Inequalities concerning polar derivative of polynomials

In this paper we obtain certain results for the polar derivative of a polynomial $p(z) = c_nz^n +\sum_{j=\mu}^n c_{n-j}z^{n-j}$, $1\leq\mu\leq n$, having all its zeros on $|z| = k$, $k\leq 1$, which generalizes the results due to Dewan and Mir, Dewan and Hans. We also obtain certain new inequalities concerning the maximum modulus of a polynomial with restricted zeros. [Editor's note: There are flaws in the paper, see M. A. Qazi, Remarks on some recent results about polynomials with restricted zeros, Ann. Univ. Mariae Curie-Skłodowska Sect. A 67 (2), (2013), 59-64

Polymorphisms in the Innate Immune IFIH1 Gene, Frequency of Enterovirus in Monthly Fecal Samples during Infancy, and Islet Autoimmunity

Interferon induced with helicase C domain 1 (IFIH1) senses and initiates antiviral activity against enteroviruses. Genetic variants of IFIH1, one common and four rare SNPs have been associated with lower risk for type 1 diabetes. Our aim was to test whether these type 1 diabetes-associated IFIH1 polymorphisms are associated with the occurrence of enterovirus infection in the gut of healthy children, or influence the lack of association between gut enterovirus infection and islet autoimmunity

Duffy Antigen Receptor for Chemokines Mediates trans-Infection of HIV-1 from Red Blood Cells to Target Cells and Affects HIV-AIDS Susceptibility

Duffy antigen receptor for chemokines (DARC) expressed on red blood cells (RBCs) influences plasma levels of HIV-1-suppressive and proinflammatory chemokines such as CCL5/RANTES. DARC is also the RBC receptor for Plasmodium vivax. Africans with DARC -46C/C genotype, which confers a DARC negative phenotype, are resistant to vivax malaria. Here, we show that HIV-1 attaches to RBCs via DARC, effecting trans-infection of target cells. In African Americans, DARC -46C/C is associated with 40% increase in the odds of acquiring HIV-1. If extrapolated to Africans, ~11% of the HIV-1 burden in Africa may be linked to this genotype. After infection occurs, however, DARC-negative RBC status is associated with slower disease progression. Furthermore, the disease-accelerating effect of a previously described CCL5 polymorphism is evident only in DARC-expressing and not in DARC-negative HIV-infected individuals. Thus, DARC influences HIV/AIDS susceptibility by mediating trans-infection of HIV-1 and by affecting both chemokine-HIV interactions and chemokine-driven inflammation

Global Prevalence of Bronchopulmonary Dysplasia in Very Low Birth Weight Neonates: A Systematic Review and Meta-Analysis

Importance: Large-scale estimates of bronchopulmonary dysplasia (BPD) are warranted for adequate prevention and treatment. However, systematic approaches to ascertain global rates of BPD are lacking. Objective: To conduct a systematic review and meta-analysis to assess the prevalence of BPD in very low birth weight (≤1,500 grams) or very low gestational age (\u3c32 \u3eweeks) neonates. Data sources: A search of MEDLINE from January 1990 until September 2019 using search terms related to BPD and prevalence was performed. Study selection: Randomized controlled trials and observational studies evaluating rates of BPD in very low birth weight or very low gestational age were eligible. Included studies defined BPD as positive pressure ventilation or oxygen requirement at 28 days (BPD28) or at 36 weeks postmenstrual age (BPD36). Data extraction and synthesis: Two reviewers independently conducted all stages of the review. Random-effects meta-analysis was used to calculate the pooled prevalence. Subgroup analyses included gestational age group, birth weight group, setting, study period, continent, and gross domestic product. Meta-regression was performed to identify the impact of significant variables on study effect. Main outcomes and measures: Prevalence of BPD defined as BPD28, BPD36, AnyBPD (BPD 28 or BPD 36), and by subgroups. Results: A total of 82 articles and 696,881 patients were included in this review. The pooled prevalence was 23% (95% CI, 17%-30%) for BPD28 (n=29 studies, 101,848 neonates), 21% (95% CI, 17%-24%) for BPD36 (n=56 studies, 584,448 neonates), and 19% (95% CI, 16%-22%) for any BPD (n=70 studies, 607,653 neonates). In subgroup meta-analyses, birth weight was the strongest driver of the pooled prevalence of BPD. Conclusions and relevance: This study provides a global estimation of BPD prevalence in very low birth weight/low gestation neonates

Copy Number Variations Due to Large Genomic Deletion in X-Linked Chronic Granulomatous Disease

Mutations in genes for any of the six subunits of NADPH oxidase cause chronic granulomatous disease (CGD), but almost 2/3 of CGD cases are caused by mutations in the X-linked CYBB gene, also known as NAD (P) H oxidase 2. Approximately 260 patients with CGD have been reported in Japan, of whom 92 were shown to have mutations of the CYBB gene and 16 to have chromosomal deletions. However, there has been very little detailed analysis of the range of the deletion or close understanding of the disease based on this. We therefore analyzed genomic rearrangements in X-linked CGD using array comparative genomic hybridization analysis, revealing the extent and the types of the deletion genes. The subjects were five Japanese X-linked CGD patients estimated to have large base deletions of 1 kb or more in the CYBB gene (four male patients, one female patient) and the mothers of four of those patients. The five Japanese patients were found to range from a patient exhibiting deletions only of the CYBB gene to a female patient exhibiting an extensive DNA deletion and the DMD and CGD phenotype manifested. Of the other three patients, two exhibited CYBB, XK, and DYNLT3 gene deletions. The remaining patient exhibited both a deletion encompassing DNA subsequent to the CYBB region following intron 2 and the DYNLT3 gene and a complex copy number variation involving the insertion of an inverted duplication of a region from the centromere side of DYNLT3 into the deleted region

Cumulative Viral Load and Virologic Decay Patterns after Antiretroviral Therapy in HIV-Infected Subjects Influence CD4 Recovery and AIDS

The impact of viral load (VL) decay and cumulative VL on CD4 recovery and AIDS after highly-active antiretroviral therapy (HAART) is unknown.Three virologic kinetic parameters (first year and overall exponential VL decay constants, and first year VL slope) and cumulative VL during HAART were estimated for 2,278 patients who initiated HAART in the U.S. Military HIV Natural History Study. CD4 and VL trajectories were computed using linear and nonlinear Generalized Estimating Equations models. Multivariate Poisson and linear regression models were used to determine associations of VL parameters with CD4 recovery, adjusted for factors known to correlate with immune recovery. Cumulative VL higher than the sample median was independently associated with an increased risk of AIDS (relative risk 2.38, 95% confidence interval 1.56-3.62, p<0.001). Among patients with VL suppression, first year VL decay and slope were independent predictors of early CD4 recovery (p = 0.001) and overall gain (p<0.05). Despite VL suppression, those with slow decay during the first year of HAART as well as during the entire therapy period (overall), in general, gained less CD4 cells compared to the other subjects (133 vs. 195.4 cells/µL; p = 0.001) even after adjusting for potential confounders.In a cohort with free access to healthcare, independent of established predictors of AIDS and CD4 recovery during HAART, cumulative VL and virologic decay patterns were associated with AIDS and distinct aspects of CD4 reconstitution