There were 142 infants in the pre-protocol group and 135 infants in the protocol group. The patients in the protocol group were heavier in weight than those in the pre-protocol group (P<.05). The Cormack-Lehane grade and the duration of operation and anesthesia were higher and longer in the pre-protocol group than in the protocol group (P<.05). Respiratory events after extubation were significantly more common in the pre-protocol group than in the protocol group [21.1 vs. 9.6%, adjusted relative risk 0.46 (95% CI 0.22-0.89), P <.01].

Among infants undergoing MDO, the standardization of extubation practices can reduce respiratory events after extubation compared with traditional management.

Among infants undergoing MDO, the standardization of extubation practices can reduce respiratory events after extubation compared with traditional management.

The purpose of this study was to identify factors that influence the need for a supplemental bone graft prior to dental implant placement at previously grafted alveolar cleft sites.

Retrospective case series of patients with cleft lip/palate who had both alveolar bone grafting (ABG) and placement of a dental implant(s) to replace a missing incisor(s) at the cleft site by the senior surgeon (BLP) at Boston Children’s Hospital from 2005 through 2020. Primary outcome variable was need for a supplemental bone graft prior to dental implant placement. Predictor variables included gender, cleft type (unilateral vs. bilateral), implant site, number of implants placed, age at ABG and implant placement, time between ABG and implant, history of maxillary expansion and whether the patient had a Le Fort I osteotomy to correct maxillary hypoplasia before implant placement. Descriptive statistics were computed and comparative analyses were performed using Pearson X

, Fisher exact, and Mann-Whitney U tests.

There wereplemental bone graft prior to implant placement.Nonalcoholic fatty liver disease often progresses to cirrhosis and causes liver cancer, but mechanisms of its progression have not been elucidated. Although nonalcoholic fatty liver disease is often associated with abnormal portal circulation, there have not been any experimental studies to test its pathogenic role. Here, whether decreased portal circulation affected the pathology of nonalcoholic steatohepatitis (NASH) was examined using congenital portosystemic shunt (PSS) in C57BL/6J mice. Whereas PSS significantly attenuated free radical-mediated carbon tetrachloride injury, it augmented pericellular fibrosis in the centrilobular area induced by a 0.1% methionine choline-deficient l-amino acid-defined high-fat diet (CDAHFD). PSS aggravated ductular reaction and increased the expression of connective tissue growth factor. Pimonidazole immunohistochemistry of the liver revealed that the centrilobular area of PSS-harboring mice was more hypoxic than that of control mice. Although tissue hypoxia was observed in the fibrotic area in CDAHFD-induced NASH in both control and PSS-harboring mice, it was more profound in the latter, which was associated with higher carbonic anhydrase 9 and vascular endothelial growth factor expression and neovascularization in the fibrotic area. Furthermore, partial ligation of the portal vein also augmented pericellular fibrosis and ductular reaction induced by a CDAHFD. These results demonstrate that decreased portal circulation, which induces hypoxia due to disrupted intralobular perfusion, is an important aggravating factor of liver fibrosis in NASH.Although hepatocellular cancer (HCC) usually occurs in the setting of liver fibrosis, the causal relationship between liver fibrosis and HCC is unclear. By studying in vivo and in vitro models of HCC using Colr/r mice (that produce a collagenase-resistant type I collagen) or wild-type (WT) mice, we aimed to assess the relationship between type I collagen, liver fibrosis, and experimental HCC. HCC was either chemically induced in WT and Colr/r mice or Hepa 1 to 6 cells were engrafted into WT and Colr/r livers. GSK1265744 mw The effect of hepatic stellate cells (HSCs) from WT and Colr/r mice on the growth of Hepa 1 to 6 cells was studied by using multicellular tumor spheroids and xenografts. Collagen type I deposition and fibrosis were increased in Colr/r mice, but they developed fewer and smaller tumors. Hepa 1 to 6 cells had reduced tumor growth in the livers of Colr/r mice. Although Colr/r HSCs exhibited a more activated phenotype, Hepa 1 to 6 growth and malignancy were suppressed in multicellular tumor spheroids and in xenografts containing Colr/r HSCs. Treatment with vitronectin, which mimics the presence of degraded collagen fragments, converted the Colr/r phenotype into a WT phenotype. Thus, although Colr/r mice have increased liver fibrosis, they exhibited decreased HCC in several models. Thus, increased liver type I collagen does not produce increased experimental HCC.Cullin (CUL) 4A and 4B ubiquitin ligases are often highly accumulated in human malignant neoplasms and are believed to possess oncogenic properties. However, the underlying mechanisms by which CUL4A and CUL4B promote pulmonary tumorigenesis remain largely elusive. This study reports that CUL4A and CUL4B are highly expressed in patients with non-small cell lung cancer (NSCLC), and high expression of both is associated with disease progression, chemotherapy resistance, and poor survival in adenocarcinomas. Depletion of CUL4A (CUL4Ak/d) or CUL4B (CUL4Bk/d) leads to cell cycle arrest at G1 and loss of proliferation and viability of NSCLC cells in culture and in a lung cancer xenograft model, suggesting that CUL4A and 4B are oncoproteins required for tumor maintenance of certain NSCLCs. Mechanistically, increased accumulation of the cell cycle-dependent kinase inhibitor p21/Cip1/WAF1 was observed in lung cancer cells on CUL4 silencing. Knockdown of p21 rescued the G1 arrest of CUL4Ak/d or CUL4Bk/d NSCLC cells and allowed proliferation to resume. These findings reveal that p21 is the primary downstream effector of lung adenocarcinoma dependence on CUL4, highlight the notion that not all substrates respond equally to abrogation of the CUL4 ubiquitin ligase in NSCLCs, and imply that CUL4Ahigh/CUL4Bhigh may serve as a prognostic marker and therapeutic target for patients with NSCLC.