The nurse's role in a patient-centered approach for reducing COVID-19 vaccine hesitancy during pregnancy: An American Academy of Nursing consensus paper.

The evidence shows that COVID-19 vaccines can reduce the risks of poor pregnancy outcomes. Yet, reluctance to vaccinate remains high in pregnant populations. In this paper, we take a precision health and patient-centered approach to vaccine hesitancy. We adopted the society-to-cells vaccine hesitancy framework to identify society, community, family, individual, and physiologic factors contributing to COVID-19 vaccine hesitancy in pregnancy. Nurses are particularly well-suited to impact the factors associated with vaccine hesitancy. Because of their proximity to the patient, nurses are positioned to provide individualized, timely health information, and clinical guidelines to assist patients with decision-making related to vaccinations. Recommendations are provided to bolster nurses' engagement in precision health and patient-centered models of care to mitigate COVID-19 vaccine hesitancy in pregnancy.

Glycoprotein hormone subunit alpha 2 (GPHA2): A pituitary stem cell-expressed gene associated with NOTCH2 signaling.

NOTCH2 is expressed in pituitary stem cells and is necessary for stem cell maintenance, proliferation, and differentiation. However, the pathways NOTCH2 engages to affect pituitary development remain unclear. In this study, we hypothesized that glycoprotein hormone subunit A2 (GPHA2), a corneal stem cell factor and ligand for the thyroid stimulating hormone receptor (TSHR), is downstream of NOTCH2 signaling. We found Gpha2 is expressed in quiescent pituitary stem cells by RNAscope in situ hybridization and scRNA seq. In Notch2 conditional knockout pituitaries, Gpha2 mRNA is reduced compared with control littermates. We then investigated the possible functions of GPHA2. Pituitaries treated with a GPHA2 peptide do not have a change in proliferation. However, in dissociated adult pituitary cells, GPHA2 increased pCREB expression and this induction was reversed by co-treatment with a TSHR inhibitor. These data suggest GPHA2 is a NOTCH2 related stem cell factor that activates TSHR signaling, potentially impacting pituitary development.

Characterization of Somatotrope Cell Expansion in Response to GHRH in the Neonatal Mouse Pituitary.

In humans and mice, loss-of-function mutations in growth hormone-releasing hormone receptor (GHRHR) cause isolated GH deficiency. The mutant GHRHR mouse model, GhrhrLit/Lit (LIT), exhibits loss of serum GH, but also fewer somatotropes. However, how loss of GHRH signaling affects expansion of stem and progenitor cells giving rise to GH-producing cells is unknown. LIT mice and wild-type littermates were examined for differences in proliferation and gene expression of pituitary lineage markers by quantitative reverse transcription polymerase chain reaction and immunohistochemistry at postnatal day 5 (p5) and 5 weeks. At p5, the LIT mouse shows a global decrease in pituitary proliferation measured by proliferation marker Ki67 and phospho-histone H3. This proliferative defect is seen in a pituitary cell expressing POU1F1 with or without GH. SOX9-positive progenitors show no changes in proliferation in p5 LIT mice. Additionally, the other POU1F1 lineage cells are not decreased in number; rather, we observe an increase in lactotrope cell population as well as messenger RNA for Tshb and Prl. In the 5-week LIT pituitary, the proliferative deficit in POU1F1-expressing cells observed neonatally persists, while the number and proliferative proportion of SOX9 cells do not appear changed. Treatment of cultured pituitary explants with GHRH promotes proliferation of POU1F1-expressing cells, but not GH-positive cells, in a mitogen-activated protein kinase-dependent manner. These findings indicate that hypothalamic GHRH targets proliferation of a POU1F1-positive cell, targeted to the somatotrope lineage, to fine tune their numbers.

Prenatal and postnatal exposure to polychlorinated biphenyls alter follicle numbers, gene expression, and a proliferation marker in the rat ovary.

