Objective:Clinical characteristics and diagnosis and treatment process was reported and analyzed of a patient with brucellosis complicated with thyroid abscess, providing reference for the clinical diagnosis of brucellosis complicated with thyroid abscess.Methods:Clinical medical records of a patient with brucellosis complicated with thyroid abscess who was treated at the General Surgery Department of Yanchi County People's Hospital in Wuzhong City, Ningxia Hui Autonomous Region in November 2021 were collected. The clinical manifestations, blood routine, brucella antibodies, thyroid function, bacterial culture, thyroid ultrasound and other examination results, as well as the diagnosis and treatment process, were comprehensively analyzed. Results:The patient was a male, 61 years old, who presented with a neck mass without typical clinical manifestations of brucellosis. Thyroid ultrasound revealed a space occupying lesion, and the preliminary diagnosis was thyroid cystadenoma. Thyroid right lobe and isthmus resection surgery was performed. During the operation, it was found that some of the thyroid glands were tightly adhered to the cervical blood vessels, so the resection surgery was changed to abscess drainage, and the drainage fluid was purulent and bloody. The bacterial culture result of thyroid purulent fluid (intraoperative puncture fluid and postoperative drainage fluid) was brucella lamblia, and the serum brucella test tube agglutination test titer was 1 ∶ 400 (+++). The patient improved and was discharged after local drainage and anti brucella treatment. Follow up for 4 months showed no abnormalities. Conclusions:Brucellosis which begins with a local infection of the thyroid gland is extremely rare, with no characteristic clinical manifestations, and is prone to misdiagnosis. Timely correction of the surgical plan during the treatment process avoids the removal of the patient's thyroid, which has a certain clinical reference value.

Objective:To construct a novel respiratory syncytial virus (RSV) vaccine based on a recombinant influenza virus vector and evaluate its immune protective effects in mice.Methods:A recombinant H1N1 influenza A virus (IAV) expressing the extracellular domain (Gecto) of RSV A2 G protein was constructed and rescued, named as PR8NAGecto/WSN. After in vitro verification of the Gecto expression and PR8NAGecto/WSN growth kinetics, a single dose of PR8NAGecto/WSN was used to immunize BALB/c mice through intranasal administration to evaluate the efficacy of PR8NAGecto/WSN by assessing humoral (IgG, neutralizing antibody), mucosal (IgA) and cellular immunity (IFN-γ ELISPOT). Four weeks after immunization, the mice were challenged with RSV A2 or RSV B9320 to evaluate the protective effects of PR8NAGecto/WSN by analyzing mouse body weight changes, lung tissue virus titers and pathological changes. Results:A single-dose intranasal immunization with PR8NAGecto/WSN induced robust humoral, mucosal and cellular immunity in mice. Moreover, the mice in the immunized group had lower lung virus loads and mild lung pathological damages following the challenge with RSV A or RSV B subtype as compared with the control group.Conclusions:A single-dose intranasal immunization with PR8NAGecto/WSN induces robust immunity and provide protection against RSV A and B challenges in mice. This study provides new ideas and reference for the development of novel mucosal vaccines against RSV.

