Objective To investigate the current situation in construction of WeChat public platform in 9 class A hospitals affiliated to Sichuan Province in Chengdu. Methods The problems and the reasons why they occurred in construction of WeChat public platform in these 9 hospitals were analyzed by literature analysis, interview, Topsis and RSR analysis, and their combination. Results The problems found in hospital WeChat public platform included imperfect management, unmatched construction level and hospital scale, insufficient government policy support and effective supervising mechanisms. Conclusion Hospitals should strengthen the construction and management of their WeChat public platform, innovatively construct their WeChat public platform, win over sufficient government policy support, and improve their supervising mechanisms.

Background and purpose:Bone marrow cytomorphology is the main approach for determination of bone marrow involvement in patients with malignant lymphomas. In recent years, with the development of detection of cellular surface markers and molecular biology, flow cytometry (FCM) and polymerase chain reaction (PCR) were gradually applied in the detection of bone marrow in malignant lymphomas. Because such systematic research has not been done domestically , we performed a study to compare diagnostic value and clinipathological signifi cance of cytomorphology of bone marrow aspirates, immunophenotype detected by flow cytometry and immunoglobulin heavy chain gene rearrangement detected by polymerase chain reaction in bone marrow of B cell lymphomas. Methods: Bone marrow cytomorphology, FCM and PCR were simultaneously carried out in 75 bone marrows of B cell lymphoma and compared with each other. Results:(1)16 were demonstrated by cytomorphology, 36 by FCM, 33 by PCR. The positive rates were 21.3%, 48% and 44% respectively. The differences among these three methods have statistical signifi cance (P

Objective To investigate dynamic metabolism in vivo of Ginkgo Folium Tablet under the guidance of sequential metabolism thoughts. Methods In situ closed-loop in rats was carried out to study sequential metabolism of Ginkgo Folium Tablet through oral digestive system, namely to investigate and compare the intestinal flora metabolism, the gut wall metabolism and hepatic metabolism, combined with chromatographic fingerprint of blood samples. Results The analysis showed that 12 peaks in Ginkgo Folium Tablet were metabolized by intestinal flora, and 7 peaks generated through the gut wall. Most components of Ginkgo Folium Tablet were metabolized in liver, and 3 original medicine components were directly into the blood. Conclusion This study conducts a qualitative description of metabolism of Ginkgo Folium Tablet in different parts of the oral route, and provides references for the quality control, mechanism explanation and secondary development for Ginkgo Folium Tablet.

Objective　To evaluate the correlation between vascular endothelial growth factor(VEGF) expression and microvessel density(MVD) in gastric carcinoma (GC) and the relationship of VEGF and MVD with clinicopathologic characteristics and prognosis of GC. Methods　The expression of VEGF and intratumoral microvessel density (MVD) in one hundred and sixteen resected specimens of the patients with GC were observed and counted, and the relationship of VEGF and MVD with clinicopathologic factors and prognosis of GC were analysed. Results　The expression of VEGF was found in 60.34% of the specimens. The MVD value was much higher in VEGF(+) group than that in VEGF(-) group (26.16±8.50 and 19.22±8.20, respectively, P<0.01). Expression of VEGF was significantly higher in patients with lymph node metastasis than that in patients without lymph node metastasis (p<0.05).Expression of VEGF was highly correlated with the stage of tumor (P<0.05). MVD correlated with lymph node metastasis (P<0.01) and abdomen metastasis (P<0.01) and increased with the TNM stage (P<0.01). The total five-year survival rate in VEGF(-) group and low MVD group were significantly higher than that in VEGF(+) group and high MVD group respectively(both P<0.01). Multivariate analysis indicated that the expression of VEGF and MVD were independent prognostic factors of GC. Conclusions　The expression of VEGF and MVD can reflect the malignant degree of GC. They may serve as the prognostic factors and guide the decisions on the therapy.

OBJECTIVETo study the genetic basis of aberrant crypt foci (ACF), which serve as a very early morphological alteration during the development of carcinogenesis by analyzing the loss of heterozygosity (LOH).

METHODSDNA from 35 colorectal carcinomas (CRC) and 34 matched ACF were isolated by microdissection. LOH of microsatellite loci at 18q12, 18q21, 5q12, 5q21, 3p21, 2p16, 17q21, 17q11 and 11p13 was detected by means of ABI-SEQUENCER and GeneScan software was applied for analysis.

