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 (0.05

Databases lack true information on metabolizable energy (ME) values of feed ingredients for broilers across phases. The current study evaluated the effect of broiler age (11 to 14 d or 25 to 28 d) on ME of three cereal grains (CG, one corn, two wheat flour [WF]), three oilseed meals (OM, one soybean meal, one peanut meal, and one cottonseed meal), three corn gluten meals (CGM, three sources of CGM differed in crude protein content), and three feather meals (FM, one enzymatical hydrolyzed FM, one expanded FM, and one hydrolyzed FM). Our study demonstrated no interactive effects between broiler age and source of feed on ME of OM and FM, but detected interactive effects for CG and CGM. Thus, the effect of age on ME can depend on the type of feed and its chemical composition. In addition, the ME of WF and OM was not affected by age, but the ME of corn, CGM, and FM increased as broilers aged. These results indicate that the ME in starter diets with corn, CGM, and FM may be overestimated if the ME values of feed ingredients are obtained from growing broilers.

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. JAK/STAT pathway is one of the most prominent intracellular signaling pathways, regulating cell proliferation, differentiation, and apoptosis. Inflammatory factors can act as the initiators of JAK/STAT pathway, which is implicated in the pathophysiological activity of chondrocyte. In this article, we provide a review on the importance of JAK/STAT pathway in the pathological development of OA. Potentially, JAK/STAT pathway becomes a therapeutic target for managing 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. However, the roles of HOTAIR in mechanical stimulation-treated chondrocytes are still unclear. In this study, we found that mechanical stimulation significantly induced apoptosis in C28/I2 cells. In addition, the expression of HOTAIR was up regulated and the expression of miR-221 was down regulated. Knockdown of HOTAIR effectively ameliorated cell apoptosis induced by mechanical stimulation. HOTAIR could interact with miR-221, which targeted to degrade BBC3. Overexpression of BBC3 could reverse the decreased apoptotic rates induced by HOTAIR knockdown. Collectively, HOTAIR promoted mechanical stimulation-induced apoptosis by regulating the miR-221/BBC3 axis in C28/I2 cells.

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. Xanthohumol (XH), a naturally occurring prenylflavonoid derived from hops and beer, shows the protective activity against OA development. However, the potential mechanisms still need great effort. In this article, mechanical stimulation could significantly increase the expression of MMP-13 and lncRNA GAS5 (GAS5) and promoting ECM degradation. These could be effectively reversed by XH administration. Suppressed expression GAS5 ameliorated mechanical stimulation-induced MMP-13 expression. MiR-27a was predicted and verified as a target of GAS5, and overexpression of miR-27a down regulated the expression of MMP-13. Collectively, XH exhibited protective effects against mechanical stimulation-induced ECM degradation by mediating the GAS5/miR-27a signaling pathway in OA chondrocytes.

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. Histologic changes in cartilaginous endplate chondrocytes were observed using hematoxylin and eosin (H&E) staining, transmission electron microscopy (TEM), and terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling. RESULTS: Radiographic findings suggested a significantly decreased cervical physiological curvature in the forward flexed neck group over the 6-week follow-up; normal cervical curves were maintained in other groups. The average cervical curvature (C2-C7) was - 7.6 ± 0.9° in the forward flexed neck group before the experiment, - 3.9 ± 0.8° at 2 weeks post-experiment, 10.7 ± 1.0° at 4 weeks post-experiment, and 20.5 ± 2.1° at the last follow-up post-experiment. Histologically, results of H&E staining unveiled that cartilaginous endplate chondrocytes were arranged in an irregular fashion, with the decreased number at the observation period; the incidence of apoptotic cells in the forward flexed neck group was noticeably higher at the 6-week follow-up than that in other groups. CONCLUSIONS: CK developed as the result of chronic forward flexed neck. Histologic changes suggested that chondrocyte apoptosis may play a critical role in the development of cervical kyphotic deformity associated with chronic forward flexed neck.

MicroRNA-142 protects MC3T3-E1 cells against high glucose-induced apoptosis by targeting ß-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. In the present study, high glucose induced the downregulation of miR-142 mRNA expression and promoted the apoptosis of MC3T3-E1 cells. miR-142-mimics significantly protected against high glucose-induced apoptosis, upregulated the expression levels of B-cell lymphoma 2 (Bcl-2) and downregulated the protein expression levels of ß-catenin, Bcl-2 associated X (Bax) and caspase-3. Furthermore, ß-catenin was identified as a direct target of miR-142 using luciferase reporter assays. Similar to the effects of miR-142 inhibitors, overexpression of ß-catenin aggravated the apoptosis of MC3T3-E1 cells, as demonstrated by the upregulation of Bax and caspase-3, and the downregulation of Bcl-2 expression levels. In conclusion, miR-142 protects MC3T3-E1 cells against high glucose-induced apoptosis by targeting ß-catenin.