Notes

Five story globin gene versions determined within several China households through next-generation sequencing.
99 and 0.98, respectively, which showed excellent reproductivity. The concord value showed consistency of various approaches relative to the gold standard method. The average concord value for TAR was 0.813, and the average concord value for ACG and ICG was 0.886 and 0.917, respectively. ACG utilizes computer graphics for measuring the size of cartilage defects of any size under an arthroscope, without reconditioning the injured cartilage. ACG showed excellent intra- and inter-observer reproducibility and satisfactory accuracy. This method would make it possible to more accurately match the graft with the defect, thereby facilitating cartilage repair.
To introduce a novel transverse tunnel (TT) in anterior talofibular ligament (ATFL) reconstruction, and assess whether it was superior to the tunnels currently used.

Thirteen fresh cadaveric lower extremities were perfused with lead-based contrast. Talar tunnels were drilled from the ATFL insertion in the following directions transversely towards the medial side (TT), towards the talar neck (TNT), and towards the anterior, distal, and posterior points of the medial malleolus (AMMT, DMMT, and PMMT, respectively). MicroCT was used to reconstruct the tali, and virtual transosseous and 20-mm blind-ended tunnels were generated. The graft bending angle, vascular compromise caused by the tunnels, and the minimum distances from the tunnels to the chondral surfaces were evaluated.

The bending angles between the ATFL and the TT, TNT, AMMT, DMMT, and PMMT were 47.3±7.9°, 41.5±7.7°, 57.0±6.0°, 63.9±11.7°, and 87.9±6.2°, respectively. The proportion of damaged intraosseous vessels was significantly less for the TT (damage than the TNT. The 20-mm blind-ended tunnels achieve less vessel damage and better drilling safety than transosseous tunnels.The human ether-à-go-go-related gene (hERG) potassium channel mediates the repolarization of ventricular action potentials. Mutations in the KCNH2 cause long QT syndrome (LQTS) and are associated with cardiac arrhythmias and sudden death. Here, we functionally analyzed a mutation of hERG potassium channel (p.L51P), gaining novel insights into clinical genotype-phenotype relationships. Potassium currents were recorded by whole-cell patch clamping in HEK293 cells transiently transfected with wild-type and/or mutant hERG potassium channel. Immunofluorescence assay and confocal imaging were undertaken to study the effects of L51P mutation on channel trafficking. The models of the protein structure of hERG and its mutations are predicted by Amber16 software. Molecular dynamics (MD) of individual protein were performed with Particle Mesh Ewald (PME). The production of MD simulations of hERG-WT and hERG-Mut at constant pressure and temperature were carried out with SHAKE. L51 was a conservative amino acid, located in the Per-Arnt-Sim (PAS) domain of the amino terminus. L51P caused loss of function via impairing channel activation. L51P was predicted to destroy hydrophobic structure in the PAS domain, thus causing the failure of channel opening. In summary, the present study identifies L51P as a novel mutation of hERG potassium channel. L51P mutation mechanistically impairs channel activation, reducing channel functionality.
To identify the significance of level IIb neck dissection for patients with clinically node-negative oral squamous cell carcinoma (OSCC).

A retrospective study was conducted with 203 patients with OSCC with no palpable lymph nodes in neck admitted to the Department of Oral Maxillofacial-Head and Neck Oncology from January 2012 through December 2014. After the diagnostic evaluations, all patients underwent wide local dissection and periodic supraomohyoid neck dissection (SOHND). In total, 115 patients underwent SOHND with IIb lymph node dissection, and 88 patients underwent elective SOHND without IIb lymph node dissection. The incidence of level IIb lymph node metastasis was evaluated by pathological and immunohistological analyses. The results were analyzed with independent sample t-tests. The incidence of complications (mainly scapular syndrome) and IIb lymph node metastasis rate (mainly for the preserving IIb group) were analyzed.

