Background and Objectives: Dental pulp stem cells (DPSCs) play an important role in the repair of tooth injuries. Electrogenic sodium bicarbonate cotransporter 1 (NBCe1) is a Na＋ -coupled HCO3− transporter encoded by the solute carrier 4A4 (SLC4A4) gene and plays a crucial role in maintaining the pH of DPSCs. Our previous research confirmed that NBCe1 is highly expressed in odontoblasts during the development of the tooth germ. Therefore, in this study, we aimed to investigate the effect of NBCe1 on odontogenic differentiation of DPSCs and further clarify the underlying mechanisms. Methods: and Results: DPSCs were isolated and identified, and the selective NBCe1 inhibitor S0859 was used to treat DPSCs. We used a cell counting Kit-8 assay to detect cell proliferative ability, and intracellular pH was assessed using confocal microscopy. Odontogenic differentiation of DPSCs was analyzed using real-time PCR and Alizarin Red S staining, and the NF-κB pathway was assessed using western blotting. Our results indicated that 10 μM S0859 was the optimal concentration for DPSC induction. Intracellular pH was decreased upon treatment with S0859. The mRNA expressions of DSPP, DMP1, RUNX2, OCN, and OPN were upregulated in the NBCe1 inhibited group compared to the controls. Moreover, NBCe1 inhibition significantly activated the NF-κB pathway, and a NF-κB inhibitor reduced the effect of NBCe1 on DPSC differentiation. Conclusions NBCe1 inhibition significantly promotes odontogenic differentiation of DPSCs, and this process may be regulated by activating the NF-κB signaling pathway.

Objective:The investigation and research on the application status of Hepatic Venous Pressure Gradient (HVPG) is very important to understand the real situation and future development of this technology in China.Methods:This study comprehensively investigated the basic situation of HVPG technology in China, including hospital distribution, hospital level, annual number of cases, catheters used, average cost, indications and existing problems.Results:According to the survey, there were 70 hospitals in China carrying out HVPG technology in 2021, distributed in 28 provinces (autonomous regions and municipalities directly under the central Government). A total of 4 398 cases of HVPG were performed in all the surveyed hospitals in 2021, of which 2 291 cases (52.1%) were tested by HVPG alone. The average cost of HVPG detection was (5 617.2±2 079.4) yuan. 96.3% of the teams completed HVPG detection with balloon method, and most of the teams used thrombectomy balloon catheter (80.3%).Conclusion:Through this investigation, the status of domestic clinical application of HVPG has been clarified, and it has been confirmed that many domestic medical institutions have mastered this technology, but it still needs to continue to promote and popularize HVPG technology in the future.

Objective To investigate the effect of improving immunity in the treatment of chronic brucellosis,and to analyze and evaluate its clinical curative effect.Methods A patient with chronic brucellosis was treated with Mongolian medicine combined with chemical drugs to enhance immunity.The clinical symptoms,serological antibodies,Brucella DNA and immune function were compared before and after treatment.The specific antibody against Brucella in serum was detected by tube agglutination test (SAT) and tiger red plate agglutination test (RBPT).Brucella DNA in serum and blood cells was detected by PCR,and the peripheral blood lymphocyte subsets were detected by flow cytometry.Immuno-luminescence technique was used to detect serum immunoglobulin and complement components.Results After treatment,the clinical symptoms such as cold back,fatigue,and joint pain disappeared completely,and the results of serum specific antibodies against Brucella were SAT 1 ∶ 50 (++)and RBPT (+) with no changes before and after treatment,and the results of cells and serum were both negative after treatment though the results of DNA detection of Brucella were cell positive and seronegative before treatment.The results of immunological function test showed that γδT cells decreased to 9.50％ after treatment compared to 14.00％ before treatment,and the percentage of monocytes and Treg cells were 5.59％ and 7.33％ after treatment,which were higher than 3.35％ and 4.72％ of before treatment,and the level of complement C3 was 0.79 g/L before treatment and 0.91 g/L after treatment that was returned to normal reference range (0.88 ～ 2.01 g/L).Conclusion The patients with chronic brucellosis can improve their clinical treatment by improving immunity.