Background The compound 6:2 chlorinated polyfluorinated ether sulfonic acids (6:2 Cl-PFESA) has been demonstrated abilities of strong bioaccumulation and placental barrier penetration, and it can also cross the blood-brain barrier. However, the mechanism of its neurodevelopmental toxicity in offspring induced by early-life exposure is still unknown. Objective To explore effects of 6:2 Cl-PFESA on the growth and the α-amino-3-hydroxy-5-methylisoxazole-4-propionic (AMPA) receptor gene expression in the hippocampus of offspring mice by establishing a 6:2 Cl-PFESA exposure animal model. Methods Thirty Kunming pregnant mice were randomly divided into five groups: control group, and 2, 10, 50, and 250 μg·L⁻¹ 6:2 Cl-PFESA exposure groups. The treatment groups were exposed to designed doses of 6:2 Cl-PFESA through drinking water from the first day of gestation until the end of lactation. The pups were weaned on postnatal day (PND) 21, and continued to be exposed to 6:2 Cl-PFESA through drinking water. Birth weight and body length of the offspring were recorded. Offspring mice were anesthetized and sacrificed respectively on PND7, PND21, and PND35, then their hippocampus was peeled from harvested brain tissue. The ultrastructure of hippocampus was observed via transmission electron microscopy; and the expression of AMPA receptors GluR1, GluR2, and GluR3 in the hippocampus was evaluated by real-time reverse transcription polymerase chain reaction. The learning and memory ability of the PND35 mice was measured by Morris water maze test before they were sacrificed. Results The birth weights and the lengths of the pups in the 10, 50, and 250 μg·L⁻¹ 6:2 Cl-PFESA exposure groups were (2.23±0.36), (1.92±0.20), (1.88±0.31) g, and (33.73±0.98), (32.91±1.30), (32.52±2.07) mm, respectively, which were lower than those in the control group, (2.78±0.35) g and (36.46±2.34) mm (P<0.05), respectively. The results of Morris water maze showed that the escape latencies in the orientation navigation experiment on the 4th day in the 250 μg·L⁻¹ 6:2 Cl-PFESA exposure group and on the 5th day in the 10, 50, and 250 μg·L⁻¹ 6:2 Cl-PFESA exposure groups were longer than those in the control group (P<0.05). In the space exploration experiment, the times of crossing platform in the 50 and 250 μg·L⁻¹ 6:2 Cl-PFESA exposure groups were decreased when compared with the control group (P<0.05), and the time of staying in the target quadrant of the 250 μg·L⁻¹ 6:2 Cl-PFESA exposure groups were also decreased (P<0.05). Via transmission electron microscopy, compared with the control group, the postsynaptic density was decreased and the synaptic cleft width was widened on PND35 in the 250 μg·L⁻¹ 6:2 Cl-PFESA exposure group. The mRNA expression levels of GluR1, GluR2, and GluR3 in the hippocampus of pups exposed to 250 μg·L⁻¹ 6:2 Cl-PFESA during different developmental stages were significantly lower than those in the control group (P<0.05). Except for the 2 μg·L⁻¹ 6:2 Cl-PFESA exposure group on PND7, the 6:2 Cl-PFESA exposure inhibited the mRNA expression levels of GluR1, GluR2, and GluR3 in the hippocampus of pups at different developmental stages (P<0.05). Among them, the 6:2 Cl-PFESA exposure during early development resulted in the highest decrease in the expression levels of GluR1 and GluR2 mRNA in the hippocampus of pups on PND7; GluR3 mRNA expression level in the hippocampus of the exposed pups on PND21 showed the maximum inhibitory effect; the expression levels of GluR1, GluR2, and GluR3 mRNA all showed the least decrease in the hippocampus of the exposure groups on PND35. Conclusion Early-life exposure to 6:2 Cl-PFESA may affect the growth and development of offspring mice, alter the hippocampal synaptic structure, and influence the learning and memory abilities, which may be related to their inhibitory effects on the expression levels of AMPA receptor subunits GluR1, GluR2, and GluR3 genes in the hippocampus of offspring mice at various developmental stages.

This study aims to obtain nanoantibody of vaccinia virus protein D8 by SUMO tag and analyze its binding activity with antigen.The sequence was designed and synthesized to construct the prokaryotic expression plasmid pKMD-SUMO-D8,which was transformed into Escherichia coli BL21(DE3)receptor cells and induced to express.Anti-SUMO-D8 with His and SUMO tags were purified,and then all tags were removed by SUMO protease to further obtain Anti-D8.Final-ly,the binding activity was detected and analyzed by indirect ELISA and IFA.The results showed that the prokaryotic expression plasmid pKMD-SUMO-D8 and recombinant strains were construc-ted.Under the condition of 30 ℃,the expression of Anti-SUMO-D8 was best when induced by IPTG with 0.1 mmol/L for 4 h.High purity Anti-SUMO-D8 and Anti-D8 nanoantibodies were ob-tained.Indirect ELISA results showed that both Anti-SUMO-D8 and Anti-D8 had binding activity with antigen.Under the same conditions,the binding activity of Anti-D8 to vaccinia virus and E8L was higher than that of Anti-SUMO-D8.Indirect IFA results showed that 48 h after infection with vaccinia virus,some nuclei of the experimental group showed green fluorescence under fluorescence microscope.Nanoantibodies of vaccinia virus protein D8 could be efficiently prepared by SUMO tag,and the prepared nanoantibodies had binding activity.This study provides new idea for the preparation of nanoantibody,and also lays a foundation for further study of the biological function of vaccinia virus protein D8 nano-antibody.

Objective To explore the practical effect of health science popularization in public hospitals based on the"four modernizations"path.Methods Based on the science popularization practice of the theme sharing system such as"Huafu Science Popularization",and relying on the application of technologies such as big data,Internet+,and multimedia,the science popularization practice model of the"Four modernizations"path of"system institutionalization","theme classification","form diversification"and"content output precision"is created.Results The health popularization practice research of sample hospi-tals proves that many excellent science popularization works have emerged under the path of"four modernizations";Won a num-ber of provincial science popularization honors;The number of people participating in popular science competitions increased by more than 25％;1/3 and above of the offline science lecture hall are senior professional title experts of Huashan Hospital;Set up more specialized clinics;The satisfaction of characteristic outpatient patients is more than 95％.Conclusion The science popu-larization practice method based on the"Four modernizations"path has a remarkable effect on highlighting the"public welfare"function of public hospitals and improving the specialty reputation.