Polychlorinated biphenyls (PCBs) were used in industrial applications until they were banned in the 1970s, but they still persist in the environment. Little is known about the long-term effects of exposure to PCB mixtures on the rat ovary during critical developmental periods. Thus, this study tested whether prenatal and postnatal exposures to PCBs affect follicle numbers and gene expression in the ovaries of F1 offspring. Sprague-Dawley rats were treated with vehicle or Aroclor 1221 (A1221) at 1 mg/kg/day during embryonic days 8-18 and/or postnatal days (PND) 1-21. Ovaries from F1 rats were collected for assessment of follicle numbers and differential expression of estrogen receptor 1 (Esr1), estrogen receptor 2 (Esr2), androgen receptor (Ar), progesterone receptor (Pgr), and Ki-67 (Ki67) at PNDs 8, 32, and 60. Sera were collected for measurement of estradiol concentrations. Prenatal exposure to A1221 significantly decreased the number of primordial follicles and the total number of follicles at PND 32 compared to control. Postnatal PCB exposure borderline increased Ki67 gene expression and significantly increased Ki67 protein levels (PND 60) compared to control. Combined prenatal and postnatal PCB exposure borderline decreased Ar expression (PND 8) compared to control. However, PCB exposure did not significantly affect the expression of Pgr, Esr1, and Esr2 or serum estradiol concentrations compared to control at any time point. In conclusion, these data suggest that PCB exposure affects follicle numbers and levels of the proliferation marker Ki67, but it does not affect expression of some sex steroid hormone receptors in the rat ovary.

Pre- and postnatal developmental exposure to the polychlorinated biphenyl mixture aroclor 1221 alters female rat pituitary gonadotropins and estrogen receptor alpha levels.

Polychlorinated-biphenyls (PCBs) are industrial compounds, which were widely used in manufacturing of electrical parts and transformers. Despite being banned in 1979 due to human health concerns, they persist in the environment. In humans and experimental model systems, PCBs elicit toxicity in part by acting as endocrine-disrupting chemicals (EDCs). Aroclor 1221 (A1221) is a weakly estrogenic PCB mixture known to alter reproductive function in rodents. EDCs can impact hormone signaling at any level of the hypothalamic-pituitary-gonadal (HPG) axis, and we investigated the effects of A1221 exposure during the prenatal and postnatal developmental periods on pituitary hormone and steroid receptor expression in female rats. Examining offspring at 3 ages, postnatal day 8 (P8), P32 and P60, we found that prenatal exposure to A1221 increased P8 neonate pituitary luteinizing hormone beta (Lhb) mRNA and LHß gonadotrope cell number while decreasing LH serum hormone concentration. No changes in pituitary hormone or hormone receptor gene expression were observed peri-puberty at P32. In reproductively mature rats at P60, we found pituitary follicle stimulating hormone beta (Fshb) mRNA levels increased by prenatal A1221 exposure with no corresponding alterations in FSH hormone or FSHß expressing cell number. Estrogen receptor alpha (ERα) mRNA and protein levels were also increased at P60, but only following postnatal A1221 dosing. Together, these data illustrate that exposure to the PCB A1221, during critical developmental windows, alters pituitary gonadotropin hormone subunits and ERα levels in offspring at different phases of maturation, potentially impacting reproductive function in concert with other components of the HPG axis.

Female-specific pituitary gonadotrope dysregulation in mice with chronic focal epilepsy.

Gonadotropin hormone release from the anterior pituitary is critical to regulating reproductive endocrine function. Clinical evidence has documented that people with epilepsy display altered levels of gonadotropin hormones, both acutely following seizures and chronically. Despite this relationship, pituitary function remains a largely understudied avenue in preclinical epilepsy research. Recently, we showed that females in the intrahippocampal kainic acid (IHKA) mouse model of temporal lobe epilepsy displayed changes in pituitary expression of gonadotropin hormone and gonadotropin-releasing hormone (GnRH) receptor genes. Circulating gonadotropin hormone levels, however, have yet to be measured in an animal model of epilepsy. Here, we evaluated the circulating levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), GnRH receptor (Gnrhr) gene expression, and sensitivity to exogenous GnRH in IHKA males and females. Although no changes in overall dynamics of pulsatile patterns of LH release were found in IHKA mice of either sex, estrus vs. diestrus changes in basal and mean LH levels were larger in IHKA females with prolonged, disrupted estrous cycles. In addition, IHKA females displayed increased pituitary sensitivity to GnRH and higher Gnrhr expression. The hypersensitivity to GnRH was observed on diestrus, but not estrus. Chronic seizure severity was not found to be correlated with LH parameters, and FSH levels were unchanged in IHKA mice. These results indicate that although there are changes in pituitary gene expression and sensitivity to GnRH in IHKA females, there may also be compensatory mechanisms that aid in maintaining gonadotropin release in the state of chronic epilepsy in this model.

