Objective:To investigate the effect of intensive hypoglycemic therapy on the frequency of recurrent periodontitis in the patients with type 2 diabetes mellitus. Methods: Totally 40 patients with type 2 diabetes mellitus and recurrent periodontal disease were randomly divided into group A and group B. Group A was treated with the periodontal basic therapy combined with the convention-al hypoglycemic therapy. Group B was treated with the periodontal basic therapy combined with the intensive hypoglycemic therapy. Af-ter 6-month treatment,the change of the probing depth of the periodontal pocket, sulcus bleeding index, incidence frequency, recovery course, body mass index, fasting blood glucose, glycosylated hemoglobin and serum C-reactive protein levels were measured before and after treatment. Results:After the treatment, the indices were improved in group A except body mass index and fasting blood glucose (P<0. 05), and in group B, the indices were improved except body mass index (P<0. 05), and the probing depth of the periodontal pocket, sulcus bleeding index, incidence frequency, body mass index, serum C-reactive protein levels, glycosylated hemoglobin and fasting blood glucose of the patients in group B were all better than those in group A (P<0. 05). Conclusion:Periodontal basic thera-py combined with intensive hypoglycemic therapy can effectively improve the periodontal health of diabetic patients, shorten the recov-ery treatment of periodontal disease, reduce the incidence frequency, and reduce blood glucose as well.

Objective To investigate effect of sorafenib on serum hepatoma marker in patients with advanced hepatocellular carcinoma. Methods 101 patients with advanced hepatocellular carcinoma were selected, and divided into two groups.50 cases in control group were treated with routine clinical treatment, and 51 cases in experimental group were treated with sorafenib on the basis of control group.The survival time, adverse reactions, VEGF, CTGF, HIF-1 and OPN levels were compared after the treatment.Results The survival time of experimental group was higher than control group (P<0.05).Compared with control group, the serum levels of VEGF、CTGF,HIF-1, OPN,AFP, CEA, and CA199 in experiment group were lower (P<0.05,P <0.01).There were no significant differences of total adverse reactions between experimental group and control group. Conclusion Sorafenib can effectively prolong survival time of patients with advanced hepatocellular carcinoma, reduce serum VEGF, CTGF, HIF-1 alpha and OPN levels.

AIM:To investigate the maturation of mice immature myeloid dendritic cells (mDCs) induced by antigen(Ag)85B of mycobacterium tuberculosis, and the expression of TSLPR and OX40L mediated by TSLP in vitro. METHODS:Recombinant mouse GM-CSF ( rmGM-CSF) and rmIL-4 were used to induce bone marrow precursor cells of C57BL/6 mice to differentiate into immature mDCs in vitro.mDCs were identified followed by purification using CD 11c binding magnetic beads .The morphological characteristic of mDCs was observed under inverted phase-contrast microscope and scanning electron microscope .The surface phenotypes of mDCs were determined by flow cytometry .To obtain the opti-mal concentrations of Ag85B and TSLP, immature mDCs were cultured with different concentrations of Ag 85B or TSLP at 0 (control group), 50, 100 and 200 μg/L for 24 h, and the expression of cell surface molecules CD 80, CD86, TSLPR and OX40L was detected by flow cytometry.In addition, the expression of TSLPR and OX40L in Ag85B and TSLP-co-stimula-ted mDCs was determined by flow cytometry .RESULTS:After 7 d of culture in vitro, the cells showed irregular dendritic protrusions under the inverted-phase contrast microscope , and had wrinkles and dendritic splits under scanning electron mi-croscope , conformed to the morphological characteristics of immature mDCs .The mDCs cells expressed higher level of spe-cific marker CD11c, lower level of co-stimulatory molecules CD80 and CD86, which conformed to the phenotype of imma-ture mDCs.The CD80 +and CD86 +cell ratios of mDCs displayed significant increases in 50, 100 and 200μg/L Ag85B or TSLP groups compared with control group (P<0.05).The ratios of TSLPR +and OX40L+cells did not differ among dif-ferent concentrations of Ag 85B groups.The ratios of TSLPR +and OX40L+cells were significantly increased in 100 μg/L and 200μg/L TSLP groups compared with control group and 50μg/L TSLP group (P<0.05).Under the circumstance of optimal Ag85B or TSLP treatment concentration at 200 μg/L, there was significantly decreased in TSLPR and OX 40L cell ratio of mDCs in Ag85B group or Ag85B combined with TSLP group when compared with TSLP group (P<0.05), and no significant difference among Ag85B group, Ag85B combined with TSLP group and control group was observed .CONCLU-SION: Ag85B enhances mDCs maturation by up-regulating the expression of co-stimulatory molecules CD80 and CD86, and inhibit the expression of pro-inflammatory specific molecules TSLPR and OX40L on TSLP-activated mDCs, indicating that Ag85B modifies the development of asthmatic airway inflammation through the pathway of TSLP -activated mDCs.

