OBJECTIVE: To explore the peripheral neural mechanism underlying representation along the distribution of stomach meridian induced by intestinal inflammatory reaction using diarrhea predominant-irritable bowel syndrome (IBS-D) mice. METHODS: Among 62 healthy male C57BL/6 mice of clean grade, 12 mice were randomly selected and divided into a control group and a model group, 6 mice in each group, additionally, 12 mice were randomly selected and divided into a Tianshu group, a Liangqiu group and a Zusanli group, 4 mice in each group. In the model group, citrobacter was administered orally to establish IBS-D model. In the control group and the model group, the visceral pain threshold was observed using fecal colorectal distension (fCRD) induced electromyography of external oblique muscle, the positive cell number of neutrophil in the colonic muscularis was detected by myeloperoxidase (MPO) staining, the number, location and distribution rule of Evans blue (EB) extravasation points were observed by injection of EB staining solution into the tail vein. In the Tianshu group, the Liangqiu group and the Zusanli group, fluorescent dye Dil was injected at bilateral "Tianshu" (ST25), "Liangqiu" (ST34) and "Zusanli" (ST36) respectively, to observe the dye-positive cell number in different dorsal root ganglion (DRG) segments. In the control group and the model group, the activation of satellite glial cells (SGCs) in different DRG segments was observed by immunofluorescence. RESULTS: Compared with the control group, in the model group, the area under curve of electromyography of external oblique muscle was increased at fCRD of 25, 50 and 75 μL distilled water (P<0.001, P<0.01); the MPO-positive cell number of neutrophil in the colonic muscularis was increased (P<0.01). Few EB extravasation points could be found in the control group, while there were much more EB extravasation points observed in the model group, which was specially distribution in the area of stomach meridian, from "Huaroumen" (ST24) to "Zusanli" (ST36), as well as the surface area dominated by L₂-L₅ segment of the spinal cord. The Dil-positive cells were mainly exhibited in the DRG of T₁₁, L₅ and L₄ segments in the Tianshu group, the Liangqiu group and the Zusanli group, respectively. Compared with the control group, the ratio of glial fibrillary acidic protein (GFAP)/glutamine synthetase (GS) co-expression was increased in the DRG of T₁₁, L₄ and L₅ segments in the model group (P<0.05, P<0.01). CONCLUSION The activation of SGCs within DRG of T₁₁, L₄ and L₅ segments may relate closely to the occurrence of the representation along the stomach meridian distribution in IBS-D mice.
Animals ; Male ; Mice ; Irritable Bowel Syndrome/therapy* ; Mice, Inbred C57BL ; Meridians ; Stomach/physiopathology* ; Humans ; Acupuncture Points ; Disease Models, Animal

High mobility group box 1 (HMGB1), when released extracellularly, plays a pivotal role in the development of spinal cord synapses and exacerbates autoimmune diseases within the central nervous system. In experimental autoimmune encephalomyelitis (EAE), a condition that models multiple sclerosis, the levels of extracellular HMGB1 and interleukin-33 (IL-33) have been found to be inversely correlated. However, the mechanism by which IL-33 deficiency enhances HMGB1 release during EAE remains elusive. Our study elucidates a potential signaling pathway whereby the absence of IL-33 leads to increased binding of P300/CBP-associated factor with HMGB1 in the nuclei of astrocytes, upregulating HMGB1 acetylation and promoting its release from astrocyte nuclei in the spinal cord of EAE mice. Conversely, the addition of IL-33 counteracts the TNF-α-induced increase in HMGB1 and acetylated HMGB1 levels in primary astrocytes. These findings underscore the potential of IL-33-associated signaling pathways as a therapeutic target for EAE treatment.
Animals ; Encephalomyelitis, Autoimmune, Experimental/metabolism* ; Astrocytes/metabolism* ; Interleukin-33/metabolism* ; HMGB1 Protein/metabolism* ; Acetylation ; Mice, Knockout ; Mice, Inbred C57BL ; p300-CBP Transcription Factors/metabolism* ; Mice ; Spinal Cord/metabolism* ; Cells, Cultured ; Female ; Signal Transduction

