This paper reports the diagnosis and treatment of a child with eustachian hairy polyp. The patient was a female, aged 1 year and 4 months, and visited our clinic due to "intermittent purulent discharge of the left ear, nasal congestion and sleep snoring for 1 year". Preoperative endoscopic examination found white masses at the posterior part of the nasal cavity on both sides. The imaging findings showed masses with streaks and circular-like mixed signal accompanied by slightly uneven enhancement at the left eustachian duct and the posterior wall of the nasopharyngeal cavity, and soft tissue density in the left tympanic antrum. Left modified radical mastoidectomy and radical endoscopic resection surgery for nasopharyngeal tumors was performed under general anesthesia. Histopathological examination revealed polyp of the left eustachian tube hair. The patient's symptoms improved after surgery, and no tumor recurrence was found after 3 months of follow-up.
Humans ; Female ; Eustachian Tube/surgery* ; Polyps/surgery* ; Infant ; Endoscopy

Objective:To evaluate the role of uncoupling protein 2 in dexmedetomidine-induced alleviation of myocardial ischemia-reperfusion (I/R) injury in diabetic mice.Methods:SPF C57BL/6 male mice, aged 6-8 weeks, weighing 20-25 g, in which the model of type 2 diabetes mellitus was established by high-fat feeding combined with intraperitoneal injection of streptozotocin, were used in this study. Ninety diabetic mice were divided into 5 groups ( n=18 each) by a random number table method: sham operation group (S group), myocardial I/R group, myocardial I/R+ UCP2 inhibitor genipin group (I/R+ G group), myocardial I/R+ dexmedetomidine group (I/R+ D group) and myocardial I/R+ dexmedetomidine+ UCP2 inhibitor genipin group (I/R+ DG group). Myocardial I/R injury model was established by ligating the left anterior descending coronary artery of diabetic mice for 60 min followed by 120 min of reperfusion. Dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D group. Genipin 100 mg/kg was intraperitoneally injected at 14 h prior to ischemia, and dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D+ G group. The concentrations of cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-10 in serum were detected by enzyme-linked immunosorbent assay at 120 min of reperfusion. The myocardial tissue was obtained for determination of the myocardial infarct size, the level of reactive oxygen species (ROS) (by flow cytometry), and the expression of UCP2, nuclear factor kappa B (NF-κB) inhibitory protein α (IκBα), phosphorylated IκBα (p-IκBα), NF-κB p65 and phosphorylated NF-κB p65 (p-NF-κB p65) (by Western blot) and for observation of the morphological structure of the myocardial tissue. The cardiac function was evaluated by echocardiography at 24 h of reperfusion. Results:Compared with group S, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α, IL-6 and IL-10 were increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the stroke volume (SV), ejection fraction (EF), and left ventricular fractional shortening (FS) were decreased ( P<0.05), and the myocardial structure was severely damaged in group I/R. Compared with group I/R, the percentage of myocardial infarct size and level of ROS were significantly decreased, the concentrations of cTnI, TNF-α and IL-6 were decreased, the concentration of IL-10 was increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were decreased, the SV, EF and FS were increased ( P<0.05), and the pathological damage was significantly attenuated in group I/R+ D. Compared with group I/R+ D, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α and IL-6 were increased, the concentration of IL-10 was decreased, the expression of UCP2 was down-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the SV, EF and FS were decreased ( P<0.05), and the pathological damage was aggravated in group I/R+ D+ G. Conclusions:Dexmedetomidine may ameliorate myocardial I/R injury by up-regulating UCP2 expression in the myocardium and inhibiting mitochondrial ROS-mediated inflammatory responses in diabetic mice.

Objective To investigate the influencing factors associated with the comorbidity of inflammatory bowel disease (IBD) and depression. Methods A case-control study was conducted based on the ^“Healthcare Big Data Platform^” of a tertiary class-A comprehensive hospital in Shandong Province. IBD comorbid with depression was served as the case group and IBD without depression was served as the control group. Propensity score matching (PSM) was performed by matching the case group with the control group in a ratio of 1:2 according to the age and gender of the patients. Conditional logistic regression model was used to explore the influencing factors associated with the comorbidity of IBD and depression. Results A total of 405 patients with IBD were enrolled in this study, including 270 patients without depression and 135 patients comorbid with depression. The results of conditional logistic regression showed that the use of immunosuppressants (OR=2.84, 95% CI: 1.00-8.07) and glucocorticoids (OR=2.05, 95% CI: 1.17-3.58), dementia (OR=5.20, 95% CI:1.59-17.05), cardiovascular disease (OR=3.58, 95% CI: 1.84-6.98) and cancer (OR=2.63, 95% CI: 1.16-5.95) were associated with the comorbidity of depression and IBD. Conclusion Attention should be paid to the use of immunosuppressants and glucocorticoids in the population of IBD comorbid with depression, and the coexistence of physical diseases such as dementia, cardiovascular disease and cancer. Early prevention and targeted treatment measures should be taken for high-risk populations to reduce their risk of depression and improve their quality of life and health.

