Gender Trends in Dental Leadership and Academics: A Twenty-Two-Year Observation

The purpose of this study was to examine gender disparities in dental leadership and academics in the United States. Nine journals that represent the dental specialties and high published impact factors were selected to analyze the percentage of female dentists’ first and senior authorship for the years 1986, 1990, 1995, 2000, 2005, and 2008. Data on appointment status and female deanship were collected from the American Dental Association (ADA) survey, and the trends were studied. The proportion of female presidents in ADA-recognized specialty organizations was also calculated. Overall, the increase in first female authorship was not statistically significant, but the increase of last female authorship was statistically significant in a linear trend over the years. The percentage of tenured female faculty members and female deans in U.S. dental schools increased by factors of 1.7 and 9, respectively, during the study period. However, female involvement in professional organizations was limited. Findings from this study indicate that female participation in authorship and leadership has increased over time. Nevertheless, females are still a minority in dental academics and leadership

Shocked Gas in IRAS F17207-0014: ISM Collisions and Outflows

We combine optical and near-infrared AO-assisted integral field observations of the merging ULIRG IRAS F17207-0014 from the Wide-Field Spectrograph (WiFeS) and Keck/OSIRIS. The optical emission line ratios [N II]/H$\alpha$, [S II]/H$\alpha$, and [O I]/H$\alpha$ reveal a mixing sequence of shocks present throughout the galaxy, with the strongest contributions coming from large radii (up to 100% at $\sim$5 kpc in some directions), suggesting galactic-scale winds. The near-infrared observations, which have approximately 30 times higher spatial resolution, show that two sorts of shocks are present in the vicinity of the merging nuclei: low-level shocks distributed throughout our field-of-view evidenced by an H$_{2}$/Br$\gamma$ line ratio of $\sim$0.6-4, and strong collimated shocks with a high H$_{2}$/Br$\gamma$ line ratio of $\sim$4-8, extending south from the two nuclear disks approximately 400 pc ($\sim$0.5 arcsec). Our data suggest that the diffuse shocks are caused by the collision of the interstellar media associated with the two progenitor galaxies and the strong shocks trace the base of a collimated outflow coming from the nucleus of one of the two disks.Comment: accepted to MNRA

State Benefit Design Choices under SCHIP - Implications for Pediatric Health Care

This policy brief1 is the second in a series of reports focusing on the design of state SCHIP programs as they near full implementation. It examines the extent to which state agencies adopt conventional insurance norms or adhere to special principles of Medicaid coverage design for children in designing separately administered (or freestanding) SCHIP programs. The issue of coverage design is particularly relevant for children with low prevalence conditions and special health care needs. Increasingly, conventional insurance uses standardized coverage norms to limit coverage and treatment. These standardized norms take the form of across-the-board treatments and exclusions, limited definitions of medical necessity, and the use of irrebuttable, standardized treatment guidelines in determining when covered treatments will be available. All of these practices are impermissible under Medicaid, which uses exceptionally broad preventive standards to determine coverage of children; such standards favor coverage of children with low prevalence problems

Using a model of group psychotherapy to support social research on sensitive topics

This article describes the exploratory use of professional therapeutic support by social researchers working on a sensitive topic. Talking to recently bereaved parents about the financial implications of their child's death was expected to be demanding work, and the research design included access to an independent psychotherapeutic service. Using this kind of professional support is rare within the general social research community, and it is useful to reflect on the process. There are likely to be implications for collection and interpretation of data, research output and the role and experience of the therapist. Here, the primary focus is the potential impact on researcher well-being

Growth, seed development and genetic analysis in wild type and Def mutant of Pisum sativum L

<p>Abstract</p> <p>Background</p> <p>The <it>def </it>mutant pea (<it>Pisum sativum </it>L) showed non-abscission of seeds from the funicule. Here we present data on seed development and growth pattern and their relationship in predicting this particular trait in wild type and mutant lines as well as the inheritance pattern of the <it>def </it>allele in F₂and F₃populations.</p> <p>Findings</p> <p>Pod length and seed fresh weight increase with fruit maturity and this may affect the abscission event in pea seeds. However, the seed position in either the distal and proximal ends of the pod did not show any difference. The growth factors of seed fresh weight (FW), width of funicles (WFN), seed width (SW) and seed height (SH) were highly correlated and their relationships were determined in both wild type and <it>def </it>mutant peas. The coefficient of determination <it>R</it>²values for the relationship between WFN and FW, SW and SH and their various interactions were higher for the <it>def </it>dwarf type. Stepwise multiple regression analysis showed that variation of WFN was associated with SH and SW. Pearson's chi square analysis revealed that the inheritance and segregation of the <it>Def </it>locus in 3:1 ratio was significant in two F₂populations. Structural analysis of the F3 population was used to confirm the inheritance status of the <it>Def </it>locus in F₂heterozygote plants.</p> <p>Conclusions</p> <p>This study investigated the inheritance of the presence or absence of the <it>Def </it>allele, controlling the presence of an abscission zone (AZ) or an abscission-less zone (ALZ) forming in wild type and mutant lines respectively. The single major gene (<it>Def</it>) controlling this phenotype was monogenic and <it>def </it>mutants were characterized and controlled by the homozygous recessive <it>def </it>allele that showed no palisade layers in the hilum region of the seed coat.</p

The cell of origin dictates the temporal course of neurofibromatosis-1 (Nf1) low-grade glioma formation.

