Resistance of MTB mosquitoes to DENV-2 is associated with a high density of <i>Wolbachia</i> in mosquito somatic tissues.

<p>The fold change in genome copy of the <i>Wolbachia</i> surface protein (WSP) gene in MTB mosquitoes is compared to APM mosquitoes. The copy number of the <i>Wolbachia</i> wsp was normalized by <i>Ae. polynesiensis</i> RPS6. In all the assays, the midguts, salivary glands, fat bodies, and ovaries of 7-day-old non-blood-fed females were dissected and used for extraction of total genomic DNA. Error bars are standard errors of the mean of twelve biological replicates.</p

Inhibition of dengue infection in the midgut of MTB mosquitoes.

<p>(<b>A</b>) At 4, 7 and 10 dpi with a blood meal containing DENV-2, mosquito midguts were collected, and the number of genome copies of the DENV-2 genome was determined by qRT-PCR using primers for the NS5 gene; the results were normalized to the <i>Ae. polynesiensis</i> RPS6. Lines indicate the median of the ten biological replicates. Significance was determined using a Mann-Whitney U test. (<b>B</b>) At 7 dpi through a blood meal, mosquito midguts were collected and fixed, and the viral antigen was detected using a mouse anti-Dengue complex monoclonal antibody by indirect fluorescence assay (IFA). One representative midgut from each category is shown. APM mosquitoes fed with dengue-infected or -uninfected blood meal was used as positive (POS.) and negative (NEG.) control, respectively. +, dengue-positive; −, dengue-negative.</p

Inhibition of dengue infection in the whole bodies of MTB mosquitoes.

<p>At 14 dpi (days post infection) through a blood meal or intrathoracic injection, the whole bodies of MTB and APM mosquitoes were collected, and the number of genome copies of the DENV genome was determined by qRT-PCR using primers for the NS5 gene; the results were normalized to the <i>Ae. polynesiensis</i> ribosomal protein S6 (RPS6). Lines indicate the median of the ten biological replicates. Significance was determined using a Mann-Whitney U test.</p

Maternal serum uric acid levels in pregnancy and fetal growth

<p><b>Objective:</b> Studies of maternal serum uric acid (UA) in pregnancy focus primarily on high levels of UA, however, both low and high UA levels can be markers of oxidative stress, a biological state potentially linked to fetal growth. We therefore aimed to test whether low and high maternal serum UA levels during pregnancy are associated with atypical fetal growth (unusually small or large) measured as birthweight (BW) for gestational age.</p> <p><b>Methods:</b> The Pregnancy Outcomes and Community Health Study enrolled 3019 pregnant women between their 16th–27th week of pregnancy from 52 clinics in five Michigan communities (1998–2004). Maternal UA levels were measured in blood collected at enrollment among a subcohort of 1291 participants. Infant BW and gestational age were used to calculate gestational age-specific BW <i>Z</i>-score. Infants were grouped as small (SGA = BW < 10th percentile), appropriate (AGA = BW 10th–90th percentile), or large (LGA) = BW > 90th percentile) for their gestational age. Analyses considered multiple potential confounders. Linear spline or multiple linear regression models were applied to evaluate the relationship between maternal UA levels and BW <i>Z</i>-score overall and within SGA, AGA, and LGA groups. Model robustness was tested through bootstrap, sensitivity analysis, and cross-validation techniques.</p> <p><b>Results:</b> The relation between maternal UA levels and BW <i>Z</i>-score varied by infant group. Among SGA infants, the relation was nonlinear (J-shape): both extremes of UA had lower BW <i>Z</i>-score with a breakpoint of 0.267 mmol/L UA (adjusted regression coefficient <i>β</i> = 2.32, <i>p</i> = .01 for lower UA; adjusted <i>β</i> = −37.38, <i>p</i> < .01 for higher UA). Among AGA infants, there was no significant association, and among LGA infants, the relation was linear (adjusted <i>β</i> = 2.86, <i>p</i> = .03).</p> <p><b>Conclusions:</b> Future research on maternal UA levels in pregnancy may benefit from considering both very low and high levels, and identifying <i>in utero</i> conditions associated with the two extremes.</p

<i>w</i>AlbB confers resistance to DENV-2 in both midguts and heads of MTB mosquitoes.

*<p>At 7 dpi through an infectious blood meal, the midguts of MTB and APM mosquitoes were collected and fixed, and the viral antigen was detected using a mouse anti-Dengue complex monoclonal antibody by indirect fluorescence assay (IFA).</p>#<p>At 14 dpi, the heads of both mosquitoes were collected to extract the total RNA. DENV-2 was diagnosed by RT-PCR using primers for the NS5 gene. Amplification of <i>Ae. polynesiensis</i> RPS6 was used to verify the quality of the RNA samples. Significance was shown in Fisher's exact test.</p