Hermansenhinrichsen4028
05). The frequency of complications in the RG was lower than that in the CG (
<0.05). The preoperative VAS score did not exhibit significant differences between the two groups (
<0.05), but the scores in the RG at T1 and T2 were significantly lower than those in the CG (
<0.001). The QOL score in the RG (76.17±8.57) was also significantly higher than in the CG (71.54±8.02) (
<0.05).
Full-threaded HCCSs are more effective and safer than APs and can effectively improve the prognosis of patients with triplane fractures of the distal tibia.
Full-threaded HCCSs are more effective and safer than APs and can effectively improve the prognosis of patients with triplane fractures of the distal tibia.
Regulated in development and DNA damage responses 1 (REDD1) is an important transcription factor regulating mitochondria homeostasis, which is the important pathological alteration of pulmonary hypertension (PH). However, it is unclear whether REDD1 regulates the PASMCs mitochondria homeostasis by the similar mechanism in pulmonary arterial remodeling induced by hypoxia.
The global REDD1-knockout rats (REDD1-KO) on Sprague-Dawley background were used to generate a chronic hypoxia model of PH. Right ventricular hypertrophy and vascular remodeling were detected after exposure to hypoxia. Additionally, proliferation, apoptosis, migration, mitochondria homeostasis, and autophagy were performed
and
.
The current research found that in human and experimental rats of PH, REDD1 expression is upregulated in the PASMCs. REDD1 gene knockout alleviated hypoxia PH and hemodynamic changes effectively and reversed hypoxic pulmonary vascular remodeling. In addition, REDD1 knockdown reduces the impairment of mitochondrial function caused by hypoxia in HPASMCs via autophagy inhibition, and this process may be regulated through the Parkin gene. Moreover, REDD1 knockdown can effectively inhibit the proliferation and migration of hypoxic PASMCs, and induce their apoptosis
and
.
Our results suggested that REDD1 might be a potential target for improved pulmonary vascular remodeling in PH.
Our results suggested that REDD1 might be a potential target for improved pulmonary vascular remodeling in PH.Chronic kidney disease (CKD) is complex and current treatment remains limited. As we know, glomerular injury plays a dominant role in kidney disease progression. However, accumulating evidence demonstrated that renal tubules, rather than being victims or bystanders, are major initiators in renal fibrosis progression. Renal tubules are rich in mitochondria and mitochondrial dysfunction may participate in renal tubular phenotypic changes and ultimately promote renal fibrosis. Previous studies have proved that artemether displayed renal protective effects, but the mechanisms remain unclear. In this experiment, we showed that artemether reduced urinary protein/creatinine ratio and attenuated renal tubular injury. Both in vivo and in vitro results indicated that artemether could restore renal tubular phenotypic alterations. Meanwhile, the unbalanced expressions of Bax and Bcl-xL in renal tubules were restored by artemether. In addition, artemether also regulated mitochondrial pyruvate metabolism, increased mitochondrial biogenesis, and improved mitochondrial function. Taken together, this study suggested that artemether could attenuate renal tubular injury by regulating mitochondrial biogenesis and function. It has great potential to be translated to the clinic as a therapeutic agent for treating kidney diseases, especially those associated with renal tubular injury.The diversity and complexity of sympathetic function highlight the importance of fundamental research. Little is known about the interaction of superior cervical sympathetic ganglion (SCG) and gut microbiota. In this study, the engagement of the sympathetic ganglia with gut microbiota was investigated. Bilateral superior cervical ganglionectomy (SCGx) significantly altered the microbiota composition in rats 14 days post-surgery, and these microbiotas may participate in several biological pathways in the host, suggesting the vital role of the cervical sympathetic ganglion in regulating the microbiome-brain axis, and further confirming that the sympathetic nervous system (SNS) regulates the microbiome-brain axis.MiR-199a-3p was previously predicted to target tumor suppressor gene BRCA1, which has been linked to cancer onset and therapeutic response. In this study, the effects of miR-199a-3p-mediated BRCA1 dysfunction on triple-negative breast cancer (TNBC) progression and chemosensitivity were assessed. The association between miR-199a-3p and BRCA1 expression was examined in TNBC tumors and verified with luciferase reporter and protein assays. Tumorigenic functions of miR-199a-3p in TNBC cells were investigated by cell proliferation, clonogenic and migration assays. The sensitivities to chemotherapeutic drugs were tested with cisplatin and PARP inhibitor (veliparib) treatments. Mouse xenograft model was used to examine the effects of miR-199a-3p on tumor growth and drug response in vivo. MiR-199a-3p was shown to directly target BRCA1 in TNBC cells, resulting its downregulation and reduced luciferase reporter activity mediated by BRCA1 3'-UTR. Ectopic miR-199a-3p in TNBC cells exerted inhibitory effects on cell proliferation, migration and xenograft tumor growth. Moreover, miR-199a-3p was shown to reverse cisplatin-resistance and sensitize TNBC cells to veliparib, which might be due to repressed DNA repair ability and induced cell apoptosis. Our results demonstrated the tumor suppressive effects of miR-199a-3p on TNBC and induction on chemotherapeutic sensitivities, which were correlated with BRCA1 gene dysfunction. These findings may provide insights into the potential prognostic and therapeutic values of miR-199a-3p in patients with TNBC.The side-effects of