Diagnostic accuracy of metagenomic next-generation sequencing in diagnosing infectious diseases: a meta-analysis.

Many common pathogens are difficult or impossible to detect using conventional microbiological tests. However, the rapid and untargeted nature of metagenomic next-generation sequencing (mNGS) appears to be a promising alternative. To perform a systematic review and meta-analysis of evidence regarding the diagnostic accuracy of mNGS in patients with infectious diseases. An electronic literature search of Embase, PubMed and Scopus databases was performed. Quality was assessed using the Quality Assessment of Diagnostic Accuracy Studies-2 tool. Summary receiver operating characteristics (sROC) and the area under the curve (AUC) were calculated; A random-effects model was used in cases of heterogeneity. A total of 20 papers were eligible for inclusion and synthesis. The sensitivity and specificity of diagnostic mNGS were 75% and 68%, respectively. The AUC from the SROC was 85%, corresponding to excellent performance. mNGS demonstrated satisfactory diagnostic performance for infections and yielded an overall detection rate superior to conventional methods.

Circ0001320 inhibits lung cancer cell growth and invasion by regulating TNFAIP1 and TPM1 expression through sponging miR-558.

Lung cancer is the most affected malignant tumor in the world, and its specific pathogenesis is still unclear. It has been confirmed that circ0001320 is down-regulated in lung cancer, but its mechanism has not been reported. Further study found that circ0001320 was down-regulated in lung cancer cells, localized in the cytoplasm, and had multiple miR-558 binding sites. Dual-luciferase reporter gene assay, RNA-pull-down, and immunoprecipitation experiments all confirmed that circ0001320 directly bound to miR-558, and then inhibit the expression of miR-558. MiR-558 was up-regulated in lung cancer cells, and bound the downstream target genes TNFAIP1 and TPM1 to inhibit their expression. Western blot showed that circ0001320 significantly up-regulated the protein levels of TNFAIP1 and TPM1, while miR-558 blocked this effect of circ0001320. Circ0001320, TNFAIP1, and TPM1 all inhibited the proliferation and invasion of lung cancer cells and promoted apoptosis, while miR-558 had the opposite effects. After transfection with circ0001320 overexpression vector, miR-558 up-regulation or down-regulation of TNFAIP1, or TPM1 expression significantly reversed the inhibition of cell growth and invasion by circ0001320. Similarly, the expression of TNFAIP1 or TPM1 was down-regulated, while miR-558 expression was inhibited, and the levels of cell proliferation, apoptosis, and invasion did not change significantly. Therefore, these fully show that circ0001320 inhibits the growth and invasion of lung cancer cells through miR-558/TNFAIP1 and TPM1 pathways, which may be closely related markers and therapeutic targets of lung cancer.

Critically ill patients with COVID-19 with ECMO and artificial liver plasma exchange: A retrospective study.

COVID-19 is an emerging infectious disease capable of causing severe pneumonia. We aimed to characterize a group of critically ill patients in a single-center study.This was a retrospective case series of 23 patients with confirmed COVID-19-related critical illness in the intensive care unit (ICU) of a hospital in Hangzhou Zhejiang Province between January 22 and March 20, 2020.Of the 23 critically ill patients, the median age was 66 years (interquartile range [IQR] 59-80 years). The median time from disease onset to ICU admission was 10 days (IQR 6-11 days), to mechanical ventilation (MV) was 11 days (IQR 7.75-13 days), to artificial liver plasma exchange was 12 days (IQR 9.75-14.75 days), and to extracorporeal membrane oxygenation (ECMO) was 22 days (IQR 17.5-30 days). Nine patients required high flow oxygen. Fourteen patients received MV. Six required ECMO. Nine received artificial liver plasma exchange. Mortality was 0 at day 28.Mortality was 0 at day 28 in our single-center study. Extracorporeal membrane oxygenation reduced the requirements for ventilator support. Artificial liver plasma exchange significantly reduced inflammatory cytokine levels. These supportive therapies helped to extend the patients' survival times and increase the chance of follow-up treatments.

Meta-analysis of vitamin D and lung function in patients with asthma.

