Therapeutic effects of ulinastatin on postoperative complications and cognitive function in elderly patients with esophageal cancer after thoracic laparoscopic surgery

Purpose: To investigate the therapeutic effect of ulinastatin on postoperative complications and cognitive function in elderly patients with esophageal cancer after thoracic laparoscopic surgery. Methods: A total of 100 elderly in-patients with esophageal cancer who had undergone thoracic laparoscopic surgery from April 2019 to December 2020 were selected and randomly assigned to control and study groups. Patients in control group received conventional treatment, while those in the study group were administered ulinastatin. The two groups were compared with respect to response, incidence of postoperative complications, Mini-Mental State Examination (MMSE) cognitive function score, Barthel Index (BI) scores; preoperative, intraoperative, 12-h and 24-h post-surgery levels of IL-1β and IL-6; levels of CD3+, CD4+ and CD8+, as well as duration of surgery and waking time. Results: Response, MMSE score, BI index, and levels of CD3+, CD4+ and CD8+ in the study group were significantly higher than those in the control group (p < 0.05). Incidence of postoperative complications, and expression levels of IL-1β and IL-6 12 h and 24 h after surgery in the study group were lower than the corresponding control levels (p < 0.05). There were no significant differences in duration of operation and waking time between the two groups (p > 0.05). Conclusion: Ulinastatin significantly reduces postoperative complications, and also improves cognitive function in elderly patients with esophageal cancer after thoracic laparoscopic surgery. This finding is of great significance in the treatment of these patients

A Comparison of Fundamental Movement Skills in Children with Autism Spectrum Disorder and Typically Developing Children

Autism Spectrum Disorders (ASD) is urodevelopmental disorder characterized by social and communication impairments as well as a wide range of behavior deficits. For years, motor disturbance reported in ASD has not been treated as a major core deficit because of the overwhelming problems in sociability and communication. Recent studies, however, reveal that motor deficits are associated with the core symptoms of ASD. Because limited studies have addressed motor behavior of children with ASD, especially in China, the purpose of this study is to explore the development of fundamental movement skills in children with ASD and compare it to that of typically developing (TD) children. A total of 108 children with ASD aged 5-14 years and 108 age- and gender-matched TD children were evaluated. FMS were assessed with the Movement Assessment Battery for Children 2nd edition (MABC-2) including manual dexterity, aiming and catching, static and dynamic balance, and overall motor skills. The results included: (1) The development of FMS of children with ASD was significantly behind that of the children with TD at the same age. About 80% of children with ASD experienced motor difficulty or were at risk for motor delay. (2) Children with ASD showed significantly lower standard scores than typically developing children at the same age on manual dexterity, ball skills, and static and dynamic balance and overall MABC-2 scores (all p \u3c 0.001), and there was no significant gender difference (all p \u3e 0.05). Besides the core areas of developmental deficits described in the diagnostic manual for ASD, clinicians should assess motor deficits when diagnosing and treating children with ASD. Evidence-based interventions on FMS should be introduced when motor deficits are present

Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-κB signaling and depleting Bcr-Abl

<p>Abstract</p> <p>Background</p> <p>Chronic myelogenous leukemia (CML) is characterized by the chimeric tyrosine kinase Bcr-Abl. Bcr-Abl-T315I is the notorious point mutation that causes resistance to imatinib and the second generation tyrosine kinase inhibitors, leading to poor prognosis. CML blasts have constitutive p65 (RelA NF-κB) transcriptional activity, and NF-κB may be a potential target for molecular therapies in CML that may also be effective against CML cells with Bcr-Abl-T315I.</p> <p>Results</p> <p>In this report, we discovered that pristimerin, a quinonemethide triterpenoid isolated from Celastraceae and Hippocrateaceae, inhibited growth and induced apoptosis in CML cells, including the cells harboring Bcr-Abl-T315I mutation. Additionally, pristimerin inhibited the growth of imatinib-resistant Bcr-Abl-T315I xenografts in nude mice. Pristimerin blocked the TNFα-induced IκBα phosphorylation, translocation of p65, and expression of NF-κB-regulated genes. Pristimerin inhibited two steps in NF-κB signaling: TAK1→IKK and IKK→IκBα. Pristimerin potently inhibited two pairs of CML cell lines (KBM5 versus KBM5-T315I, 32D-Bcr-Abl versus 32D-Bcr-Abl-T315I) and primary cells from a CML patient with acquired resistance to imatinib. The mRNA and protein levels of Bcr-Abl in imatinib-sensitive (KBM5) or imatinib-resistant (KBM5-T315I) CML cells were reduced after pristimerin treatment. Further, inactivation of Bcr-Abl by imatinib pretreatment did not abrogate the TNFα-induced NF-κB activation while silencing p65 by siRNA did not affect the levels of Bcr-Abl, both results together indicating that NF-κB inactivation and Bcr-Abl inhibition may be parallel independent pathways.</p> <p>Conclusion</p> <p>To our knowledge, this is the first report to show that pristimerin is effective <it>in vitro </it>and <it>in vivo </it>against CML cells, including those with the T315I mutation. The mechanisms may involve inhibition of NF-κB and Bcr-Abl. We concluded that pristimerin could be a lead compound for further drug development to overcome imatinib resistance in CML patients.</p

