An Atlas for Schistosoma mansoni Organs and Life-Cycle Stages Using Cell Type-Specific Markers and Confocal Microscopy

Schistosomiasis (bilharzia) is a tropical disease caused by trematode parasites (Schistosoma) that affects hundreds of millions of people in the developing world. Currently only a single drug (praziquantel) is available to treat this disease, highlighting the importance of developing new techniques to study Schistosoma. While molecular advances, including RNA interference and the availability of complete genome sequences for two Schistosoma species, will help to revolutionize studies of these animals, an array of tools for visualizing the consequences of experimental perturbations on tissue integrity and development needs to be made widely available. To this end, we screened a battery of commercially available stains, antibodies and fluorescently labeled lectins, many of which have not been described previously for analyzing schistosomes, for their ability to label various cell and tissue types in the cercarial stage of S. mansoni. This analysis uncovered more than 20 new markers that label most cercarial tissues, including the tegument, the musculature, the protonephridia, the secretory system and the nervous system. Using these markers we present a high-resolution visual depiction of cercarial anatomy. Examining the effectiveness of a subset of these markers in S. mansoni adults and miracidia, we demonstrate the value of these tools for labeling tissues in a variety of life-cycle stages. The methodologies described here will facilitate functional analyses aimed at understanding fundamental biological processes in these parasites

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

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Protective Mechanisms for Depression among Racial/Ethnic Minority Youth: Empirical Findings, Issues, and Recommendations

We (1) review empirical studies that report findings regarding putative protective mechanisms when exposed to risk of depression in African American and Hispanic adolescents; (2) identify key protective mechanisms for different risk contexts that garner empirical support; (3) synthesize the mechanisms identified as protective against depression among racial/ethnic minority adolescents; and (4) discuss improved methods for advancing understanding of resilience against depression in minority youth. The studies were selected from PsycINFO searches that met the following inclusion criteria: participants between 12 and 21 years of age, inclusions of racial/ethnic minority members, examining protection through an interaction with a risk factor, and outcome measures of depression, depressed mood, or depressive symptomatology. We found 39 eligible studies; 13 of which included multiple racial/ethnic groups. The following were supported as protective mechanisms, at least preliminarily, for at least one racial/ethnic group and in at least one risk context: employment, extracurricular activities, father–adolescent closeness, familism, maternal support, attending predominately minority schools, neighborhood composition, non-parent support, parental inductive reasoning, religiosity, self-esteem, social activities, and positive early teacher relationships. To investigate protective mechanisms more comprehensively and accurately across individual, social, and community levels of influence, we recommend incorporating multilevel modeling or multilevel growth curve analyses and large diverse samples

Opioid-Sparing Multimodal Analgesia Efficacy in Hispanic Patients Undergoing Total Knee Arthroplasty

Background:. Adequate pain control after total knee arthroplasty (TKA) has been associated with improved patient mobility and satisfaction, and is a task that has historically relied on opioids. Multimodal analgesic regimens can be considered a therapeutic alternative for postoperative pain control to avoid opioid consumption and its adverse side effects. This study aimed to evaluate the use of a multimodal analgesia protocol based on nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen as an alternative to reduce opioid consumption in Hispanic patients undergoing primary TKA. Methods:. An institutional review board-approved, randomized controlled trial evaluated postoperative pain control after TKA in a Hispanic population. The experimental opioid-sparing group received 30-mg ketorolac intravenously every 6 hours and 1-g acetaminophen orally every 6 hours as the patient requested. The experimental group had the option to use morphine and oxycodone combined with acetaminophen as a rescue therapy. The control group received opioids in the form of 0.1-mg/kg morphine intravenously every 6 hours and/or oxycodone combined with acetaminophen (2.5 and 325 mg), 2 tablets orally every 6 hours, as the patient requested. Sociodemographic, operative, and immediate postoperative data and pain intensity measurements according to the numerical rating scale (NRS) were compared between groups. Analgesic efficacy was assessed according to the NRS scores at 12, 24, and 48 hours postoperatively. Results:. Eighty-one Hispanic patients met inclusion criteria: 42 patients in the experimental group and 39 patients in the control group. None of the patients in the experimental group requested oxycodone combined with acetaminophen as a rescue therapy. Only 2 patients in the experimental group used a mean of 3.0 ± 1.4 mg of rescue morphine; in comparison, the control group consumed a mean of 28.0 ± 7.9 mg of morphine and 64.8 ± 26.0 mg of oxycodone per patient. A pain intensity decrease was observed in the experimental and control groups, with no postoperative evaluation differences at 12 hours (6.7 ± 2.9 compared with 5.9 ± 2.8; p = 0.209), 24 hours (6.2 ± 2.0 compared with 6.1 ± 2.2; p = 0.813), and 48 hours (4.7 ± 2.1 compared with 4.6 ± 1.7; p = 0.835). Conclusions:. The use of a multimodal analgesic regimen based on intravenous ketorolac and oral acetaminophen was adequate in reducing postoperative pain and opioid consumption in Hispanic patients undergoing TKA. Level of Evidence:. Therapeutic Level I. See Instructions for Authors for a complete description of levels of evidence

Implications of the Estrogen Receptor Coactivators SRC1 and SRC2 in the Biological Basis of Gender Incongruence

ABSTRACT: Introduction: Brain sexual differentiation results from the effects of sex steroids on the developing brain. The presumptive route for brain masculinization is the direct induction of gene expression via activation of the estrogen receptors α and β and the androgen receptor through their binding to ligands and to coactivators, regulating the transcription of multiple genes in a cascade effect. Aim: To analyze the implication of the estrogen receptor coactivators SRC-1, SRC-2, and SRC-3 in the genetic basis of gender incongruence. Main Outcome Measures: Analysis of 157 polymorphisms located at the estrogen receptor coactivators SRC-1, SRC-2, and SRC-3, in 94 transgender versus 94 cisgender individuals. Method: Using SNPStats software, the allele and genotype frequencies were analyzed by χ2, the strength of the association was measured by binary logistic regression, estimating the odds ratio for each genotype. Measurements of linkage disequilibrium and haplotype frequencies were also performed. Results: We found significant differences at level P < .05 in 8 polymorphisms that correspond to 5.09% of the total. Three were located in SRC-1 and 5 in SRC-2. The odds ratio analysis showed significant differences at level P < .05 for multiple patterns of inheritance. The polymorphisms analyzed were in linkage disequilibrium. The SRC-1 haplotypes CGA and CGG (global haplotype association P < .009) and the SRC-2 haplotypes GGTAA and GGTAG (global haplotype association P < .005) were overrepresented in the transgender population. Conclusion: The coactivators SRC-1 and SRC-2 could be considered as candidates for increasing the list of potential genes for gender incongruence. Ramírez KDV, Fernández R, Delgado-Zayas E, et al. Implications of the Estrogen Receptor Coactivators SRC1 and SRC2 in the Biological Basis of Gender Incongruence. Sex Med 2021;9:100368