Prenatal exposure to the phthalate DEHP impacts reproduction-related gene expression in the pituitary.

Phthalates are chemicals used in products including plastics, personal care products, and building materials, leading to widespread contact. Previous studies on prenatal exposure to Di-(2-ethylhexyl) phthalate (DEHP) in mice and humans demonstrated pubertal timing and reproductive performance could be affected in exposed offspring. However, the impacts at the pituitary, specifically regarding signaling pathways engaged and direct effects on the gonadotropins LH and FSH, are unknown. We hypothesized prenatal exposure to DEHP during a critical period of embryonic development (e15.5 to e18.5) will cause sex-specific disruptions in reproduction-related mRNA expression in offspring's pituitary due to interference with androgen and aryl hydrocarbon receptor (AhR) signaling. We found that prenatal DEHP exposure in vivo caused a significant increase in Fshb specifically in males, while the anti-androgen flutamide caused significant increases in both Lhb and Fshb in males. AhR target gene Cyp1b1 was increased in both sexes in DEHP-exposed offspring. In embryonic pituitary cultures, the DEHP metabolite MEHP increased Cyp1a1 and Cyp1b1 mRNA in both sexes and Cyp1b1 induction was reduced by co-treatment with AhR antagonist. AhR reporter assay in GHFT1 cells confirmed MEHP can activate AhR signaling. Lhb, Fshb and Gnrhr mRNA were significantly decreased in both sexes by MEHP, but co-treatment with AhR antagonist did not restore mRNA levels in pituitary culture. In summary, our data suggest phthalates can directly affect the function of the pituitary by activating AhR signaling and altering gonadotropin expression. This indicates DEHP's impacts on the pituitary could contribute to reproductive dysfunctions observed in exposed mice and humans.

Iodoacetic Acid, a Water Disinfection Byproduct, Disrupts Hypothalamic, and Pituitary Reproductive Regulatory Factors and Induces Toxicity in the Female Pituitary.

Iodoacetic acid (IAA) is a water disinfection byproduct (DBP) formed by reactions between oxidizing disinfectants and iodide. In vitro studies have indicated that IAA is one of the most cyto- and genotoxic DBPs. In humans, DBPs have been epidemiologically associated with reproductive dysfunction. In mouse ovarian culture, IAA exposure significantly inhibits antral follicle growth and reduces estradiol production. Despite this evidence, little is known about the effects of IAA on the other components of the reproductive axis: the hypothalamus and pituitary. We tested the hypothesis that IAA disrupts expression of key neuroendocrine factors and directly induces cell damage in the mouse pituitary. We exposed adult female mice to IAA in drinking water in vivo and found 0.5 and 10 mg/l IAA concentrations lead to significantly increased mRNA levels of kisspeptin (Kiss1) in the arcuate nucleus although not affecting Kiss1 in the anteroventral periventricular nucleus. Both 10 mg/l IAA exposure in vivo and 20 µM IAA in vitro reduced follicle stimulating hormone (FSHß)-positive cell number and Fshb mRNA expression. IAA did not alter luteinizing hormone (LHß) expression in vivo although exposure to 20 µM IAA decreased expression of Lhb and glycoprotein hormones, alpha subunit (Cga) mRNA in vitro. IAA also had toxic effects in the pituitary, inducing DNA damage and P21/Cdkn1a expression in vitro (20 µM IAA) and DNA damage and Cdkn1a expression in vivo (500 mg/l). These data implicate IAA as a hypothalamic-pituitary-gonadal axis toxicant and suggest the pituitary is directly affected by IAA exposure.

Associations between Physiological Biomarkers and Psychosocial Measures of Pregnancy-Specific Anxiety and Depression with Support Intervention.

