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1.
Acad Psychiatry ; 48(3): 244-248, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38570407

ABSTRACT

OBJECTIVE: Mental health treatment is often initiated in primary care settings, but many primary care providers (PCPs), residents, and medical students report discomfort in managing psychiatric conditions. This study evaluated the effect of an educational workshop that featured an evidence-based psychopharmacology clinical decision support tool (CDST) on trainee confidence and willingness to treat psychiatric conditions. METHODS: Participants completed pre- and post-workshop surveys. Nine months after the workshop, a subset of trainees participated in a focus group. RESULTS: Of the participants, 62.5% of the obstetrics-gynecology (OB-GYN) resident physicians (10/16) and 100% of the medical students (18/18) completed both pre- and post-surveys. Following the workshop, OB-GYN resident physicians reported significantly improved confidence in treating psychiatric disorders (p < 0.001), sense of having psychiatric support tools (p < 0.001), and knowledge of treating psychiatric disorders (p = 0.021). Medical students reported significantly improved confidence in treating psychiatric disorders (p < 0.001), willingness to devise treatment plans for psychiatric disorders (p = 0.024), sense of having psychiatric support tools (p < 0.001), knowledge of treating psychiatric disorders (p < 0.001), and comfort in presenting a psychiatric treatment plan to an attending (p = 0.003). Most focus group participants (93.75%; 15/16) reported that they continued to use the CDST, and it increased their confidence in formulating psychiatric treatment plans. CONCLUSIONS: These findings suggest that educational workshops that introduce high-quality psychopharmacology CDSTs may be an effective method for improving provider comfort in treating psychiatric disorders.


Subject(s)
Internship and Residency , Students, Medical , Humans , Students, Medical/psychology , Female , Primary Health Care , Male , Adult , Clinical Competence , Psychiatry/education , Obstetrics/education , Focus Groups , Gynecology/education , Attitude of Health Personnel , Psychopharmacology/education , Mental Disorders/therapy , Surveys and Questionnaires , Decision Support Systems, Clinical , Education
2.
J Assist Reprod Genet ; 40(5): 1063-1070, 2023 May.
Article in English | MEDLINE | ID: mdl-36943574

ABSTRACT

PURPOSE: Many countries prohibit payment for gamete donation, which means fertility clinics do not have to compensate donors. However, acquiring and utilizing donor sperm can still be expensive for fertility clinics. This study evaluates international fertility workers' views on charging patients for altruistically donated sperm. METHODS: Using social media and email, we disseminated a SurveyMonkey survey with a question that was specifically focused on opinions about charging patients for altruistically donated sperm. Clinicians were able to select multiple pre-populated answer choices as well as write answers that reflected their views as an open-ended response. Snowball sampling was utilized to reach international fertility clinicians. RESULTS: Of 112 respondents from 14 countries, 88% believe it is acceptable to charge for altruistically donated sperm based on one or more of four different assenting categories: so patients appreciate that sperm is valuable, because it generates funds for the running of the clinic, to cover specific costs associated with sperm, and to make a profit for the clinic. CONCLUSIONS: The consensus that charging for altruistically donated sperm is acceptable was not surprising since recruiting and processing donor sperm can be expensive for clinics. However, there were geographical differences for specific assenting answer choices which may be based on countries' income, and healthcare system, as well as religious and cultural beliefs.


Subject(s)
Fertility Clinics , Semen , Humans , Male , Pilot Projects , Tissue Donors , Spermatozoa
3.
Front Immunol ; 14: 1196453, 2023.
Article in English | MEDLINE | ID: mdl-37600782