therapeutic drugs and the intrinsic or acquired cisplation resistance are considered impediments in the clinic treatment of human epithelial ovarian cancer, which contribute heavily to the startlingly high mortality. It is imperative to look for drugs to inhibit cancer and minimize the chemotherapy resistance safely and effectively from the Chinese herbal medicine. In the present study, we evaluated the anti-cancer effect of Tripterygium glycosides (GTW) and its sensitizing effect with cisplation (DDP) both in vitro and in vivo. The 5-ethynyl-2'-deoxyuridine (EdU) proliferation assay, transwell assay, and scratch wound healing assay demonstrated that GTW and DDP+GTW prominently inhibited the proliferation, migration, and invasion of SKOV3/DDP cells. In addition, treatment using GTW and DDP+GTW for 24 h significantly decreased the expression of ILK, p-AKT, p-GSK3β, N-Cadherin, and Slug, and markedly enhanced the expression of E-cadherin. Moreover, animal results confirmed that GTW and DDP+GTW significantly inhibited the tumor volume, increased the apoptosis of tumors cells and reduced the production of tumor markers CA125 and HE4 in mice serum. Similar to the results in vitro, GTW and DDP+GTW significantly inhibited the expression of proteins in epithelial-mesenchymal transition (EMT) and ILK/GSK3β/Slug signal pathway in tumors in vivo. In conclusion, our results indicated that GTW may be served as a potential therapeutic drug combination with DDP to treat drug resistant ovarian cancer via regulating ILK/GSK3β/Slug signal pathway.
As the most frequent type of birth defect in humans, congenital heart disease (CHD) leads to a large amount of morbidity and mortality as well as a tremendous socioeconomic burden. Accumulating studies have convincingly substantiated the pivotal roles of genetic defects in the occurrence of familial CHD, and deleterious variations in a great number of genes have been reported to cause various types of CHD. However, owing to pronounced genetic heterogeneity, the hereditary components underpinning CHD remain obscure in most cases. This investigation aimed to identify novel genetic determinants underlying CHD.
A four-generation pedigree with high incidence of autosomal-dominant CHD was enrolled from the Chinese Han race population. Using whole-exome sequencing and Sanger sequencing assays of the family members available, a novel
variation in heterozygous status, NM_031439.4 c.310C>T; p.(Gln104*), was discovered to be in co-segregation with the CHD phenotype in the whole family. The truncating variant was absent in 500 unrelated healthy subjects utilized as control individuals. Functional measurements by dual-luciferase reporter analysis revealed that Gln104*-mutant SOX7 failed to transactivate its two important target genes,
and
, which are both responsible for CHD. In addition, the nonsense variation invalidated the cooperative transactivation between SOX7 and NKX2.5, which is another recognized CHD-causative gene.
The present study demonstrates for the first time that genetically defective
predisposes to CHD, which sheds light on the novel molecular mechanism underpinning CHD, and implies significance for precise prevention and personalized treatment in a subset of CHD patients.
The present study demonstrates for the first time that genetically defective SOX7 predisposes to CHD, which sheds light on the novel molecular mechanism underpinning CHD, and implies significance for precise prevention and personalized treatment in a subset of CHD patients.
Sparganosis is a serious parasitic zoonosis triggered by intake of and wound contact with frog flesh or the water infected or contaminated by sparganum.
The prevalence of Sparganum infection in wild frogs was assessed. A questionnaire survey was also conducted among the residents in Hainan Province to evaluate people's awareness of the medical and epidemiological relevance of sparganosis.
A total of 1556 wild frogs were collected to examine Sparganum infection in different organs. AP-III-a4 research buy A total of 201 (12.92%) were found to be infected with spargana of the genus
. There were 612 spargana found in those frogs, and the average infection rate was 3.04 per frog. The infection rate in the central region of Hainan Island is higher than that in other regions. Most spargana were found in the hind legs of frog, and the infection rate was not related to the weight of frogs. About 37.05% of the residents on Hainan Island have the knowledge of sparganosis and sparganum infection, and the internet was a major way to lea in frogs and its association with sparganosis, as well as advocate healthy diet concepts and habits, and abandon the capture, sale and purchase of wild frogs to prevent and decrease the incidence of sparganosis.
Radical prostatectomy is a treatment for prostate cancer (PC), but most patients suffer urinary incontinence, decreased urinary control function, and poor prognoses after the surgery. Specific nursing intervention is a nursing model based on the patients' individual conditions and disease progression.
To investigate the effects of specific nursing intervention on the urinary control functions and self-efficacy of radical prostatectomy patients.
From April 1, 2016 to June 30, 2019, 149 patients who underwent radical prostatectomies in our hospital were retrospectively selected for this observational study and assigned to two groups in accordance with the different nursing intervention method each patient underwent. Seventy-six patients who underwent specific nursing intervention were included in the observation group (OG), and 73 patients who underwent routine nursing intervention were included in the control group (CG). The clinical symptoms, the urodynamic indexes, the recoveries of urinary control function, the incidences of urinary incontinence, and the complications were observed in both groups.