Escherichia coli(E.coli)is a key pathogenic bacterium responsible for postpartum endo-metritis,with its colonization in the reproductive tract closely associated with endometrial damage and disruption of the ovarian cycle.This ultimately leads to infertility,causing significant economic losses to the dairy industry.Macrophages play a pivotal role in the inflammatory response.This study aims to investigate the mRNA expression profile of bovine bone marrow-derived macropha-ges following E.coli infection using RNA sequencing(RNA-seq)technology.Additionally,it seeks to identify the biological functions and signaling pathways of differentially expressed genes(DEGs)through Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analyses.The results demonstrated that E.coli infection induced differential expression of 4 522 genes,with 2 141 upregulated and 2 381 downregulated.These genes were primarily asso-ciated with inflammatory responses,where TLR2,TLR4,NLRP3,and PTGS2 played pivotal roles.PGD2 synthesis was mediated by TLR2,TLR4,and NLRP3.Transcriptome sequencing of bovine bone marrow-derived macrophages infected with E.coli and treated with a PGD2 inhibitor revealed a marked downregulation of TLR2 and TLR4 gene expression.qPCR validation results were highly consistent with the RNA-seq findings.This study elucidates the interactive regulatory roles of TLR2,TLR4,and NLRP3 in conjunction with PGD2,which collectively modulate bovine endome-tritis.These findings offer significant molecular insights that enhance our understanding of the pathological mechanisms underlying bovine endometritis,thereby informing its prevention and treatment strategies.

Escherichia coli(E.coli)is a key pathogenic bacterium responsible for postpartum endo-metritis,with its colonization in the reproductive tract closely associated with endometrial damage and disruption of the ovarian cycle.This ultimately leads to infertility,causing significant economic losses to the dairy industry.Macrophages play a pivotal role in the inflammatory response.This study aims to investigate the mRNA expression profile of bovine bone marrow-derived macropha-ges following E.coli infection using RNA sequencing(RNA-seq)technology.Additionally,it seeks to identify the biological functions and signaling pathways of differentially expressed genes(DEGs)through Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analyses.The results demonstrated that E.coli infection induced differential expression of 4 522 genes,with 2 141 upregulated and 2 381 downregulated.These genes were primarily asso-ciated with inflammatory responses,where TLR2,TLR4,NLRP3,and PTGS2 played pivotal roles.PGD2 synthesis was mediated by TLR2,TLR4,and NLRP3.Transcriptome sequencing of bovine bone marrow-derived macrophages infected with E.coli and treated with a PGD2 inhibitor revealed a marked downregulation of TLR2 and TLR4 gene expression.qPCR validation results were highly consistent with the RNA-seq findings.This study elucidates the interactive regulatory roles of TLR2,TLR4,and NLRP3 in conjunction with PGD2,which collectively modulate bovine endome-tritis.These findings offer significant molecular insights that enhance our understanding of the pathological mechanisms underlying bovine endometritis,thereby informing its prevention and treatment strategies.

