Objective Early presentation and prompt diagnosis of acute appendicitis are necessary to prevent progression of disease leading to complicated appendicitis. We hypothesize that patients had a delayed presentation of acute appendicitis during the COVID-19 pandemic, which affected severity of disease on presentation and outcomes. Patients and methods We conducted a retrospective review of all patients who were treated for acute appendicitis at Morgan Stanley Children's Hospital (MSCH) between March 1, 2020 and May 31, 2020 when the COVID-19 pandemic was at its peak in New York City (NYC). For comparison, we reviewed patients treated from March 1, 2019 to May 31, 2019, prior to the pandemic. Demographics and baseline patient characteristics were analyzed for potential confounding variables. Outcomes were collected and grouped into those quantifying severity of illness on presentation to our ED, type of treatment, and associated post-treatment outcomes. Fisher's Exact Test and Kruskal-Wallis Test were used for univariate analysis while cox regression with calculation of hazard ratios was used for multivariate analysis. Results A total of 89 patients were included in this study, 41 patients were treated for appendicitis from March 1 to May 31 of 2019 (non-pandemic) and 48 were treated during the same time period in 2020 (pandemic). Duration of symptoms prior to presentation to the ED was significantly longer in patients treated in 2020, with a median of 2 days compared to 1 day (p = 0.003). Additionally, these patients were more likely to present with reported fever (52.1% vs 24.4%, p = 0.009) and had a higher heart rate on presentation with a median of 101 beats per minute (bpm) compared to 91 bpm (p = 0.040). Findings of complicated appendicitis on radiographic imaging including suspicion of perforation (41.7% vs 9.8%, p < 0.001) and intra-abdominal abscess (27.1% vs 7.3%, p = 0.025) were higher in patients presenting in 2020. Patients treated during the pandemic had higher rates of non-operative treatment (25.0% vs 7.3%, p = 0.044) requiring increased antibiotic use and image-guided percutaneous drain placement. They also had longer hospital length of stay by a median of 1 day (p = 0.001) and longer duration until symptom resolution by a median of 1 day (p = 0.004). Type of treatment was not a predictor of LOS (HR = 0.565, 95% CI = 0.357–0.894, p = 0.015) or duration until symptom resolution (HR = 0.630, 95% CI = 0.405–0.979, p = 0.040). Conclusion Patients treated for acute appendicitis at our children's hospital during the peak of the COVID-19 pandemic presented with more severe disease and experienced suboptimal outcomes compared to those who presented during the same time period in 2019. Level of Evidence III
Limits to sustained energy intake (SusEI) during lactation are important because they provide an upper boundary below which females must trade off competing physiological activities. To date, SusEI is thought to be limited either by the capacity of the mammary glands to produce milk (the peripheral limitation hypothesis) or by a female's ability to dissipate body heat (the heat dissipation hypothesis). In the present study, we examined the effects of litter size and ambient temperature on a set of physiological, behavioral and morphological indicators of SusEI and reproductive performance in lactating Swiss mice. Our results indicate that energy input, energy output and mammary gland mass increased with litter size, whereas pup body mass and survival rate decreased. The body temperature increased significantly, while food intake (18 g day −1 at 21°C versus 10 g day −1 at 30°C), thermal conductance (lower by 20-27% at 30°C than 21°C), litter mass and milk energy output decreased significantly in the females raising a large litter size at 30°C compared with those at 21°C. Furthermore, an interaction between ambient temperature and litter size affected females' energy budget, imposing strong constraints on SusEI. Together, our data suggest that the limitation may be caused by both mammary glands and heat dissipation, i.e. peripheral limitation is dominant at room temperature, but heat dissipation is more significant at warm temperatures. Further, the level of the heat dissipation limits may be temperature dependent, shifting down with increasing temperature.
Human riboflavin transporter 2 (RFT2) encoded by the SLC52A3 gene is a member of the SLC52 family that has been shown to play a key role in riboflavin homeostasis. Recently, a number of studies have shown that RFT2 is important in the development of several cancers, including esophageal squamous cell carcinoma, gastric cancer, and cervical cancer. However, its expression and function in glioma have not yet been explored. In this study, we found that RFT2 was overexpressed in glioma samples compared with normal brain tissue. Furthermore, RFT2 expression was correlated with WHO grade (P<0.001). Silencing of RFT2 resulted in inhibition of glioma cell proliferation through promotion of cell cycle arrest and apoptosis. Expression of proteins known to regulate cell cycle or apoptosis including p21, p27, BCL-2, and BAX was notably altered in RFT2-depleted cells. Furthermore, silencing of RFT2 impeded the migration and invasion of glioma cells through suppression of matrix metalloproteinase-2 and matrix metalloproteinase-9 expression. In addition to blocking cell proliferation in vitro, reduction of RFT2 levels also decreased tumor growth in vivo. These data suggest that RFT2 could be an attractive therapeutic target for the treatment of glioma.
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