Objective:To analyze the gene mutations of 18 patients with plasminogen (PLG) deficiency and to explore the clinical manifestations caused by PLG gene mutations.Methods:This study belongs to observational study-descriptive study: case series.Clinical data from 18 patients with PLG deficiency admitted to the First Affiliated Hospital of Wenzhou Medical University from January 1st, 2021 to May 31st, 2025 were collected. The age ranged from 16 to 70 years old, with an average of 48 years old. Among them, there were 10 males and 8 females. Anticoagulant blood samples were taken before treatment to measure and analyze plasminogen activity (PLG:A), plasminogen antigen (PLG:Ag), protein C activity, protein S activity, fibrinogen, antithrombin activity, D-dimer, and fibrin (fibrinogen) degradation products. PCR direct sequencing was used to analyze the 19 exons and flanking sequences of the PLG gene in these patients, and reverse sequencing was employed to verify the suspected mutations.Results:For the 18 patients, cranial MRI showed fresh cerebral infarction lesions, and PLG:A levels ranged from 19% to 67%, while no other lab indicators showed significant abnormalities, all presenting with dysplasminogenemia. Genetic analysis revealed five types of PLG gene mutations: c.1858G>A (p.Ala620Thr) heterozygous mutation, c.1858G>A (p.Ala620Thr) homozygous mutation, c.398A>G (p.His133Arg) heterozygous mutation, c.2108G>A (p.Gly703Asp) heterozygous mutation, and c.1702G>A (p.Gly568Arg) heterozygous mutation. Among the above, the c.1858G>A heterozygous mutation was the most common, and c.398A>G and c.1702G>A were identified for the first time.Conclusion:Patients with plasminogen deficiency caused by PLG gene defects are prone to occur cerebral infarction events, which may be related to impaired fibrinolytic function due to PLG gene mutations.

Objective:To develop the Nurse Parenting Stress Scale and evaluate its reliability and validity.Methods:Based on Abidin's Parenting Stress Theory, scale items were generated through literature review and semi-structured interviews. The initial version was constructed via Delphi expert consultation. Using a convenience sampling method, nurses from six hospitals in Shandong Province were surveyed between August and October 2024. The first survey collected 314 questionnaires (308 valid, effective recovery rate 98.1%) for item analysis and exploratory factor analysis (EFA). The second survey collected 458 questionnaires (447 valid, effective recovery rate 97.6%) for confirmatory factor analysis (CFA) .Results:The Nurse Parenting Stress Scale consists of 4 dimensions and 31 items. The Cronbach's α coefficient of the total scale was 0.951, split-half reliability was 0.782, and test-retest reliability was 0.926. EFA extracted four common factors explaining 70.241% of the cumulative variance. CFA demonstrated a good model fit. The item-level content validity index ( I- CVI) ranged from 0.889 to 1.000, the scale-level universal agreement content validity index ( S- CVI/ UA) was 0.903, and the scale-level average content validity index ( S- CVI/ Ave) was 0.989. Conclusions:The Nurse Parenting Stress Scale shows strong reliability and validity and can serve as an effective tool for assessing parenting stress among nurses.

Objective:To develop the Nurse Parenting Stress Scale and evaluate its reliability and validity.Methods:Based on Abidin's Parenting Stress Theory, scale items were generated through literature review and semi-structured interviews. The initial version was constructed via Delphi expert consultation. Using a convenience sampling method, nurses from six hospitals in Shandong Province were surveyed between August and October 2024. The first survey collected 314 questionnaires (308 valid, effective recovery rate 98.1%) for item analysis and exploratory factor analysis (EFA). The second survey collected 458 questionnaires (447 valid, effective recovery rate 97.6%) for confirmatory factor analysis (CFA) .Results:The Nurse Parenting Stress Scale consists of 4 dimensions and 31 items. The Cronbach's α coefficient of the total scale was 0.951, split-half reliability was 0.782, and test-retest reliability was 0.926. EFA extracted four common factors explaining 70.241% of the cumulative variance. CFA demonstrated a good model fit. The item-level content validity index ( I- CVI) ranged from 0.889 to 1.000, the scale-level universal agreement content validity index ( S- CVI/ UA) was 0.903, and the scale-level average content validity index ( S- CVI/ Ave) was 0.989. Conclusions:The Nurse Parenting Stress Scale shows strong reliability and validity and can serve as an effective tool for assessing parenting stress among nurses.