Stress and anxiety significantly impact the hypothalamic-pituitary axis, and in pregnancy, the subsequent maternal-fetal response can lead to poor outcomes. The objective of this study was to assess the association between psychosocial measures of pregnancy-specific anxiety and physiologic inflammatory responses. Specifically, to determine the effectiveness of the Mentors Offering Maternal Support (M-O-M-STM) program to reduce psychosocial anxiety and associated inflammatory response. In conjunction with measures of pregnancy-specific anxiety and depression, serum biomarkers (IL-2, IL-6, IL-10, IL1-B, TNF-α, CRH, CRP, and cortisol) were analyzed for each trimester throughout pregnancy. Results demonstrated that women receiving the M-O-M-STM intervention had longitudinally sustained lower TNF-α/IL-10 ratios than the control group, and it was significantly associated with psychosocial measures of anxiety, specifically for fears of labor and spouse/partner relationships. Additionally, the anxiety of spouse/partner relationships was significantly associated with IL-6/IL-10 ratios. The findings highlight the important counter-regulatory relationship between anti- and pro-inflammatory cytokines and provide insight into the distinct physiologic responses to pregnancy-specific anxiety with early prenatal intervention.

Risk of Preterm Birth and Newborn Low Birthweight in Military Women with Increased Pregnancy-Specific Anxiety.

INTRODUCTION: Prenatal maternal anxiety and depression have been implicated as possible risk factors for preterm birth (PTB) and other poor birth outcomes. Within the military, maternal conditions account for 15.3% of all hospital bed days, and it is the most common diagnostic code for active duty females after mental disorders. The majority of women (97.6%) serving on active duty are women of childbearing potential. Understanding the impact that prenatal maternal anxiety and depression can have on PTB and low birthweight (LBW) in a military population is critical to providing insight into biological pathways that alter fetal development and growth. The purpose of the study was to determine the impact of pregnancy-specific anxiety and depression on PTB and LBW within a military population. MATERIAL AND METHODS: Pregnancy-specific anxiety and depression were measured for 246 pregnant women in each trimester. Individual slopes for seven different measures of pregnancy anxiety and one depression scale were calculated using linear mixed models. Logistic regression, adjusted and unadjusted models, were applied to determine the impact on PTB and LBW. RESULTS: For each 1/10 unit increase in the anxiety slope as it related to well-being, the risk of LBW increased by 83% after controlling for parity, PTB, and active duty status. Similarly, a 1/10 unit rise in the anxiety slope related to accepting pregnancy, labor fears, and helplessness increased the risk of PTB by 37%, 60%, and 54%, respectively. CONCLUSIONS: Pregnancy-specific anxiety was found to significantly increase the risk of PTB and LBW in a military population. Understanding this relationship is essential in developing effective assessments and interventions. Results emphasize the importance of prenatal maternal mental health to fetal health and birth outcomes. Further research is needed to determine the specific physiological pathways that link prenatal anxiety and depression with poor birth outcomes.

Genistein inhibits proliferation and induces senescence in neonatal mouse pituitary gland explant cultures.

Genistein is an isoflavone abundant in soybean and infants are exposed to high levels of genistein in soy-based formula. It is known that genistein mediates estrogen receptor (ER) signaling, and exposure during neonatal development could cause acute and long term endocrine effects. We assayed genistein's impact on the neonatal mouse pituitary gland because it is an endocrine signaling hub and is sensitive to endocrine disruption during critical periods. Pituitary explant cultures, which actively proliferate and differentiate, were exposed to 0.06 µM-36 µM genistein and assayed for mRNA and protein changes. Genistein induced mRNA expression of the ERα regulated gene, Cckar, to the same magnitude as estradiol (E2) but with less potency. Interestingly, 36 µM genistein strongly inhibited pituitary proliferation, measured by a reduction in mKi67 mRNA and phospho-Histone H3 immunostaining. Examining cell cycle dynamics, we found that 36 µM genistein decreased Ccnb1 (Cyclin B1) mRNA; while mRNA for the cyclin dependent kinase inhibitor Cdkn1a (p21) was upregulated, correlated with an apparent increase in p21 immunostained cells. Strikingly, we observed a robust onset of cellular senescence, permanent cell cycle exit, in 36 µM genistein treated pituitaries by increased senescence activated ß-galactosidase staining. We also found that 36 µM genistein decreased Bcl2 mRNA levels, a gene protective against apoptosis. Taken together these data suggest that genistein exposure during the neonatal period could initiate senescence and halt proliferation during a time when the proper numbers of endocrine cells are being established for mature gland function.