The ninth edition of TNM staging for lung cancer has been announced at the 2023 World Lung Cancer Congress and implemented from January 1, 2024. The focus of the ninth TNM staging change is dividing N2 into N2a and N2b, as well as M1c into M1c1 and M1c2. Although the T staging has not changed, it has played an important role in verifying the eighth edition of the T staging. The subdivision of stage N2 has led some patients with ⅢA of the eighth edition to experience ascending or descending stages, which will more accurately help to assess the condition and prognosis of patients with mediastinal lymph node metastasis, as well as the design of related clinical studies. Modifying the M1c staging will help define oligometastasis and explore new treatment models in the future. The ninth edition of the TNM staging system provides a more detailed division of different tumor loads, but there is no clear explanation for the staging of lung cancer after neoadjuvant therapy. Further data analysis is needed, and it is expected to be answered in the tenth edition of TNM staging.

The ninth edition of TNM staging for lung cancer has been announced at the 2023 World Lung Cancer Congress and implemented from January 1, 2024. The focus of the ninth TNM staging change is dividing N2 into N2a and N2b, as well as M1c into M1c1 and M1c2. Although the T staging has not changed, it has played an important role in verifying the eighth edition of the T staging. The subdivision of stage N2 has led some patients with ⅢA of the eighth edition to experience ascending or descending stages, which will more accurately help to assess the condition and prognosis of patients with mediastinal lymph node metastasis, as well as the design of related clinical studies. Modifying the M1c staging will help define oligometastasis and explore new treatment models in the future. The ninth edition of the TNM staging system provides a more detailed division of different tumor loads, but there is no clear explanation for the staging of lung cancer after neoadjuvant therapy. Further data analysis is needed, and it is expected to be answered in the tenth edition of TNM staging.

Life science and medical research involving human beings cannot be separated from the support of research participants.The safety,health,and rights and interests of research participants are the primary considerations in clinical research,and their rights and interests include the right of compensation,privacy protection,health and so on.Protecting the compensation rights of research participants is a necessary responsibility of the research-related departments and personnel.Based on laws and regulations and literature review,and combined with practical experience,this paper made an in-depth discussion on compensation rights.It puts forward the types of compensation(conventional compensation,research-related damage compensation),compensation principles(necessity,timeliness,appropriateness,fairness),compensation elements(method,amount,plan,consent,notification,and reference of compensation),compensation under special circumstances(compensation for participants without or with limited informed consent ability and withdraw from the study midway),protection measures of compensation right(sponsor/contract research organizations,research institutions,research management departments,(main)researchers and research teams,ethics(review)committee).The compensation rights should be implemented to protect research participants.

Objective:To investigate the role and mechanism of miR-146b in the proliferation, metastasis and apoptosis of thyroid papillary carcinoma cells.Methods:qRT-PCR was used to detect the expression of miR-146b in thyroid papillary carcinoma cells (NPA, GLAG-66, ONCNO-DG1 and B-CPAP) and normal human thyroid cell line HTori3. After B-CPAP cells were transfected with miR-146b inhibitor, the inhibition efficiency was detected by qRT-PCR, the effect of miR-146b on PTC cells proliferation was detected by MTT assay, the effect of miR-146b on PTC cells invasion was studied by Transwell assay, and the effect of miR-146b on tumor cell apoptosis was detected by flow cytometry. SiRNA-IRAK1 was transfected into B-CPAP cell line. The cell proliferation rate, migration ability and apoptosis rate were detected by MTT, cell scratch test and flow cytometry respectively. The target gene of miR-146b, interleukin-1 associated receptor kinase 1 (IRAK1) , was predicted by bioinformatics software, and the regulatory effect of miR-146b on IRAK1 was verified by double fluorescein reporter gene experiment.Results:QRT-PCR showed that the expression of miR-146b in NPA87, KAT-5, FTC-133 and B-CPAP cell lines was significantly higher than that in normal cell HTori3, especially B-CPAP ( P<0.05) . MiR-146b inhibitor transfection could significantly reduce the expression level of miR-146b in B-CPAP cells ( P<0.01) . MTT results showed that miR-146b inhibitor could inhibit the proliferation of B-CPAP cells ( P<0.05) . Flow cytometry showed that miR-146b inhibitor could promote the apoptosis of B-CPAP cells ( P<0.05) . Transwell results showed that miR-146b inhibitor could reduce the invasive ability of B-CPAP cells ( P<0.05) . After transfection with siRNA-IRAK1, the proliferation rate of B-CPAP cells increased significantly (MTT test) , the migration ability increased (cell scratch test) , and the apoptosis rate decreased significantly (flow cytometry) ( P<0.05) . The results of double luciferase reporter gene showed that irak1 was the target gene of miR-146b, and miR-146b inhibitor could significantly up regulate the expression level of irak1 protein in B-CPAP cells. Conclusion:miR-146b may play a role in promoting the proliferation and metastasis and inhibiting cell apoptosis of PTC cells by inhibiting the downstream target protein IRAK1.

