Patients with Kashin-Beck Disease Obtained Lower Functional Activities but Better Satisfaction Than Patients with Osteoarthritis After Total Knee Arthroplasty: A Retrospective Study.

Background: Increasingly, patient satisfaction after total knee arthroplasty (TKA) is being recognized as an important measure of health-care quality in osteoarthritis (OA) patients. But satisfaction after TKA has not yet been reported in Kashin-Beck disease (KBD). We aim to examine satisfaction and clinical efficacy of TKA in the treatment of OA and KBD. Methods: Retrospectively review of 37 KBD patients (45 knees) and 52 OA patients (58 knees) who underwent TKA from January 2015 to January 2017. Data of outcome measures such as Knee Society knee score (KSKS) and function score (KSFS), Western Ontario and McMaster Universities Arthritis Index (WOMAC), and radiographic evaluation were collected preoperatively and during the last follow-up. Satisfaction was compared using the 2011 Knee Society Scoring System. Results: There were no differences in age, gender, BMI and Follow-up time. KBD patients had significantly worse preoperative range of motion, KSKS, and mechanical lateral distal femoral angle (mLDFA) compared with OA patients (P < 0.05). At the last follow-up, the KSKS, KSFS, WOMAC score, and radiographic parameters of all patients significantly improved (P < 0.05), but the satisfaction was higher in KBD patients than in OA (P < 0.05). Further analysis showed that KSFS, WOMAC total, pain, stiffness, and function scores were significantly worse for KBD (P < 0.05). Conclusion: Patient satisfaction was greater but clinical outcomes were inferior in KBD than in OA. This study also demonstrated that TKA is an effective surgical procedure for KBD, but how to improve functional outcomes needs to be further studied.

Shikonin inhibits proliferation and induces apoptosis in glioma cells via downregulation of CD147.

Shikonin, a traditional Chinese medicine, has been identified as being capable of inducing apoptosis in various tumors, including glioma, and is thus considered to be a promising therapeutic agent for tumor therapy. However, little is known about the molecular mechanism of shikonin in glioma. The present study investigated the influence of shikonin on the proliferation and apoptosis of glioma cells U251 and U87MG and explored the potential molecular mechanisms. It was identified that shikonin was able to induce apoptosis in human glioma cells in a time­ and dose­dependent manner, and a decreased expression level of cluster of differentiation (CD)147 was observed in shikonin­treated U251 and U87MG cells. Knockdown of CD147 inhibited U251 and U87MG cell growth, whereas CD147 overexpression enhanced cell growth and decreased shikonin­induced apoptosis. Additionally, an increased expression level of CD147 suppressed the elevated production of reactive oxygen species and mitochondrial membrane potential levels induced by shikonin. The data indicated that shikonin­induced apoptosis in glioma cells was associated with the downregulation of CD147 and the upregulation of oxidative stress. CD147 may be an optional target of shikonin­induced cell apoptosis in glioma cells.

Drug development for Alzheimer's disease: review.

Alzheimer's disease (AD) is a chronic neurodegenerative disease, which is considered as one of the most intractable medical problems with heavy social and economic costs. The current drugs for AD, including acetylcholinesterase inhibitors (AChEIs) and memantine, a NMDA receptor antagonist, only temporarily ameliorate cognitive decline, but are unable to stop or reverse the progression of dementia. This paper reviewed the recent advance in AD drug development. The drug discovery programs under clinical trials targeting cholinergic system, α7 nicotinic acetylcholine receptors (nAChRs), N-methyl-d-aspartate receptor (NMDAR), ß-secretase, γ-secretase modulators, tau, inflammatory mediators and glucagon-like peptide-1 (GLP-1) were discussed. Though several drug discovery programs are ongoing, the high failure rate is an outstanding issue. Novel techniques and strategies are desperately needed to significantly accelerate this process.

Aerobic exercise promotes the expression of ERCC1 to prolong lifespan: A new possible mechanism.

Aerobic exercise can delay aging and extend lifespan, but its specific mechanism still remains unclear. One popular theory is that with age and the cell division times increasing, DNA damage will inevitably accumulate, leading to dysfunction and failure of various tissues and organs, which will eventually lead to aging. Thus, repairing damaged DNA is a key strategy to extend lifespan. Excision repair cross-complementary gene 1 (ERCC1) is a DNA repair enzyme that recognizes, excises and repairs damaged DNA. Defects or reduced activity of the enzyme can lead to DNA damage accumulation. This study provides that aerobic exercise can significantly extend rats' lifespan and increase the expression of ERCC1 in heart, brain, liver and kidney. Therefore, based on our experiments, we propose the following scientific hypothesis: aerobic exercise can up-regulate the expression of ERCC1 and then may reduce DNA damage accumulation to maintain genomic integrity and stability, thereby delaying aging and prolonging lifespan in humans.

Aerobic exercise-stimulated Klotho upregulation extends life span by attenuating the excess production of reactive oxygen species in the brain and kidney.

Aerobic exercise induces many adaptive changes in the whole body and improves metabolic characteristics. Klotho, an anti-aging gene, is mainly expressed in the brain and kidney. The roles of Klotho in the brain and kidney during aerobic exercise remain largely unknown. The present study aimed to determine whether aerobic exercise could influence the expression of Klotho, decrease reactive oxygen species (ROS) and prolong life span. Sprague Dawley rats were exercised on a motor treadmill. Klotho mRNA and protein expression levels in rat brain and kidney tissues were examined using reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. ROS production was detected following intermittent aerobic exercise (IAE) or continuous aerobic exercise (CAE). Kaplan-Meier curve analysis demonstrated that aerobic exercise significantly improved rat survival (P<0.001). The ROS levels in rat brain and kidney tissues were decreased in the aerobic exercise groups compared with the control group (P<0.05). In addition, Klotho mRNA and protein expression levels were increased significantly following aerobic exercise compared with controls (P<0.05). There was no significant difference between the IAE and CAE groups in any experiments (P>0.05). These results suggest that aerobic exercise-stimulated Klotho upregulation extends the life span by attenuating the excess production of ROS in the brain and kidney. As Klotho exhibits a potential anti-aging effect, promoting Klotho expression through aerobic exercise may be a novel approach for the prevention and treatment of aging and aging-related diseases.