Background::Hepatic ischemia-reperfusion injury (HIRI) remains a common complication during liver transplantation (LT) in patients. As a key downstream effector of the Hippo pathway, Yes-associated protein (YAP) has been reported to be involved in various physiological and pathological processes. However, it remains elusive whether and how YAP may control autophagy activation during ischemia-reperfusion.Methods::Human liver tissues from patients who had undergone LT were obtained to evaluate the correlation between YAP and autophagy activation. Both an in vitro hepatocyte cell line and in vivo liver-specific YAP knockdown mice were used to establish the hepatic ischemia-reperfusion models to determine the role of YAP in the activation of autophagy and the mechanism of regulation. Results::Autophagy was activated in the post-perfusion liver grafts during LT in patients, and the expression of YAP positively correlated with the autophagic level of hepatocytes. Liver-specific knockdown of YAP inhibited hepatocytes autophagy upon hypoxia-reoxygenation and HIRI ( P <0.05). YAP deficiency aggravated HIRI by promoting the apoptosis of hepatocytes both in the in vitro and in vivo models ( P <0.05). Attenuated HIRI by overexpression of YAP was diminished after the inhibition of autophagy with 3-methyladenine. In addition, inhibiting autophagy activation by YAP knockdown exacerbated mitochondrial damage through increasing reactive oxygen species ( P <0.05). Moreover, the regulation of autophagy by YAP during HIRI was mediated by AP1 (c-Jun) N-terminal kinase (JNK) signaling through binding to the transcriptional enhanced associate domain (TEAD). Conclusions::YAP protects against HIRI by inducing autophagy via JNK signaling that suppresses the apoptosis of hepatocytes. Targeting Hippo (YAP)-JNK-autophagy axis may provide a novel strategy for the prevention and treatment of HIRI.

Objective:To analyze the risk factors of hypoparathyroidism after thyroid cancer surgery.Methods:The clinical data of 430 patients who underwent total thyroidectomy and central lymph node dissection due to thyroid cancer from Jan. 2021 to Dec. 2021 in the First Ward of Head and Neck Surgery of Sichuan Cancer Hospital were collected. They were divided into two groups according to their parathyroid hormone levels at day 1 and 6 months after surgery: temporary hypoparathyroidism group ( n = 174) and permanent hypoparathyroidism group ( n = 11). and patients with normal parathyroid function were selected as control group (256 cases on postoperative day 1 and 419 cases on postoperative month 6). Gender, age, body mass index, tumor diameter, invasion, central lymph node dissection, parathyroid transplantation, Hashimoto’s thyroiditis, and lymph node dissection in lateral neck region were monitored. The suspicious risk factors of hypoparathyroidism were evaluated by χ2 test and multivariate logistic regression analysis. Results:Univariate analysis showed that women (86.21% vs 77.34%, χ2 = 5.73, P = 0.022) and parathyroid autotransplantation (44.83% vs 28.91%, χ2 = 11.49, P = 0.001) were associated with postoperative transient hypoparathyroidism. The posterior capsule of tumor invasion (81.82% vs 45.11%, χ2 = 5.81, P = 0.016) was associated with postoperative hypoparathyroidism.Multivariate analysis showed that the independent risk factors of transient hypoparathyroidism were female ( P=0.028, OR=1.870), the largest diameter of tumor ( P=0.043, OR=1.595), extravasation of tumor ( P=0.018, OR=1.587), and parathyroid transplantation ( P=0.001, OR=1.966). The independent risk factor of permanent parathyroidism was the posterior capsule of tumor invasion ( P=0.046, OR=4.658) . Conclusions:Female, the largest tumor diameter, tumor invasion and parathyroid transplantation are independent risk factors for transient hypoparathyroidism after total thyroidectomy. The posterior capsule of tumor invasion is an independent risk factor for permanent hypoparathyroidism after total thyroidectomy.

