Objective To systematically analyze the domestic and foreign literature related to interventional nursing care for patients with coronary heart disease in the past 10 years and to make a further understanding of the research status,hot spots and trends in this field so as to provide useful reference for the in-depth research in this field.Methods A computerized retrieval of academic papers concerning the interventional nursing care for patients with coronary heart disease from the databases of CNKI,Wanfang,VIP-CMJD,PubMed and Web of Science was conducted.The retrieval time period was from 1 January,2014 to February 27,2024.NoteExpress and CiteSpace software were used to make visualization analysis for the literature meeting the inclusion and exclusion criteria.Results A total of 4 098 Chinese articles and 381 English articles were enrolled in the analysis.Between 2014 and 2021,the number of domestic and foreign documents was on the rise.The number of foreign publications continued to increase in 2022,thereafter,the number of publications was declined in 2023.The authors with the most published academic papers were WANG Jing(15 articles)and Ayman Elbadawi(7 articles).The research keywords involved a wide range,and the research focus was on the characteristics and perioperative care of coronary heart disease,including quality of life,evidence-based nursing care,complications,myocardial infarction,outcome,mortality,etc.The obvious trend of research was to emphasize the psychological nursing,continuation nursing and rehabilitation nursing for patients with coronary heart disease receiving interventional treatment.Conclusion Although the number of research publications concerning the interventional nursing care for patients with coronary heart disease in the past decade is very large,the authors and institutions lack effective communication and collaboration.In order to improve the overall health,self-care ability and quality of life of patients,the future studies should further strengthen the quality of research,focus on key population,and innovate nursing pattern.

The acute combination fractures of the atlas and axis in adults have a higher rate of neurological injury and early death compared with atlas or axial fractures alone. Currently, the diagnosis and treatment choices of acute combination fractures of the atlas and axis in adults are controversial because of the lack of standards for implementation. Non-operative treatments have a high incidence of bone nonunion and complications, while surgeries may easily lead to the injury of the vertebral artery, spinal cord and nerve root. At present, there are no evidence-based Chinese guidelines for the diagnosis and treatment of acute combination fractures of the atlas and axis in adults. To provide orthopedic surgeons with the most up-to-date and effective information in treating acute combination fractures of the atlas and axis in adults, the Spinal Trauma Group of Orthopedic Branch of Chinese Medical Doctor Association organized experts in the field of spinal trauma to develop the Evidence-based guideline for clinical diagnosis and treatment of acute combination fractures of the atlas and axis in adults ( version 2023) by referring to the "Management of acute combination fractures of the atlas and axis in adults" published by American Association of Neurological Surgeons (AANS)/Congress of Neurological Surgeons (CNS) in 2013 and the relevant Chinese and English literatures. Ten recommendations were made concerning the radiological diagnosis, stability judgment, treatment rules, treatment options and complications based on medical evidence, aiming to provide a reference for the diagnosis and treatment of acute combination fractures of the atlas and axis in adults.

Objective To understand the etiological features of diarrhea in Xiangyang city and to provide a scientific basis for the prevention and control of diarrhea. Methods A total of 1 142 stool samples were collected from diarrheal patients admitted to the First People's Hospital of Xiangyang from 2013 to 2017 anwere tested for pathogens. The pathogenic composition, population characteristics and time distribution of diarrheal patients were analyzed. Results Of the 1 142 diarrheal patients, 737 patients (64.54%) were tested negatively. Of the 405 patients tested positively, adenovirus was the most prevalent, with proportion of 38.27% (155 patients), followed by norovirus and rotavirus. Only 20 patients (4.94%) were tested as bacterial infection. Infectious diarrhea showed obvious seasonality, with largest infectious proportion in April-June. Patients younger than 1 year old were the most susceptible to infectious diarrhea and the proportion was 29.63% (120 patients). Conclusions The majority of infectious diarrhea was viral diarrhea, and the main pathogen was adenovirus and norovirus. Only a very small proportion of diarrhea was due to bacterial infection. The guidance for infant's feeding and the surveillance and control of virus diarrhea for infants should be strengthened.

OBJECTIVE: To explore the genetic basis for a child featuring X-linked intellectual disability. METHODS: The 1-year-and-6-month-old child presented with growth retardation, intellectual disability and bilateral alternating squint. With DNA extracted from the child and his parents' peripheral venous blood samples, whole exome sequencing was carried out to identify potential variants that can explain his condition. Suspected variants were validated by Sanger sequencing. The impact of variants was predicted by bioinformatic tools. RESULTS: The child was found to harbor a de novo nonsense c.3163C>T (p.Arg1055*) variant of the IQSEC2 gene. The variant, unreported previously, was predicted to be pathogenic based on MutationTaster, PROVEAN and SIFT. Analysis using a HomoloGene system suggested Arg1055 in IQSEC2 residues to be highly conserved evolutionarily, and that replacement of Arg1055 may cause destroy of the PH domain (AA 951-1085) and serious damage to the function of IQSEC2 protein. Analysis with UCSF chimera software suggested that the c.3163C>T (p.Arg1055*) variant can induce serious damages to the secondary structures of IQSEC2 protein, causing loss of its function. CONCLUSION The patient's condition may be attributed to the de novo nonsense variant c.3163C>T (p.Arg1055*) of the IQSEC2 gene.