BACKGROUND: There is growing literature suggesting a link between vitamin D and asthma lung function, but the results from systematic reviews are conflicting. We conducted this meta-analysis to investigate the relation between serum vitamin D and lung function in asthma patients. METHODS: Major databases, including OVID, MEDLINE, Web of Science and PUBMED, were searched until 10th October 2018. All published observational studies related to vitamin D and asthma were extracted. All meta-analyses were performed using Review Manager 5.3.5. RESULTS: This quantitative synthesis found that asthma patients with low vitamin D levels had lower forced expiratory volume In 1 s (FEV1) (mean difference (MD) = - 0.1, 95% CI = - 0.11 to - 0.08,p < 0.01;I2 = 49%, p = 0.12) and FEV1% (MD = - 10.02, 95% CI = - 11 to - 9.04, p < 0.01; I2 = 0%, p = 0.82) than those with sufficient vitamin D levels. A positive relation was found between vitamin D and FEV1 (r = 0.12, 95% CI = 0.04 to 0.2, p = 0.003; I2 = 59%,p = 0.01), FEV1% (r = 0.19, 95% CI = 0.13 to 0.26, p < 0.001; I2 = 42%, p = 0.11), forced vital capacity (FVC) (r = 0.17, 95% CI = 0.00 to 0.34, p = 0.05; I2 = 60%, p = 0.04), FEV1/FVC (r = 0.4, 95% CI = 0.3 to 0.51, p < 0.001; I2 = 48%, p = 0.07), and the asthma control test (ACT) (r = 0.33, 95% CI = 0.2 to 0.47, p < 0.001; I2 = 0%, p = 0.7). Subgroup analysis indicated that the positive correlation between vitamin D and lung function remained significant in both children and adults. CONCLUSIONS: Our meta-analysis suggested that serum vitamin D levels may be positively correlated with lung function in asthma patients. Future comprehensive studies are required to confirm these relations and to elucidate potential mechanisms.

Food Insecurity and Hunger: Quiet Public Health Problems on Campus.

Food insecurity and hunger are gaining traction as recognized public health problems on college campuses in the United States. Data from recent publications and reports suggest the prevalence of food insecurity among U.S. undergraduate students ranges from 14.1 to 58.8%, compared to 12.3% of U.S. households. Undergraduate students (N=1,069) were surveyed at the University of Texas at Austin in 2014-2015. The survey questionnaire included the validated 6-item short-form of the USDA food security module, was distributed and completed in class and answered anonymously. The demographic characteristics of the sample are representative of all undergraduates on campus. Food insecurity was reported by 23.5% of students surveyed; ever being hungry by 31% and 12.5% of the ever-hungry also report being food-insecure. Importantly, most of the food insecure (96%) did not report experiencing food insecurity prior to matriculation. In multiple logistic regression models, the factors associated with a higher odds ratio of food insecurity include: being a first-generation college student; Hispanic ethnicity; third-born child or later in the family; and less confident about financial management skills. The factors associated with a higher adjusted odds ratio of hunger include: being of Asian or other ethnicity (vs. non-Hispanic white) and having limited confidence about financial management skills. The results, from one of the largest surveys of food insecurity and hunger among undergraduate students on a single campus in the U.S., suggest that transition to college is a vulnerable window for the emergence of food insecurity and hunger. More research is needed on the long-term effects of food insecurity in this population and the effectiveness of campus policy and interventions addressing food insecurity and hunger.

Household Food Insecurity is Associated with Childhood Asthma.

BACKGROUND: In 2013, 20% of U.S. households with children experienced food insecurity. Asthma afflicts over 7 million children; prevalence has steadily increased while incidence peaks in young children. Asthma and food insecurity share the determinants of poverty and race that are associated with weight, yet limited research on the relation between food insecurity and asthma exists. OBJECTIVE: The objective of this study was to determine the association between food insecurity and asthma in a diverse sample of children. METHODS: Cross-sectional data from grade 3 of the Early Childhood Longitudinal Study-Kindergarten Cohort were analyzed (n = 11,099). Food security based on the USDA module and asthma diagnosis were reported by parents; anthropometric factors were measured. Multivariate logistic regression models of food security and asthma were analyzed overall and by race/ethnicity. RESULTS: Children in food-insecure households had a 4% higher adjusted odds of asthma (95% CI: 1.02, 1.06). Adjusted odds of asthma were also higher by 70% for males (95% CI: 1.69, 1.71), 53% for non-Hispanic black (NHB) children (95% CI: 1.51, 1.54), 20% for Hispanic children (95% CI: 1.19, 1.21), 38% for overweight children (95% CI: 1.36, 1.39), 67% for obese children (95% CI: 1.65, 1.68), 23% for low-birth weight children (95% CI: 1.21, 1.24), 24% if mothers had a high school diploma (95% CI: 1.23, 1.26), and 33% if mothers had some college education (95% CI: 1.32, 1.35). High-birth weight children (OR: 0.84; 95% CI: 0.83, 0.85) and those with foreign-born mothers (OR: 0.52; 95% CI: 0.51, 0.53) had lower odds of asthma. Being food-insecure remained positively associated with asthma in non-Hispanic whites and Hispanics but was inversely associated with odds among NHBs. Odds of asthma doubled (OR: 2.00; 95% CI: 1.97, 2.03) for all children in households that were both food-insecure and poor; this relation remained positive in race/ethnicity-specific models. CONCLUSIONS: Food insecurity is positively associated with asthma in U.S. third graders, and household poverty strengthens the association.

In utero preeclampsia exposure, milk intake and pubertal development.