RESULTSThe rate of LOH in ACF (41.18%) was less than that in carcinoma (68.57%) (P < 0.05). The profile of LOH rates at loci 18q12, 5q12, 3p21, 17q21, 17q11, 11p13 and 2p16 in ACF was similar to that in carcinoma. The LOH frequencies on 18q12, 18q21, 5q12, 5q21, and 3p21 were higher than that on 17q11 and 11p13. However the rate at 18q21 and 5q21 in ACF was much lower than that in the carcinoma (P < 0.05). The co-existing carcinomas displayed more polypoid growth pattern and located more at the sigmoid colon and rectum. LOH in carcinomas did not correlate with the location, size, type of the carcinoma and Duke's stage.

CONCLUSIONSACF are putative preneoplastic lesions that might represent the earliest morphological lesion with the alteration at molecular genetic level. Our study provides further genetic evidence in the pathogenesis of colorectal carcinomas.

Chromosomes ; Chromosomes, Human, Pair 11 ; Chromosomes, Human, Pair 17 ; Chromosomes, Human, Pair 18 ; Chromosomes, Human, Pair 2 ; Chromosomes, Human, Pair 3 ; Chromosomes, Human, Pair 5 ; Colorectal Neoplasms ; genetics ; pathology ; Humans ; Loss of Heterozygosity ; Precancerous Conditions

Objective:To study the clinical phenotype and molecular genetic characteristics of a Chinese Han family with X-linked retinoschisis (XLRS), and to determine the associated gene variations.Methods:A pedigree investigation was performed.The clinical characteristics and pedigree analysis of a Han Chinese family line with XLRS was conducted in August 2021 at the Xiamen Eye Center Affiliated to Xiamen University.All patients and the carriers underwent comprehensive medical history collection and routine ophthalmological examinations, including visual acuity, non-contact tonometer, slit lamp microscope, direct ophthalmoscope, and optical coherence tomography.The proband and some patients underwent medical optometry, fundus photography or wide-angle fundus photography, and electroretinogram examination.Peripheral venous blood samples were collected from the family members, and whole exome sequencing (WES) analysis was performed on the proband samples.For variants screened by WES, the expanded verification in other patients and normal persons in the family was carried out by Sanger sequencing.Multiple bioinformatic tools were used to analyze the pathogenicity of variants.This study protocol was approved by the Ethics Committee of Xiamen Eye Center of Xiamen University (No.XMYKZX-KY-2021-012). Written informed consent forms were obtained from each subject or guardian of minors.CADD, FATHMM and other bioinformatics tools were used to analyze the pathogenicity of the variation sites.Results:The Han XLRS pedigree consisted of 8 individuals in 3 generations.Out of the 3 cases diagnosed with XLRS based on clinical evaluation, all were male.The mother of the proband was a carrier of related genes.There were 5 persons with normal phenotypes.There was no history of consanguineous marriages within the family, and the disease was shown to be intergenerational, which is consistent with the recessive inheritance of the X chromosome.None of the patients had a history of systemic disease or any other abnormal manifestations.The prevailing feature of ophthalmopathy was poor binocular vision since childhood.The proband and his younger brother had spoke split in the macula, and their grandfather showed atrophy of retinal nerve fibers.Genetic analysis revealed a hemizygous variation c. 214G>C: p.Glu72Gln in the RS1 gene in all the patients in this family.The proband's mother was heterozygous at this site, and all other phenotypically normal family members exhibited wild type at this site.This variant was predicted to be a deleterious variation and likely to cause disease based on bioinformatics analysis. Conclusions:The proband and patients in this Han Chinese family have the known c. 214G>C: p.Glu72Gln hemizygous variation of the RS1 gene and exhibit mild XLRS, which was consistent with the recessive inheritance of X chromosome.