OBJECTIVE: To identify potential mutation of PMM2 gene in an infant with congenital disorders of glycosylation type 1a (CDG-1a). METHODS: Genomic DNA was extracted from peripheral blood sample of the patient. All coding exons (exons 1-8) and splicing sites of the PMM2 gene were amplified with PCR. Potential variants were detected by direct sequencing of the PCR products and comparing the results against the ESP and SNP human gene databases. A protein BLAST system was employed to analyze cross-species conservation of the variants amino acid. A PubMed BLAST CD-search system was employed to identify functional domains damaged by variants of the PMM2 gene. Impact of potential variants was analyzed using software including PolyPhen-2 SIFT and Mutation Taster. Whole exome sequencing was used to identify additional variants of the PMM2 gene which may explain the condition of the patient. RESULTS: The child was found to carry compound heterozygous variants (c.458_462delTAAGA and c.395T>C) of the PMM2 gene, which were inherited respectively from his father and mother. The c.458_462delTAAGA has not been reported previously and may result in disruption of 10 functional domains within the PMM2 protein. The c.395T>C mutation has been recorded by a SNP database with frequency unknown. Both mutations were predicted as "probably damaging". Whole exome sequencing has identified no additional disease-causing variant which can explain the patient's condition. CONCLUSION The patient's condition may be attributed to the compound heterozygous variants c.458_462delTAAGA and c.395T>C of the PMM2 gene. Above results has facilitated molecular diagnosis for the patient.
Congenital Disorders of Glycosylation ; genetics ; Exons ; Humans ; Infant ; Mutation ; Phosphotransferases (Phosphomutases) ; genetics

Objective     To investigate predictors for mortality among patients with Stanford type A acute aortic dissection (AAD) and to establish a predictive model to estimate risk of in-hospital mortality. Methods     A total of 999 patients with Stanford type A AAD enrolled between 2010 and 2015 in our hospital were included for analysis. There were 745 males and 254 females with a mean age of 49.8±12.0 years. There were 837 patients with acute dissection and 182 patients (18.22%) were preoperatively treated or waiting for surgery in the emergency department and 817 (81.78%) were surgically treated. Multivariable logistic regression analysis was used to investigate predictors of in-hospital mortality. Significant risk factors for in-hospital death were used to develop a prediction model. Results     The overall in-hospital mortality was 25.93%. In the multivariable analysis, the following variables were associated with increased in-hospital mortality: increased age (OR=1.04, 95% CI 1.02 to 1.05, P<0.000 1), acute aortic dissection (OR=2.49, 95% CI 1.30 to 4.77, P=0.006 1), syncope (OR=2.76, 95% CI 1.15 to 6.60, P=0.022 8), lower limbs numbness/pain (OR=7.99, 95% CI 2.71 to 23.52, P=0.000 2), type Ⅰ DeBakey dissection (OR=1.72, 95% CI 1.05 to 2.80, P=0.030 5), brachiocephalic vessels  involvement (OR=2.25, 95% CI 1.20 to 4.24, P=0.011 7), acute liver insufficiency (OR=2.60, 95% CI 1.46 to 4.64, P=0.001 2), white blood cell count (WBC)>15×109 cells/L (OR=1.87, 95% CI 1.21 to 2.89, P=0.004 9) and massive pericardial effusion (OR=4.34, 95% CI 2.45 to 7.69, P<0.000 1). Based on these multivariable results, a reliable and simple bedside risk prediction tool was developed. Conclusion     Different clinical manifestations and imaging features of patients with Stanford type A AAD predict the risk of in-hospital mortality. This model can be used to assist physicians to quickly identify high risk patients and to make reasonable treatment decisions.