In total, 7 (6.09%) of the 115 patients who underwent SOHND had level I resection are not necessary during SOHND, which thereby protects the accessory nerve and its branches from damage and improves patient quality of life.With the development of radiology and minimally invasive technology, vertebroplasty has become the mainstream treatment for Kummell's disease. However, the catastrophic complication of bone cement displacement appears occasionally. We use robot-assisted pediculoplasty combined with vertebroplasty to avoid such complications. From January 2015 to January 2018, 87 patients suffering from thoracolumbar Kummell's disease without neurological symptoms were treated by robot-assisted pediculoplasty combined with vertebroplasty. Pediculoplasty as a "bridge" allows the bone cement at the anterior edge of the vertebral body to be fixed in the vertebral body through the intrapedicular cement, which can effectively prevent bone cement displacement. The clinical efficacy was evaluated based on the statistical analysis results of vertebral body index (VBI), Cobb angle, visual analogue scale (VAS), and Oswestry disability index (ODI) at 3, 6, 12, 18, and 24 months after treatment. The average operation time was 85.23±10.48 hotic deformity improvement.Cardiovascular complications have been well documented as the downside to conventional cancer chemotherapy. As a notable side effect of cisplatin, cardiotoxicity represents a major obstacle to the successful treatment of cancer. It has been reported that kaempferol (KPF) possesses cardioprotective and anti-inflammatory qualities. However, the effect of KPF on cardiac damage caused by conventional cancer chemotherapy remains unclear. In this study, we clarified the protective effect of KPF on cisplatin-induced heart injury, and conducted in-depth research on the molecular mechanism underlying this effect. The results showed that KPF protected against cardiac dysfunction and injury induced by cisplatin in vivo. In H9c2 cells, KPF dramatically reduced cispaltin-induced apoptosis and inflammatory response by modulating STING/NF-κB pathway. In conclusion, these results showed that KPF had great potential in attenuating cisplatin-induced cardiac injury. Besides, greater emphasis should be placed in the future on natural active compounds containing KPF with anti-inflammatory effects for the treatment of these diseases.Adora2B (adenosine receptor 2B) has been reported as one of the key modulators during cardiac remodeling after acute myocardial infarction (AMI). However, the molecular mechanism involved has not been well investigated. Thus, our study aims to investigate whether Adora2B contributes to cardiac remodeling after AMI and its underlying mechanisms. Adenovirus harboring Adora2B or shAdora2B was injected in the border zone in a mouse model of AMI experimentally produced by permanent ligation of left anterior descending (LAD) coronary artery. Decreased Adora2B expression protected the cardiomyocytes from MI-induced autophagic flux obstacle, improved cardiac function, and reduced fibrosis after MI. Adora2B downregulation attenuated the accumulation of LC3-II and p62, which are autophagy substrate proteins. UAMC-3203 cost An adenovirus containing mRFP-GFP-LC3 showed that decreased expression of Adora2B restored the autophagic flux by enhancing autophagosome conversion to autophagolysosome. Also, Adora2B knockdown improved cardiomyocytes' survival and protected mitochondrial function of cardiomyocytes insulted with hypoxia. Notably, the effect of Adora2B on autophagy flux and cardiomyocyte protection could be mitigated by autophagy inhibitor chloroquine. Our results demonstrate that decreased expression of Adora2B protected cardiomyocytes from impaired autophagy flux induced by MI. Modulation Adora2B expression plays a significant role in blunting the worsening of heart function and reducing scar formation, suggesting therapeutic potential by targeting Adora2B in AMI for the infarct healing.Coronary heart disease (CHD) is a fatal disease associated with coronary atherosclerosis. Although triptolide (TTL) has been reported to protect against CHD, the mechanism has not yet been determined. This study intended to explore its molecular regulation mechanism in CHD. It is shown in this study that TTL contributed to the proliferation and migration of in vitro cell models of CHD (endothelial cells) and the inhibition of apoptosis, and had an improvement effect on apoptosis factors and endoplasmic reticulum stress (ERS). From its mechanisms, TTL evidently downregulates miR-24-3p which is elevated in CHD, and evidently upregulates BCL2-like 11 (BCL2L11) which is suppressed in CHD, as well as affects the activation of peroxisome proliferator-activated receptors (PPARs)-Peroxisome proliferator activated receptor-γ co-activator-1α (PGC-1α) pathway of nuclear receptor transcription factors. In addition, miR-24-3p-BCL2L11-PPARs-PGC1α axis regulates protective effects of TTL against CHD.Epilepsy, one of the most common neurological diseases with spontaneous recurrent seizures, is a severe health problem globally. The present study aimed to study the role and upstream mechanism of 26S proteasome non-ATPase regulatory subunit 11 (Psmd11) in epilepsy. In the current paper, epileptic mice models were successfully established. Hematoxylin and eosin (HE) staining was performed to reveal morphology of hippocampal tissues. Nissl's staining was performed for detection of neuron injury. Enzyme-linked immunosorbent assay (ELISA) was conducted to detect concentrations of pro-inflammatory cytokines. The expression of Psmd11 was downregulated in the hippocampal tissues of epileptic mice, and overexpression of Psmd11 improved the spatial learning and memory of epileptic mice. Further, upregulation of Psmd11 protected epileptic hippocampal neurons from injury. Moreover, Psmd11 overexpression inhibited cell apoptosis, suppressed the activities of microglia and astrocytes, as well as reduced inflammatory response in epileptic hippocampi. Psmd11 was a downstream target of miR-490-3p. Long noncoding RNA (lncRNA) Peg13 bound with miR-490-3p to upregulate Psmd11. Subsequently, rescue experiments revealed that Peg13 suppressed the progression of epilepsy via upregulating Psmd11. Furthermore, Psmd11 was verified to inactivate the Wnt/β-catenin pathway. Peg13 repressed the Wnt/β-catenin pathway via upregulation of Peg13. In conclusion, this paper illuminated the function and upstream mechanism of Psmd11 in epilepsy. Psmd11 was upregulated by Peg13 at a miR-490-3p dependent way, thus inactivating the Wnt/β-catenin pathway and alleviating epilepsy course in mice, which may be a promising approach for epilepsy treatment.
To probe into the role and regulatory mechanisms of INSR in pathogenesis of osteoarthritis (OA).

KLF4 and INSR expression was detected in cartilage tissues of 40 OA patients and 10 controls using RT-qPCR. IL-1β-induced OA chondrocytes and anterior cruciate ligament transection (ACLT)-induced OA models were respectively constructed. After overexpressing or silencing KLF4 or INSR, flow cytometry assay was utilized to detect chondrocyte apoptosis. Furthermore, JAK2/STAT3, cartilage markers and OA-related markers were examined by western blot. Dual luciferase report and CHIP assay were carried out to verify the interactions between KLF4 and INSR, followed by functional gain and loss assay. INSR promoter methylation was assessed by MS-PCR.

Both KLF4 and INSR were down-regulated both in OA chondrocytes and cartilage tissues. Knockdown of KLF4 or INSR accelerated apoptosis of IL-1β-induced OA chondrocytes. However, overexpression of KLF4 or INSR ameliorated OA progression both in OA chondrocytes and OA mouse models.
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