Background: In order to establish an effective screening method for respiratory inhibition after crying (RIAC), we prospectively studied the correlations between infant RIAC and perinatal factors.
Methods: We monitored infants (n=141) born from May through July 2009 with polygraphy and evaluated the presence of RIAC and respiratory pause that occurred when feeding was initiated immediately after crying with a decrease in oxygen saturation (SpO(2) ) to <60%. The infants were screened for increased echogenicity, a cyst in the ganglionic eminence (GE), or a subependymal cyst by cranial ultrasound. Furthermore, we evaluated the correlations between RIAC and perinatal factors.
Results: Eleven infants displayed RIAC and 31 experienced respiratory pause during feeding with a decrease in SpO(2) to <60%. There were no significant correlations between RIAC and perinatal factors. Forty infants had ultrasound abnormalities (increased echogenicity in the GE, 26; cyst in the GE, nine; and subependymal cyst, seven). Sensitivity, specificity, and efficiency of abnormal cranial ultrasound findings for RIAC were 1.00, 0.777, and 0.794, respectively. The odds ratio, sensitivity, specificity, and efficiency of the combination of abnormal cranial ultrasound findings and respiratory pause during feeding with a decrease in SpO(2) to <60% and RIAC were 35.9 (P<0.001), 0.727, 0.931, and 0.915, respectively.
Conclusion: The combination of abnormal cranial ultrasound findings and respiratory pause during feeding with a decrease in SpO(2) appears to be an effective method of screening for RIAC.
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http://dx.doi.org/10.1111/j.1442-200X.2010.03205.x | DOI Listing |
Sci Rep
December 2024
Department of Respiratory Medicine, Hunan Provincial People's Hospital (The First-Affiliated Hospital of Hunan Normal University), No. 61 Jiefang Xi Road, Changsha, Hunan, 410219, China.
Pulmonary arterial hypertension (PAH) is a serious medical condition that causes a failure in the right heart. Two-pore channel 2 (TPC2) is upregulated in PAH, but its roles in PAH remain largely unknown. Our investigation aims at the mechanisms by which TPC2 regulates PAH development.
View Article and Find Full Text PDFSci Rep
December 2024
Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), Department of Chronic Diseases and Metabolism, KU Leuven, Leuven, Belgium.
The lungs of people with cystic fibrosis (PwCF) are characterized by recurrent bacterial infections and inflammation. Infections in cystic fibrosis (CF) are left unresolved despite excessive neutrophil infiltration. The role of CFTR in neutrophils is not fully understood.
View Article and Find Full Text PDFVet Res
December 2024
Key Laboratory of Animal Diseases Diagnostic and Immunology, Ministry of Agriculture, MOE International Joint Collaborative Research Laboratory for Animal Health & Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, China.
Cell Death Dis
December 2024
Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Radiotherapy resistance is one of the main reasons for the dismal clinical outcome of patients with esophageal squamous cell carcinoma (ESCC). Therefore, clarifying the targets and molecular mechanisms of radiotherapy resistance in ESCC is of great theoretical and clinical significance to enhance the efficacy of radiotherapy. In this study, GPR37 was identified as a key factor facilitating ESCC radiosensitization.
View Article and Find Full Text PDFJ Gastroenterol Hepatol
December 2024
Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut, USA.
Aim: The goal of this study was to determine the role of histone deacetylase 9 (HDAC9) in the development of diet-induced metabolic dysfunction-associated steatohepatitis (MASH) and white adipose tissue (WAT) dysfunctions.
Methods: We fed male and female mice with global Hdac9 knockout (KO) and their wild-type (WT) littermates an obesogenic high-fat/high-sucrose/high-cholesterol (35%/34%/2%, w/w) diet for 20 weeks.
Results: Hdac9 deletion markedly inhibited body weight gain and liver steatosis with lower liver weight and triglyceride content than WT in male mice but not females.
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