Primary biliary cholangitis (PBC) is an autoimmune liver disease with unclear pathogenesis.The amino acid composition and sequence in the complementarity-determining region 3 of T cell receptor (TCR) and B cell receptor (BCR) are highly diverse, which forms a large antigen recognition receptor repertoire, i.e., immune repertoire.In recent years, second-generation sequencing techniques combined with multiplex PCR or amplicon rescue multiplex PCR have been used to study the features of immune repertoire in PBC patients, and it has been found that PBC patients have clonal expansion of specific CD4+ T lymphocytes, clonal diversity of B lymphocytes, somatic hypermutation, and reduction in class switch, as well as increase in clonal diversity after treatment with ursodeoxycholic acid.These findings need to be confirmed by large-scale in vivo and in vitro studies and different immune repertoire research strategies.

Objective: To analyze the characteristics of immunoglobulin heavy chain complementarity-determining region (IgH-CDR3) repertoire of peripheral B cells in a patient with primary biliary cholangitis (PBC) and to investigate the diversity of the immune system. Methods: Arm-PCR was used to amplify the IgH-CDR3 region of circulating B cells isolated from a PBC patient, and high-throughput sequencing was used to analyze the amplified product. The characteristics of immune repertoire were analyzed by bioinformatics. Results: In total, 329219 sequence reads were generated from the sample, with 325540 total CDR3 sequences and 72774 distinct CDR3 sequences, and the D50 of IGH-CDR3 was 7.7. The dominant CDR3 length of the sample was 45 nt (9.6%); the N addition with the highest frequency ranged from 13 to 14 nt (5.25%); the J trimming with the highest frequency was 0 nt (12.7%); the three most frequent V alleles were V4-59 (9.5%), V3-23 (8.1%), and V1-69 (6.4%). Conclusion The diversity of IgH-CDR3 repertoire is relatively low in this patient with PBC, with several B-cell clonal expansions. The specificity needs to be further verified after increasing the sample size.

[ ABSTRACT] AIM:To investigate the preventive effects of Clostridium butyricum ( C.butyricum) on the type of pylorus ligated gastric ulcer ( GU) in mice and the underlying mechanisms.METHODS:ICR mice were randomly divided into 4 groups:sham operation group, model group, C.butyricum pretreatment group and omeprazole pretreatment group. Gastric pyloric ligation was adopted to establish GU model in mice.The gastric juice was collected to measure the content of gastric free mucus, the pH of gastric juice and the activity of pepsin.The gastric tissues were collected for routine HE stai-ning to observe the pathological changes.The content of glycogen was detected by PAS staining.The protein expression of Bax and Bcl-2 in the gastric mucosa was also assessed by immunohistochemical staining.RESULTS: The HE and PAS staining showed that the C.butyricum pretreatment obviously attenuated the mucosa lesion induced by ligation.Compared with model group, the pH of gastric juice was significantly raised.The activity of pepsin fell off in C.butyricum group, which was lower than that in omeprazole group.In comparison with model group, the content of gastric free mucus was dra-matically increased and PAS staining showed a significant rise in C.butyricum group, but not in omeprazole group.The protein expression of Bax was decreased and the protein expression of Bcl-2 was upgraded in C.butyricum group than those in model group.CONCLUSION:C.butyricum protects gastric mucosa against the challenge of pylorus ligation in mice and its mechanism may be related to inhibiting gastric acid secretion and the activation of pepsin, increasing the production of gastric free mucus, strengthening the expression of bcl-2 gene and inhibiting the expression of bax gene.

Objective To investigate the clinical features of aortic dissection (AD) and emergency treatments. Methods Data from 784 patients with aortic dissection were collected in the Department of Emergency from January 2000 through December 2009. A retrospective analysis was carried out to determine the survival rate, mortality rate and treatment efficiency. Results Pain was the most common onset symptom (77.7% , 609/784). The majority of patients (86.5%) had essential hypertension (678/784). All the patients with preoperative diagnosis of aortic dissection underwent emergency medical intervention by internists resulting in 81.5% survival rate (639/784) and 18.5% mortality rate (145/784). There were 157 patients without improvement (20.0% ) and the total efficiency rate was (83. 1% ). The efficiency rate of conventional treatment was 76.4% , while the efficiency rate of triple four-procedure treatment was 89. 8% (P<0.05). Of them, 139 patients (17. 7% ) died in the hospital. Among them,. 26 patients died within 24 hours (18.4% ) and 47 cases died within 48 hours (33. 8% ) and 66 patients died within 72 hours (47.2% ). There were 92 patients who refused treatments after diagnosis, and among them, 81 patients died within 72 hours (88.04% ). The difference in mortality rate between two groups was significant (P<0.05). Conclusions The diagnosis of aortic dissection depends on detailed history, physical examination and CT or MRI imaging. Analgesia, sedation and control of blood pressure are essential for emergency treatments. Early diagnosis and effective emergency treatments are the critical strategy for the early surgical intervention and time window for further treatment to improve the survival rate of AD.