Objective:To explore the clinical features and pathogenic causes of a Chinese Han family with Wagner syndrome, and to analyze the relationship between VCAN gene mutation and patient phenotype. Methods:The method of family pedigree investigation was adopted.A Chinese Han family with Wagner syndrome in 3 generations including 13 family members was collected in Xiamen Eye Center of Xiamen University in January 2020, and 5 patients from 3 generations were diagnosed.All members underwent a comprehensive medical history collection and routine ophthalmological examinations, including visual acuity, intraocular pressure, slit lamp microscopy, and ophthalmoscopy to analyze the condition of anterior segment and fundus.Anterior segment photography, fundus photography, optical coherence tomography and ultrasound biological microscopy were carried out in the proband and some patients to analyze the condition of anterior segment, fundus and anterior chamber angle.The peripheral venous blood of all family members was collected for genomic DNA extraction, and pathogenic gene variation analysis for verification was through high-throughput target region capture sequencing and Sanger sequencing.Variants were scored using the American College of Medical Genetics and Genomics (ACMG) guidelines, and the structure and function of variants were predicted through PredictProtein.This study adhered to the Declaration of Helsinki.The study protocol was approved by the Ethics Committee of Xiamen Eye Center of Xiamen University (No.MR-35-22-002800).Written informed consent was obtained from each subject.Results:The Chinese pedigree with Wagner syndrome was in accordance with autosomal dominant inheritance pattern, and all patients had no history of systemic disease or other abnormal manifestations.The common ophthalmic features of the patients were abnormal suspensory ligament, premature cataract, vitreous cavity, vitreous condensation, veil-like proliferative membrane in the vitreous cavity, retinal choroid atrophy and thinning, tractional retinal detachment, and retinal pigmentation.The proband had binocular cataract surgery, and binocular intraocular lens dislocation occurred after the operation.Genetic analysis revealed that a heterozygous splice site variation c.9265+ 1G>A in the VCAN gene in this family was co-segregated with the disease phenotype and graded as a likely pathogenic variant by the ACMG guidelines.This variant base pair substitution could cause the formation of a protein product with 1 754 amino acids shorter, resulting in insufficient haploid dosage and severe reduction of glycosaminoglycan attachment sites, making the versican protein dysfunctional. Conclusions:It is the first time to report a Chinese family with Wagner syndrome in China, and it is confirmed that the family has a heterozygous variation in the VCAN gene c.9265+ 1G>A by molecular genetic analysis.

Objective:To analyze the clinical and molecular genetic characteristics of a Chinese family with congenital cataract-microcornea syndrome.Methods:The method of pedigree investigation was adopted.A Chinese Han family with congenital cataract-microcornea syndrome was recruited in Xiamen Eye Center of Xiamen University.All the family members received detailed ophthalmologic examination including the best corrected visual acuity, intraocular pressure measurement by handheld applanation tonometry, slit lamp biomicroscopy, color fundus photography, B-scan ultrasonography, corneal diameter, anterior segment optical coherence tomography, ultrasound biomicroscopy, corneal endoscopy, and corneal topography.Genomic DNA was extracted from peripheral venous blood from some patients and unaffected family members.Targeted high-throughput DNA sequencing was performed on the proband.The sequencing chip contained 188 known pathogenic genes related to lens abnormalities.Suspected pathogenic genes were verified by Sanger sequencing in phenotypically normal family members to identify the co-segregation and the disease-causing gene.Bioinformatics analysis was performed to analyze the pathogenicity of variants by REVEL.Conserved protein domains were analyzed by InterPro.Physicochemical property of the mutant protein was analyzed by ProtParam.The deleteriousness of the protein was predicted by PolyPhen-2.Homology of the variants in pathogenic gene was analyzed by NCBI website to compare the conservation among various species.This study followed the Declaration of Helsinki.The study protocol was approved by the Ethics Committee of Xiamen Eye Center of Xiamen University (No.XMYKZX-LW-2009-003).Written informed consent was obtained from each subject prior to entering the study cohort.Results:There were 39 members of 4 generations in this family including 11 patients with an autosomal dominant inheritance pattern.Clinical features of the patients included congenital cataract and microcornea.No obvious abnormality was found in ophthalmic and general examination.A heterozygous mutation c. 61C>T in the CRYAA gene was found, resulting in the mutation of the amino acid from arginine to tryptophan (p.Arg21Trp) at position 21, consistent with co-segregation.The number of cationic cluster in the mutant protein decreased, and the hydrophilicity and stability were reduced.The variant was predicted to be deleterious and was highly conserved in multiple species. Conclusions:A novel heterozygous mutation c.61C>T p. Arg21Trp in CRYAA gene is considered as the causal gene of this family.It is the first time this variant has been reported in China.