Flexibility in Faculty Work-Life Policies at Medical Schools in the Big Ten Conference: A Ten-Year Follow-up Study.

Background: Flexible work-life policies for medical school faculty are necessary to support career progress, advancement, retention, and job satisfaction. Objective: Our objective was to perform a 10-year follow-up descriptive assessment of the availability of flexible work-life policies for faculty in medical schools in the Big Ten Conference. Design: In this descriptive study, a modified objective scoring system was used to evaluate the flexibility of faculty work-life policies at 13 medical schools in the Big Ten Conference. Policy information was obtained from institutional websites and verified with the human resources offices. Scores from the 2011 study and 2020 were compared. Results: Michigan State and Ohio State Universities offered the most flexible policies (score 17.75/22) with the Universities of Maryland and Minnesota following (score 16/22). The largest delta scores, indicating more flexible policies in the past decade, were at University of Minnesota (5.25) and University of Michigan (5). Policies for parental leave and part-time faculty varied widely. Most schools earned an additional point in the newly added category of "flexible scheduling and return-to-work policies." Nearly every institution reported dedicated lactation spaces and improved childcare options. Limitations : Limitations included missing policy data and interpretation bias in reviewing the policy websites, unavailable baseline data for schools that joined the Big Ten after the 2011 study, and unavailable baseline data for the additional category of return-to-work policies. Conclusions: While progress has been made, every institution should challenge themselves to review flexibility in work-life policies for faculty. It is important to advance a healthy competition with the goal to achieve more forward-thinking policies that improve retention, recruitment, and advancement of faculty. Big Ten institutions can continue to advance their policies by providing greater ease of access to options, further expansion of parental leave and childcare support, and offering more flexible policies for part-time faculty.

Flexible Scheduling Policy for Pregnant and New Parent Residents: A Descriptive Pilot Study.

OBJECTIVES: Many physicians complete residency training during optimal childbearing years. The literature shows that working nights or on call can lead to pregnancy complications including miscarriage, preterm labor, and preeclampsia. In addition, infant-parent bonding in the postpartum period is crucial for breastfeeding, health, and well-being. No national standards exist for flexible scheduling options for pregnant or new parent residents. Our project objectives are 1) to describe a policy for scheduling pregnant and new parent residents in an emergency medicine (EM) residency and 2) to report pilot outcomes to assess feasibility of implementation, resident satisfaction, and pregnancy outcomes. METHODS: An EM residency task force developed a proposal of scheduling options for pregnant and new parent residents based on best practice recommendations and resident input. The policy included prenatal scheduling options for pregnant residents and postpartum scheduling options for all new resident parents. Resident support for the policy was evaluated via an anonymous survey. It was piloted for 2 months in an EM residency program. RESULTS: Policy development resulted in 1) an opt-out prenatal pregnancy work hour option policy with no nights or call during the first and third trimesters, 2) a 6-week new parent flexible scheduling policy, and 3) clarified sick call options. A majority of residents approved the new policy. During the 2-month pilot period, four residents (of 73 total) utilized the policy. The chief residents reported no added burden in scheduling. Of the residents who utilized the policy, all reported high satisfaction. There were no reported pregnancy or postpartum complications. CONCLUSIONS: We successfully adopted a new scheduling policy for pregnant residents and new parents in one of the largest EM residency training programs in the country. This policy can serve as a national model for other graduate medical education programs.

First-time Diabetic Ketoacidosis in Type 2 Diabetics With Covid-19 Infection: A Novel Case Series.

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 is a novel coronavirus first diagnosed in U.S. hospitals in January 2020. Typical presenting symptoms include fever, dry cough, dyspnea, and hypoxia. However, several other symptoms have been reported, including fatigue, weakness, diarrhea, and abdominal pain. We have identified a series of patients with diabetic ketoacidosis (DKA) likely precipitated by coronavirus disease 2019 (COVID-19). CASE SERIES: We describe 5 patients with previously known type 2 diabetes and no history of DKA, who presented to the emergency department with new-onset DKA and COVID-19. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Diabetes mellitus is a known risk factor for poor outcomes in viral respiratory illnesses, including COVID-19. Infection may precipitate DKA in patients with type 2 diabetes. Aggressive management of these patients is recommended; however, management guidelines have not yet been put forth for this unique subset of patients.

