RESUMEN
Objective: To explore risk factors affecting treatment for deep neck space infections (DNSIs) so as to provide guidance for appropriate early managements. Methods: A retrospective cohort study was conducted on inpatients with DNSIs admitted to the Department of Otolaryngology, Head and Neck Surgery, Affiliated Hospital of Qingdao University from March 2013 to February 2021. Patients were divided into surgical and non-surgical groups based on whether they had surgery or not. Information collected included demographic data, disease-related signs and symptoms, treatment history, systemic comorbidities, imaging data and laboratory indicators. Hypothesis testing, univariate Logistic regression and multivariate Logistic regression were used for data processing. Resuts A total of 61 patients were included, including 37 males and 24 females, aged 6-96 years. There were 35 cases (57.4%) in the surgical group and 26 cases (42.6%) in the non-surgical group. Multivariate analysis showed that risk factors for surgery as followings: neck dyskinesia (OR=0.03, 95%CI: 0.00-0.24), dysphagia (OR=0.10, 95%CI: 0.02-0.72), serum white blood cell count≥16.74×109/L (OR=1.18, 95%CI: 1.01-1.39) and interspace gas (OR=0.03, 95%CI: 0.00-0.30). Conclusion: Clinicians should be alert to these risk factors for surgery in the course of treatment and timely surgical treatment for patients who meet the conditions.
Asunto(s)
Masculino , Femenino , Humanos , Estudios Retrospectivos , Cuello/cirugía , Factores de Riesgo , Trastornos de DegluciónRESUMEN
E3 ubiquitin ligase TRIM21(tripartite motif containing 21) plays an important role in regulating cell biological functions and clinical prognosis as oncogene or tumor suppressor in different types of tumors. However,the biological functions and molecular mechanism of TRIM21 in hypopharyngeal squamous cell carcinoma (HPSCC) are still unclear.Our results showed that TRIM21 is highly expressed in moderately and well differentiated HPSCC, suggesting the role of TRIM21 in tumor differentiation. Overexpression and knockdown of TRIM21 inhibited or promoted cell proliferation and migration. Meanwhile, the expression of differentiation markers including KRT10 (keratin 10), IVL (involucrin) and TGM1 (transglutaminase 1) were increased and decreased upon TRIM21 overexpression or knockdown, respectively. The bioinformatics analysis of TRIM21 interacting protein identified by co-immunoprecipitation combined with mass spectrometry suggested that TRIM21 may be closely related to the regulation of cytoskeleton protein. We further demonstrated that TRIM21 interacted with KRT10. The inhibition of protein synthesis by cycloheximide led to upregulation of KRT10 in TRIM21 overexpressing FaDu cells, and ectopic expression of TRIM21 enhanced the ubiquitination level of KRT10. In summary, our results suggest that TRIM21 may promote the HPSCC differentiation by mediating ubiquitination of cytoskeleton proteins to improve the protein stability.
RESUMEN
Objective To study the prevalence of plasmid-mediated quinolone resistance (PMQR) genes in carbapenem-resistant Enterobacteriaceae (CRE) and its resistance mechanism.Methods Clinically isolated CRE strains in a hospital from March 2015 to March 2018 were collected, then identified and performed antimicrobial susceptibility test by VITEK2 Compact analyzer, carriage of PMQR genes qnrA, qnrB, qnrS, qepA and acc (6') Ib-cr were determined by polymerase chain reaction (PCR) and sequencing, the horizontal transfer of PMQR genes were verified by plasmid conjugation test.Results Resistance rates of carbapenem-resistant Escherichia coli and carbapenem-resistant Klebsiella pneumoniae to quinolones were 100％ and 15.56％-33.33％ respectively.Detection rate of acc (6') Ib-cr gene was the highest (87.72％), followed by qnrB (77.19％) and qnrS (17.54％), 2 strains (3.51％) carried qnrA gene, qepA gene was not isolated, 84.21％ of strains harbored 2 or 3 PMQR genes.PMQR gene was transfected into all the 8 conjugated strains, but minimum inhibitory concentration value of quinolones didn't change significantly.Conclusion The detection rate of PMQR genes in CRE in this hospital is high, but there is a certain sensitivity to quinolones.
RESUMEN
<p><b>OBJECTIVE</b>To explore the molecular mechanism of exocrine immune inflammatory injury of Sjögren's Syndrome and the intervention of Banxia Qinlian Decoction (BQD).</p><p><b>METHODS</b>Totally 18 female NOD mice were randomly divided into the model group, the positive drug group, and the BQD group, 6 in each group. Six female BALB/c mice were recruited as a blank control group. Mice in the blank control group and the model group were gavaged with deionized water at the daily dose of 0.1 mL/10 g body weight. Tripterygium Tablet was administered by gastrogavage to mice in the positive group at the daily dose of 10 mg/kg. BQD was administered by gastrogavage to mice in the BQD group at the daily dose of 60 g crude drugs/kg. After 12 weeks of medication, mice were sacrificed. Their eyeballs were excised and blood collected. Tissues of bilateral parotids and submandibular glands were kept. mRNA transcriptional levels of IL-17, IL-6, type 3 muscarinic acetylcholine receptors (M3R), aquaporin protein-5 (AQP5) were detected by RT-PCR. Expression levels of M3R and AQP5 protein were detected by Western blot. Protein expression levels of IL-17 and IL-6 were detected by ELISA.</p><p><b>RESULTS</b>Compared with the normal group, mRNA transcriptional levels and protein expression levels of IL-17, IL-6, M3R, and AQP5 were significantly up-regulated in the model group (P < 0.01). Compared with the model group, mRNA transcriptional levels and protein expression levels of IL-17, IL-6, M3R, and AQP5 were significantly down-regulated in the positive drug group and the BQD group with statistical difference (P < 0.01, P < 0.05). Compared with the BQD group, mRNA-transcriptional levels of IL-17, IL-6, and M3R, as well as M3R and AQP5 protein expression levels were significantly down-regulated in the positive drug group (all P < 0.01).</p><p><b>CONCLUSION</b>The molecular mechanism of BQD in inhibiting SS exocrine neurotoxic injury might be possibly related to regulating Th17/IL-17 immune inflammatory way.</p>