Objective:To evaluate the role of uncoupling protein 2 in dexmedetomidine-induced alleviation of myocardial ischemia-reperfusion (I/R) injury in diabetic mice.Methods:SPF C57BL/6 male mice, aged 6-8 weeks, weighing 20-25 g, in which the model of type 2 diabetes mellitus was established by high-fat feeding combined with intraperitoneal injection of streptozotocin, were used in this study. Ninety diabetic mice were divided into 5 groups ( n=18 each) by a random number table method: sham operation group (S group), myocardial I/R group, myocardial I/R+ UCP2 inhibitor genipin group (I/R+ G group), myocardial I/R+ dexmedetomidine group (I/R+ D group) and myocardial I/R+ dexmedetomidine+ UCP2 inhibitor genipin group (I/R+ DG group). Myocardial I/R injury model was established by ligating the left anterior descending coronary artery of diabetic mice for 60 min followed by 120 min of reperfusion. Dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D group. Genipin 100 mg/kg was intraperitoneally injected at 14 h prior to ischemia, and dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D+ G group. The concentrations of cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-10 in serum were detected by enzyme-linked immunosorbent assay at 120 min of reperfusion. The myocardial tissue was obtained for determination of the myocardial infarct size, the level of reactive oxygen species (ROS) (by flow cytometry), and the expression of UCP2, nuclear factor kappa B (NF-κB) inhibitory protein α (IκBα), phosphorylated IκBα (p-IκBα), NF-κB p65 and phosphorylated NF-κB p65 (p-NF-κB p65) (by Western blot) and for observation of the morphological structure of the myocardial tissue. The cardiac function was evaluated by echocardiography at 24 h of reperfusion. Results:Compared with group S, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α, IL-6 and IL-10 were increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the stroke volume (SV), ejection fraction (EF), and left ventricular fractional shortening (FS) were decreased ( P<0.05), and the myocardial structure was severely damaged in group I/R. Compared with group I/R, the percentage of myocardial infarct size and level of ROS were significantly decreased, the concentrations of cTnI, TNF-α and IL-6 were decreased, the concentration of IL-10 was increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were decreased, the SV, EF and FS were increased ( P<0.05), and the pathological damage was significantly attenuated in group I/R+ D. Compared with group I/R+ D, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α and IL-6 were increased, the concentration of IL-10 was decreased, the expression of UCP2 was down-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the SV, EF and FS were decreased ( P<0.05), and the pathological damage was aggravated in group I/R+ D+ G. Conclusions:Dexmedetomidine may ameliorate myocardial I/R injury by up-regulating UCP2 expression in the myocardium and inhibiting mitochondrial ROS-mediated inflammatory responses in diabetic mice.

Objective: To provide high-quality clinical evidence of the efficacy of Tibetan medicine Honghua Ruyi (HHRY) pills for endometriosis-associated dysmenorrhea. Methods: This study constitutes a multicenter, randomized, double-blind, placebo-controlled trial encompassing a three-menstrual cycle intervention followed by a three-menstrual cycle follow-up period. A total of 164 eligible females with endometriosis-associated dysmenorrhea were randomly divided into HHRY pills and placebo groups in a 1:1 ratio. The primary outcome included dysmenorrhea symptoms assessed using Visual Analog Scale (VAS) scores and quality of life, whereas the secondary outcome measures included the maximum VAS for non-menstrual pelvic pain, duration of pain episodes (in days), frequency and quantity of the consumption of ibuprofen sustained-release capsules (or other non-steroidal anti-inflammatory drugs), and days off work/study for staff/student due to dysmenorrhea, ovarian cyst, and/or pelvic nodule size. The safety was monitored throughout the treatment period. All the analyses were based on the intention-to-treat principle. For continuous outcomes, simple or multiple linear regressions were used to estimate the differences between the HHRY pills and placebo groups, with categorical data expressed as the number and percentage of occurrences. Differences were compared using the chi-square test or Fisher's exact test. The predefined analysis was adjusted for concomitant treatment, a variable considered to be associated with outcomes but unaffected by treatment allocation. Estimates of treatment effects were reported with 95% confidence intervals. Two-tailed P values ≤ .05 were considered statistically significant. Conclusion Positive results from this trial, upon completion would provide robust evidence for the efficacy and safety of HHRY pills in treating dysmenorrhea in patients with endometriosis.

