Browsing by Subject "Acute inflammation"

Now showing 1 - 2 of 2
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    Molecular testing for gastrointestinal pathogens in intestinal tissue of infants with necrotizing enterocolitis or spontaneous intestinal perforation
    (Springer Nature, 2024) Talavera-Barber, Maria M.; Sánchez, Pablo J.; Conces, Miriam; Kaptsan, Irina; Everhart, Kathy; Leber, Amy; Malleske, Daniel T.; Moallem, Mohannad; Panesso-Gómez, Santiago; Shimamura, Masako; Pediatrics, School of Medicine
    Objective: The objective of this study was to determine the frequency of common gastrointestinal bacterial, parasitic, and viral pathogen detection in necrotizing enterocolitis (NEC) or spontaneous intestinal perforation (SIP) -associated intestinal tissue. Study design: Retrospective cohort study examined formalin fixed, paraffin embedded (FFPE) surgical or autopsy intestinal tissue from NEC or SIP specimens. DNA and RNA were extracted and analyzed by multiplex PCR panel (GIFA Biofire). DNA or RNA from stool samples containing each pathogen were extracted for positive controls. Results: The total number of intestinal tissue samples were 193 from 310 infants (156 NEC, 37 SIP). Six (3%) infants with stage III NEC tested positive for a target pathogen; 2, C. difficile; 3, Enteroaggregtive E. coli; and 1, Giardia. No gastrointestinal viral pathogens were detected. Conclusion: Molecular testing yielded few GI pathogens suggesting that these organisms are likely not major causes or facilitators of NEC or SIP.
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    Sex as Biological Variable in Cardiac Mitochondrial Bioenergetic Responses to Acute Stress
    (MDPI, 2022-08-18) Scott, Susan R.; Singh, Kanhaiya; Yu, Qing; Sen, Chandan K.; Wang, Meijing; Surgery, School of Medicine
    Cardiac dysfunction/damage following trauma, shock, sepsis, and ischemia impacts clinical outcomes. Acute inflammation and oxidative stress triggered by these injuries impair mitochondria, which are critical to maintaining cardiac function. Despite sex dimorphisms in consequences of these injuries, it is unclear whether mitochondrial bioenergetic responses to inflammation/oxidative stress are sex-dependent. We hypothesized that sex disparity in mitochondrial bioenergetics following TNFα or H2O2 exposure is responsible for reported sex differences in cardiac damage/dysfunction. Methods and Results: Cardiomyocytes isolated from age-matched adult male and female mice were subjected to 1 h TNFα or H2O2 challenge, followed by detection of mitochondrial respiration capacity using the Seahorse XF96 Cell Mito Stress Test. Mitochondrial membrane potential (ΔΨm) was analyzed using JC-1 in TNFα-challenged cardiomyocytes. We found that cardiomyocytes isolated from female mice displayed a better mitochondrial bioenergetic response to TNFα or H2O2 than those isolated from male mice did. TNFα decreased ΔΨm in cardiomyocytes isolated from males but not from females. 17β-estradiol (E2) treatment improved mitochondrial metabolic function in cardiomyocytes from male mice subjected to TNFα or H2O2 treatment. Conclusions: Cardiomyocyte mitochondria from female mice were more resistant to acute stress than those from males. The female sex hormone E2 treatment protected cardiac mitochondria against acute inflammatory and oxidative stress.