Cord blood insulin-like growth factor-1 (IGF-1) concentrations are lower in preeclamptic (PE) than normotensive (NT) pregnancies. PE offspring have increased risk of cardiovascular disease and decreased risk of some cancers including breast. We examined the effects of PE exposure in utero, infant feeding and childhood diet at 3-5 years on IGF-1 and breast development in 194 female offspring who were followed from birth until follow-ups at 10.8 and 12.9 years. Diet was not associated with serum IGF-1 levels at 10.8 years. PE exposure was associated with reduced odds of thelarche at 10.8 years only among exclusively breastfed girls. Milk, butter and ice cream consumption at 3-5 years was inversely related to the OR of breast development at 10.8 years. Child's weight and maternal overweight were positively associated with breast development at 10.8 years; child's height and weight were positively associated with breast development at 12.9 years.

Do longer formula feeding and later introduction of solids increase risk for pediatric acute lymphoblastic leukemia?

Milk formula feeding can elevate insulin-like growth factor-1 levels, possibly impacting leukemogenesis. The intent of the current study is to examine the associations between infant feeding practices and age at introduction of solids on risk of childhood acute lymphoblastic leukemia (ALL). Incident cases of infant and childhood (aged ≤14 years) ALL (n = 142) were enrolled in a case-control study. Cases were frequency matched on age, sex, race, and ethnicity to two sets of controls (n = 284 total). Multivariable logistic regression was used to determine the association between infant feeding practices and age at the introduction of solids and the odds ratio of ALL. In adjusted multivariable analyses, each additional month of formula feeding was associated with a 1.17 (1.09-1.25) odds ratio; each additional month of age at introduction of solids was associated with a 1.18 (1.07-1.30) odds ratio. In this study, longer duration of formula feeding and later age at the introduction of solid foods were independently associated with increased risk of ALL. Additional studies are needed to address the factors influencing duration of formula feeding and delayed introduction of solids. The results support the potential role of energy balance in early life as a contributor to risk for pediatric acute lymphoblastic leukemia.

Dietary alpha-, beta-, gamma- and delta-tocopherols in lung cancer risk.

Studies of vitamin E and cancer have focused on the alpha-tocopherol form of the vitamin. However, other forms of vitamin E, in particular gamma-tocopherol may have unique mechanistic characteristics relevant to lung cancer prevention. In an ongoing study of 1,088 incident lung cancer cases and 1,414 healthy matched controls, we studied the associations between 4 tocopherols (alpha-, beta-, gamma-, and delta-tocopherol) in the diet and lung cancer risk. Using multiple logistic regression analysis, the adjusted odds ratios (OR) and 95% confidence intervals (CI) of lung cancer for increasing quartiles of dietary alpha-tocopherol intake were 1.0, 0.63 (0.50-0.79), 0.58 (0.44-0.76) and 0.39 (0.28-0.53), respectively (p-trend < 0.0001). For dietary intake of beta-tocopherol, the OR and 95% CI for all subjects were: 1.0, 0.79 (0.63-0.98), 0.59 (0.45-0.78) and 0.56 (0.42-0.74), respectively (p-trend < 0.0001). Similar results for dietary gamma-tocopherol intake were observed: 1.0, 0.84 (0.67-1.06), 0.76 (0.59-0.97) and 0.56 (0.42-0.75), respectively (p- trend = 0.0002). No significant association between delta-tocopherol intake and lung cancer risk was detected. When the 4 tocopherols were summed as total tocopherol intake, a monotonic risk reduction was also observed. When we entered the other tocopherols in our model, only the association with dietary alpha-tocopherol intake remained significant; i.e., increasing intake of dietary alpha-tocopherol accounted for 34-53% reductions in lung cancer risk. To the best of our knowledge, this is the first report of the independent associations of the 4 forms of dietary tocopherol (alpha-, beta-, gamma- and delta-tocohperol) on lung cancer risk. Given the limitations with case-control studies, these findings need to be confirmed in further investigations.

Dietary magnesium and DNA repair capacity as risk factors for lung cancer.

Magnesium (Mg) is required for maintenance of genomic stability; however, data on the relationship between dietary Mg intake and lung cancer are lacking. In an ongoing lung cancer case-control study, we identified 1139 cases and 1210 matched healthy controls with data on both diet and DNA repair capacity (DRC). Dietary intake was assessed using a modified Block-NCI food frequency questionnaire and DRC was measured using the host-cell reactivation assay to assess repair in lymphocyte cultures. After adjustment for potential confounding factors including DRC, the odds ratios (ORs) and 95% confidence intervals (CIs) for lung cancer with increasing quartiles of dietary Mg intake were 1.0, 0.83 (0.66-1.05), 0.64 (0.50-0.83) and 0.47 (0.36-0.61), respectively, for all subjects (P-trend < 0.0001). Similar results were observed by histology and clinical stage of lung cancer. Low dietary Mg intake was associated with poorer DRC and increased risk of lung cancer. In joint effects analyses, compared with those with high dietary Mg intake and proficient DRC, the OR (95% CI) for lung cancer in the presence of both low dietary Mg and suboptimal DRC was 2.36 (1.83-3.04). Similar results were observed for men and women. The effects were more pronounced among older subjects (>60 years), current or heavier smokers, drinkers, those with a family history of cancer in first-degree relatives, small cell lung cancer and late-stage disease. These intriguing results need to be confirmed in prospective studies.