Incidence and risk factors associated with negative postoperative behavioral changes in children undergoing painless gastroscopy.

OBJECTIVE: To investigate the incidence of and risk factors associated with negative postoperative behavioral changes (NPOBCs) in children undergoing painless gastroscopy. METHODS: Inclusion criteria: ASA I-II and outpatients aged 6-12 years undergoing painless gastroscopy. EXCLUSION CRITERIA: history of surgery or anesthesia, children with developmental or intellectual abnormalities, refusal to participate, preoperative abdominal pain score > 3 points, history of chronic abdominal pain of > 3 months duration, and serious intraoperative complications. On the 1st, 14th, and 30th day after the gastroscopy, the Post Hospitalization Behavior Questionnaire for Ambulatory Surgery (PHBQ-AS) was used to assess NPOBCs in children. RESULTS: A total of 1,670 children were included in this prospective observational cohort study. The incidence rates of NPOBCs were 14.13%, 4.55%, and 2.14% on the 1st, 14th, and 30th day after gastroscopy, respectively. The risk factors for the first day were female sex (OR 1.34, 95% CI 1.00-1.79), parental anxiety (OR 2.23, 95% CI 1.75-3.12), and severe anxiety in children (OR 2.83, 95% CI 1.96-4.07). The risk factors on the 14th day were parental anxiety (OR 3.71, 95% CI 2.19-6.29), a parental educational level above high school (OR 1.65, 95% CI 1.00-2.70), and severe anxiety in children (OR 11.87, 95% CI 5.85-24.07). The risk factors on the 30th day were female sex (OR 2.99, 95% CI 1.41-6.34), being an only child (OR 4.42, 95% CI 2.18-8.95), a parental educational level above high school (OR 2.66, 95% CI 1.27 NPOBCs 5.56), and severe anxiety in children (OR 6.84, 95% CI 2.84-16.49). CONCLUSION: In children undergoing painless gastroscopy, the incidence rates of NPOBCs on the 1st, 14th, and 30th day were 14.13%, 4.55%, and 2.14%, respectively. The risk factors for NPOBCs were severe anxiety in children, female sex, parental anxiety, and a parental educational level above high school. In particular, severe preoperative anxiety in children was a persistent risk factor for NPOBCs within 30 days.

Stilbene B10 induces apoptosis and tumor suppression in lymphoid Raji cells by BTK-mediated regulation of the KRAS/HDAC1/EP300/PEBP1 axis.

Lymphoma is a cancer of the lymphoid cells that originated in matured B or T cells. The bioactive natural compounds can efficiently treat this disease with lesser side effects. Thus, in this study, a natural stilbene B10 (3-methoxy 5-hydroxy stilbene) isolated from Cajanus cajan (Pigeon Pea) was screened for its anti-proliferative efficacy against 13 cancer cell lines. B10 showed a potential effect on the human lymphoma (Raji) cells. Cytotoxicity analysis of B10 has revealed IC50 concentrations in Raji cells at low doses (18 µM) than other cancer cell lines. The B10 could significantly cause dose and time-dependent inhibition in the proliferation of Raji cells triggering intrinsic apoptosis and S/G1 phase cellular arrest. There was an increased expression of phospho-γ-H2A.X and decreased expression of cyclin D1, causing DNA damage and cell cycle arrest, post- B10 treatments. The mitochondrial membrane potential (MMP) variations observed after B10 treatment led to changes in Bax/Bcl-2 ratio, cytochrome C release, and enhanced expression of cleaved caspase3, 9, PARP-1, and APAF-1. The B10 inhibited the proliferation of Raji cells by significantly downregulating the expression of KRAS, BTK, MDM2, P-JAK2, P-STAT3, PI3K, HDAC1/2, SIRT7, and EP300. The treatment upregulated the tumor suppressor genes PEBP1 and SAP18. Thus, the study could reveal the selective inhibitory effects of B10 on lymphoma, suggesting it as a probable innovative chemotherapeutic agent.

Retrospective Study of the Etiology and Risk Factors of Systemic Inflammatory Response Syndrome After Systematic Transrectal Ultrasound-Guided Prostate Biopsy.

