Publications by authors named "Lahari Vuppaladhadiam"

Objective: To evaluate the relationship between duration of labor during second-trimester medication abortion and adverse outcomes.

Methods: We conducted a retrospective cohort study including all individuals with a singleton gestation undergoing second-trimester medication abortion without evidence of advanced cervical dilation, rupture of membranes, or preterm labor at four centers. The primary exposure was duration of labor (ie, hours spent from receiving misoprostol to fetal expulsion).

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Background: Op-ed writing can be a powerful and accessible advocacy tool for physicians, but training is lacking in undergraduate medical education.

Aim: To train and engage first-year medical students in op-ed writing.

Setting: Midwestern research-intensive medical school.

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Objective: This study aimed to assess if the use of mechanical dilation at the time of induction termination is associated with changes in the time from initiation of labor to expulsion of the fetus (induction-to-expulsion interval) and with the frequency of health complications when compared with medication management alone.

Data Sources: PubMed, CINAHAL, Scopus, and the Cochrane Central Register of Controlled Trials were queried from January 2000 to May 2023.

Study Eligibility Criteria: We included randomized controlled trials of individuals who were assigned to undergo mechanical dilation (ie, laminaria, Dilapan-S, and intracervical Foley balloon catheter) in combination with the use of medication and compared it with the outcomes of medication use (eg, prostaglandins, antiprogestins, oxytocin) alone.

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The mitochondrial response to changes in cellular energy demand is necessary for cellular adaptation and organ function. Many genes are essential in orchestrating this response, including the transforming growth factor (TGF)-β1 target gene Mss51, an inhibitor of skeletal muscle mitochondrial respiration. Although Mss51 is implicated in the pathophysiology of obesity and musculoskeletal disease, how Mss51 is regulated is not entirely understood.

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Maternal stress during pregnancy is linked to several negative birth outcomes. The placenta, a unique pregnancy-specific organ, not only nourishes and protects the fetus but is also the major source of progesterone and estrogens. As the placenta becomes the primary source of maternal progesterone (P4) and estradiol between 6-9 weeks of gestation, and these hormones are critical for maintaining pregnancy, maternal stress may modulate levels of these steroids to impact birth outcomes.

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No organ in the body is impervious to the effects of stress, and a coordinated response from all organs is essential to deal with stressors. A dysregulated stress response that fails to bring systems back to homeostasis leads to compromised function and ultimately a diseased state. The components of the corticotropin-releasing factor (CRF) family, an ancient and evolutionarily conserved stress hormone-receptor system, helps both initiate stress responses and bring systems back to homeostasis once the stressors are removed.

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