Objective:To study on the effect of ultrasound-guided thoracic paravertebral nerve (TPVB) block on quality of recovery from general anesthesia in tuberculosis patients with fiberboard exfoliation in post anesthesia recovery unit (PACU).Methods:From May 2018 to December 2019, 40 tuberculosis patients in Changsha Central Hospital with pulmonary fibreboard exfoliation and focal abscess lesions cleaning were randomly divided into two groups, with 20 patients in each group. The patients in group A received endobronchial general anesthesia and in group B received ultrasound-guided TPVB combined with endobronchial general anesthesia. Patients in the two groups were maintained under anesthesia by propofol, and the bispectral index (BIS) was maintained within the range of 40-50. The dosage of propofol and sufentanil was adjusted according to changes in BIS and hemodynamics. The mean arterial pressure (MAP), heart rate (HR) in two groups of patients were recorded at before anesthesia induction (T 0), before cutting leather (T 1), cut skin after (T 2), the end of operation (T 3), extubation time (T 4), and T 5 (time of leaving PACU). The visual analogue scale (VAS) of all patients in resting and cough state was recorded at 5, 30 min after extubation and the time of leaving PACU. The dosage of propofol and sufentanil in the operation and the additional dosage of sufentanil in PACU were recorded in both two groups. And the respiratory recovery time, consciousness recovery time, extubation time and sedation agitation scale(SAS) were observed. The adverse reactions such as nausea, vomiting, drowsiness and hypotension were observed in PACU. Results:Compared with group A, MAP and HR of patients at T 2, T 3, T 4, T 5 in group B were more stable during anesthesia, and VAS of patients in group B were lower than that in group A at each time point after extubation ( P<0.05). The dosage of sufentanil and propofol in group B were (35.92±8.12)μg and (749.56±95.30)mg respectively, which were significantly lower than those in group A [(45.74±4.42)μg and (862.83±105.34)mg, P<0.05]; the dosage of sufentanil in postoperative anesthesia recovery room of group B was (5.26±2.10)μg, significantly less than that of group A (10.35±5.86)μg ( P<0.05). The respiratory recovery time, consciousness recovery time and extubation time in group B were (12.92±5.12) min, (20.56±5.10) min and (26.87 ± 6.16) min, which were shorter than those in group A [(15.74±4.72)min, (25.83±5.34)min and (35.35±5.80)min, P<0.05]. The incidence of postoperative nausea, vomiting, lethargy and hypotension in group B were 10%, 10%, 35% and 20%, which were significantly lower than those in group A (30%, 20%, 75% and 45%, P<0.05). Conclusions:Ultrasound-guided paravertebral nerve block may significantly reduce the dosage of opioid analgesics for general anesthesia in tuberculosis patients with fiberboard exfoliation, accelerate the speed of anesthesia recovery, reduce the agitation during recovery, and improve the quality of anesthesia recovery.