Inflammation is recently recognized as one of the hallmarks of human cancer. Chronic inflammatory response plays a critical role in cancer development, progression, metastasis, and resistance to chemotherapy. Conversely, the oncogenic aberrations also generate an inflammatory microenvironment, enabling the development and progression of cancer. The molecular mechanisms of action that are responsible for inflammatory cancer and cancer-associated inflammation are not fully understood due to the complex crosstalk between oncogenic and pro-inflammatory genes. However, molecular mediators that regulate both inflammation and cancer, such as NF-κB and STAT have been considered as promising targets for preventing and treating these diseases. Recent works have further demonstrated an important role of oncogenes (e.g., NFAT1, MDM2) and tumor suppressor genes (e.g., p53) in cancer-related inflammation. Natural products that target these molecular mediators have shown anticancer and anti-inflammatory activities in preclinical and clinical studies. Sesquiterpenoids (STs), a class of novel plant-derived secondary metabolites have attracted great interest in recent years because of their diversity in chemical structures and pharmacological activities. At present, we and other investigators have found that dimeric sesquiterpenoids (DSTs) may exert enhanced activity and binding affinity to molecular targets due to the increased number of alkylating centers and improved conformational flexibility and lipophilicity. Here, we focus our discussion on the activities and mechanisms of action of STs and DSTs in treating inflammation and cancer as well as their structure-activity relationships.
Animals ; Anti-Inflammatory Agents ; pharmacology ; Antineoplastic Agents, Phytogenic ; pharmacology ; Humans ; Inflammation ; drug therapy ; etiology ; NF-kappa B ; antagonists & inhibitors ; NFATC Transcription Factors ; antagonists & inhibitors ; Neoplasms ; drug therapy ; etiology ; Proto-Oncogene Proteins c-mdm2 ; antagonists & inhibitors ; physiology ; Sesquiterpenes ; chemistry ; pharmacology ; Structure-Activity Relationship

Objective To compare the application of Shikani optical stylet(SOS)and Clarus Video Sty-let(Tracway)in patient with cervical spine immobilization in tracheal intubation. Method Sixty patients,ASAⅠ~Ⅱ,undergoing cervical internal fixation operation,were randomly divided into Shikani optical stylet group (Group S,n = 30)and Clarus Video Stylet group(Group T,n = 30). MAP,HR and RPP(The rate-pressure product)were recorded at the point before induction of anesthesia(T1),before intubation(T2),at the immediate time of intubation(T3)and 1 min(T4),3 mins(T5),and 5 mins after intubation(T6).The intubation time,one-time success rate of intubation,the number of intubation times and the incidence of sore throat and other complica-tions were observed. Results The one-time intubation time in group S was obviously shorter than that in group T (P<0.05).The incidence of mild sore throat and intubation throat injury rate were lower in group S than those in group T(P<0.05).Compared with those at T1,MAP and RPP decreased significantly at point of T2~T6in both of two groups(P<0.05).There was no significantly difference in MAP,HR and RPP at any points of time between the two groups. The one-time success rate of intubation,the number of intubation times and the incidence of air-way complications in two groups(P>0.05)were no significantly different. Conclusions Compared with Clarus Video Stylet(Tracway),Shikani optical stylet can shorten the intubation time in patients with cervical spine immo-bilization,but no difference was found in regard to the hemodynamic influence on intubation,success rate of intu-bation,the intubation times,the sore throat and the other related complications.

Objective To evaluate the effect of dexmedetomidine on gastric mucosal injury induced by intestinal ischemia-reperfusion (I/R) in rats.Methods Thirty-six healthy male Sprague-Dawley rats,aged 4-5 months,weighing 200-250 g,were randomly divided into 4 groups (n =9 each) using a random number table:sham operation group (group S),intestinal I/R group (group I/R),low-dose dexmedetomidine group (group LD),and high-dose dexmedetomidine group (group HD).Intestinal I/R was produced by occlusion of the superior mesenteric artery for 1 h followed by 2 h reperfusion in anesthetized rats.Dexmedetomidine 2.5 and 5.0 μg · kg-1 · h-1 were infused via the caudal vein for 1 h starting from 1 h before ischemia in LD and HD groups,respectively.The rats were sacrificed at 2 h of reperfusion,and the gastric mucosa was obtained for examination of the pathological changes (with light microscope) and for determination of the expression of serine/threonine kinase (Akt),phosphorylated Akt (p-Akt),activated caspase-3 and caspase-3 (by Western blot).The ratio of p-Akt to Akt (p-Akt/Akt)was calculated to reflect the phosphorylation of Akt.The ratio of activated caspase-3 to easpase-3 (activated caspase-3/caspase-3) was calculated to reflect the activation of caspase-3.Results Compared with group S,the expression of Akt was significantly up-regulated,the expression of p-Akt was significantly downregulated,the phosphorylation of Akt was significantly decreased,and the activation of caspase-3 was significantly increased in group I/R,and the expression of p-Akt was significantly up-regulated,and the phosphorylation of Akt and activation of caspase-3 were significantly increased in LD and HD groups (P＜0.05).Compared with group I/R,the expression of Akt was significantly down-regulated,the expression of p-Akt was significantly up-regulated,the phosphorylation of Akt was significantly increased,and the activation of caspase-3 was significantly decreased in LD and HD groups (P＜0.05).The degree of gastric mucosal injury was significantly lower in LD and HD groups than in group I/R,and there was no significant difference in the degree of gastric mucosal injury between group LD and group HD.Conclusion Dexmedetomidine can attenuate gastric mucosal injury induced by intestinal I/R,and the mechanism may be related to activation of PI3K/Akt signaling pathways and inhibition of cell apoptosis in rats.