The age-related metabolizable energy of cereal grains, oilseed meals, corn gluten meals, and feather meals for broilers.

A 2 × 3 factorial arrangement of treatments with two ages of broilers (11 to 14 or 25 to 28 d of age) and three samples of feed ingredients was utilized to compare metabolizable energy (ME) and ratio of ME to gross energy (GE) in each group of three cereal grains (CG, including one corn, two wheat flour), three oilseed meals (OM, including one soybean meal, one peanut meal, and one cottonseed meal), three corn gluten meals (CGM A, B, and C), and three feather meals (FM A, B, and C). Each treatment contained six replicates of four Arbor Acre male broilers in energy balance experiments. Trends toward interactions between age and source of CG were observed on the ME and ME/GE of CG (0.

The potential roles of JAK/STAT signaling in the progression of osteoarthritis.

Osteoarthritis (OA) is an age-related chronic progressive degenerative disease that induces persistent pain and disabilities. The development of OA is a complex process, and the risk factors are various, including aging, genetics, trauma and altered biomechanics. Inflammation and immunity play an important role in the pathogenesis of OA.

Long non-coding RNA HOTAIRincreased mechanical stimulation-induced apoptosis by regulating microRNA-221/BBC3 axis in C28/I2 cells.

Abnormal mechanical stimulation contributes to articular cartilage degeneration and osteoarthritis (OA) development. Many long noncoding RNAs (lncRNAs) are involved in mechanical force-induced cartilage degeneration. LncRNA HOTAIR (HOTAIR) has been demonstrated to increase osteoarthritis progression.

Xanthohumol Inhibited Mechanical Stimulation-Induced Articular ECM Degradation by Mediating lncRNA GAS5/miR-27a Axis.

Osteoarthritis (OA) is histopathologically marked by extracellular matrix (ECM) degradation in joint cartilage. Abnormal mechanical stimulation on joint cartilage may result in ECM degeneration and OA development. Matrix metalloproteinase 13 (MMP-13) is one of the catabolic enzymes contributing to the degradation of ECM, and it has become the potential biomarker for the therapeutic management of OA.

Apoptosis of endplate chondrocytes in cervical kyphosis is associated with chronic forward flexed neck: an in vivo rat bipedal walking model.

Background: This study was undertaken to establish a rat bipedal walking model of cervical kyphosis (CK) associated with chronic forward flexed neck and assess the effects of chronic forward flexed neck on endplate chondrocytes.

Methods: Forty-eight 1-month-old Sprague-Dawley rats were randomly divided into 3 groups: forward flexed neck group (n = 16), bipedal group (n = 16), and normal group (n = 16). Cervical curves were analyzed on a lateral cervical spine X-ray using Harrison's posterior tangent method before the experiment and at 2-week intervals for a 6-week period.

MicroRNA-142 protects MC3T3-E1 cells against high glucose-induced apoptosis by targeting β-catenin.

Osteoporosis, characterized by decreased mineral density and bone mass, is triggered by various detrimental factors and often causes further complications, including fractures. Aberrant expression of microRNAs (miRs) has been associated with the pathogenesis of osteoporosis. Recently, miR-142 was reported to be downregulated in osteoblasts; however, the underlying mechanism of miR-142 in mediating the development of osteoporosis remains unclear.