However, further patient-level evaluation of treatment at low- versus high-volume hospitals demonstrated that hospital volume did not predict the risk of developing perioperative systemic (OR, 1.28; 95 percent CI, 0.75 to 2.18; p = 0.36) or microsurgical complications (OR, 1.06; 95 percent CI, 0.78 to 1.44; p = 0.73).

Perioperative complications after free flap breast reconstruction did not differ between patients treated at low- versus high-volume hospitals after in-depth multiprong analysis. Patient outcomes are more likely associated with surgeon and programmatic experience. Overall annual hospital volume should not serve as a proxy for high-quality breast free flap care. .

Risk, III.

Risk, III.In utero transmission of severe acute respiratory syndrome coronavirus 2 infection is a point of debate. We report a case of severe acute respiratory syndrome coronavirus 2 vertical transmission from asymptomatic mother, with molecular detection in mother’s blood at delivery and neonatal nasopharyngeal swabs at 5 and 28 hours of life and later IgG seroconversion. The newborn was asymptomatic.Multisystem inflammatory syndrome in children (MIS-C) is an emerging entity during the coronavirus disease 2019 pandemic. Medium- and large-vessel changes are present in MIS-C; however, microcirculatory impairment has not been documented. We report a case of MIS-C in a toddler that presented with persistent fever, gastrointestinal symptoms and rash. Nailfold videocapillaroscopy was abnormal, suggesting microcirculatory disease in the setting of MIS-C.

Meningococcal serogroup B (MenB) is the leading cause of invasive meningococcal disease among US adolescents and young adults, accounting for 62% of cases in 16-23-year-olds in 2018. Since 2015, the Advisory Committee on Immunization Practices (ACIP) has recommended vaccination of healthy adolescents against MenB based on shared clinical decision-making (previously called „Category B“ or individual clinical decision-making). However, MenB vaccine coverage and series completion rates remain low. Herein we examine implementation experience of adolescent MenB vaccination in the United States under this nonroutine ACIP recommendation.

PubMed was searched for English-language articles published after 2015 examining MenB vaccination implementation in the United States. Studies reporting MenB vaccination awareness, coverage, knowledge of recommendations and implementation barriers or access disparities were included.

Identified studies provided evidence that ACIP’s MenB vaccination recommendation is poorly undr MenB vaccines is partly responsible for low vaccine coverage. Further, inconsistent implementation of ACIP recommendations could be limiting access to MenB vaccines. Providers need additional support and guidance to implement the shared clinical decision-making recommendation, in turn ensuring equitable access for vaccine-eligible adolescents to enable comprehensive protection against meningococcal disease.We analyzed 19 cases of breakthrough candidemia from a referral pediatric cancer center in Brazil. All patients had neutropenia and were under antifungal prophylactic regimens, mostly micafungin (68%). Most of the patients were treated with amphotericin B formulations and 30-day mortality was 21%. Candida parapsilosis was the main etiologic agent (63%), and horizontal transmission was not evidenced by microsatellite analysis.

Surveillance is essential to all aspects of management of healthcare-associated infections (HAIs) in critically ill children, where data are limited. We conducted an active surveillance study to elucidate epidemiology, resistance, antimicrobial treatment practices and outcomes of pediatric intensive care unit-acquired HAIs in a southern European country.

Four Greek pediatric intensive care unit encounters (153 patients, 2183 patient-days) during a 6-month period participated using the European Centre for Disease Prevention and Control HAI-net ICU (v2.2) protocol. Bloodstream infections and device-associated HAIs were recorded. Clinical severity, isolated pathogens, antimicrobial resistance and antibiotic prescriptions were collected on a daily basis. Mortality and excess length of stay due to HAI were also assessed.

Overall rate of HAIs was 18.3 per 1000 patient-days. Aggregate rates for device-associated HAI were catheter-related bloodstream infection 2.32, intubation-associated pneumonia 10.5, and catn critically ill children in Greece. Using a well-standardized system facilitates inter- and intra-countries reliable recordings and comparative assessments of infection control programs.We describe a 6-week-old male-term infant with a pulmonary aspergilloma diagnosed following lobectomy for suspected pleuropulmonary blastoma, with characteristic histopathologic findings and Aspergillus detected by polymerase chain reaction. Intensive testing did not reveal primary or secondary immunodeficiency. During 5 weeks treatment with voriconazole including regular therapeutic drug monitoring and dose adjustment, a level in the target range was never achieved. When the patient developed photosensitivity, treatment was stopped without relapse over 12 months follow-up. Voriconazole dosing is notoriously challenging in children. We review the cumulative published experience with voriconazole use in infants to highlight even greater difficulty in infants. Pulmonary aspergillosis is typically a disease affecting immunocompromised or critically ill patients. In children, it is well described in those with chronic granulomatous disease (CGD) as a complication of immunosuppressive antineoplastic chemotherapy and rarely in extremely- or very-low birthweight premature neonatal intensive care patients. The diagnosis is extremely rare in children without underlying risk factors. To our knowledge, this is the first report of a pulmonary aspergilloma in an immunocompetent infant.

This research plans to address the function of miR-204-5p/tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma (YWHAG) in cerulein-induced acute pancreatitis (AP).