Objective To investigate the effect of spirolactone on cardiac function and serum brain natriuretic peptide in patients with chronic heart failure( CHF). Methods Eighty-four patients with CHF were randomly divided into control group( n=42 )and observation group( n=42 ). The patients in the control group were given conventional therapy,while in the observation group were given spirolactone( 20 mg/times,2 times/day)based on treatment of the control group for six months. The clinical effects and left ventricular end diastolic diameter( LVEDd ),left ventricular ejection fraction( LVEF ) and serum brain natriuretic peptide( BNP ) of pretherapy and post-treatment between the two groups were recorded and compared. Results The total effective rate of observation group was 95. 2%(40/42),obviously higher than that of control group(80. 9%(34/42),χ2=6. 468,P=0. 028). The levels of LVEDd and BNP in two groups after treatment were(57. 8 ± 6. 2)mm and (62. 4 ± 7. 8)mm,(364. 4 ± 32. 8)ng/L and(457. 4 ± 43. 2)ng/L,significantly lower than those at before treatment((64. 6 ± 7. 4)mm and(64. 8 ± 7. 6)mm,(867. 8 ± 78. 5)ng/L and(864. 4 ± 74. 8)ng/L),while LVEF in two groups after treatment were( 49. 8 ± 5. 4 )% and( 42. 6 ± 4. 6 )%,significantly higher than those before treatment((35. 2 ± 3. 9)% and(35. 4 ± 3. 5)%),and the differences were significant(t = -3. 264, 4. 626,-5. 373,-3. 932,5. 438,-6. 548;P﹤0. 05). Moreover the changes in observation group were obvious than those in control group in terms of LVEDd,BNP and LVEF( t = -3. 425,3. 644,-2. 846;P ﹤0. 05 ) . Conclusion Spironolactone can effectively decrease the serum brain natriuretic peptide levels,improve the cardiac function in patients with chronic heart failure,and it is worthy of popularization and application.

Objective To analyze a rare genotype with β-thalassemia intermadia.Methods Phenotypic analysis was performed using routine hematological tests to measure red blood cell parameters and high performance liquid chromatography (HPLC)was used to measure hemoglobin fractions.The β-globin gene mutations were conducted using reverse-dot-blot and DNA sequencing of the breakpoint region were characterized with gap-PCR.Results The proband had a trait of thalassemia intermedia with reduced hemoglobin (86 g/L).The proband's father had a trait of microcytic hypochromic with reduced mean corpuscular volume(MCV),mean corpuscular hemoglobin (MCH) (63.7 fl and 20.4 pg,respectively) and an elevated level of HbA2.He had the phenotype of heterozygosity for β-thalassemia.The preband's mother,grandmother and sister had a trait of heterezygote for hereditary persistence of fetal hemoglobin (HPFH) with elevated level of HbF,which were 28.3%,21.1% and 33.7%,respectively.After molecular characterization of the family members,the proband was identified as a patient with β-thalassemia intermedia caused by co-existence of β-thalassemia(β41-42) and HPFH-6.The father was heterozygoas for β-thaiassemia (β41-42/βN) and the mother,grandmother and sister were all heterozygons for HPFH-6.Condusions A rare β-thalassemia intermedia case resulting from compound heterezygote of β41-42 with HPFH-6 is found.This study may provide clinical experiences for antenatal diagnosis.

Background: High concentrations of particulate matter less than 2.5 μm in diameter (PM2.5) in poultry houses is an important cause of respiratory disease in animals and humans. Pseudomonas aeruginosa is an opportunistic pathogen that can induce severe respiratory disease in animals under stress or with abnormal immune functions. When excessively high concentrations of PM2.5 in poultry houses damage the respiratory system and impair host immunity, secondary infections with P. aeruginosa can occur and produce a more intense inflammatory response, resulting in more severe lung injury. Objectives: In this study, we focused on the synergistic induction of inflammatory injury in the respiratory system and the related molecular mechanisms induced by PM2.5 and P. aeruginosa in poultry houses. Methods: High-throughput 16S rDNA sequence analysis was used for characterizing the bacterial diversity and relative abundance of the PM2.5 samples, and the effects of PM2.5 and P. aeruginosa stimulation on inflammation were detected by in vitro and in vivo. Results: Sequencing results indicated that the PM2.5 in poultry houses contained a high abundance of potentially pathogenic genera, such as Pseudomonas (2.94%). The lung tissues of mice had more significant pathological damage when co-stimulated by PM2.5 and P. aeruginosa, and it can increase the expression levels of interleukin (IL)-6, IL-8, and tumor necrosis factor-α through nuclear factor (NF)-κB pathway in vivo and in vitro. Conclusions The results confirmed that poultry house PM2.5 in combination with P. aeruginosa could aggravate the inflammatory response and cause more severe respiratory system injuries through a process closely related to the activation of the NF-κB pathway.

Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer's disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. β-Amyloid (Aβ) and ibotenic acid (IBO)-induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed Aβ + IBO-induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in Aβ + IBO-induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against Aβ + IBO-induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine A₁ receptor-specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the Aβ + IBO-induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of A₁R is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.
Action Potentials ; Adenosine ; Alzheimer Disease ; Fires ; Ibotenic Acid ; Membranes ; Neurons ; Neuroprotection ; Neuroprotective Agents ; Patch-Clamp Techniques ; Pyramidal Cells

Taking the Department of Obstetrics and Gynecology as an example, this paper expounds a series of practices of online education, in the process from pre-course training, platform selection, curriculum design, to student evaluation, etc. From that, we can provide a reference for carrying out online teaching in response to the epidemic for clinical medical colleges which have not been exposed to the online course. Furthermore, it is a new attempt to explore a way to make a change of the traditional teaching method and deepen the reform of clinical teaching in our hospital after the epidemic, not only in professional medical education, but also in the popularization of medical knowledge.

OBJECTIVE: To investigate the clinical phenotype and genetic basis of a child with epilepsy and global developmental delay. METHODS: A child with epilepsy and global developmental delay who had visited West China Second University Hospital, Sichuan University on April 1, 2021 was selected as the study subject. Clinical data of the child were reviewed. Genomic DNA was extracted from peripheral blood samples of the child and his parents. Whole exome sequencing (WES) was carried out for the child, and candidate variant was verified by Sanger sequencing and bioinformatic analysis. A literature review was also carried out by searching databases such as Wanfang data knowledge service platform, China National Knowledge Infrastructure, PubMed, ClinVar and Embase to summarize the clinical phenotypes and genotypes of the affected children. RESULTS: The child was a 2-year-and-2-month-old male with epilepsy, global developmental delay and macrocephaly. Results of WES showed that the child has harbored a c.1427T>C variant of the PAK1 gene. Sanger sequencing confirmed that neither of his parents has carried the same variant. Only one similar case had been recorded by the dbSNP, OMIM, HGMD, and ClinVar databases. No frequency for this variant among Asian population was available in the ExAC, 1000 Genomes, and gnomAD databases. Prediction with IFT, PolyPhen-2, LRT, Mutation Taster, and FATHMM online software suggested that this variant is deleterious to the function of encoded protein. Based on the Standards and Guidelines for the Interpretation of Sequence Variants: A Joint Consensus Recommendation of the American College of Medical Genetics and Genomics (ACMG), the PAK1 gene c.1427T>C variant was determined to be likely pathogenic. CONCLUSION The PAK1 gene c.1427T>C variant probably underlay the epilepsy and global developmental delay in this child, which has provided a reference for the clinical diagnosis and genetic counseling in children with similar disorders.
Humans ; Male ; China ; Computational Biology ; Consensus ; Epilepsy/genetics* ; Genotype ; Mutation ; p21-Activated Kinases/genetics* ; Child, Preschool

OBJECTIVE: To explore the clinical phenotype and genetic characteristics of two children with developmental epileptic encephalopathy type 66. METHODS: Genomic DNA was extracted from peripheral blood samples of the two children and their parents. Whole exome sequencing (WES) was carried out and suspected variant was verified by Sanger sequencing. RESULTS: The main manifestations of the two children were neonatal onset seizures, hypotonia, global developmental delay, and facial dysmorphisms. Cranial MRI showed delayed myelination in case 1 and cerebellar dysgenesis in case 2. WES has identified a de novo pathogenic variant in the PACS2 gene in both patients, namely c.625G>A (p.Glu209Lys)(NM_001100913.3), which was reported as a pathogenic variant before. This variant was predicted to be pathogenic according to the American College of Medical Genetics and Genomics guideline (PS2+PM2+PP3). The seizures were controlled after combination treatment of sodium valproate and levetiracetam in both cases. At last follow-up, the motor and intellectual development of the 2 cases were improved. Compared with the cases reported, the clinical symptoms and signs of our cases were relatively mild, and the treatment effects were fairly good. CONCLUSION The variant of c.625G>A (p.Glu209Lys) in PACS2 gene is a hotspot variant of developmental epileptic encephalopathy 66. Gene testing can facilitate the clinical diagnosis and treatment.
Child ; Epilepsy, Generalized ; Family ; Genetic Testing ; Humans ; Magnetic Resonance Imaging ; Vesicular Transport Proteins/genetics* ; Whole Exome Sequencing