Objective:To analyze the gene mutations of 18 patients with plasminogen (PLG) deficiency and to explore the clinical manifestations caused by PLG gene mutations.Methods:This study belongs to observational study-descriptive study: case series.Clinical data from 18 patients with PLG deficiency admitted to the First Affiliated Hospital of Wenzhou Medical University from January 1st, 2021 to May 31st, 2025 were collected. The age ranged from 16 to 70 years old, with an average of 48 years old. Among them, there were 10 males and 8 females. Anticoagulant blood samples were taken before treatment to measure and analyze plasminogen activity (PLG:A), plasminogen antigen (PLG:Ag), protein C activity, protein S activity, fibrinogen, antithrombin activity, D-dimer, and fibrin (fibrinogen) degradation products. PCR direct sequencing was used to analyze the 19 exons and flanking sequences of the PLG gene in these patients, and reverse sequencing was employed to verify the suspected mutations.Results:For the 18 patients, cranial MRI showed fresh cerebral infarction lesions, and PLG:A levels ranged from 19% to 67%, while no other lab indicators showed significant abnormalities, all presenting with dysplasminogenemia. Genetic analysis revealed five types of PLG gene mutations: c.1858G>A (p.Ala620Thr) heterozygous mutation, c.1858G>A (p.Ala620Thr) homozygous mutation, c.398A>G (p.His133Arg) heterozygous mutation, c.2108G>A (p.Gly703Asp) heterozygous mutation, and c.1702G>A (p.Gly568Arg) heterozygous mutation. Among the above, the c.1858G>A heterozygous mutation was the most common, and c.398A>G and c.1702G>A were identified for the first time.Conclusion:Patients with plasminogen deficiency caused by PLG gene defects are prone to occur cerebral infarction events, which may be related to impaired fibrinolytic function due to PLG gene mutations.

Patients with deep vein thrombosis require long-term anticoagulant therapy to prevent the spread or recurrence of the thrombus. Self-management can enhance patients' awareness of the disease and adherence to anticoagulant therapy, reducing the recurrence rate. This study reviews the current status, evaluation tools, intervention methods, and influencing factors of self-management in patients with deep vein thrombosis, providing reference for improving the home self-management ability of patients with deep vein thrombosis.

Changes in nuclear morphology are common in malignant tumors, but the underlying molecular mechanisms remain poorly understood. Lamins is involved in supporting nuclear structure, and the expression of Lamins is the molecular basis for nuclear morphological changes during tumor progression. In recent years, the research on the relationship between Lamins and malignant tumors has made great progress. Lamins is of great value in the diagnosis, treatment, and prognosis of various malignant tumors.
Cell Nucleus ; Humans ; Lamins/genetics* ; Neoplasms/genetics* ; Prognosis

Objective:To investigate the role of advanced oxidation protein products (AOPPs) in epithelial - mesenchymal transition (EMT) of small intestinal epithelial cells, and provide basis for the study of mechanism of intestinal fibrosis (IF) in intestinal bowel disease (IBD) .Methods:The small intestinal crypt epithelial cells IEC-6 were cultured in vitro. AOPPs was made by hypochlorous acid oxidation of rat serum albumin (RSA) in vitro. IEC-6 cells were divided into blank control group, AOPPs group and RSA group. The different concentrations (50, 100, 200, 400 μg/ml) of AOPPs were used to interfere with IEC-6 cells respectively in AOPPs group, 50, 100, 200, 400 μg/ml RSA were used to interfere with IEC-6 cells respectively in RSA group and no intervention in blank control group. The morphological changes of IEC-6 cells were observed and apoptosis was detected by flow cytometry in 3 groups 24 h after intervention. When the apoptosis rate was highest, the concentration of AOPPs were analyzed statistically and used to interfere IEC-6 for 48 and 72 h. The difference of apoptosis rate were analyzed between the different times. The mRNA expression of E-cadherin, Fibronectin, Snail, Slug and Collagen Ⅰ were detected in blank control group, AOPPs group and RSA group by fluorescence quantitative PCR.Results:AOPPs could induce the apoptosis of IEC-6 cells with time- and concentration-dependent effects ( P<0.05) . The apoptosis rate was (17.30 ± 1.03) %, which reached the peak by the intervention of 400 μg/ml AOPPs for 72 h. AOPPs significantly decreased the mRNA expression of E-cadherin in IEC-6 cells, significantly increased the mRNA expression of Fibronectin and CollagenⅠ, and significantly increased the mRNA expression of transcription factor Snail and Slug (all P<0.05) . Conclusions:AOPPs can promote the ECT of small intestinal epithelial cells and play a role in IF of IBD by inducing the apoptosis of IEC-6 cells, inhibiting of the transcription of E-cadherin, up-regulating the gene expression of the transcription factors Snail and Slug, while increasing the gene expression of Fibronectin and CollagenⅠ.