ABSTRACT

Background: Fetal inflammatory response mediated by the influx of immune cells and activation of pro-inflammatory transcription factor NF-κB in feto-maternal uterine tissues is the major determinant of infection-associated preterm birth (PTB, live births < 37 weeks of gestation). Objective: To reduce the incidence of PTB by minimizing inflammation, extracellular vesicles (EVs) were electroporetically engineered to contain anti-inflammatory cytokine interleukin (IL)-10 (eIL-10), and their efficacy was tested in an ascending model of infection (vaginal administration of E. coli) induced PTB in mouse models. Study design: EVs (size: 30-170 nm) derived from HEK293T cells were electroporated with recombinant IL-10 at 500 volts and 125 Ω, and 6 pulses to generate eIL-10. eIL-10 structural characters (electron microscopy, nanoparticle tracking analysis, ExoView [size and cargo content] and functional properties (co-treatment of macrophage cells with LPS and eIL-10) were assessed. To test efficacy, CD1 mice were vaginally inoculated with E. coli (1010CFU) and subsequently treated with either PBS, eIL-10 (500ng) or Gentamicin (10mg/kg) or a combination of eIL-10+gentamicin. Fetal inflammatory response in maternal and fetal tissues after the infection or treatment were conducted by suspension Cytometer Time of Flight (CyTOF) using a transgenic mouse model that express red fluorescent TdTomato (mT+) in fetal cells. Results: Engineered EVs were structurally and functionally stable and showed reduced proinflammatory cytokine production from LPS challenged macrophage cells in vitro. Maternal administration of eIL-10 (10 µg/kg body weight) crossed feto-maternal barriers to delay E. coli-induced PTB to deliver live pups at term. Delay in PTB was associated with reduced feto-maternal uterine inflammation (immune cell infiltration and histologic chorioamnionitis, NF-κB activation, and proinflammatory cytokine production). Conclusions: eIL-10 administration was safe, stable, specific, delayed PTB by over 72 hrs and delivered live pups. The delivery of drugs using EVs overcomes the limitations of in-utero fetal interventions. Protecting IL-10 in EVs eliminates the need for the amniotic administration of recombinant IL-10 for its efficacy.


Subject(s)
Extracellular Vesicles , Interleukin-10 , Pregnancy Complications, Infectious , Animals , Female , Humans , Mice , Pregnancy , Cytokines , Disease Models, Animal , Escherichia coli , Fetus , HEK293 Cells , Interleukin-10/pharmacology , Lipopolysaccharides , NF-kappa B , Premature Birth , Recombinant Proteins/pharmacology , Inflammation , Pregnancy Complications, Infectious/drug therapy
4.
Cell Rep ; 41(13): 111879, 2022 12 27.
Article in English | MEDLINE | ID: mdl-36577368

ABSTRACT

Phosphorylation of Neurospora crassa eukaryotic initiation factor 2 α (eIF2α), a conserved translation initiation factor, is clock controlled. To determine the impact of rhythmic eIF2α phosphorylation on translation, we performed temporal ribosome profiling and RNA sequencing (RNA-seq) in wild-type (WT), clock mutant Δfrq, eIF2α kinase mutant Δcpc-3, and constitutively active cpc-3c cells. About 14% of mRNAs are rhythmically translated in WT cells, and translation rhythms for ∼30% of these mRNAs, which we named circadian translation-initiation-controlled genes (cTICs), are dependent on the clock and CPC-3. Most cTICs are expressed from arrhythmic mRNAs and contain a P-body (PB) localization motif in their 5' leader sequence. Deletion of SNR-1, a component of cytoplasmic messenger ribonucleoprotein granules (cmRNPgs) that include PBs and stress granules (SGs), and the PB motif on one of the cTIC mRNAs, zip-1, significantly alters zip-1 rhythmic translation. These results reveal that the clock regulates rhythmic translation of specific mRNAs through rhythmic eIF2α activity and cmRNPg metabolism.


Subject(s)
Circadian Clocks , Circadian Clocks/genetics , RNA, Messenger/genetics , RNA, Messenger/metabolism , Phosphorylation , Protein Processing, Post-Translational , Cytoplasmic Granules/metabolism , Protein Biosynthesis , Eukaryotic Initiation Factor-2/metabolism
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