Cellular fate decisions in the developing female anteroventral periventricular nucleus are regulated by canonical Notch signaling.

The hypothalamic anteroventral periventricular nucleus (AVPV) is the major regulator of reproductive function within the hypothalamic-pituitary-gonadal (HPG) axis. Despite an understanding of the function of neuronal subtypes within the AVPV, little is known about the molecular mechanisms regulating their development. Previous work from our laboratory has demonstrated that Notch signaling is required in progenitor cell maintenance and formation of kisspeptin neurons of the arcuate nucleus (ARC) while simultaneously restraining POMC neuron number. Based on these findings, we hypothesized that the Notch signaling pathway may act similarly in the AVPV by promoting development of kisspeptin neurons at the expense of other neuronal subtypes. To address this hypothesis, we utilized a genetic mouse model with a conditional loss of Rbpj in Nkx2.1 expressing cells (Rbpj cKO). We noted an increase in cellular proliferation, as marked by Ki-67, in the hypothalamic ventricular zone (HVZ) in Rbpj cKO mice at E13.5. This corresponded to an increase in general neurogenesis and more TH-positive neurons. Additionally, an increase in OLIG2-positive early oligodendrocytic precursor cells was observed at postnatal day 0 in Rbpj cKO mice. By 5 weeks of age in Rbpj cKO mice, TH-positive cells were readily detected in the AVPV but few kisspeptin neurons were present. To elucidate the direct effects of Notch signaling on neuron and glia differentiation, an in vitro primary hypothalamic neurosphere assay was employed. We demonstrated that treatment with the chemical Notch inhibitor DAPT increased mKi67 and Olig2 mRNA expression while decreasing astroglial Gfap expression, suggesting Notch signaling regulates both proliferation and early glial fate decisions. A modest increase in expression of TH in both the cell soma and neurite extensions was observed after extended culture, suggesting that inhibition of Notch signaling alone is enough to bias progenitors towards a dopaminergic fate. Together, these data suggest that Notch signaling restricts early cellular proliferation and differentiation of neurons and oligodendrocytes both in vivo and in vitro and acts as a fate selector of kisspeptin neurons.

Mentors Offering Maternal Support Reduces Prenatal, Pregnancy-Specific Anxiety in a Sample of Military Women.

OBJECTIVE: To determine the efficacy of the Mentors Offering Maternal Support (MOMS) program to reduce pregnancy-specific anxiety and depression and build self-esteem and resilience in military women. DESIGN: Randomized controlled trial with repeated measures. SETTING: Large military community in Texas. PARTICIPANTS: Pregnant women (N = 246) in a military sample defined as active duty or spouse of military personnel. METHODS: Participants were randomized in the first trimester to the MOMS program or normal prenatal care. Participants attended eight 1-hour sessions every other week during the first, second, and third trimesters of pregnancy. Pregnancy-specific anxiety, depression, self-esteem, and resilience were measured in each trimester. Linear mixed models were used to compare the two-group difference in slope for prenatal anxiety, depression, self-esteem, and resilience. RESULTS: The Prenatal Self-Evaluation Questionnaire was used to measure perinatal anxiety. Rates of prenatal anxiety on the Identification With a Motherhood Role (p = .049) scale and the Preparation for Labor (p = .017) scale were significantly reduced for participants in MOMS. Nulliparous participants showed significantly lower anxiety on the Acceptance of Pregnancy scale and significantly greater anxiety on the Preparation for Labor scale. Single participants had significantly greater anxiety on the Well-Being of Self and Baby in Labor scale, and participants with deployed husbands had significantly greater anxiety on the Identification With a Motherhood Role scale. CONCLUSION: Participation in the MOMS program reduced pregnancy-specific prenatal anxiety for the dimensions of Identification With a Motherhood Role and Preparation for Labor. Both dimensions of anxiety were previously found to be significantly associated with preterm birth and low birth weight. Military leaders have recognized the urgent need to support military families.