Tubulointerstitial fibrosis(TIF)is a common pathological feature of end-stage kidney disease.Previous studies showed that upregulation of TGFβ1 notably contributed to the chronic renal injury and irbesartan halted the development of TIF in rats with 5/6 renal mass reduction.This study was to investigate the effects of irbesartan on chronic TIF and the mechanism involved TGFβ1 in the rodent model of chronic renal failure involving 5/6 nephrectomy.The results showed that irbesartan significantly attenuated the rise in blood pressure and tubulointerstitial injury observed in this model.Masson staining of the renal tissue revealed that there appeared severe renal tubule atrophy and fibrosis in operation group,but the lesion was attenuated mostly in irbesartan-treated group.Immunohistochemistry showed that irbesartan treatment apparently decreased the protein expression of TGFβ1 which was up-regulated in operation groups.Western blot showed that irbesartan treatment down-regulated the expression of TGFβ1,phosphorylated smad2(p-smad2),AT1R and phosphorylated p38(p-p38)MAPK,but significantly up-regulated the protein expression of smad6 as compared with operation group.These findings suggest that irbesartan attenuates hypertension and reduces the development of TIF in rats with 5/6 renal mass reduction via changes in the expression of these proteins at least including smad6,TGF-β1,p-smad2,AT1 and p-p38 MAPK.

Objectives The present study aimed to investigate the associations between genetic polymorphism of methylenetetrahydrofolate reductase ( MTHFR) G1793A, plasma homocysteine (Hcy) levels, vitamin status and ulcerative colitis ( UC) in a cohort of patients in Hubei Han nationality. Methods Two hundred and ninty-nine UC patients and 764 age- and sex-matched healthy controls were recruited in this study. Polymorphism of MTHFR G1793A was examined using a PCR-RELP method.Plasma levels of Hcy, folate and vitamin B12 were determined by enzymatic cycling assay and corpuscle immune chemiluminescence assay, respectively.Results Both variant allele and genotype frequencies in MTHFR G1793A gene were significantly higher in the UC patients compared to the controls (22.24% vs 14.20% , P<0.001 ;42.81% vs 26.97%, P < 0.001, respectively).Plasma Hcy levels were increased in UC patients compared to the controls [(20.67 ±6.42)mmol/L vs (13.21 ±5.11)mmol/L, P <0.001] while folate and vitamin B12 concentrations were significantly decreased [(11.37±6.34) nmol/L vs (14.89±7.21) nmol/L, P < 0.001; (324.15±127.53 ) pmol/L vs (421.54±128.45 ) pmol/L, P < 0.001, respectively].Furthermore, hyperhomocysteinaemia (HHcy) and folate deficiency were also more prevalent in the UC patients (32.44% vs 25.78% , P = 0.029; 23.41% vs 17.01%, P =0.016, respectively).Conclusions Genetic polymorphism of MTHFR G1793A Wag strongly associated with UC.HHcy,folate deficiency and low vitamin B12 concentration were common phenomena in the UC patients of Hubei Han nationality.Our findings demonstrate that the genes relmed to Hey metabolism may play an important role in the pathogenesis of UC.

Tubulointerstitial fibrosis (TIF) is a common pathological feature of end-stage kidney disease. Previous studies showed that upregulation of TGFbeta1 notably contributed to the chronic renal injury and irbesartan halted the development of TIF in rats with 5/6 renal mass reduction. This study was to investigate the effects of irbesartan on chronic TIF and the mechanism involved TGFbeta1 in the rodent model of chronic renal failure involving 5/6 nephrectomy. The results showed that irbesartan significantly attenuated the rise in blood pressure and tubulointerstitial injury observed in this model. Masson staining of the renal tissue revealed that there appeared severe renal tubule atrophy and fibrosis in operation group, but the lesion was attenuated mostly in irbesartan-treated group. Immunohistochemistry showed that irbesartan treatment apparently decreased the protein expression of TGFbeta1 which was up-regulated in operation groups. Western blot showed that irbesartan treatment down-regulated the expression of TGFbeta1, phosphorylated smad2 (p-smad2), AT1R and phosphorylated p38 (p-p38) MAPK, but significantly up-regulated the protein expression of smad6 as compared with operation group. These findings suggest that irbesartan attenuates hypertension and reduces the development of TIF in rats with 5/6 renal mass reduction via changes in the expression of these proteins at least including smad6, TGF-beta1, p-smad2, AT1 and p-p38 MAPK.