Objective:To evaluate the effect of propofol on parvalbumin (PV) neurons in the medical prefrontal cortex(mPFC)of rats with social behavior disorders induced by chronic sleep deprivation.Methods:Forty-two SPF male Sprague-Dawley rats, aged 8 weeks, weighing 200-250 g, were divided into 3 groups ( n=14 each) using a random number table method: control group (group Con), chronic sleep deprivation plus natural sleep group (group CSD+ NS), and chronic sleep deprivation plus propofol group (group CSD+ Pro). Sleep deprivation model was established by the modified multiple platform method, the rats were placed in the sleep-deprivation tank for 20 h a day (14: 00-10: 00), and allowed to sleep naturally for 4 h (10: 00-14: 00) a day for 28 consecutive days. Propofol 40 mg/kg was intraperitoneally injected for 28 consecutive days after sleep deprivation in CSD+ Pro group. While the equal volume of 10% fat emulsion was given in Con and CSD+ NS groups. After the end of sleep deprivation, a three-box social experiment was used to detect the social behavior of rats, and the number of the PV positive cells and density of the perineuronal network (PNN) in the mPFC area were measured by immunofluorescence. Results:Compared with group Con, the pertentage of rapid eye movement sleep and sniffing time preference coefficients for the strange rat 1 in the first stage and for the strange rat 2 in the second stage were significantly decreased, and the number of the PV positive cells and density of PNN in the mPFC area were decreased in group CSD+ NS ( P<0.05). Compared with group CSD+ NS, the sniffing time preference coefficients for the strange rat 1 in the first stage and for the strange rat 2 in the second stage were significantly increased, the number of the PV positive cells and density of PNN in the mPFC area were increased( P<0.05), and no significant change was found in the percentage of the rapid eye movement sleep in group CSD+ Pro. Conclusions:Propofol probably increases the number and function of PV neurons in the mPFC and ameliorates sleep deprivation-induced social behavior disorders in sleep-deprived rats.

Tumor immunotherapy has become the main treatment method for cancer after surgery, radiotherapy and chemotherapy. With the in-depth study of tumor immunology, cell biology and molecular technology, the tumor microenvironment was found to be immunosuppressive, and tumor development and metastasis are closely related to it. Tumor immunotherapy uses the body’s own immune system to kill tumor cells. At present, there are mainly mainstream tumor immunotherapy methods, namely monoclonal antibody therapy, immune checkpoint inhibitor therapy, immunocell therapy, and tumor vaccines. In this paper, the advantages and limitations of these four immunotherapies were mainly discussed, and the current status of their marketing and clinical research was also reviewed.

Objective:To explore the relevance between secondary retroperitoneal infection, as well as the outcomes, and the approach of intensive care unit (ICU) admission for the patients suffered from acute pancreatitis.Methods:Patients with acute pancreatitis admitted to the ICU of the Second Affiliated Hospital of Anhui Medical University from January 2013 to July 2022 were retrospectively analyzed. According to ICU admission approaches, the patients were divided into the emergency group (first admission or transferred from the emergency department) and the delayed group (transferred from the general wards due to disease evolution). Patients were also divided into retroperitoneal infection group and non-retroperitoneal infection group according to whether retroperitoneal infection was accompanied. Patients' baseline data including gender, age, underlying diseases, laboratory test indicators, acute physiology and chronic health evaluationⅡ score (APACHEⅡ), sequential organ failure assessment (SOFA), computed tomography severity index (CTSI), bedside index of severity in acute pancreatitis (BISAP), and acute complications were collected. Univariate and multivariate logistic regression was used to analyze the risk factors of retroperitoneal infection in patients with acute pancreatitis.Results:A total of 271 patients with acute pancreatitis were enrolled, including 95 cases in the emergency group and 176 cases in the delayed group. The cohort included 71 cases with and 200 cases without retroperitoneal infection development. The incidence of retroperitoneal infection and the 30-day mortality of patients in the delayed group, which was observed with a significantly longer ICU stay (days), [(15.4±21.3) vs. (8.6±10.8), P<0.05], were significantly higher than those in the emergency group [retroperitoneal infection incidence rate: 31.82% (56/176) vs.15.79%(15/95), 30-day mortality: 13.64%(24/176) vs. 4.21%(4/95), both P<0.05]. Univariate Logistic analysis showed significant differences in diabetes, APACHEⅡ, SOFA, CTSI and BISAP score, urea nitrogen, creatinine, blood calcium, D-D dimer, peritoneal puncture catheter drainage and ICU transferred from general wards due to disease evolution between the retroperitoneal infection group and the non-retroperitoneal infection group. Multivariate Logistic regression analysis showed that diabetes, SOFA score, CTSI score, peritoneal puncture catheter drainage and transfered from general wards to ICU due to disease evolution were independent risk factor for retroperitoneal infection in acute pancreatitis patients[odds ratio were 3.379, 1.150, 1.358, 3.855, 2.285, respectively]. Conclusions:Acute pancreatitis patients in ICU transferred from general wards are more likely to develop retroperitoneal infection, and have a higher risk of mortality and a longer ICU stay. Delayed admission to ICU, diabetes, SOFA score, CTSI score and peritoneal puncture catheter drainage are independent risk factors for retroperitoneal infection in patients with acute pancreatitis.