Isoliquiritigenin exhibits anti-proliferative properties in the pituitary independent of estrogen receptor function.

The plant flavonoid isoliquiritigenin (ISL) is a botanical estrogen widely taken as an herbal supplement to ease the symptoms of menopause. ISL has been also shown to have anti-tumor properties in a number of cancer cell backgrounds. However, the effects of ISL on normal cells are less well known and virtually unstudied in the context of the pituitary gland. We have established a pituitary explant culture model to screen chemical agents for gene expression changes within the pituitary gland during a period of active proliferation and differentiation. Using this whole-organ culture system we found ISL to be weakly estrogenic based on its ability to induce Cckar mRNA expression, an estrogen receptor (ER) mediated gene. Using a range of ISL from 200nM to 200µM, we discovered that ISL promoted cell proliferation at a low concentration, yet potently inhibited proliferation at the highest concentration. ICI 182,780 failed to antagonize ISL's repression of pituitary cell proliferation, indicating the effect is independent of ER signaling. Coincident with a decrease in proliferating cells, we observed down-regulation of transcript for cyclin D2 and E2 and a strong induction of mRNA and protein for the cyclin dependent kinase inhibitor Cdkn1a (p21). Importantly, high dose ISL did not alter the balance of progenitor vs. differentiated cell types within the pituitary explants and they seemed otherwise healthy; however, TUNEL staining revealed an increase in apoptotic cell death in ISL treated cultures. Our results merit further examination of ISL as an anti-tumor agent in the pituitary gland.

Icam5 Expression Exhibits Sex Differences in the Neonatal Pituitary and Is Regulated by Estradiol and Bisphenol A.

Endocrine-disrupting chemicals are prevalent in the environment and can impair reproductive success by affecting the hypothalamic-pituitary-gonadal axis. The developing pituitary gland is sensitive to exposure to endocrine-disrupting chemicals, such as bisphenol A (BPA), and sex-specific effects can occur. However, effects on the critical window of neonatal pituitary gland development in mice have not been explored. Therefore, this study determined baseline gene expression in male and female pituitaries and consequences of environmental exposure to 17ß-estradiol (E2) and BPA on transcription of genes exhibiting sex differences during the neonatal period. Through microarray and quantitative RT-PCR analysis of pituitaries at postnatal day (PND)1, 3 genes were differentially expressed between males and females: Lhb, Fshb, and intracellular adhesion molecule-5 (Icam5). To see whether E2 and BPA exposure regulates these genes, pituitaries were cultured at PND1 with 10(-8) M E2 or 4.4 × 10(-6) M BPA. E2 decreased expression of Lhb, Fshb, and Icam5 mRNA in females but only significantly decreased expression of Icam5 in males. BPA decreased expression of Icam5 similarly to E2, but it did not affect Lhb or Fshb. Importantly, in vivo exposure to 50-µg/kg · d E2 from PND0 to PND7 decreased expression of Lhb, Fshb, and Icam5 mRNA in both males and females, whereas 50-mg/kg · d BPA exposure during the same time frame decreased expression of Icam5 in females only. Overall, we have uncovered that genes differentially expressed between the sexes can be regulated in part by hormonal and chemical signals in vivo and directly at the pituitary and can be regulated in a sex-specific manner.

Assessment of family history of substance abuse for preventive interventions with patients experiencing chronic pain: A quality improvement project.

This quality improvement project demonstrates that RN Care Managers, in a chronic pain programme, can assess for a family history of substance abuse in 5-10 min. Information informs treatment based on specific high risk criteria. Benefits include heightened awareness of the genetic and environmental risks associated with a family history of substance abuse, an opportunity to participate in motivational interventions to prevent or minimize consequences of substance use disorders, and likely substantial overall health-care cost savings.

Mentors offering maternal support: a support intervention for military mothers.

