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Hypospadias is one of the most common congenital anomalies. Trends of hypospadias prevalence by severity are not well reported. Most prevalence studies consist of pooled data from different countries or states suffer from low data quality due to inconsistent methodologies, limited variables, and lack of categorization of hypospadias severity. The objective of this study is to examine the prevalence of hypospadias by degrees of severity and associated risk factors using combined data sources from a stable and well-defined population. The study population includes infants born with hypospadias to mothers residing in Arkansas from 1997 to 2016. Cases were identified from an active population-based surveillance program of birth defects. Identified hypospadias cases from surveillance data were linked to birth certificate and to a clinical database. These two data sources provide more details on the location of the defect and maternal and infant characteristics. The prevalence and 95% confidence intervals were calculated using total male live births as denominator. Chi-square test was used to assess the association of nominal variables. Logistic regression was used to calculate adjusted odds ratio. A total 3230 hypospadias cases were identified from 1997 to 2016. The overall prevalence is 83.0 per 10,000 male births. A majority of cases (56.7%) were classified as first degree with the others having second degree (22.8%), third degree (4.7%) or not otherwise specified (15.6%). The highest prevalence of hypospadias was observed among Non-Hispanic whites. Higher prevalence also was observed among mothers in the older age group with no prenatal care in the first trimester and with gestational hypertension or diabetes. Premature or small for gestational age infants tend to have higher prevalence across all levels of severity. The number of hypospadias cases increased over time. After maternal age, race and education were adjusted, higher risk persisted for infants of restricted fetal growth, mothers with gestational hypertension or diabetes and the cohort of 2013–2016. There is an increase of hypospadias cases in Arkansas. Several maternal and infant characteristics associated with higher prevalence for all levels of severity are worth further investigation. Summary Table Prevalence of hypospadias per 10 000 by severity and selected characteristics 1997-2016. Summary Table 1st degree 2nd degree 3rd degree Not otherwise specified Cases Prevalence (95% CI) Cases Prevalence (95% CI) Cases Prevalence (95% CI) Cases Prevalence (95% CI) Maternal Race Non Hispanic–White 1442 53.9 (51.1–56.7) 551 20.6 (18.9–22.4) 91 3.4 (2.7–4.2) 385 14.4 (13.0–15.9) Non Hispanic–Black 232 31 (27.2–35.3) 123 16.4 (13.7–19.6) 39 5.2 (3.7–7.1) 80 10.7 (8.5–13.3) Maternal age 30–34 356 53.6 (48.2–59.4) 133 20 (16.8–23.7) 22 3.3 (2.1–5) 93 14 (11.3–17.1) 35+ 178 56.7 (48.7–65.6) 63 20.1 (15.4–25.7) 19 6.1 (3.6–9.4) 45 14.3 (10.5–19.2) Fetal growth Small for gestational age 213 61.7 (53.7–70.5) 112 32.4 (26.7–39) 61 17.7 (13.5–22.7) 78 22.6 (17.9–28.2) Appropriate gestational age 1373 43.7 (41.4–46.1) 540 17.2 (15.8–18.7) 79 2.5 (2.0–3.1) 370 11.8 (10.6–13) Gestational hypetension 113 58.7 (48.4–70.5) 48 24.9 (18.4–33.0) 28 14.5 (9.7–21) 42 21.8 (15.7–29.5) Gestational diabetes 73 53.9 (42.3–67.8) 33 24.4 (16.8–34.2) 8 5.9 (2.6–11.6) 20 14.8 (9.0–22.8) Birth cohort 2002–2006 546 56 (51.4–60.9) 149 15.3 (12.9–17.9) 37 3.8 (2.7–5.2) 93 9.5 (7.7–11.7) 2007–2011 430 42.5 (38.5–46.7) 228 22.5 (19.7–25.6) 45 4.4 (3.2–5.9) 153 15.1 (12.8–17.7) 2012–2016 505 52.5 (48.0–57.2) 256 26.6 (23.4–30.1) 46 4.8 (3.5–6.4) 118 12.3 (10.1–14.7) CI=Confidence Intervel [ABSTRACT FROM AUTHOR]

Objective: To assess whether the severity of cases of spina bifida changed after the institution of mandatory folic acid fortification in the US.Study Design: Six active population-based birth defects programs provided data on cases of spina bifida for 1992-1996 (prefortification period) and 1999-2016 (postfortification period). The programs contributed varying years of data. Case information included both a medical record verbatim text description of the spina bifida diagnosis and spina bifida codes (International Classification of Diseases, Clinical Modification, or a modified birth defects surveillance coding system). Comparing the prefortification and postfortification periods, aORs for case severity (upper-level lesions [cervical, thoracic] vs lower-level lesions [lumbar, sacral]) and prevalence ratios (PRs) were estimated.Results: A total of 2593 cases of spina bifida (out of 7 816 062 live births) met the inclusion criteria, including 573 cases from the prefortification period and 2020 cases from the postfortification period. Case severity decreased by 70% (aOR, 0.30; 95% CI, 0.26-0.35) between the fortification periods. The decrease was most pronounced for non-Hispanic White mothers. Overall spina bifida prevalence declined by 23% (PR, 0.77; 95% CI, 0.71-0.85), with similar reductions seen across the early, mid, and recent postfortification periods. A statistically significant decrease in upper-level lesions occurred in the postfortification period compared with the prefortification period (PR, 0.28; 95% CI, 0.22-0.34), whereas the prevalence of lower-level lesions remained relatively similar (PR, 0.94; 95% CI, 0.84-1.05).Conclusions: The severity of spina bifida cases decreased after mandatory folic acid fortification in the US. Further examination is warranted to better understand the potential effect of folic acid on spina bifida severity. [ABSTRACT FROM AUTHOR]

Plant hormones are crucial signaling molecules that coordinate all aspects of plant growth, development and defense. A great deal of attention has been attracted from biologists to study the molecular mechanisms for perception and signal transduction of plant hormones during the last two decades. Tremendous progress has been made in identifying receptors and key signaling components of plant hormones. The holistic picture of hormone signaling pathways is extremely complicated, this review will give a general overview of perception and signal transduction mechanisms of auxin, gibberellin, cytokinin, abscisic acid, ethylene, brassinosteroid, and jasmonate. [ABSTRACT FROM AUTHOR]