OBJECTIVE: To explore the risk factors, pathogenic bacteria distribution and drug resistance of systematic transrectal ultrasound-guided prostate biopsy (TRUS-Bx), 329 cases of TRUS-Bx were collected, retrospectively, in the Second Affiliated Hospital, Army Military Medical University, from April 2017 to October 2019. METHODS: A total of 329 cases were all qualified and grouped into the SIRS group (25 cases) and the non-SIRS group (304 cases). Of all the cases, incidence and risk factors of systemic inflammatory response syndrome (SIRS) were analyzed. Urine and blood samples of patients with SIRS after TRUS-Bx were also collected for bacterial culture and drug sensitivity test. RESULTS: Multivariate logistic regression analysis showed that BMI ≥ 25 kg/m2 (OR = 1.66, 95% CI = 1.34-2.12, P <0.001), history of diabetes (OR = 5.48, 95% CI = 1.53-19.68, P = 0.008), urinary infection before operation (OR = 9.19, 95% CI = 2.92-20.93, P < 0.001) and erythrocyte sedimentation (ESR) ≥ 20 mm/h (OR = 1.04, 95% CI = 1.01-1.08, P = 0.039) were independent risk factors of SIRS after TURS-PB. CONCLUSION: The incidence of SIRS and urinary sepsis was 7.59% and 2.13%, respectively, and major pathogens of SIRS after TRUS-Bx were Escherichia coli (58.33%), Klebsiella pneumoniae (12.5%) and Pseudomonas aeruginosa (12.5%). Imipenem, meropenem, tigecycline, piperacillin/tazobactam, teicoplanin, vancomycin, amikacin and cefoperazone/sulbactam had a very strong inhibitory effect to those pathogenic bacteria (sensitivity 85.72%~100%). Levofloxacin, ciprofloxacin, gentamicin, penicillin G, compound neonomine and second-generation cephalosporins showed less but also worked as a good inhibitor to pathogenic bacteria (42.86%~80.95%).

UNC45A localizes to centrosomes and regulates cancer cell proliferation through ChK1 activation.

The UCS family of proteins regulates cellular functions through their interactions with myosin. Here we show that one member of this family, UNC45A, is also a novel centrosomal protein. UNC45A is required for cellular proliferation of cancer cell in vitro and for tumor growth in vivo through its ability to bind and regulate ChK1 nuclear-cytoplasmic localization in an Hsp90-independent manner. Immunocytochemical and biochemical fractionation studies revealed that UNC45A and ChK1 co-localize to the centrosome. Inhibition of UNC45A expression reduced ChK1 activation and its tethering to the centrosome, events required for proper centrosome function. Lack of UNC45A caused the accumulation of multi-nucleated cells, consistent with a defect in Chk1 regulation of centrosomes. These findings identify a novel centrosomal function for UNC45A and its role in cell proliferation and tumorigenesis.

Molecular phylogenetic evidence for paraphyly of Ceratovacuna and Pseudoregma (Hemiptera, Hormaphidinae) reveals late Tertiary radiation.

Ceratovacuna and Pseudoregma are important groups in Cerataphidini (Hemiptera, Hormaphidinae) that not only produce soldier aphids in galls on the primary hosts but also produce horned soldiers on the herbaceous secondary hosts. However, due to sampling bias in previous studies, the phylogenetic relationships of these two genera remain inconclusive. In this study, based on more extensive sampling and examination of both mitochondrial (cytochrome c oxidase subunit I (COI); cytochrome b (Cytb)) and nuclear (elongation factor-1α (EF-1α); long-wavelength opsin (LWO)) genes, we reconstructed the phylogenetic relationships of Ceratovacuna and Pseudoregma. Phylogenetic analyses, along with morphological evidence, suggested that these two genera belong to the paraphyletic groups with species clustered into three main groups. The monophyly of Ceratovacuna and Pseudoregma as a whole was generally supported by all analyses. Monophyly of Pseudoregma was also supported. The estimated divergence times demonstrated that diversification of Ceratovacuna and Pseudoregma occurred approximately at 10 mya. The relatively low resolution for the basal relationships of the three main clades may indicate that these two genera have experienced a rapid radiation along with speciation burst of their secondary hosts during the late Tertiary.

Acute lung injury in patients with severe acute pancreatitis.

BACKGROUND/AIMS: Severe acute pancreatitis can result in acute lung injury. This study aims to investigate the clinical characteristics and possible prediction index of acute lung injury in severe acute pancreatitis. MATERIALS AND METHODS: We retrospectively evaluated 184 patients with severe acute pancreatitis admitted between April 2007 and July 2010. There were 51 patients who developed acute lung injury with a rate of 27.7% (51/184). Clinical data of the acute lung injury and non-acute lung injury patients were compared, and the characteristics of acute lung injury were also analyzed. Meanwhile, we validated a few possible prediction indexes to identify the patients at high risk for acute lung injury at the time of hospital admission. RESULTS: The severity index, hospital day, and the incidence of infectious complications were significantly higher in the acute lung injury patients than in the nonacute lung injury patients (p<0.05). The differences between the non-acute lung injury and acute lung injury groups in mortality (3% vs. 11.8%, p<0.05), operation (5.3% vs. 15.7%, p<0.05), and incidence of renal failure (15.8% vs. 33.3%, p<0.05), cardiovascular failure (3.8% vs. 15.7%, p<0.05), and pancreatic cyst (18% vs. 37.3%, p<0.05) were statistically significant. The patients with higher level of severity index score, acidosis, tachypnea, smoking history, and obesity were prone to develop acute lung injury. conclusion: Acute lung injury occurrence in patients with severe acute pancreatitis varies according to predisposing conditions and independently carries poor prognosis.