Prevalence and genotyping of Norovirus in environment and food handlers of catering services and hotels

Objective To investigate the prevalence and genotyping of Norovirus in environment and food handlers in catering services and hotels. Methods A total of 40 catering services and 10 hotels were selected as the sampling sites in this study and 4 environment samples and 2 food-handler fecal samples were collected from each site. RNA was extracted and preliminary analyzed for Norovirus by real-time polymerase chain reaction (PCR). Partial opening reading frames 1 (ORF1) sequences were amplified by reverse transcription-polymerase chain reaction (RT-PCR), followed by sequence and phylogenetic analysis. Results One mop sink swab out of 200 environment samples (0.5%, 1/200) and 3 out of 100 food handlers fecal samples (3.0%, 3/100) were positive for Norovirus. The genotyping of Norovirus revealed that one belonged to GII. 17 genotype and two belonged to GI. 3 genotype. Conclusion The transmission risk of Norovirus in catering services and hotels should be paid more attention to and hygienic management should be strengthened. Health education of food handlers to prevent the transmission of Norovirus should be strengthened

Loss of Fructose-1,6-Bisphosphatase Induces Glycolysis and Promotes Apoptosis Resistance of Cancer Stem-Like Cells: An Important Role in Hexavalent Chromium-Induced Carcinogenesis

Hexavalent chromium (Cr(VI)) compounds are confirmed human carcinogens for lung cancer. Our previous studies has demonstrated that chronic exposure of human bronchial epithelial BEAS-2B cells to low dose of Cr(VI) causes malignant cell transformation. The acquisition of cancer stem cell-like properties is involved in the initiation of cancers. The present study has observed that a small population of cancer stem-like cells (BEAS-2B-Cr-CSC) exists in the Cr(VI)-transformed cells (BEAS-2B-Cr). Those BEAS-2B-Cr-CSC exhibit extremely reduced capability of generating reactive oxygen species (ROS) and apoptosis resistance. BEAS-2B-Cr-CSC are metabolic inactive as evidenced by reductions in oxygen consumption, glucose uptake, ATP production, and lactate production. Most importantly, BEAS-2B-Cr-CSC are more tumorigenic with high levels of cell self-renewal genes, Notch1 and p21. Further study has found that fructose-1,6-bisphosphatase (FBP1), an rate-limiting enzyme driving glyconeogenesis, was lost in BEAS-2B-Cr-CSC. Forced expression of FBP1 in BEAS-2B-Cr-CSC restored ROS generation, resulting in increased apoptosis, leading to inhibition of tumorigenesis. In summary, the present study suggests that loss of FBP1 is a critical event in tumorigenesis of Cr(VI)-transformed cells

Interkingdom Gene Transfer May Contribute to the Evolution of Phytopathogenicity in Botrytis Cinerea

The ascomycete Botrytis cinerea is a phytopathogenic fungus infecting and causing significant yield losses in a number of crops. The genome of B. cinerea has been fully sequenced while the importance of horizontal gene transfer (HGT) to extend the host range in plant pathogenic fungi has been recently appreciated. However, recent data confirm that the B. cinerea fungus shares conserved virulence factors with other fungal plant pathogens with narrow host range. Therefore, interkingdom HGT may contribute to the evolution of phytopathogenicity in B. cinerea. In this study, a stringent genome comparison pipeline was used to identify potential genes that have been obtained by B. cinerea but not by other fungi through interkingdom HGT. This search led to the identification of four genes: a UDP-glucosyltransferase (UGT), a lipoprotein and two alpha/beta hydrolase fold proteins. Phylogenetic analysis of the four genes suggests that B. cinerea acquired UGT from plants and the other 3 genes from bacteria. Based on the known gene functions and literature searching, a correlation between gene acquision and the evolution of pathogenicity in B. cinerea can be postulated