White Families' Communications About and Around Race: Conversations Between white Adolescents and Their Mothers.

Though there is substantial research on racial socialization in families of color, there is less on such socialization in white families. To investigate racial socialization in white families, the current study analyzed mixed-methods data from 46 mother-adolescent dyads. Though white parents and their adolescent children largely claimed to not talk about race, they in fact communicated about and around race through various strategies that in effect, maintained white privilege and failed to challenge systems of racial oppression. Very few families in our sample discussed racial discrimination or white privilege, and fewer rooted both at the systems level. Our results highlight situations that prompt conversations about race as well as the ways white families talk about and around race and white privilege.

Lessons of Resistance from Black Mothers to their Black Sons.

In negotiating the anti-Black oppression, Black mothers communicate lessons of resistance in their racial socialization messages to their Black adolescent boys. We investigate whether distinct strategies of resistance for survival, characterized by individual-focused immediate strategies of resistance, and resistance for liberation, strategies of resistance that disrupt systems of anti-Black oppression rooted in furthering collective Black empowerment, are employed in Black mothers' messages to their sons. In this manuscript, we use longitudinal data of Black mothers' of adolescent boys interviews (N = 31) across three time points (6th-11th grade). Our findings indicate the presence of various strategies of resistance for survival and resistance for liberation within Black mothers' preparation for bias socialization.

A randomized, double-blind, placebo-controlled trial on intravenous ibuprofen L-lysine for the early closure of nonsymptomatic patent ductus arteriosus within 72 hours of birth in extremely low-birth-weight infants.

A multicenter, double-blind, randomized, placebo-controlled trial was conducted to evaluate the efficacy and safety of intravenous (IV) ibuprofen (L-lysine) for the early closure of nonsymptomatic patent ductus arteriosus (PDA) within 72 hours of birth in extremely low-birth-weight (ELBW) infants with evidence of ductal shunting by echocardiogram. Eleven sites enrolled 136 infants with nonsymptomatic early PDA (gestational age < 30 weeks; body weight 500 to 1000 g) to receive a 3-day course (10 mg/kg, 5 mg/kg, and 5 mg/kg) of IV ibuprofen ( N = 68) or placebo ( N = 68). Cardiac echocardiogram was performed on study days 1 and 14, and with rescue. Infants were followed to 36 weeks postconceptional age. Patient demographics, mean (standard deviation), were similar between ibuprofen and placebo: birth weight: 798.5 g (128.7) versus 797.3 g (132.8); gestational age: 26.1 weeks (1.3) versus 26.2 weeks (1.4); and age at first dose: 1.5 days (0.7). The intent-to-treat analysis of the primary endpoint, subjects rescued, died, or dropped through study day 14, was 21/68 (30.9%) with ibuprofen and 36/68 (52.9%) for placebo ( P = 0.005). Death, intraventricular hemorrhage, necrotizing enterocolitis, daily fluid intake/output, liver function, bronchopulmonary dysplasia, and retinopathy of prematurity did not differ. A trend toward decreased periventricular leukomalacia by ibuprofen was noted. IV ibuprofen was effective and safe in the early closure of PDA in preterm neonates.

Mechanisms modulating estrogen-induced uterine vasodilation.

Estrogen, a potent vasodilator, has its greatest effects in reproductive tissues, e.g., increasing uterine blood flow (UBF) 5- to 10-fold within 90 min after a bolus dose. High-conductance potassium channels and nitric oxide (NO) contribute to the uterine responses, but other factors may be involved. We examined the role of ATP-dependent (ATP-sensitive) and voltage-gated (Kv) potassium channels and new protein synthesis in ovariectomized ewes with uterine artery flow probes, infusing intraarterial inhibitors glibenclamide (GLB; KATP), 4-aminopyridine (4-AP; Kv) or cycloheximide, respectively, into one uterine horn before and/or after systemic estradiol-17 beta (E2 beta, 1 microgram/kg i.v.). E2 beta alone increased UBF > 5-fold and heart rate by 10-25% (P < .01) within 90 min; mean arterial pressure (MAP) was unaffected. GLB did not alter basal hemodynamic parameters or responses to E2 beta. Basal UBF and heart rate were unaffected by 4-AP, but MAP increased by 10% and 25% at 30 and 120 min of infusion (P < .01), respectively. Although E2 beta-induced rises in UBF were unaffected in the control uterine horn, 4-AP dose-dependently inhibited UBF responses in the infused horn (R = .83, P = .003, n = 10). Cycloheximide not only dose-dependently inhibited UBF responses (R = .57, P = .01, n = 18) and increases in uterine cGMP secretion, 23.4 +/- 10.7 versus 340 +/- 60 pmol/min (P < .001), but also decreased UBF by 50% and cGMP by approximately 90% at the time of maximum UBF. Mechanisms modulating estrogen-induced uterine vasodilation involve signaling pathways that include NO, smooth muscle cGMP, smooth muscle potassium channels and new protein synthesis.