Rat pancreatic acinar cell AR42J was stimulated by 100 nmol/L of cerulein to mimic the situation in AP. Gene Expression Omnibus database was used to select differentially expressed genes. StarBase database and Kyoto Encyclopedia of Genes and Genomes enrichment analysis were used to select the target genes of miR-204-5p, which were further affirmed by dual luciferase assay. The biological behaviors of AR42J cells were measured by cell proliferation and flow cytometry assays. Quantitative real-time polymerase chain reaction and western blot assays were executed to assess YWHAG expression. The secretion of C-C Motif Chemokine Ligand 2/Timp metallopeptidase inhibitor 1 in AR42J cells was evaluated by enzyme-linked immunosorbent assay. The protein expression of YAP1/p-YAP1/PI3K/p-PI3K was measured by western blot.

miR-204-5p expression was profoundly reduced in cerulein-induced AP model. YWHAG was upregulated in cerulein-induced AP model and related to C-C Motif Chemokine Ligand 2/Timp1. In addition to the negative association between miR-204-5p and YWHAG, the alleviation impact of miR-204-5p mimic on cerulein-induced AR42J cell damage was blocked by YWHAG overexpression and PI3K/Hippo signaling pathways activation.

These observations indicated that the alleviation impact of miR-204-5p on cerulein-induced AR42J cell damage was mediated via YWHAG and PI3K/Hippo signaling pathways.

These observations indicated that the alleviation impact of miR-204-5p on cerulein-induced AR42J cell damage was mediated via YWHAG and PI3K/Hippo signaling pathways.

The mechanisms underlying hypothermia-induced pancreatic injury are unclear. Thus, we investigated the pathophysiology of hypothermia-induced pancreatic injury.

We created a normal circulatory model with body surface cooling in rats. We divided the rats into control (36°C-38°C), mild hypothermia (33°C-35°C), moderate hypothermia (30°C-32°C), and severe hypothermia (27°C-29°C) (n = 5 per group) groups. Then, we induced circulatory failure with a cooling model using high-dose inhalation anesthesia and divided the rats into control (36°C-38°C) and severe hypothermia (27°C-29°C) (n = 5 per group) groups. Serum samples were collected before the introduction of hypothermia. Serum and pancreatic tissue were collected after maintaining the target body temperature for 1 hour.

Hematoxylin and eosin staining of the pancreas revealed vacuoles and edema in the hypothermia group. Serum amylase (P = 0.056), lactic acid (P < 0.05), interleukin 1β (P < 0.05), interleukin 6 (P < 0.05), and tumor necrosis factor α (P = 0.13) levels were suppressed by hypothermia. The circulatory failure model exhibited pancreatic injury.

Hypothermia induced bilateral effects on the pancreas. Morphologically, hypothermia induced pancreatic injury based on characteristic pathology typified by vacuoles. Serologically, hypothermia induced protective effects on the pancreas by suppressing amylase and inflammatory cytokine levels.

Hypothermia induced bilateral effects on the pancreas. Morphologically, hypothermia induced pancreatic injury based on characteristic pathology typified by vacuoles. Serologically, hypothermia induced protective effects on the pancreas by suppressing amylase and inflammatory cytokine levels.

Elucidation of the regulatory mechanisms of gemcitabine sensitivity is needed to improve the therapeutic effects of this drug in pancreatic cancer.

PANC-1 cells were transfected with small hairpin RNA against PVT1 or microRNA (miR)-143 mimics or inhibitor. The gemcitabine sensitivity of pancreatic cancer was evaluated. Autophagosomes were analyzed with an immunofluorescence assay. Cell viability and proliferation were examined with MTT assays. Quantitative reverse transcription-polymerase chain reaction and Western blotting were used to analyze the expression of PVT1, miR-143, HIF-1α, VMP1, LC3I/II, p62, and Beclin-1. The interactions of PVT1/miR-143 and miR-143/HIF-1α were assessed by dual-luciferase reporter assays.

PVT1 was upregulated while miR-143 was downregulated in pancreatic cancer. Both PVT1 knockdown and miR-143 overexpression suppressed autophagy and improved gemcitabine sensitivity in pancreatic cancer. PVT1 directly sponged miR-143 to regulate HIF-1α expression. MiR-143 inhibitor reversed the effect of PVT1 knockdown on autophagy and gemcitabine sensitivity.

PVT1 knockdown inhibited autophagy and improved gemcitabine sensitivity via the miR-143/HIF-1α/VMP1 axis in pancreatic cancer. H89 Our investigation elucidated a novel regulatory mechanism of gemcitabine sensitivity and may contribute to improve the therapeutic effects of chemotherapy drugs on pancreatic cancer.

PVT1 knockdown inhibited autophagy and improved gemcitabine sensitivity via the miR-143/HIF-1α/VMP1 axis in pancreatic cancer. Our investigation elucidated a novel regulatory mechanism of gemcitabine sensitivity and may contribute to improve the therapeutic effects of chemotherapy drugs on pancreatic cancer.

Pancreatic ductal adenocarcinoma is the fourth-leading cause of cancer death in the United States, and there is an urgent need for effective therapies. Stearoyl-CoA desaturase (SCD) is an enzyme localized in the endoplasmic reticulum and generates monounsaturated fatty acid from saturated fatty acid. In this study, we examined the role of SCD in pancreatic cancer.

We isolated epithelial cell adhesion molecule-positive pancreatic tumors from the Pdx1Cre;LSL-KrasG12D mouse and formed organoids in Matrigel. Using a SCD inhibitor, A939572, we tested its effects on growth and cell death in tumor organoids, tumors developed in the Pdx1Cre;LSL-KrasG12D mouse, and a human pancreatic ductal adenocarcinoma cell line, PANC-1.

A939572 treatment rapidly induced degeneration of mouse tumor organoids and activated the unfolded protein response (UPR). Cotreatment of oleic acid, but not stearic acid, reduced the UPR in the organoids and rescued the inhibitory effect of the SCD inhibitor on their growth. Administration of A939572 to Pdx1Cre;LSL-KrasG12D mice caused cell death in early pancreatic tumors, but not in acini or islets.