👤 D J Lew

Trainees are facing isolation and burnout, due to the fear of contracting and transmitting novel coronavirus-19 (COVID-19). There has been a reduction in clinical activities of residents. The purpose of this paper is to measure and compare the psychological well-being of dental versus medical residents during the COVID-19 outbreak. This is a cross-sectional study whereby trainees of a hospital in New York City were sent a questionnaire. Participants were from the dental and medical departments. Psychological measures of depression and post traumatic stress disorder were assessed utilizing the Patient Health Questionnaire-9 (PHQ-9) and The Impact of Event Scale-Revised (IES-R) questionnaire. Other variables compared were age, gender, smoking status, living situation and comorbidities. Data analysis utilized chi-squared (X The survey was sent to 19 dental (Dental) and 171 medical (MD) residents. There were 66 participants. The response rate was 63.16 and 35.09% for the Dental and MD residents, respectively. The mean age for the Dental and MD residents, respectively, was 29.62 ± 2.09 and 34.82 ± 9.32 (P = .014). Eighty-one percent of the Dental respondents were male and 33.3% of the MD respondents were male (P < .001). The mean PHQ-9 score was 18.29 ± 2.88 vs 7.24 ± 7.41 for Dental and MD residents, respectively (P < .001). A higher score represents increased severity of depression. The Dental residents scored 61.9 ± 3.90 on the IES-R vs 30.36 ± 24.67 (P < .001). A higher score indicates a greater frequency of intrusive thoughts and avoidance. Forty-two percent of Dental and 13.3% of MD residents tested positive; 25% of Dental and 28.9% of MD residents self-reported symptoms for COVID-19. Being positive or symptomatic resulted in statistically significant higher IES-R and PHQ-9 scores. Dental residents and being positive or symptomatic for COVID-19 resulted in higher PHQ-9 and IES-R scores. Being aware of the impact of COVID-19 is an important step in providing intervention. Show less

Analysis of cell cycle regulation in the budding yeast Saccharomyces cerevisiae has shown that a central regulatory protein kinase, Cdc28, undergoes changes in activity through the cell cycle by associating with distinct groups of cyclins that accumulate at different times. The various cyclin/Cdc28 complexes control different aspects of cell cycle progression, including the commitment step known as START and mitosis. We found that altering the activity of Cdc28 had profound effects on morphogenesis during the yeast cell cycle. Our results suggest that activation of Cdc28 by G1 cyclins (Cln1, Cln2, or Cln3) in unbudded G1 cells triggers polarization of the cortical actin cytoskeleton to a specialized pre-bud site at one end of the cell, while activation of Cdc28 by mitotic cyclins (Clb1 or Clb2) in budded G2 cells causes depolarization of the cortical actin cytoskeleton and secretory apparatus. Inactivation of Cdc28 following cyclin destruction in mitosis triggers redistribution of cortical actin structures to the neck region for cytokinesis. In the case of pre-bud site assembly following START, we found that the actin rearrangement could be triggered by Cln/Cdc28 activation in the absence of de novo protein synthesis, suggesting that the kinase may directly phosphorylate substrates (such as actin-binding proteins) that regulate actin distribution in cells. Show less

Growth of S. cerevisiae cells by budding gives rise to asymmetric progeny cells: a larger "mother" cell and a smaller "daughter" cell. The mother cell transits a brief G1 phase before forming a new bud and beginning DNA replication. The daughter cell stays in G1 for a longer period, growing in size before initiating a new cell cycle. We show that the timing of cell cycle initiation in mother and daughter cells is governed by different G1 cyclins. In daughter cells, transcription of CLN1 and CLN2 is induced in a size-dependent manner, and these cyclins are necessary for the normal timing of cell cycle initiation. CLN3 is not required in daughter cells, but is crucial for mother cells, in which the G1 phase is much longer in the absence of this cyclin. Show less