To examine the expression of forkhead transcription factor O4 (FOXO4) in prostate cancer and to explore its effect on prostate cancer cell invasion.
 Methods: Immunohistochemistry was used to detect the expression of FOXO4 in prostate hyperplasia tissues and prostate cancer tissues. Western blot was used to detect the expression of FOXO4 in prostate hyperplasia cell line BPH-1 and prostate cancer cell lines: PC-3 and DU145. PC-3 cells with high relative expression of FOXO4 were transfected with FOXO4 siRNA and scramble siRNA; DU145 cells with low expression of FOXO4 were transfected with FOXO4 plasmid and blank vector. Matrigel Transwell assay was used to detect the invasive ability of transfected cells. The expression of endothelial-mesenchymal transition (EMT)-related proteins E-cadherin, N-cadherin, and vimentin in the transfected cells was detected by Western blot.
 Results: The expression of FOXO4 in prostate cancer cells and tissues was significantly lower than that in the prostate hyperplasia cells and tissues (both P<0.05). In the prostate cancer tissues, the expression of FOXO4 in cancer tissues with prostate cancer specific antigen (PSA) value <4 was significantly higher than that in the tissues with 4≤PSA≤10 and PSA>10 (all P<0.05). The expression of FOXO4 in cancer tissues with Gleason score <8 was significantly higher than that in the cancer tissues with Gleason ≥8 (P<0.05). The expression of FOXO4 in clinical stage T1-T2 prostate cancer tissues was higher than that in the clinical stage T3-T4 prostate cancer tissues (P<0.05). The expression of FOXO4 in prostate cancer tissues without lymph node metastasis was significantly higher than that in the prostate cancer tissues with lymph node metastasis (P<0.05). Down-regulation of FOXO4 in PC-3 cells could significantly promote the EMT and invasion, with the decreased expression of E-cadherin and the increased expression of N-cadherin and vimentin (all P<0.05); Up-regulation of FOXO4 in DU145 cells could inhibit the EMT and invasion of cells, with the increased expression of E-cadherin and the decreased expression of N-cadherin and vimentin (all P<0.05).
 Conclusion: FOXO4 is involved in prostate cancer progression, and it can inhibit prostate cancer cell invasion by regulating EMT of prostate cancer cells.
Cadherins ; genetics ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Neoplasm Invasiveness ; genetics ; Prostatic Neoplasms ; genetics ; Transcription Factors ; genetics

Objective To investigate the polymorphisms of human cytomegalovirus ( HCMV ) UL146 gene in asymptomatic children. Methods Urine samples were collected from 47 asymptomatic chil-dren who were positive for HCMV DNA. PCR was performed to amplify the open reading frame ( ORF) of UL146 gene. Positive bands were sequenced and variations in UL146 gene were analyzed by using bioinfor-matics software. Results Seventeen samples were successfully amplified and sequenced. Variations spread all over the sequence of UL146 gene and the variability in nucleotide and amino acid sequences ranged from 0％ to 42. 5％ and 0％ to 67. 7％ respectively. Compared with the Towne strain, there was diversity in sig-nal sequence and C-terminal region. Phylogenetic analysis indicated that UL146 in the 17 asymptomatic chil-dren belonged to four genotypes, which were G1, G8, G9 and G11. Forms of post-translational modification varied greatly among the four genotypes, while the important functional region of ELRCXC chemokine was highly conservative. Secondary structure prediction showed that random-coli conformation was the predomi-nant structure of active proteins. Isoelectric point ( PI) and molecular weight ( MW) were dissimilar among the four genotypes. Conclusion HCMV UL146 gene in asymptomatic children was hypervariable in both nucleotide sequence and amino acid structure. However, the important functional region was highly con-served. The predominant genotypes of UL146 in these children were G1, G8, G9 and G11, and the geno-type distribution in them showed no significant difference with previous findings in children with symptomatic HCMV infection.

Objective To investigate the risk factors for early hypoglycemia and its relationship with prognosis of patients with cerebral infarction.Methods A total of 273 patients with cerebral infarction were divided into the normal blood glucose(NBG) and severe hypoglycemia (SHG)and mild hypoglycemia(MHG) groups in our hospital.Biochemical indicators,the National Institute of Health stroke scale(NIHSS)and mortality were compared between the three groups.According to prognosis,patients were divided into death group and survival group.The NIHSS score,blood glucose concentration and incidence of hypoglycemia were compared between death and survival groups.Pearson relationship between hypoglycemia and NIHSS score,and spearman rank correlation between hypoglycemia severity and mortality were analyzed.Results Levels of lactic acid (6.3 ± 2.8) mmol/L,creatinine(268.7 ± 63.9) mmol/L,urea nitrogen (13.8 ± 3.7) mmol/L,albumin (25.6 ±4.9) g/L,alanine aminotransferase (150 ± 19.7) U/L,NIHSS (22.3 ± 9.2) scores,and mortality rates (38.1 ％)were higher in severe hypoglycemia group than in both NBG group and severe hypoglycemia group[(lactic acid:4.7±2.3 mmol/L and 3.3±1.5 mmol/L),(creatinine 134.8±51.3 mmol/L and 78.7±40.8 mmol/L),(urea nitrogen 7.9±4.2 mmol/L and 7.7±3.3 mmol/L),(albumin 36.9±3.8 g/L and 35.6±4.3 g/L),(alanine aminotransferase 85.8± 18.3U/L and 46.3± 13.8U/L),(NHISS 14.6±5.9 scores and 10.5 ± 5.4 scores)and(mortality rates 20.8％,11.0％)] (all P＜0.01).There was a negative correlation between hypoglycemia and NIHSS score(r=-0.45,P＜＜0.05).There was a positive correlation between hypoglycemic severity and mortality (r =0.41,P ＜ 0.05).Multiple Logistic regression showed that creatinine and alanine aminotransferase were correlated with hypoglycemia and prognosis of patients with cerebral infarction(both P＜0.05).Conclusions Early hypoglycemia in patients with severe cerebral infarction is closely correlated with the liver and kidney insufficiency,and a severe cerebral infarction combined with hypoglycemia often indicate a poor prognosis.