Adenoid hypertrophy (AH) is a common disorder in children, resulting in chronic nasal congestion. This chronic congestion should be evaluated carefully because it can lead to chronic upper airway obstruction. Many authors have suggested that increased nasal resistance to respiration may cause disturbances in the pulmonary ventilation and carry the risk of cardiopulmonary diseases. Mean platelet volume (MPV) is a marker of platelet function and is positively associated with indicators of platelet activity. Mean platelet volume is an indicator of larger and more reactive platelets and has been shown to be increased in patients with vascular disease, including peripheral, pulmonary, and coronary artery disease. Recently, MPV levels have also been shown to be increased in patients with severe obstructive sleep apnea, and marked nasal septal deviation. Moreover, increased MPV has also been shown to have a prognostic role in cardiovascular disease. We investigated whether MPV is higher in patients with AH and whether higher MPV levels can be reduced by adenoidectomy. To the best of our knowledge, this is the first study to investigate MPV in patients with AH. Our results suggest that MPV, a determinant of platelet activation, is elevated in patients with AH and adenoidectomy is an effective therapeutic measure in such patients. Increased platelet activation may be related to an increase of cardiopulmonary risk in patients with AH.
Evisceration of the small intestine through the anus is an extremely rare event in children. We report a 2-year-old boy who sustained transanal small bowel evisceration associated with bilateral diaphragmatic rupture, left diaphragmatic herniation, and spinal cord injury without radiographic abnormality which happened after crushing by motor vehicle. We reviewed children with transanal small bowel evisceration and discussed etiological differences between children and adult. We also discussed the basic principles of management and follow up in these patients.
We consider that it is reasonable to wait up to an age at which the child could understand and participate in the decision of the concept and timing of circumcision.
Abstract. Glucose-regulated protein 78 kDa/binding immunoglobulin protein (GRP78/BIP) is a well-known endoplasmic reticulum (ER) chaperone protein regulating ER stress by facilitating protein folding, assembly and Ca 2+ binding. GRP78 is also a member of the heat shock protein 70 gene family and induces tumor cell survival and resistance to chemotherapeutics. Bortezomib is a highly specific 26S proteasome inhibitor that has been approved as treatment for patients with multiple myeloma. The present study first examined the dose-and time-dependent effects of bortezomib on GRP78 expression levels in the highly metastatic mouse breast cancer 4T1 cell line using western blot analysis. The analysis results revealed that GRP78 levels were significantly increased by bortezomib at a dose as low as 10 nM. Time-dependent experiments indicated that the accumulation of GRP78 was initiated after a 24 h incubation period following the addition of 10 nM bortezomib. Subsequently, the present study determined the half maximal inhibitory concentration of intracellular calcium chelator BAPTA-AM (13.6 µM) on 4T1 cells. The combination effect of BAPTA-AM and bortezomib on the 4T1 cells was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and WST-1 assays and an iCELLigence system. The results revealed that the combination of 10 nM bortezomib + 5 µM BAPTA-AM is more cytotoxic compared with monotherapies, including 10 nM bortezomib, 1 µM BAPTA-AM and 5 µM BAPTA-AM. In addition, the present results revealed that bortezomib + BAPTA-AM combination causes cell death through the induction of apoptosis. The present results also revealed that bortezomib + BAPTA-AM combination-induced apoptosis is associated with a clear increase in the phosphorylation of stress-activated protein kinase/Jun amino-terminal kinase SAPK/JNK. Overall, the present results suggest that bortezomib and BAPTA-AM combination therapy may be a novel therapeutic strategy for breast cancer treatment.
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