the result of complex interactions of environmental and genetic factors. Because pulmonary surfactant components play important roles in normal lung function, innate host defence, and inflammation in the lung, this study investigated the hypothesis that the surfactant protein genes are involved in certain cases of COPD.Genotype analysis of surfactant protein (SP)-A, SP-B, SP-B-linked microsatellite, and SP-D marker alleles was performed in patients with COPD (n=97) and smoker (n=82) or nonsmoker (n=99) controls. Univariate and multiple logistic regression analyses were performed.The regression analysis results between COPD and smokers revealed several COPD susceptibility alleles (AA62_A, B1580_C, D2S388_5), based on an odds ratio (OR w2.5). The predictive ability of this model for developing COPD is good (c=0.926). Allele-allele (B1580_C and D2S388_5) and allele-environment (i.e. smoking) interactions were detected. When smoker controls were compared to nonsmoker controls, marker D2S388_5 appeared to be smoking-independent (p=0.874), whereas marker alleles AA62_A (p=0.045) and B1580_5 (p=0.007) were smoking-dependent. Males were at higher risk (OR=6.05, p=0.001), and smoking (w50 packs?yr -1 ) increased risk (OR=5.38, p=0.007). Males and alleles of loci flanking SP-B were associated with more severe cases (forced expiratory volume in one second/forced vital capacity ¡40%).The present results indicate that the surfactant protein alleles may be useful in chronic obstructive pulmonary disease by either predicting the disease in a subgroup and/or by identifying disease subgroups that may be used for therapeutic intervention. These observations should now be confirmed in a larger study, designed according to strict epidemiological criteria.

Highlights: Patients with coronavirus disease 2019 (COVID-19) had altered inflammatory markers. High sensitivity C-reactive protein-(pre)albumin ratios positively correlated with severe COVID-19. Prognostic nutritional index negatively correlated with risk of severe COVID-19. Nomogram combining the three factors reliably predicted the progression of COVID-19. High sensitivity C-reactive protein-prealbumin and -albumin ratios helped estimate duration of hospitalization.

Background Visceral adiposity and obstructive sleep apnoea (OSA) may be independently associated with daytime sleepiness/low performance, insulin resistance, hypercytokinaemia, and/or hypertension. The objectives of this study are to simultaneously test these associations at baseline and after 3 months of continuous positive airway pressure (CPAP) therapy. Materials and methods Sixteen obese men with OSA; 13 non-apnoeic, obese controls, and 15 non-obese controls were monitored in the sleep laboratory for four consecutive nights. Objective measures of daytime sleepiness and performance, serial 24 h plasma measures of interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), TNF receptor 1 (TNF-r1) and adiponectin, fasting blood glucose and insulin, visceral adiposity and blood pressure were obtained. Sleep apnoeics were re-assessed using the same protocol after 3 months of CPAP. Results At baseline, IL-6, TNF-r1, and insulin resistance were highest in OSA patients, intermediate in obese controls, and lowest in non-obese controls (P < 0·05). Visceral fat was significantly greater in sleep apnoeics than obese controls and predicted insulin resistance and IL-6 levels, whereas OSA predicted TNF-r1 levels (P < 0·05). CPAP decreased daytime sleepiness and blood pressure (P < 0·05), but did not affect fasting glucose or insulin or around the clock adiponectin, IL-6, TNF-α, or TNF-r1 levels. Conclusions In obese sleep apnoeics, visceral fat is strongly associated with insulin resistance and inflammation. CPAP decreases sleepiness and moderates hypertension but does not affect visceral adiposity, insulin resistance, hypoadiponectinaemia or hypercytokinaemia, all of which are independent risk factors for cardiovascular disease and diabetes.

No abstract

Surface‐enhanced Raman spectroscopy (SERS) is a surface‐sensitive technique that enhances Raman scattering by molecules adsorbed on nanostructures. The advantages of using SERS include high detection sensibility and fast analysis, thus it is a potentially promising tool for sensing metabolic cancer molecules in trace amounts. To explore this new method of lung cancer detection, we analyzed saliva samples from 61 lung cancer patients and 66 healthy controls. An SERS system and a nano‐modified chip were used in this study. Statistics were analyzed using support vector machine (SVM) and random forest algorithms. The leave‐one‐out algorithm was used based on SVM results to analyze differences in saliva between lung cancer patients and controls. There was a significant difference between the saliva of patients with lung cancer and healthy controls using the Raman spectrum; the intensity of the spectral line in lung cancer patients was weaker than in controls and 12 characteristic peaks were detected. Saliva SERS peaks have been characterized to refer to tissues, body fluids, and biological standard Raman peaks, but it is difficult to identify molecules with current information. The sensitivity and specificity of Raman spectroscopy data and SVM classification results of lung cancer patients and normal saliva samples were both 100%. Using the leave‐one‐out algorithm, the sensitivity was 95.08% and the specificity was 100%. The sensitivity of the random forest method was 96.72% and specificity was 100%. Our results show that SERS has the potential to detect lung cancer.

The results suggest the existence of vaginopathic C. albicans strains with enhanced virulence and tropism for the vagina and the high possibility of sexual transmission of genital C. albicans infection. Identification of specific genotypes that correlate with severity of VVC is also of diagnostic and therapeutic significance.