Expectations for Tinnitus Treatment and Outcomes: A Survey Study of Audiologists and Patients.

BACKGROUND: Roughly 10-15% of the general population is affected by tinnitus and this percentage is estimated to rise in future. Because there is currently no cure for tinnitus, treatment is limited and is primarily achieved through management of symptoms and counseling. PURPOSE: This study compared audiologists' and patients' responses to related survey questions about their expectations regarding tinnitus treatment. Two separate surveys were created, one for patients with tinnitus, and one for practicing audiologists who may treat such patients. The surveys included several related questions, such that comparison of the two could reveal where patients' and audiologists' expectations for tinnitus care were in agreement and areas in which they differed. RESEARCH DESIGN: The surveys for audiologists and adults with tinnitus were 31- and 38-item questionnaires, respectively. Both surveys comprised demographic questions followed by several tinnitus-related questions in either multiple-choice or Likert-scale format. STUDY SAMPLE: We received 230 completed Patient Surveys and 68 completed Audiologist Surveys. DATA COLLECTION AND ANALYSIS: All survey recruitment was completed online. Responses were collected via the Survey Monkey web tool (http://www.surveymonkey.com/). Responses were analyzed within and between surveys and grouped into topical categories (assessment, counseling, current available tinnitus information, satisfaction and expectations, improving tinnitus management). For data within each survey, descriptive statistics and correlation analyses were used. For selected comparisons between surveys, cross-tabulations were used. Hierarchical regression modeling was conducted to further explore (1) the perceived effectiveness of treatment received, and (2) how each group defined treatment success. RESULTS: Differences were noted between the two groups' responses to the question on the definition of treatment success; audiologists reported decreased awareness (77%), stress/anxiety relief (63%), and increased knowledge of tinnitus (63%) most commonly, whereas patients reported reduction of tinnitus loudness (63%) and complete elimination of tinnitus (57%) most often. The topic of greatest agreement was the desire for more information on tinnitus; 62% of patients felt more information from their healthcare provider would be the most important factor for improved tinnitus management, and 67% of audiologists reported currently having "some access" or less to appropriate resources for tinnitus treatment. Modeling results for effective tinnitus management and definitions of treatment success highlighted the importance of resource access and information sharing for both audiologists and patients. CONCLUSIONS: Patients and audiologists differed in terms of their expectations for successful treatment, with the patients focusing on perceptual factors and the audiologists on the reaction to the sound. Patient satisfaction with tinnitus treatment may be improved through access to more information, specifically, more information about current tinnitus treatment options and how these focus on the patient's reaction to the tinnitus rather than the percept itself. Providing credible tinnitus information resources to audiologists, and focusing resources on training a small number of tinnitus specialist audiologists could greatly improve patient satisfaction with the current state of tinnitus palliative care.

Cbk1 regulation of the RNA-binding protein Ssd1 integrates cell fate with translational control.

Spatial control of gene expression, at the level of both transcription and translation, is critical for cellular differentiation [1-4]. In budding yeast, the conserved Ndr/warts kinase Cbk1 localizes to the new daughter cell, where it acts as a cell fate determinant. Cbk1 both induces a daughter-specific transcriptional program and promotes morphogenesis in a less well-defined role [5-8]. Cbk1 is essential in cells expressing functional Ssd1, an RNA-binding protein of unknown function [9-11]. We show here that Cbk1 inhibits Ssd1 in vivo. Loss of this regulation dramatically slows bud expansion, leading to highly aberrant cell wall organization at the site of cell growth. Ssd1 associates with specific mRNAs, a significant number of which encode cell wall remodeling proteins. Translation of these messages is rapidly and specifically suppressed when Cbk1 is inhibited; this suppression requires Ssd1. Transcription of several of these Ssd1-associated mRNAs is also regulated by Cbk1, indicating that the kinase controls both the transcription and translation of daughter-specific mRNAs. This work suggests a novel system by which cells coordinate localized expression of genes involved in processes critical for cell growth and division.

