Effect of vitamin D3 supplementation in winter on physical performance of university students: a one-month randomized controlled trial.

BACKGROUND: There is epidemiological evidence which suggests an association between 25-hydroxyvitamin D [25(OH)D] levels and bone and muscle function; however, it is unclear whether vitamin D supplementation has an added benefit beyond bone health. Here, we investigated the effects of vitamin D3 supplementation (1 month) on physical performance in Chinese university students in winter. METHODS: One hundred and seventeen eligible subjects with 25(OH)D (19.2 ± 7.8 ng/mL) were randomly assigned to either vitamin D3 supplement (N = 56; 1000 IU/day) or the control (N = 61) group for 1 month. Pre- and post-measurements included: 1) serum levels of 25(OH)D; 2) musculoskeletal and pulmonary function [vertical jump height (VJH) and right handgrip strength (RHS), forced vital capacity (FVC), and forced expiratory volume at 1s (FEV1)]; 3) bone turnover markers [parathyroid hormone (PTH), n-terminal osteocalcin (N-MID), and calcium]; 4) hemoglobin-related parameters [hemoglobin (Hb), hematocrit (HCT), red blood cells (RBC), and red cell distribution width (RDW)]; 5) lipid parameters [total triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C)]; 6) Fatigue-related indicators [serum creatine kinase (CK), lactate dehydrogenase (LDH), and total testosterone (T)]. In addition, aerobic capacity was assessed by measuring maximal oxygen uptake (VO2max) at baseline. RESULTS: During wintertime, supplementation with 1000 IU/d of vitamin D3 significantly increased serum 25(OH)D levels (from 18.85 ± 7.04 to 26.98 ± 5.88 ng/mL, p < 0.05), accompanied by a decrease of PTH (p < 0.05). However, vitamin D3 supplementation did not significantly impact the physical performance, serum lipid parameters, and bone turnover markers of students. Furthermore, 25(OH)D was found to be positively correlated with VJH and negatively correlated with PTH and TC at the beginning and end of the study (p < 0.05). In addition, the multiple linear regression analysis showed that 25(OH)D combined with athletic, gender, height, weight, Hb, and FVC could account for 84.0% of the VO2max value. CONCLUSIONS: The study demonstrated that one-month of 1000 IU/d of vitamin D3 supplementation during the winter had beneficial effects on 25(OH)D status and PTH. However, vitamin D3 intervention was not sufficient to improve physical performance. Furthermore, 25(OH)D levels combined with athletic, Hb and FVC could be a predictor of VO2max.

Role of the mechanosensitive piezo1 channel in intervertebral disc degeneration.

Intervertebral disc degeneration (IDD) is a multifactorial skeletal disease involving mechanical, genetic, systemic, and biological factors, and it is characterized by apoptosis of the nucleus pulposus cells and breakdown of the extracellular matrix (ECM), which will impair the structure and function of the intervertebral disc (IVD), and cause low back pain. Recently, the piezo1 is recognized as a critical mechanically activated ion channel of IDD. Numerous studies have reported that the piezo1 ion channel was aberrantly activated in the degenerated disc tissues and deeply participated in the pathogenesis of IDD. Inactivating or interfering with the piezo1 channel could effectively prevent the progression of IDD under the experimental conditions. It may be a promising target for the prevention and treatment of the disabling disease. Therefore, we have to make a comprehensive investigation and understanding of the mechanisms and functions of the piezo1 in the biomechanics of the spine. This study mainly elucidates the role of the piezo1 channel in IDD, which may facilitate the development of therapeutic targets for this disease.

Exosomes: A promising therapeutic strategy for intervertebral disc degeneration.

As a common problem all over the world, low back pain (LBP) places a huge social and economic burden on people. Intervertebral disc degeneration (IDD) is often considered to be the main cause of low back pain. The current methods of treating disc degenerative diseases mainly focus on relieving symptoms, including surgery and conservative treatment, but none of them can be treated with the etiology, which means that the normal structure of the intervertebral disc cannot be fundamentally restored. With the development of tissue engineering and regenerative medicine, exosomes from different sources, especially mesenchymal stem cell-derived exosomes (MSC-exos) as active biological substances for intercellular communication have made rapid progress due to their potency in promoting tissue regeneration. The study of exosomes in the field of treatment of IDD has yielded many surprising results. This paper mainly reviews the mechanism and function of exosomes in the study of delaying or reversing IDD, as well as gives the prospects and challenges of exosomes.

The Mechanism and Function of miRNA in Intervertebral Disc Degeneration.

Intervertebral disc degeneration (IDD) disease has been considered as the main cause of low back pain (LBP), which is a very common symptom and the leading cause of disability worldwide today. The pathological mechanism of IDD remains quite complicated, and genetic, developmental, biochemical, and biomechanical factors all contribute to the development of the disease. There exists no effective, non-surgical treatment for IDD nowadays, which is largely related to the lack of knowledge of the specific mechanisms of IDD, and the lack of effective specific targets. Recently, non-coding RNA, including miRNA, has been recognized as an important regulator of gene expression. Current studies on the effects of miRNA in IDD have confirmed that a variety of miRNAs play a crucial role in the process of IDD via nucleus pulposus cells (NPC) apoptosis, abnormal proliferation, inflammatory factors, the extracellular matrix (ECM) degradation, and annulus fibrosus (AF) degeneration. In the past 10 years, research on miRNA has been quite active in IDD. This review summarizes the current research progression of miRNA in the IDD and puts forward some prospects and challenges on non-surgical treatment for IDD.

Histone demethylase KDM5A promotes tumorigenesis of osteosarcoma tumor.

Osteosarcoma is a primary bone malignancy with a high rate of recurrence and poorer prognosis. Therefore, it is of vital importance to explore novel prognostic molecular biomarkers and targets for more effective therapeutic approaches. Previous studies showed that histone demethylase KDM5A can increase the proliferation and metastasis of several cancers. However, the function of KDM5A in the carcinogenesis of osteosarcoma is not clear. In the current study, KDM5A was highly expressed in osteosarcoma than adjacent normal tissue. Knockdown of KDM5A suppressed osteosarcoma cell proliferation and induced apoptosis. Moreover, knockdown of KDM5A could increase the expression level of P27 (cell-cycle inhibitor) and decrease the expression of Cyclin D1. Furthermore, after knockout of KDM5A in osteosarcoma cells by CRISPR/Cas9 system, the tumor size and growth speed were inhibited in tumor-bearing nude mice. RNA-Seq of KDM5A-KO cells indicated that interferon, epithelial-mesenchymal transition (EMT), IL6/JAK/STAT3, and TNF-α/NF-κB pathway were likely involved in the regulation of osteosarcoma cell viability. Taken together, our research established a role of KDM5A in osteosarcoma tumorigenesis and progression.