Influence of Ag Photodeposition Conditions over SERS Intensity of Ag/ZnO Microspheres for Nanomolar Detection of Methylene Blue.

Surface enhanced Raman spectroscopy (SERS) is considered a versatile and multifunctional technique with the ability to detect molecules of different species at very low molar concentration. In this work, hierarchical ZnO microspheres (ZnO MSs) and Ag/ZnO MSs were fabricated and decorated by hydrothermal and photodeposition methods, respectively. For Ag deposition, precursor molar concentration (1.9 and 9.8 mM) and UV irradiation time (5, 15, and 30 min) were evaluated by SEM, TEM, X-ray diffraction and Raman spectroscopy. X-ray diffraction showed a peak at 37.9° corresponding to the (111) plane of Ag, whose intensity increases as precursor concentration and UV irradiation time increases. SEM images confirmed the formation of ZnO MSs (from 2.5 to 4.5 µm) building by radially aligned two-dimensional ZnO nanosheets with thicknesses below 30 nm. The Raman spectra of Ag/ZnO MSs exhibited a vibration mode at 486 cm-1 which can be directly associated to Ag deposition on ZnO MSs surface. The performance of SERS substrate was evaluated using rhodamine 6G. The SERS substrate grown at 9.8 mM during 30 min showed the best SERS activity and the ability to detect methylene blue at 10-9 M.

High Rate of Non-Human Feeding by Aedes aegypti Reduces Zika Virus Transmission in South Texas.

Mosquito-borne viruses are emerging or re-emerging globally, afflicting millions of people around the world. Aedes aegypti, the yellow fever mosquito, is the principal vector of dengue, Zika, and chikungunya viruses, and has well-established populations across tropical and subtropical urban areas of the Americas, including the southern United States. While intense arboviral epidemics have occurred in Mexico and further south in the Americas, local transmission in the United States has been minimal. Here, we study Ae. aegypti and Culex quinquefasciatus host feeding patterns and vertebrate host communities in residential environments of South Texas to identify host-utilization relative to availability. Only 31% of Ae. aegypti blood meals were derived from humans, while 50% were from dogs and 19% from other wild and domestic animals. In Cx. quinquefasciatus, 67% of blood meals were derived from chicken, 22% came from dogs, 9% from various wild avian species, and 2% from other mammals including one human, one cat, and one pig. We developed a model for the reproductive number, R0, for Zika virus (ZIKV) in South Texas relative to northern Mexico using human disease data from Tamaulipas, Mexico. We show that ZIKV R0 in South Texas communities could be greater than one if the risk of human exposure to Ae. aegypti bites in these communities is at least 60% that of Northern Mexico communities. The high utilization of non-human vertebrates and low risk of human exposure in South Texas diminishes the outbreak potential for human-amplified urban arboviruses transmitted by Ae. aegypti.

Chronic Binge Alcohol Exposure During Pregnancy Alters mTOR System in Rat Fetal Hippocampus.

BACKGROUND: Gestational alcohol exposure can contribute to fetal alcohol spectrum disorders (FASD), an array of cognitive, behavioral, and physical developmental impairments. Mammalian target of rapamycin (mTOR) plays a key role in regulating protein synthesis in response to neuronal activity, thereby modulating synaptic plasticity and long-term memory formation in the brain. Based on our previous quantitative mass spectrometry proteomic studies, we hypothesized that gestational chronic binge alcohol exposure alters mTOR signaling and downstream pathways in the fetal hippocampus. METHODS: Pregnant Sprague-Dawley rats were assigned to either a pair-fed control (PF-Cont) or a binge alcohol (Alcohol) treatment group. Alcohol dams were acclimatized via a once-daily orogastric gavage of 4.5 g/kg alcohol (peak BAC, 216 mg/dl) from GD 5-10 and progressed to 6 g/kg alcohol (peak BAC, 289 mg/dl) from GD 11-21. Pair-fed dams similarly received isocaloric maltose dextrin. RESULTS: In the Alcohol group, following this exposure paradigm, fetal body weight and crown-rump length were decreased. The phosphorylation level of mTOR (P-mTOR) in the fetal hippocampus was decreased in the Alcohol group compared with controls. Alcohol exposure resulted in dysregulation of fetal hippocampal mTORC1 signaling, as evidenced by an increase in total 4E-BP1 expression. Phosphorylation levels of 4E-BP1 and p70 S6K were also increased following alcohol exposure. P-mTOR and P-4E-BP1 were exclusively detected in the dentate gyrus and oriens layer of the fetal hippocampus, respectively. DEPTOR and RICTOR expression levels in the fetal hippocampus were increased; however, RAPTOR was not altered by chronic binge alcohol exposure. CONCLUSION: We conclude that chronic binge alcohol exposure during pregnancy alters mTORC1 signaling pathway in the fetal hippocampus. We conjecture that this dysregulation of mTOR protein expression, its activity, and downstream proteins may play a critical role in FASD neurobiological phenotypes.