OBJECTIVE: To evaluate the effectiveness of the Mentors Offering Maternal Support (MOMS) program to promote maternal fetal attachment, maternal adaptation to pregnancy, self-esteem, and perceived community support in women within a military environment. DESIGN: A randomized, controlled, repeated measured pilot study compared two groups of pregnant military wives, a control group receiving standard prenatal care and an intervention group receiving a structured eight-session MOMS program. SETTING: The study was conducted at two Air Force installations in Florida having joint (Air Force, Army, and Navy) operations and high deployment requirements. PARTICIPANTS: Sixty-five military wives in their first trimester of pregnancy (control group, n = 36 and intervention group, n = 29) completed all aspects of the study. METHODS: Women randomized to the MOMS program received eight structured classes starting in the first trimester of pregnancy and occurring every other week until the third trimester. Outcome measures were obtained in each trimester. The women in the control group received usual prenatal care. RESULTS: No statistically significant differences were found between the two groups for any of the outcome variables. The interaction of the amount of contact the women had with their deployed husbands and group assignment was statistically different for two variables, the Relationship with Husband Scale and the Rosenberg Self-Esteem Inventory.

The relationship of military imposed marital separations on maternal acceptance of pregnancy.

The effect of military deployment and perceived availability and source of community support on women's acceptance of pregnancy were examined in each trimester of pregnancy at four military bases. The sample was 503 primigravida or multigravida women eligible for care in the military medical system. Military deployment and community support had a statistically significant effect on pregnancy acceptance. Gravidas with deployed husbands had higher conflict for accepting pregnancy than gravidas without deployed spouses. Community support had a significant positive effect on pregnancy acceptance. Women perceiving support predominantly from off-base versus on-base communities had significantly higher conflict with acceptance of pregnancy. Findings point to improved maternal acceptance of pregnancy with paternal presence and community support in the event of military deployment.

Calcium channel gamma6 subunits are unique modulators of low voltage-activated (Cav3.1) calcium current.

The calcium channel gamma (gamma) subunit family consists of eight members whose functions include modulation of high voltage-activated (HVA) calcium currents in skeletal muscle and neurons, and regulation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propanoic acid (AMPA) receptor targeting. Cardiac myocytes express at least three gamma subunits, gamma(4), gamma(6) and gamma(7), whose function(s) in the heart are unknown. Here we compare the effects of the previously uncharacterized gamma(6) subunit with that of gamma(4) and gamma(7) on a low voltage-activated calcium channel (Cav3.1) that is expressed in cardiac myocytes. Co-expression of both the long and short gamma(6) subunit isoforms, gamma(6L) and gamma(6S), with Cav3.1 in HEK-293 cells significantly decreases current density by 49% and 69%, respectively. Two other gamma subunits expressed in cardiac myocytes, gamma(4) and gamma(7), have no significant effect on Cav3.1 current. Neither gamma(6L), gamma(6S), gamma(4) nor gamma(7) significantly affect the voltage dependency of activation or inactivation or the kinetics of Cav3.1 current. Transient expression of gamma(6L) in an immortalized atrial cell line (HL-1) significantly reduces the endogenous low voltage-activated current in these cells by 63%. Green fluorescent protein tagged gamma(6L) is localized primarily in HEK-293 cell surface membranes where it is evenly distributed. Expression of gamma(6L) does not affect the level of Cav3.1 mRNA or the amount of total Cav3.1 protein in transfected HEK-293 cells. These results demonstrate that the gamma(6) subunit has a unique ability to inhibit Cav3.1 dependent calcium current that is not shared with the gamma(4) and gamma(7) isoforms and is thus a potential regulator of cardiac low voltage-activated calcium current.

Asthma management across the life span: the childbearing woman with asthma.

Asthma can pose a serious threat to the pregnant mother and her fetus if not treated appropriately. Studies analyzing the causes of death in severe asthma have shown that most occur outside of the hospital with neither the physician nor the patient appreciating the seriousness of the symptoms [31]. For this reason, a pregnant woman with a diagnosis of asthma must be evaluated thoroughly and managed aggressively by an obstetrician and pulmonary specialist or a maternal-fetal medicine specialist trained in high-risk pregnancies. Any evaluation or assessment of the pregnant asthmatic must be interpreted in light of pregnancy-induced changes. Treatment must be focused on set goals to correct maternal hypoxia, relieve bronchospasm, ensure adequate ventilation, and optimize uteroplacental exchange preventing fetal hypoxia.