Objective:To investigate the role of advanced oxidation protein products (AOPPs) in epithelial - mesenchymal transition (EMT) of small intestinal epithelial cells, and provide basis for the study of mechanism of intestinal fibrosis (IF) in intestinal bowel disease (IBD) .Methods:The small intestinal crypt epithelial cells IEC-6 were cultured in vitro. AOPPs was made by hypochlorous acid oxidation of rat serum albumin (RSA) in vitro. IEC-6 cells were divided into blank control group, AOPPs group and RSA group. The different concentrations (50, 100, 200, 400 μg/ml) of AOPPs were used to interfere with IEC-6 cells respectively in AOPPs group, 50, 100, 200, 400 μg/ml RSA were used to interfere with IEC-6 cells respectively in RSA group and no intervention in blank control group. The morphological changes of IEC-6 cells were observed and apoptosis was detected by flow cytometry in 3 groups 24 h after intervention. When the apoptosis rate was highest, the concentration of AOPPs were analyzed statistically and used to interfere IEC-6 for 48 and 72 h. The difference of apoptosis rate were analyzed between the different times. The mRNA expression of E-cadherin, Fibronectin, Snail, Slug and Collagen Ⅰ were detected in blank control group, AOPPs group and RSA group by fluorescence quantitative PCR.Results:AOPPs could induce the apoptosis of IEC-6 cells with time- and concentration-dependent effects ( P<0.05) . The apoptosis rate was (17.30 ± 1.03) %, which reached the peak by the intervention of 400 μg/ml AOPPs for 72 h. AOPPs significantly decreased the mRNA expression of E-cadherin in IEC-6 cells, significantly increased the mRNA expression of Fibronectin and CollagenⅠ, and significantly increased the mRNA expression of transcription factor Snail and Slug (all P<0.05) . Conclusions:AOPPs can promote the ECT of small intestinal epithelial cells and play a role in IF of IBD by inducing the apoptosis of IEC-6 cells, inhibiting of the transcription of E-cadherin, up-regulating the gene expression of the transcription factors Snail and Slug, while increasing the gene expression of Fibronectin and CollagenⅠ.

OBJECTIVETo investigate the polymorphism in the promoter region of PCA3 gene and its relationship with risk of prostate cancer (PCa).

METHODSThe promoter region of PCA3 gene of the DNA of peripheral blood mononuclear cells was detected by sequence analysis in the 186 PCa and 141 BPH patients and 135 healthy control individuals. If the samples were detected with polymorphism of insection/deletion, clone sequence analysis was used with pBS-T carrier to verify it.

RESULTSThere were 5 polymorphisms. TAAA repeat times: 4, 5, 6, 7, 8, and 8 genotypes (TAAA 4/5, TAAA 4/6, TAAA 5/5, TAAA 5/6, TAAA 5/7, TAAA 5/8, TAAA 6/6, and TAAA 6/7) were detected in the promoter region of PCA3 gene. The eight genotypes were divided into three groups: ≤10TAAA, 11TAAA, ≥12TAAA. Unconditional logistic regression analysis models were used to analyze the relationship between different genotypes and cancer risks adjusted by sex and age. The type 11TAAA and ≥12TAAA was associated with higher relative risk for prostate cancer than the group ≤10TAAA [OR=1.74, 95% CI=1.06-2.87 (for type 11TAAA); OR=5.63, 95% CI=1.85-17.19 (for type ≥12TAAA)]. In the 186 PCa patients, there was 62.4% allele of PCA3 gene with AG/CA mutation found in the promoter 18-19 bp region of PCA3 gene and it had a close relation with the development of prostate cancer.

CONCLUSIONSShort tandem repeats are found in the promoter region of the PCA3 gene in PCa patients, and the increase of TAAA repeat sequences highly enhance the relative risk of prostate cancer development. The occurrence of such STR might be related to the mutations in their upstream loci.

Antigens, Neoplasm ; genetics ; metabolism ; Base Sequence ; Genes, Neoplasm ; physiology ; Genotype ; Humans ; Leukocytes, Mononuclear ; Male ; Microsatellite Repeats ; Mutation ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Prostatic Neoplasms ; epidemiology ; genetics ; Risk

OBJECTIVETo identify potential mutations in a family affected with inherited factor Ⅶ (FⅦ) deficiency.

METHODSProthrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen, FⅦ activity (FⅦ:C) and other coagulant parameters of the proband and 15 family members were measured. Potential mutations were screened in the pedigree by polymerase chain reaction and direct DNA sequencing.

RESULTSThe PT of the proband and his younger brother was significantly prolonged to 39.0 s and 30.1 s, respectively. FⅦ:C of the proband and his younger brother was obviously reduced to 2% and 3%, respectively. FⅦ:C of his grandmother, maternal grandmother, aunt, father, mother, maternal uncle and maternal aunt was all below the normal range (80%-108%), which measured 68%, 54%, 71%, 73%, 62%, 72% and 59%, respectively. The other coagulant parameters were in the normal range. Two heterozygous mutations, g.11349G>A and g.11482T>G, both reside in exon 8 of the F7 gene, have resulted in p.Arg304Gln and p.His348Gln substitutions, were identified in the proband. The same mutations were also found in the proband's younger brother. Four maternal members in this family (grandmother, mother, maternal uncle and maternal aunt of the proband) were heterozygous for the p.Arg304Gln mutation, while three paternal members (grandmother, aunt and father of the proband) were heterozygous for the p.His348Gln mutation.

CONCLUSIONThe proband had inherited two independent mutations of the F7 gene including g.11349G>A and g.11482T>G from his mother and father, respectively. The compound heterozygous mutation probably explains the low FⅦ concentrations in this pedigree.

Adult ; Base Sequence ; Blood Coagulation Tests ; Factor VII ; genetics ; metabolism ; Factor VII Deficiency ; blood ; genetics ; Female ; Genetic Testing ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; Pedigree ; Young Adult