Distribution of Phosphatidylethanol in Maternal and Fetal Compartments After Chronic Gestational Binge Alcohol Exposure.

BACKGROUND: Phosphatidylethanol (PEth) is a promising biomarker for gestational alcohol exposure. Studies show PEth accumulation in maternal and fetal blood following alcohol exposure; however, distribution of specific PEth homologues (16:0/18:1, 16:0/18:2, 16:0/20:4) in maternal and fetal blood is unknown. Additionally, PEth levels in highly vulnerable FASD targets in maternal and fetal compartments remain unexplored. We hypothesized that all 3 major PEth homologues will be detectable in the maternal and fetal blood, the maternal uterine artery (a reproductive tissue that delivers oxygen and nutrients to fetoplacental unit), and fetal brain regions following gestational binge alcohol exposure and that homologue distribution profiles will be tissue-specific. METHODS: Pregnant rats received once-daily orogastric gavage of alcohol (Alcohol; BAC 216 mg/dl@4.5g/kg/d; BAC 289 mg/dl@6g/kg/d) or iso-caloric maltose dextrin (Pair-fed control) from gestation days (GD) 5 to 20 or 21. Following chronic exposure, maternal and fetal tissues were analyzed for PEth homologue concentrations utilizing LC-MS/MS technology. RESULTS: All 3 PEth homologues were detected in alcohol-exposed maternal blood, fetal blood, maternal uterine artery, and fetal brain regions (hippocampus, cerebral cortex, and cerebellum). In both maternal and fetal blood, respectively, PEth 16:0/18:2 was more abundant compared to 16:0/18:1 (p < 0.0001,~66%,↑; p = 0.0159, 20.4%↑) and 16:0/20:4 (p = 0.0072,~25%↑; p = 0.0187, 19.4%↑). Maternal PEth 16:0/20:4 was ~ 42% higher than 16:0/18:1 (p = 0.0015). Maternal PEth 16:0/18:2 and 16:0/20:4 were ~ 25%↑ and ~ 20%↑ higher than in fetal blood (p < 0.05). No homologue differences were detected in the maternal uterine artery. In all fetal brain regions, PEth 16:0/18:1 was significantly higher (p < 0.0001) than 16:0/18:2 (~48 to 78%↑) and 16:0/20:4 (~31 to 62%↑) concentrations. PEth 16:0/20:4 was ~ 18% higher than 16:0/18:1 (p < 0.05) in the fetal hippocampus and cortex. CONCLUSION: All major PEth homologues were detected in maternal and fetal blood following chronic gestational binge alcohol exposure; homologue distribution profiles were tissue-specific. This study also provides insights into PEth accumulation in critical FASD targets, specifically the maternal uterine artery and fetal brain.

Gestational binge alcohol-induced alterations in maternal uterine artery transcriptome.

Binge alcohol exposure during pregnancy results in diminished vessel function and altered proteome in the maternal uterine artery. We aimed to utilize high throughput RNA-seq deep-sequencing to characterize specific effects of binge alcohol exposure during pregnancy on the uterine artery transcriptome, and gain insight into mechanisms underlying alcohol-mediated uterine artery dysfunction. Pregnant Sprague-Dawley rats assigned to Pair-Fed Control or Alcohol groups, received a once-daily orogastric gavage in a binge paradigm. RNA-sequencing using Illumina NextSeq 500, identified 13,941 genes; 40 significantly altered genes were altered by log2(fold change) > 2; 27 genes were upregulated and 13 were downregulated in the Alcohol group. Transcripts altered included those which encode for aldehyde dehydrogenases, matrix metalloproteases, and molecules vital for vasodilation and vascular remodeling. Biological pathways that were disproportionally altered by alcohol were proline and citrulline biosynthesis/metabolism. Disruption of these pathways suggests candidate mechanism(s) for alcohol-mediated impairments to the proteome and vascular function.

Hippocampal transcriptome reveals novel targets of FASD pathogenesis.