Low-grade gliomas are one of the most common brain tumors in children, where they frequently form within the optic pathway (optic pathway gliomas; OPGs). Since many OPGs occur in the context of the Neurofibromatosis Type 1 (NF1) cancer predisposition syndrome, we have previously employed Nf1 genetically-engineered mouse (GEM) strains to study the pathogenesis of these low-grade glial neoplasms. In the light of the finding that human and mouse low-grade gliomas are composed of Olig2+ cells and that Olig2+ oligodendrocyte precursor cells (OPCs) give rise to murine high-grade gliomas, we sought to determine whether Olig2+ OPCs could be tumor-initiating cells for Nf1 optic glioma. Similar to the GFAP-Cre transgenic strain previously employed to generate Nf1 optic gliomas, Olig2+ cells also give rise to astrocytes in the murine optic nerve in vivo. However, in contrast to the GFAP-Cre strain where somatic Nf1 inactivation in embryonic neural progenitor/stem cells (Nf1flox/mut; GFAP-Cre mice) results in optic gliomas by 3 months of age in vivo, mice with Nf1 gene inactivation in Olig2+ OPCs (Nf1flox/mut; Olig2-Cre mice) do not form optic gliomas until 6 months of age. These distinct patterns of glioma latency do not reflect differences in the timing or brain location of somatic Nf1 loss. Instead, they most likely reflect the cell of origin, as somatic Nf1 loss in CD133+ neural progenitor/stem cells during late embryogenesis results in optic gliomas at 3 months of age. Collectively, these data demonstrate that the cell of origin dictates the time to tumorigenesis in murine optic glioma

Sodium-activated potassium channels shape peripheral auditory function and activity of the primary auditory neurons in mice

Potassium (K+) channels shape the response properties of neurons. Although enormous progress has been made to characterize K+ channels in the primary auditory neurons, the molecular identities of many of these channels and their contributions to hearing in vivo remain unknown. Using a combination of RNA sequencing and single molecule fluorescent in situ hybridization, we localized expression of transcripts encoding the sodium-activated potassium channels K(Na)1.1(SLO2.2/Slack) and K(Na)1.2 (SLO2.1/Slick) to the primary auditory neurons (spiral ganglion neurons, SGNs). To examine the contribution of these channels to function of the SGNs in vivo, we measured auditory brainstem responses in K(Na)1.1/1.2 double knockout (DKO) mice. Although auditory brainstem response (wave I) thresholds were not altered, the amplitudes of suprathreshold responses were reduced in DKO mice. This reduction in amplitude occurred despite normal numbers and molecular architecture of the SGNs and their synapses with the inner hair cells. Patch clamp electrophysiology of SGNs isolated from DKO mice displayed altered membrane properties, including reduced action potential thresholds and amplitudes. These findings show that K(Na)1 channel activity is essential for normal cochlear function and suggest that early forms of hearing loss may result from physiological changes in the activity of the primary auditory neurons

Statin use and adverse effects among adults \u3e 75 years of age: Insights from the Patient and Provider Assessment of Lipid Management (PALM) registry

Background: Current statin use and symptoms among older adults in routine community practice have not been well characterized since the release of the 2013 American College of Cardiology/American Heart Association guideline. Methods and results: We compared statin use and dosing between adults \u3e75 and ≤75 years old who were eligible for primary or secondary prevention statin use without considering guideline-recommended age criteria. The patients were treated at 138 US practices in the Patient and Provider Assessment of Lipid Management (PALM) registry in 2015. Patient surveys also evaluated reported symptoms while taking statins. Multivariable logistic regression models examined the association between older age and statin use and dosing. Among 6717 people enrolled, 1704 (25%) were \u3e75 years old. For primary prevention, use of any statin or high-dose statin did not vary by age group: any statin, 62.6% in those \u3e75 years old versus 63.1% in those ≤75 years old (P=0.83); high-dose statin, 10.2% versus 12.3% in the same groups (P=0.14). For secondary prevention, older patients were slightly less likely to receive any statin (80.1% versus 84.2% [P=0.003]; adjusted odds ratio, 0.81; 95% confidence interval, 0.66-1.01 [P=0.06]), but were much less likely to receive a high-intensity statin (23.5% versus 36.2% [PP=0.0001]). Among current statin users, older patients were slightly less likely to report any symptoms (41.3% versus 46.6%; P=0.003) or myalgias (27.3% versus 33.3%; Conclusions: Overall use of statins was similar for primary prevention in those aged \u3e75 years versus younger patients, yet older patients were less likely to receive high-intensity statins for secondary prevention. Statins appear to be similarly tolerated in older and younger adult

Oxidative Toxicity in Neurodegenerative Diseases: Role of Mitochondrial Dysfunction and Therapeutic Strategies

Besides fluorine, oxygen is the most electronegative element with the highest reduction potential in biological systems. Metabolic pathways in mammalian cells utilize oxygen as the ultimate oxidizing agent to harvest free energy. They are very efficient, but not without risk of generating various oxygen radicals. These cells have good antioxidative defense mechanisms to neutralize these radicals and prevent oxidative stress. However, increased oxidative stress results in oxidative modifications in lipid, protein, and nucleic acids, leading to mitochondrial dysfunction and cell death. Oxidative stress and mitochondrial dysfunction have been implicated in many neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, and stroke-related brain damage. Research has indicated mitochondria play a central role in cell suicide. An increase in oxidative stress causes mitochondrial dysfunction, leading to more production of reactive oxygen species and eventually mitochondrial membrane permeabilization. Once the mitochondria are destabilized, cells are destined to commit suicide. Therefore, antioxidative agents alone are not sufficient to protect neuronal loss in many neurodegenerative diseases. Combinatorial treatment with antioxidative agents could stabilize mitochondria and may be the most suitable strategy to prevent neuronal loss. This review discusses recent work related to oxidative toxicity in the central nervous system and strategies to treat neurodegenerative diseases