Phosphoregulation of Cbk1 is critical for RAM network control of transcription and morphogenesis.

The budding yeast regulation of Ace2 and morphogenesis (RAM) network integrates cell fate determination and morphogenesis. Its disruption impairs polarized growth and causes mislocalization of the transcription factor Ace2, resulting in failure of daughter cell-specific transcription required for cell separation. We find that phosphoregulation of the conserved AGC family kinase Cbk1 is critical for RAM network function. Intramolecular autophosphorylation of the enzyme's activation loop is critical for kinase activity but is only partially required for cell separation and polarized growth. In marked contrast, phosphorylation of a C-terminal hydrophobic motif is required for Cbk1 function in vivo but not for its kinase activity, suggesting a previously unappreciated level of control for this family of kinases. Phosphorylation of the C-terminal site is regulated over the cell cycle and requires the transcription factor Ace2 as well as all RAM network components. Therefore, Ace2 is not only a downstream target of Cbk1 but also reinforces activation of its upstream regulator.

Two isoforms of tissue transglutaminase mediate opposing cellular fates.

Opposing cellular responses are typically regulated by distinct sets of genes. However, tissue transglutaminase (TGase) provides an interesting example of a single gene product that has been implicated both in affording protection against cellular insults as well as in promoting cell death. Here, we shed some light on how these conflicting activities might be manifested by demonstrating that alternative transcripts of TGase differentially affect cell viability. We show that although the full-length TGase protein affords strong protection against cell death signals, a shorter version of TGase that is truncated at the 3' end, and thus called TGase-short (TGase-S), is cytotoxic. The apoptotic activity of TGase-S is not dependent on its transamidation activity because the mutation of a cysteine residue that is essential for catalyzing this reaction does not compromise the ability of TGase-S to induce cell death. Intriguingly, TGase-S undergoes inappropriate oligomer formation in cells before cell death, suggesting a novel mechanism for the apoptotic effects of this protein.

Augmentation of tissue transglutaminase expression and activation by epidermal growth factor inhibit doxorubicin-induced apoptosis in human breast cancer cells.

Tissue transglutaminase (TGase) exhibits both a GTP binding/hydrolytic capability and an enzymatic transamidation activity. Increases in TGase expression and activation often occur in response to stimuli that promote cellular differentiation and apoptosis, yet the signaling mechanisms used by these stimuli to regulate TGase expression and activation and the role of TGase in these cellular processes are not well understood. Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Here we investigate whether EGF also antagonized RA-induced TGase expression in breast cancer cells. We found that EGF stimulation affected TGase expression and activation very differently in these cancer cells. Not only did EGF fail to block RA-induced TGase expression, but also EGF alone was sufficient to potently up-regulate TGase expression and activation in SKBR3 cells, as well as MDAMB468 and BT-20 cells. Inhibiting phosphoinositide 3-kinase activity severely diminished the ability of EGF and RA to increase TGase protein levels, whereas a constitutively active form of phosphoinositide 3-kinase potentiated the induction of TGase expression by EGF in SKBR3 cells. Because EGF is an established antiapoptotic factor, we examined whether the protection afforded by EGF was dependent on its ability to up-regulate TGase activity in SKBR3 and BT-20 cells. Exposure of cells to a TGase inhibitor or expression of a dominant-negative form of TGase potently inhibited EGF-mediated protection from doxorubicin-induced apoptosis. Moreover, expression of exogenous TGase in SKBR3 cells mimicked the survival advantage of EGF, suggesting that TGase activation is necessary and sufficient for the antiapoptotic properties of EGF. These findings indicate for the first time that EGF can induce TGase expression and activation in human breast cancer cells and that this contributes to their oncogenic potential by promoting chemoresistance.