INTRODUCTION: Prenatal alcohol exposure can contribute to fetal alcohol spectrum disorders (FASD), characterized by a myriad of developmental impairments affecting behavior and cognition. Studies show that many of these functional impairments are associated with the hippocampus, a structure exhibiting exquisite vulnerability to developmental alcohol exposure and critically implicated in learning and memory; however, mechanisms underlying alcohol-induced hippocampal deficits remain poorly understood. By utilizing a high-throughput RNA-sequencing (RNA-seq) approach to address the neurobiological and molecular basis of prenatal alcohol-induced hippocampal functional deficits, we hypothesized that chronic binge prenatal alcohol exposure alters gene expression and global molecular pathways in the fetal hippocampus. METHODS: Timed-pregnant Sprague-Dawley rats were randomly assigned to a pair-fed control (PF) or binge alcohol (ALC) treatment group on gestational day (GD) 4. ALC dams acclimatized from GDs 5-10 with a daily treatment of 4.5 g/kg alcohol and subsequently received 6 g/kg on GDs 11-20. PF dams received a once daily maltose dextrin gavage on GDs 5-20, isocalorically matching ALC counterparts. On GD 21, bilateral hippocampi were dissected, flash frozen, and stored at -80° C. Total RNA was then isolated from homogenized tissues. Samples were normalized to ~4nM and pooled equally. Sequencing was performed by Illumina NextSeq 500 on a 75 cycle, single-end sequencing run. RESULTS: RNA-seq identified 13,388 genes, of these, 76 genes showed a significant difference (p < 0.05, log2 fold change ≥2) in expression between the PF and ALC groups. Forty-nine genes showed sex-dependent dysregulation; IPA analysis showed among female offspring, dysregulated pathways included proline and citrulline biosynthesis, whereas in males, xenobiotic metabolism signaling and alaninine biosynthesis etc. were altered. CONCLUSION: We conclude that chronic binge alcohol exposure during pregnancy dysregulates fetal hippocampal gene expression in a sex-specific manner. Identification of subtle, transcriptome-level dysregulation in hippocampal molecular pathways offers potential mechanistic insights underlying FASD pathogenesis.

Chronic exposure to e-cig aerosols during early development causes vascular dysfunction and offspring growth deficits.

Increasing popularity of electronic cigarettes (e-cigs), including among women of reproductive age, is attributed to its perceived safety compared to conventional tobacco. However, there is a major knowledge gap surrounding the effects of e-cig aerosols on pregnancy and fetal development. We aimed to evaluate the effects of vaping e-cigs during gestation on offspring growth and to asses if growth deficits are accompanied by altered maternal and fetal vascular hemodynamics. Sprague-Dawley dams were assigned to Pair-Fed Control, Pair-Fed Juice, or Juice+Nicotine groups, and then underwent either a prenatal or prenatal+postnatal exposure paradigm in a custom-engineered vaping system. Mass spectrometry identified major aerosolized constituents from e-cig vaping. The Juice+Nicotine group exhibited significantly decreased fetal weight and crown-rump length (↓46.56%, and ↓23.83%, respectively). Pre- and postnatal exposure to Juice+Nicotine resulted in decreased pup weight at postnatal day (PND) 4-10. Crown-rump length was decreased by 24.71% on PND 10. Blood flow in the Juice+Nicotine group was decreased in the maternal uterine and fetal umbilical circuits by 49.50% and 65.33%, respectively. We conclude that chronic exposure to e-cig aerosols containing nicotine during early development can have deleterious health effects on the exposed offspring. Vaping e-cigs containing nicotine during pregnancy lead to a reduction in offspring weight and crown-rump length, associated with a marked decrease in blood flow in both the maternal uterine and fetal umbilical circulation (a strong indicator of growth restriction). Thus, chronic exposure to e-cig aerosols containing nicotine can lead to potentially harmful developmental effects in early life.

Dengue fever seroprevalence and risk factors, Texas-Mexico border, 2004.

Reported autochthonous dengue fever transmission in the United States has been limited to 5 south Texas border counties since 1980. We conducted a cross-sectional serosurvey in Brownsville, Texas, and Matamoros, Tamaulipas, Mexico (n = 600), in 2004 to assess dengue seroprevalence. Recent dengue infection was detected in 2% (95% confidence interval [CI] 0.5%-3.5%) and 7.3% (95% CI 4.3%-10.3%) of residents in Brownsville and Matamoros, respectively. Past infection was detected in 40% (95% CI 34%-45%) of Brownsville residents and 78% (95% CI 74%-83%) of Matamoros residents. For recent infection, only weekly family income