Predictors for the use of traditional Chinese medicine among inpatients with first-time stroke: a population-based study.

BACKGROUND: Stroke is one of the major causes of death and disability. The treatments that are provided to patients during hospitalization after an acute stroke are very important in stabilizing their medical condition and enabling the recovery of their motor functions. However, limited information is available regarding the use of traditional Chinese medicine (TCM) during hospitalization for first-time stroke patients. The researchers aimed to investigate the factors affecting TCM use and to provide clinicians with comprehensive information on TCM use among first-time stroke inpatients in Taiwan. METHODS: The researchers collected and analyzed data, including patient characteristics, TCM use, and TCM prescription patterns, from the National Health Insurance Research Database in Taiwan for first-time stroke inpatients between 2006 and 2012. RESULTS: Among the 89,162 first-time stroke patients, 7455 were TCM users, and 81,707 were TCM nonusers. The predictors for TCM use were as follows: age, 45-64 or < 45 years; men; living in a level 2, 4, or 7 urbanized area; insured amount ≥ 576 USD per month; ischemic stroke; hospitalized for first-time stroke for 8-14 days, 15-28 days, or ≥ 29 days; stroke severity index score 0-9 or 10-19; Charlson-Deyo comorbidity index score 0 or 1-2; hospitalization in a regional or community hospital; receiving rehabilitation; and previous experience with outpatient TCM use. An increase in the number of TCM users was observed from 2006 to 2012. Furthermore, 68.8-79.7% of TCM users used acupuncture only, while 17.8-26.1% used both acupuncture and Chinese herbal medicine. CONCLUSIONS: An increasing number of first-time stroke patients have been choosing TCM as a complementary treatment during hospitalization. Moreover, TCM use is associated with demographic, clinical, and socioeconomic characteristics. These findings may help clinicians comprehensively understand the trend and the important factors affecting TCM utilization among patients who are hospitalized due to first-time stroke.

Folate Deficiency Triggered Apoptosis of Synoviocytes: Role of Overproduction of Reactive Oxygen Species Generated via NADPH Oxidase/Mitochondrial Complex II and Calcium Perturbation.

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.

Lysophosphatidic acid enhanced the angiogenic capability of human chondrocytes by regulating Gi/NF-kB-dependent angiogenic factor expression.

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.

Clinical use of high-resolution ultrasonography for the diagnosis of type II accessory navicular bone.

Medial foot pain is a common complaint in rehabilitation clinics. The differential diagnoses include many musculoskeletal disorders like tendonitis and inflammation of ossicles. Posterior tibialis tendonitis is a common cause of foot pain in adults. The accessory navicular (AN) bone is occasionally observed and considered as a secondary ossification center of the navicular bone. Occasionally, posterior tibialis tendonitis and AN bone may cause acute or chronic medial foot pain with varying degrees of dysfunction. Previously, the diagnosis of an AN bone in a painful medial foot was based on clinical presentation and radiographic examinations such as plain radiography, bone scintigraphy, and magnetic resonance imaging. However, the application of soft-tissue ultrasonography for the diagnosis of posterior tibialis tendonitis associated with an AN bone has not been documented. Here, we report the case of a 60-yr-old woman with painful medial foot which had a diagnosis of posterior tibialis tendonitis associated with an AN bone by high-resolution ultrasonography.