Objective To discuss the morphological features and diagnosis of congenial double orifice mitral valve (DOMV) deformity by echocardiography.Methods Twenty consecutive patients were examined.The changes of the morphology and flow dynamics of DOMV were studied,and other congenital cardiac abnormalities were also observed.These results were compared with those of surgery.Results Thirteen cases of adult patients were all with significant hemodynamic abnormalities,and underwent mitral replacement.One case of school child with muscular ventricular septal defect underwent mitral replacement because of obvious hemodynamic changes.Six cases were under 2 years old,2 cases with complete endocardial cushion defect accompanied with pulmonary hypertension,1 case with partial endocardial cushion defect accompanied with coarctation of the aorta underwent corrective operation.No significant hemodynamic abnormalities in 2 cases,1 case was associated with coarctation of the aorta and patent ductus arteriosus,the other patient with membranous ventricular septal defect.Severe stenosis in 1 case with papillary muscle dysplasia,because there was no suitable operation and take conservative therapy.Seventeen cases were confirmed by the results of open-heart surgery.Conclusions Echocardiography can provide an accurate method to diagnose DOMV and evaluate the hemodynamic changes.

PURPOSE: Clinical studies have reported a correlation between pelvic ischemia and voiding dysfunction in elderly men. The aim of this study was to identify and compare prostate structural modifications in cultured cells and in a rabbit model after exposure to hypoxia, oxidative stress, and chronic ischemia. MATERIALS AND METHODS: Cultured human prostate smooth muscle cells (SMCs), epithelial cells (ECs), and stromal cells (SCs) were incubated under normoxia, hypoxia, and oxidative stress conditions by use of a computerized oxycycler system. We developed a rabbit model of chronic prostate ischemia by creating aorto-iliac arterial atherosclerosis. Markers of oxidative stress were examined by using fluorometric analysis and enzyme immunoassay. Prostate structure was examined by using Masson's trichrome staining and transmission electron microscopy (TEM). RESULTS: Lipid peroxidation was found in SMCs exposed to hypoxia and in all cell types exposed to oxidative stress. We identified protein oxidation in ECs exposed to hypoxia and in all cell types exposed to oxidative stress. Markers indicating oxidative damage were present in chronically ischemic rabbit prostate tissue. These reactions were associated with DNA damage. Prostate ischemia resulted in epithelial atrophy, loss of smooth muscle, and diffuse fibrosis. TEM showed swollen mitochondria with degraded cristae, loss of membrane, loss of Golgi bodies, degenerated nerves, and disrupted cell-to-cell junctions. CONCLUSIONS: Human prostate cells exhibited differential reactions to hypoxia and oxidative stress with widespread DNA damage. Structural modifications in ischemic prostate tissue were similar to those in cells exposed to oxidative stress. Structural changes due to ischemia and oxidative stress may contribute to prostatic noncompliance in aging men.
Animals ; Anoxia/*complications ; Atherosclerosis/complications ; Biomarkers ; Cells, Cultured ; DNA Damage ; Disease Models, Animal ; Epithelial Cells/ultrastructure ; Fibrosis ; Humans ; Ischemia/*complications ; Lipid Peroxidation ; Male ; Myocytes, Smooth Muscle/ultrastructure ; Nerve Degeneration ; *Oxidative Stress ; Prostate/*anatomy & histology/*cytology ; Rabbits ; Stromal Cells/ultrastructure ; Urinary Bladder Neck Obstruction/complications

