BackgroundStroke complications can occur not only in the acute ward but also during the subsequent rehabilitation period. However, existing studies have not adequately addressed the incidence of various complications among stroke in patients undergoing rehabilitation using a longitudinal method. We aimed to investigate the longitudinal impact of age on complication rates in patients undergoing inpatient stroke rehabilitation at different disease stages.MethodsFive hundred and sixty-eight first-time stroke patients transferred to the rehabilitation ward between July 2002 and June 2012 were included in the study. Patients were stratified into age groups for comparison: <65 years (young), 65 years to <75 years (younger old), and ≥75 years (older old). In total, 30 different complication types were recorded for analysis.ResultsConstipation, shoulder pain, symptomatic urinary tract infection (UTI), and fever were common complications during initial stay in the rehabilitation ward, and incidence was >10% in all three age groups. The frequency of incidence of upper gastrointestinal bleeding (UGIB) was higher in the younger old (17.9%) and older old (20.6%) groups than in the young group (4.1%) during initial stay in the rehabilitation ward (p < 0.001). The incidence of UGIB was higher in the younger old (8.04%) and older old (8.33%) groups than in the young group (0.19%) during subsequent stay in the rehabilitation ward (p = 0.011). The incidence of symptomatic UTI was higher in the younger old (21.0%) and older old (20.0%) groups than in the young group (11.5%) during initial stay in the rehabilitation ward (p = 0.019). The incidence of symptomatic UTI was higher in the older old group (29.17%) than in the younger old (9.21%) and young (3.14%) groups during subsequent stay in the rehabilitation ward (p < 0.001).ConclusionsAge does not affect every complication type. UGIB and symptomatic UTI occurred more frequently in stroke patients aged ≥65 years during their stay in the rehabilitation ward.
Lysophosphatidic acid (LPA) has been found to mediate myeloid differentiation, stimulate osteogenesis, alter cell proliferation and migration, and inhibit apoptosis in chondrocytes. The effect of LPA on the angiogenic capability of chondrocytes is not clear. This study aimed to investigate its effect on the angiogenic capability of human chondrocytes and the underlying mechanism of these effects. Human chondrocyte cell line, CHON-001, commercialized human chondrocytes (HC) derived from normal human articular cartilage, and human vascular endothelial cells (HUVECs) were used as cell models in this study. The angiogenic capability of chondrocytes was determined by capillary tube formation, monolayer permeability, cell migration, and cell proliferation. An angiogenesis protein array kit was used to evaluate the secretion of angiogenic factors in conditioned medium. Angiogenin, insulin-like growth factor-binding protein 1 (IGFBP-1), interleukin (IL)-8, monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase (MMP)-9, and vascular endothelial growth factor (VEGF) mRNA and protein expressions were evaluated by Q-RT-PCR and EIA, respectively. LPA receptor (LPAR) expression was determined by RT-PCR. Signaling pathways were clarified using inhibitors, Western blot analysis, and reporter assays. The LPA treatment promoted the angiogenic capability of CHON-001 cells and HC, resulting in enhanced HUVEC capillary tube formation, monolayer permeability, migration, and cell growth. Angiogenin, IGFBP-1, IL-8, MCP-1, MMP-9, and VEGF mRNA and protein expressions were significantly enhanced in LPA-treated chondrocytes. LPA2, 3, 4 and 6 were expressed in CHON-001 and HC cells. Pretreatment with the Gi/o type G protein inhibitor, pertussis toxin (PTX), and the NF-kB inhibitor, PDTC, significantly inhibited LPA-induced angiogenin, IGFBP-1, IL-8, MCP-1, MMP-9, and VEGF expressions in chondrocytes. The PTX pretreatment also inhibited LPA-mediated NF-kB activation, suggesting the presence of active Gi/NF-kB signaling in CHON-001 and HC cells. The effect of LPA on the angiogenesis-inducing capacity of chondrocytes may be due to the increased angiogenesis factor expression via the Gi/NF-kB signaling pathway.
Despite a plethora of literature has documented that osteoarthritis (OA) is veritably associated with oxidative stress-mediated chondrocyte death and matrix degradation, yet the possible involvement of synoviocyte abnormality as causative factor of OA has not been thoroughly investigated. For this reason, we conduct the current studies to insight into how synoviocytes could respond to an episode of folate-deprived (FD) condition. First, when HIG-82 synoviocytes were cultivated under FD condition, a time-dependent growth impediment was observed and the demise of these cells was demonstrated to be apoptotic in nature mediated through FD-evoked overproduction of reactive oxygen species (ROS) and drastically released of cytosolic calcium (Ca2+) concentrations. Next, we uncovered that FD-evoked ROS overproduction could only be strongly suppressed by either mitochondrial complex II inhibitors (TTFA and carboxin) or NADPH oxidase (NOX) inhibitors (AEBSF and apocynin), but not by mitochondrial complex I inhibitor (rotenone) and mitochondrial complex III inhibitor (antimycin A). Interestingly, this selective inhibition of FD-evoked ROS by mitochondrial complex II and NOX inhibitors was found to correlate excellently with the suppression of cytosolic Ca2+ release and reduced the magnitude of the apoptotic TUNEL-positive cells. Taken together, we present the first evidence here that FD-triggered ROS overproduction in synoviocytes is originated from mitochondrial complex II and NOX. Both elevated ROS in tandem with cytosolic Ca2+ overload serve as final arbitrators for apoptotic lethality of synoviocytes cultivated under FD condition. Thus, folate supplementation may be beneficial to patients with OA.
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