Pretreatment of yellow pine in an acidic ionic liquid: extraction of hemicellulose and lignin to facilitate enzymatic digestion.

The acidic ionic liquid 1-H-3-methylimidazolium chloride can effectively pretreat yellow pine wood chips under mild conditions for enzymatic saccharification. Wood samples were treated at temperatures between 110 and 150°C for up to 5 h in the ionic liquid and three fractions collected; a cellulose rich fraction, lignin, and an aqueous fraction. This treatment caused the hemicellulose and the lignin to be degraded and dissolved from the cell walls of the pine wood. The lignin was depolymerized and subsequently dissolved in the ionic liquid. This process occurred more quickly at higher temperatures, although at the highest temperatures tested, significant cellulose degradation also occurred. The cellulose rich fraction was saccharified using cellulase from Trichoderma viride, with longer pretreatment times at 130°C resulting in higher glucose yields.

Depolymerization of oak wood lignin under mild conditions using the acidic ionic liquid 1-H-3-methylimidazolium chloride as both solvent and catalyst.

Oak wood lignin, which was separated from the wood using dissolution in the ionic liquid 1-methyl-3-ethylimidazolium acetate and subsequent precipitation, was successfully depolymerized in the acidic ionic liquid 1-H-3-methylimidazolium chloride under mild conditions (110-150 °C). Based on gel permeation chromatography results, an increase in temperature from 110 to 150 °C increased the rate of reaction, but did not significantly change the final size of the lignin fragments. Nuclear magnetic resonance and infrared spectroscopy were utilized to demonstrate that the depolymerization proceeded via a hydrolysis reaction that cleaved the alkyl-aryl ether linkages. Coupling of the lignin fragments was also shown to occur in the reaction mixture. These hydrolysis results are consistent with the literature on acid catalyzed depolymerization of lignin in conventional solvents and with recent model compound studies involving guaiacylglycerol-ß-guaiacyl ether and veratrylglycerol-ß-guaiacyl ether done in acidic ionic liquids.

Cleaving the ß--O--4 bonds of lignin model compounds in an acidic ionic liquid, 1-H-3-methylimidazolium chloride: an optional strategy for the degradation of lignin.

The hydrolysis of ß--O--4 bonds in two lignin model compounds was studied in an acidic ionic liquid, 1-H-3-methylimidazolium chloride. The ß--O--4 bonds of both guaiacylglycerol-ß-guaiacyl ether and veratrylglycerol-ß-guaiacyl ether underwent catalytic hydrolysis to produce guaiacol as the primary product with more than 70 % yield at 150 °C. Up to 32 wt % substrate concentration could be treated in the system without a decrease in guaiacol production. The ionic liquid could be reused without loss of activity in guaiacol production from both guaiacylglycerol-ß-guaiacyl ether and veratrylglycerol-ß-guaiacyl ether. A possible mechanism accounting for the guaiacol production is presented.

Vascular development in early ovine gestation: carotid smooth muscle function, phenotype, and biochemical markers.

Vascular smooth muscle (VSM) maturation is developmentally regulated and differs between vascular beds. The maturation and contribution of VSM function to tissue blood flow and blood pressure regulation during early gestation are unknown. The carotid artery (CA) contributes to fetal cerebral blood flow regulation and well being. We studied CA VSM contractility, protein contents, and phenotype beginning in the midthird of ovine development. CAs were collected from early (88-101 day of gestation) and late (138-150 day; term = day 150) fetal (n = 14), newborn (6-8 day old; n = 7), and adult (n = 5) sheep to measure forces in endothelium-denuded rings with KCl, phenylephrine, and ANG II; changes in cellular proteins, including total and soluble protein, actin and myosin, myosin heavy chain isoforms (MHC), filamin, and proliferating cell nuclear antigen; and vascular remodeling. KCl and phenylephrine elicited age- and dose-dependent contraction responses (P < 0.001) at all ages except early fetal, which were unresponsive. In contrast, ANG II elicited dose responses only in adults, with contractility increasing greater than fivefold vs. that shown in fetal or neonatal animals (P < 0.001). Increased contractility paralleled age-dependent increases (P < 0.01) in soluble protein, actin and myosin, filamin, adult smooth muscle MHC-2 (SM2) and medial wall thickness and reciprocal decreases (P < 0.001) in nonmuscle MHC-B, proliferating cell nuclear antigen and medial cellular density. VSM nonreceptor- and receptor-mediated contractions are absent or markedly attenuated in midgestation and increase age dependently, paralleling the transition from synthetic to contractile VSM phenotype and, in the case of ANG II, paralleling the switch to the AT(1) receptor. The mechanisms regulating VSM maturation and thus blood pressure and tissue perfusion in early development remain to be determined.

Large-conductance Ca2+-dependent K+ channels regulate basal uteroplacental blood flow in ovine pregnancy.

