Distal radius fracture is recognized as an osteoporosis-related fracture in aged population. If another osteoporosis-related fracture occurs in a short period, it represents a prolonged hospitalization and a considerable economic burden to the society. We evaluated the relationship between distal radius fracture and subsequent hip fracture within 1 year, especially in the critical time and age. We identified newly diagnosed distal radius fracture patients in 2000 to 2006 as an exposed cohort (N = 9,986). A comparison cohort (N = 81,227) was randomly selected from patients without distal radius fracture in the same year of exposed cohort. The subjects were followed up for 1 year since the recruited date. We compared the sociodemographic factors between two cohorts. Furthermore, the time interval following the previous distal radial fracture and the incidence of subsequent hip fracture was studied in detail. The incidence of hip fracture within 1 year increased with age in both cohorts. The risk was 5.67 times (84.6 vs. 14.9 per 10,000 person-years) greater in the distal radial fracture cohort than in the comparison cohort. The multivariate Cox proportional hazard regression analyses showed the hazard ratios of hip fracture in relation to distal radial fracture was 3.45 (95% confidence interval = 2.59–4.61). The highest incidence was within the first month after distal radial fracture, 17-fold higher than the comparison cohort (17.9 vs. 1.05 per 10,000). Among comorbidities, age > 60 years was also a significant factor associated with hip fracture (hazard ratio = 8.67, 95% confidence interval = 4.51–16.7). Patients with distal radius fracture and age >60 years will significantly increase the incidence of subsequent hip fracture, especially within the first month. Prognostic/epidemiologic study, level II.

Alzheimer’s disease is a neurodegenerative disease that was conventionally thought to be related to the sedimentation of beta‐amyloids, but drugs designed according to this hypothesis have generally failed. That FKBP52 can reduce the accumulation of tau proteins, and that Tacrolimus can reduce the pathological changes of tau proteins are new directions away from the long held amyloid‐beta‐centric concept. Therefore, the screening of traditional Chinese medicine compounds for those with higher affinity towards FKBP52 than Tacrolimus may be a new direction for treating Alzheimer’s disease. This study utilizes ligand‐based and structure‐based methods as the foundation. By utilizing dock scores and the predicted pIC50 from SVM, MLR, and Bayesian Network, several TCM compounds were selected for further analysis of their protein‐ligand interactions. Daphnetoxin has higher affinity and complex structure stability than Tacrolimus; Lythrancine II exhibits the most identical trends in FKBP52 interactions as Tacrolimus, and 20‐O‐(2′E,4′E‐decadienoyl)ingenol may be further modified at its hydrocarbon chain to promote interaction with FKBP52. In addition, we observed the residue Tyr113 of FKBP52 may play a key role in protein‐ligand interaction. Our results indicate that Daphnetoxin, 20‐O‐(2′E,4′E‐decadienoyl)ingenol, and Lythrancine II may be starting points for further modification as a new type of non‐amyloid‐beta‐centric drug for Alzheimer’s disease.

Platelet activation and its interaction with leukocytes play an important role in atherothrombosis. Cardiovascular diseases resulted from atherothrombosis remain the major causes of death worldwide. Gallic acid, a major constituent of red wine and tea, has been believed to have properties of cardiovascular protection, which is likely to be related to its antioxidant effects. Nonetheless, there were few and inconsistent data regarding the effects of gallic acid on platelet function. Therefore, we designed thisin vitrostudy to determine whether gallic acid could inhibit platelet activation and the possible mechanisms. From our results, gallic acid could concentration-dependently inhibit platelet aggregation, P-selectin expression, and platelet-leukocyte aggregation. Gallic acid prevented the elevation of intracellular calcium and attenuated phosphorylation of PKCα/p38 MAPK and Akt/GSK3βon platelets stimulated by the stimulants ADP or U46619. This is the first mechanistic explanation for the inhibitory effects on platelets from gallic acid.

Parkinson’s disease (PD) is the second most common age-related neurodegenerative disorder with limited clinical treatments. The occurrence of PD includes both genetic and environmental toxins, such as the pesticides paraquat (PQ), as major contributors to PD pathology in both invertebrate and mammalian models. Calycosin, an isoflavone phytoestrogen, has multiple pharmacological properties, including neuroprotective activity. However, the paucity of information regarding the neuroprotective potential of calycosin on PQ-induced neurodegeneration led us to explore whether calycosin can mitigate PD-like phenotypes and the underlying molecular mechanisms. We used a PQ-induced PD model in Drosophila as a cost-effective in vivo screening platform to investigate the neuroprotective efficacy of natural compounds on PD. We reported that calycosin shows a protective role in preventing dopaminergic (DA) neuronal cell death in PQ-exposed Canton S flies. Calycosin-fed PQ-exposed flies exhibit significant resistance against PQ-induced mortality and locomotor deficits in terms of reduced oxidative stress, loss of DA neurons, the depletion of dopamine content, and phosphorylated JNK-caspase-3 levels. Additionally, mechanistic studies show that calycosin administration improves PQ-induced mitochondrial dysfunction and stimulates mitophagy and general autophagy with reduced pS6K and p4EBP1 levels, suggestive of a maintained energy balance between anabolic and catabolic processes, resulting in the inhibition of neuronal cell death. Collectively, this study substantiates the protective effect of calycosin against PQ-induced neurodegeneration by improving DA neurons’ survival and reducing apoptosis, likely via autophagy induction, and it is implicated as a novel therapeutic application against toxin-induced PD pathogenesis.