Objective:To compare the value of coronary CT angiography, congenital heart disease CT, and transthoracic echocardiography (TTE) in the diagnosis of sinus venosus atrial septal defect (SVASD), to summarize the CT image features of SVASD, and to explore its significance in guiding the selection of surgical procedures.Methods:A total of 443 patients of SVASD diagnosed by surgical procedures from January 2017 to December 2021 were retrospectively analyzed. All patients underwent coronary CT angiography or congenital heart disease CT examination and TTE before surgery. Using surgical results as the gold standard, McNemar test was used to analyze the differences between CT and TTE in distinguishing SVASD and pulmonary venous drainage. The difference of pulmonary venosus drainage was analyzed between superior sinus venosus atrial septal defect (ASD) and inferior sinus venosus ASD. The image features of SVASD were summarized and the corresponding surgical procedures were analyzed.Results:No significant difference was found between CT and TTE for the diagnostic accuracy of the SVASD (63.21%, 57.56%, P=0.065). There were 159 patients (35.89%) with PAPVC and 284 patients (64.11%) without PAPVC in the 443 SVASD patients. The diagnostic accuracy of CT and TTE in diagnosing pulmonary venous drainage was statistically significantly different (98.42%, 73.81%, P<0.001). Among 145 patients with superior sinus venosus ASD, 101 (69.66%) were associated with PAPVC; in contrast, among 298 patients with inferior sinus venosus ASD, 58 (19.46%) had PAPVC. The difference between the two groups was statistically significant ( χ 2=106.79, P<0.001), indicating a higher prevalence of PAPVC in patients with superior sinus venosus ASD. The CT imaging features of SVASD can be categorized into four types. The first type was SVASD alone without PAPVC, comprising 284 patients (64.11%). Surgical intervention for this type typically involved direct suturing or closure using a patch. The second type was SVASD with concomitant PAPVC, encompassing 151 patients (34.09%). This type included superior sinus venosus ASD with anomalous pulmonary venous low connection and inferior sinus venosus ASD with PAPVC. During the repair of the defect, it was necessary to redirect the anomalous pulmonary veins into the left atrium. The third type was superior sinus venosus ASD in 7 patients (1.58%). The position of pulmonary vein draining into superior vena cava was too high to be directly corrected to the left atrium, requiring Warden′s technique. The fourth type was rare (1 patient, 0.22%). The anomalous pulmonary vein drained into the coronary sinus. The surgery included incision of the roof of the coronary sinus to redirect pulmonary vein flow to the left atrium, reconstruction of the roof of the sinus to drain coronary vein back to the right atrium, and repair of the ASD. Conclusions:Both CT and TTE can diagnose the type of SVASD, and CT is more accurate than TTE in the diagnosis of PAPVC. CT image features of SVASD can provide valuable information for surgical procedures and guide the selection of surgical procedures.

Duodenal cancer is a clinically rare gastrointestinal malignant tumor. Its early symptoms lack specificity, making it difficult to diagnose clinically and easy to be misdiagnosed and missed. The treatment of duodenal cancer is mainly surgery, supplemented by radiotherapy and chemotherapy. Most patients have already experienced local invasion or distant metastasis at the time of first diagnosis, and lack of effective treatment, the prognosis is extremely poor. In recent years, a series of studies have pointed out that targeted therapy and immunotherapy can improve the prognosis of patients with duodenal cancer. This article reviews the progress of diagnosis and treatment of duodenal cancer, hoping to help guide clinical diagnosis and treatment and develop new treatment options.

Additional sex combs-like 1 (ASXL1) interacts with BRCA1-associated protein 1 (BAP1) deubiquitinase to oppose the polycomb repressive complex 1 (PRC1)-mediated histone H2A ubiquitylation. Germline BAP1 mutations are found in a spectrum of human malignancies, while ASXL1 mutations recurrently occur in myeloid neoplasm and are associated with poor prognosis. Nearly all ASXL1 mutations are heterozygous frameshift or nonsense mutations in the middle or to a less extent the C-terminal region, resulting in the production of C-terminally truncated mutant ASXL1 proteins. How ASXL1 regulates specific target genes and how the C-terminal truncation of ASXL1 promotes leukemogenesis are unclear. Here, we report that ASXL1 interacts with forkhead transcription factors FOXK1 and FOXK2 to regulate a subset of FOXK1/K2 target genes. We show that the C-terminally truncated mutant ASXL1 proteins are expressed at much higher levels than the wild-type protein in ASXL1 heterozygous leukemia cells, and lose the ability to interact with FOXK1/K2. Specific deletion of the mutant allele eliminates the expression of C-terminally truncated ASXL1 and increases the association of wild-type ASXL1 with BAP1, thereby restoring the expression of BAP1-ASXL1-FOXK1/K2 target genes, particularly those involved in glucose metabolism, oxygen sensing, and JAK-STAT3 signaling pathways. In addition to FOXK1/K2, we also identify other DNA-binding transcription regulators including transcription factors (TFs) which interact with wild-type ASXL1, but not C-terminally truncated mutant. Our results suggest that ASXL1 mutations result in neomorphic alleles that contribute to leukemogenesis at least in part through dominantly inhibiting the wild-type ASXL1 from interacting with BAP1 and thereby impairing the function of ASXL1-BAP1-TF in regulating target genes and leukemia cell growth.