OBJECTIVES: The mechanisms regulating basal uteroplacental blood flow (UBF) and the greater than 30-fold increase observed in normal pregnancy remain unclear. Although vascular growth contributes in early gestation, vasodilation accounts for the exponential rise seen in the last third of pregnancy. Large conductance potassium channels (BK(Ca)) are expressed in uterine vascular smooth muscle (VSM), but the extent of their role in regulating UBF in pregnancy is unclear. Therefore, we determined if BK(Ca) regulate basal UBF during ovine pregnancy. METHODS: Studies were performed at 113 to 127 days and 135 to 150 days of gestation in eight pregnant ewes instrumented with uterine artery flow probes and uterine arterial and venous catheters. Tetraethylammonium chloride (TEA), a BK(Ca)-specific inhibitor at less than 1.0 mM, was infused intra-arterially into the pregnant uterine horn over 60 minutes to achieve levels of 0.001-0.35 mM while continuously monitoring UBF, arterial pressure (MAP), and heart rate (HR). Uterine arterial and venous blood was collected simultaneously to measure uterine cyclic guanosine monophosphate (cGMP) synthesis. RESULTS: Intra-arterial TEA dose-dependently decreased basal UBF in the early (R = 0.81, n = 36, P <.001) and late (R = 0.72, n = 31, P <.001) study periods without altering contralateral UBF, MAP, and HR. The IC(50) was 0.2 mM and basal UBF decreased >or=80% at 0.35 mM in both periods. Although UBF fell greater than 40% at estimated plasma TEA levels of 0.3 mM, uterine arterial cGMP was unchanged, uterine venous cGMP rose, and uterine cGMP synthesis was unchanged; therefore, upstream events associated with BK(Ca) activation were unaffected by blockade. CONCLUSIONS: These are the first data demonstrating that BK(Ca) are essential in the maintenance of basal UBF in the last third of ovine pregnancy.

Vessel-specific regulation of angiotensin II receptor subtypes during ovine development.

Umbilical and systemic responses to angiotensin II differ in term fetal sheep, and peripheral vascular responses are attenuated or absent before and after birth. These observations may reflect developmental differences in angiotensin II receptor (AT) subtypes in vascular smooth muscle (VSM). Studies of AT subtype ontogeny and regulation are generally limited to the aorta, which may not be extrapolated to other arteries, and neither is completely described during ovine development. We therefore characterized VSM AT subtype expression and regulation throughout an extended period of development in umbilical and carotid artery and aorta from fetal (85-146 d gestation), postnatal (5-23 d), and adult sheep, measuring AT(1) and AT(2) mRNA and protein and performing immunohistochemistry. Parallel increases in umbilical AT(1) mRNA and protein began early in gestation and continued to term, and although AT(2) mRNA was unchanged, protein levels decreased >90% at term. Fetal carotid AT(1) mRNA was <40% of adult values and unchanged before birth; however, AT(1) protein rose >2-fold at term. After birth, AT(1) mRNA increased to 85% of adult values and was associated with another 2-fold rise in protein. In contrast, carotid AT(2) mRNA and protein fell in parallel throughout development and were barely detectable in the newborn and the adult. Immunostaining was consistent with observations in both arteries. A third pattern occurred in aortic VSM. The ontogeny of AT subtype expression and regulation is vessel specific, with changes in umbilical VSM beginning very early in development. Although the mechanisms that regulate mRNA and protein expression are unclear, these changes parallel differences in VSM maturation and function and local blood flow.

Angiotensin II mediates uterine vasoconstriction through alpha-stimulation.

Intravenous angiotensin II (ANG II) increases uterine vascular resistance (UVR), whereas uterine intra-arterial infusions do not. Type 2 ANG II (AT(2)) receptors predominate in uterine vascular smooth muscle; this may reflect involvement of systemic type 1 ANG II (AT(1)) receptor-mediated alpha-adrenergic activation. To examine this, we compared systemic pressor and UVR responses to intravenous phenylephrine and ANG II without and with systemic or uterine alpha-receptor blockade and in the absence or presence of AT(1) receptor blockade in pregnant and nonpregnant ewes. Systemic alpha-receptor blockade inhibited phenylephrine-mediated increases in mean arterial pressure (MAP) and UVR, whereas uterine alpha-receptor blockade alone did not alter pressor responses and resulted in proportionate increases in UVR and MAP. Although neither systemic nor uterine alpha-receptor blockade affected ANG II-mediated pressor responses, UVR responses decreased >65% and also were proportionate to increases in MAP. Systemic AT(1) receptor blockade inhibited all responses to intravenous ANG II. In contrast, uterine AT(1) receptor blockade + systemic alpha-receptor blockade resulted in persistent proportionate increases in MAP and UVR. Uterine AT(2) receptor blockade had no effects. We have shown that ANG II-mediated pressor responses reflect activation of systemic vascular AT(1) receptors, whereas increases in UVR reflect AT(1) receptor-mediated release of an alpha-agonist and uterine autoregulatory responses.