Objective:To investigate the prognosis of severe hyperbilirubinemia in full-term infants who met the exchange transfusion criteria and were treated by blood exchange transfusion and phototherapy.Methods:A total of 168 full-term infants with severe hyperbilirubinemia who met the criteria for exchange transfusion and were hospitalized in the Neonatology Department of seven tertiary hospitals in Hebei Province from June 2017 to December 2018 were retrospectively included. According to the treatment protocol, they were divided into two groups: exchange transfusion group (38 cases) and phototherapy group (130 cases). Two independent sample t-test and Chi-square test were used to compare the clinical manifestations and follow-up results between the two groups. Multivariate logistic regression was used to analyze the risk factors for poor prognosis. Results:Neonatal severe hyperbilirubinemia in the exchange transfusion and phototherapy group were both mainly caused by hemolytic disease [42.1%(16/38) and 29.2%(38/130)], sepsis [28.9%(11/38) and 11.5%(15/130)] and early-onset breastfeeding jaundice [15.8%(6/38) and 11.5%(15/130)]. Total serum bilirubin level on admission in the exchange transfusion group was significantly higher than that in the phototherapy group [(531.7±141.3) vs (440.0±67.4) μmol/L, t=3.870, P<0.001]. Moreover, the percentage of patients with mild, moderate and severe acute bilirubin encephalopathy in the exchange transfusion group were higher than those in the phototherapy group [15.8%(6/38) vs 3.8%(5/130), 7.9%(3/38) vs 0.8%(1/130), 13.2%(5/38) vs 0.0%(0/130); χ2=29.119, P<0.001]. Among the 168 patients, 135 were followed up to 18-36 months of age and 12 showed poor prognosis (developmental retardation or hearing impairment) with four in the exchange transfusion group (12.9%, 4/31) and eight in the phototherapy group (7.7%, 8/104). Multivariate logistic regression analysis showed that for full-term infants with severe hyperbilirubinemia who met the exchange transfusion criteria, phototherapy alone without blood exchange transfusion as well as severe ABE were risk factors for poor prognosis ( OR=14.407, 95% CI: 1.101-88.528, P=0.042; OR=16.561, 95% CI: 4.042-67.850, P<0.001). Conclusions:Full-term infants who have severe hyperbilirubinemia and meet the exchange transfusion criteria should be actively treated with blood exchange transfusion, especially for those with severe ABE, so as to improve the prognosis.

Objective? To construct the "Internet +" based health management model for physical examination population. Methods? From September 2016 to September 2017, we constructed the primary"Internet +" health management model by literature review. Two rounds of consultation with 25 experts were carried out with the Delphi method to construct the "Internet +" health management model for physical examination population. Results? Among two rounds of consultation, the recovery rate of questionnaire was all 100%. The expert authority coefficient (Cr) was 0.87. The final "Internet +" health management model included 3 first-level indicators, 7 second-level indicators and 26 third-level indicators. Conclusions? The "Internet +"based health management model is reliable which can be intervention for health management model of physical examination population.

Secalonic acid D (SAD) could inhibit cell growth in not only sensitive cells but also multidrug resistant (MDR) cells. However, the molecular mechanisms need to be elucidated. Here, we identified that SAD possessed potent cytotoxicity in 3 pairs of MDR and their parental sensitive cells including S1-MI-80 and S1, H460/MX20 and H460, MCF-7/ADR and MCF-7 cells. Furthermore, SAD induced cell G2/M phase arrest the downregulation of cyclin B1 and the increase of CDC2 phosphorylation. Importantly, JNK pathway upregulated the expression of c-Jun in protein level and increased c-Jun phosphorylation induced by SAD, which was linked to cell apoptosis c-Jun/Src/STAT3 pathway. To investigate the mechanisms of upregulation of c-Jun protein by SAD, the mRNA expression level and degradation of c-Jun were examined. We found that SAD did not alter the mRNA level of c-Jun but inhibited its proteasome-dependent degradation. Taken together, these results implicate that SAD induces cancer cell death through c-Jun/Src/STAT3 signaling axis by inhibiting the proteasome-dependent degradation of c-Jun in both sensitive cells and ATP-binding cassette transporter sub-family G member 2 (ABCG2)-mediated MDR cells.