Injury-Admission Time is an Independent Risk Factor for Deep Vein Thrombosis in Older Patients with Osteoporotic Hip Fracture.

BACKGROUND Deep vein thrombosis is a common pre- and post-operative complication in older patients with osteoporotic hip fractures. Pre-operative thrombus can increase the risk of surgery. This study examined the association between the time from fracture to admission (injury-admission time) and deep vein thrombosis in older patients with osteoporotic hip fractures. MATERIAL AND METHODS Doppler ultrasound screening of deep lower-extremity veins was performed in patients with osteoporotic hip fractures between June 2019 and December 2021. Clinical data, including medical history, injury-admission time, and laboratory tests, were collected retrospectively. RESULTS Of the 439 patients, deep vein thrombosis was found in 139 (31.66%). The injury-admission time was significantly longer in the thrombosis group, which was positively associated with deep vein thrombosis (odds ratio 1.010, 95% confidence interval 1.003-1.017). The area under the curve to predict deep vein thrombosis was 0.619. The best cut-off value, sensitivity, and specificity were 21 h, 46.76%, and 75%, respectively. When the injury-admission period exceeded 21 h, the prevalence of deep vein thrombosis was 45.8% and the thrombosis incidence was significantly higher than in the <21 h group (24.9%). CONCLUSIONS Our results suggest that screening for deep vein thrombosis should be routinely performed for patients with osteoporotic hip fractures, particularly for those with injury-admission time ≥21 h.

The prevalence of osteoporosis in postmenopausal women in urban Tianjin, China and its related factors.

OBJECTIVES: The aims of the study are to understand the prevalence of osteoporosis in postmenopausal women in urban Tianjin, China and its related factors through a questionnaire and to assess the correlation between individual characteristics, physical mobility, psychological and emotional well-being, and prevalence, as well as people's awareness of osteoporosis. METHODS: We selected 240 postmenopausal women from 12 randomly selected streets in 6 administrative districts of Tianjin for bone mineral density measurement and a face-to-face questionnaire survey to obtain the relevant data. Female residents who had lived in the communities under the jurisdiction of the incorporated streets for more than 10 years and had been in menopause for 2 years were included. The women were made aware of the study, there were no communication barriers, and they were willing to undergo dual-energy absorptiometry and cooperate in completing the questionnaire. We used one-way analysis of variance, Fisher exact test, and Pearson correlation analysis for the statistical analysis. RESULTS: The overall prevalence of osteoporosis in postmenopausal women in the six districts of Tianjin was found to be 52.08%, and the χ 2 test for trend showed a clear trend of increasing with age ( P = 0.035). Body mass index was found to be the most significant personal characteristic affecting the prevalence of osteoporosis; the mean values of the nonosteoporosis and osteoporosis group were (25.45 ± 3.09) and (23.85 ± 3.16), respectively ( P < 0.001); previous fractures were closely associated with the prevalence of osteoporosis. Awareness about osteoporosis had not disseminated among the population, and 9.17% of the participants had never heard of the disease. While 75.42% and 72.92% of the participants, respectively, believe that the harm of osteoporosis cannot be compared with heart disease and cerebral infarction, 56.67% had never had an examination for osteoporosis and paid little to no attention to this disease. People still had major misconceptions about the hazards of osteoporosis and common-sense precautions that needed to be followed. CONCLUSIONS: Although osteoporosis is prevalent among postmenopausal women in urban Tianjin and is strongly linked to both history of fracture and body mass index, most women are only familiar with the disease's name and lack an understanding of the dangers it poses as well as the importance of early diagnosis and treatment. To ensure the prevention and control of osteoporosis, it is crucial to focus on increasing the examination and treatment rates and spreading awareness of the three-level diagnosis and treatment pattern among the public.

Danthron ameliorates obesity and MAFLD through activating the interplay between PPARα/RXRα heterodimer and adiponectin receptor 2.

Obesity and associated metabolic associated fatty liver diseases (MAFLD) are strongly associated with dysfunction of glucose and lipid metabolism. AMPKα and PPARα are key regulators in the lipid and glucose homeostasis, indicating that novel agents to activate them are promising therapeutic approaches for metabolic syndrome. Noticeably, as a natural anthraquinone derivative extracted from rhubarb, danthron can activate AMPKα in vitro. However, the protective effect of danthron on obesity and associated MAFLD in vivo, as well as the underlying mechanism remains unknown. In this study, obesity and associated MAFLD was induced in C57BL/6J mice by high fat diet (HFD), which were subjected to evaluations on the parameters of systematic metabolism. Simultaneously, the molecular mechanism of danthron on lipid metabolism was investigated in 3T3-L1-derived adipocytes and HepG2 cells in vitro. In vivo, danthron significantly attenuated the obesity and MAFLD by enhancing hepatic fatty acid oxidation, decreasing lipid synthesis, and promoting mitochondrial homeostasis. Mechanistically, danthron significantly promoted combination of RXRα and PPARα, enhanced the binding of RXRα/PPARα heterodimer to the promoter of adiponectin receptor 2 (AdipoR2), by which activating the AMPKα and PPARα pathway. Moreover, PPARα and AdipoR2 can interplay in a loop style. Collectively, this study demonstrates that danthron can substantially ameliorate obesity and associated hepatic steatosis via AdipoR2-mediated dual PPARα/AMPKα activation, which suggests that danthron might be a novel therapeutic approach for inhibition of obesity and hepatic steatosis.

Influences of phosphorus concentration and porewater advection on phosphorus dynamics in carbonate sands around the Weizhou Island, northern South China Sea.

A series of flow-through reactor experiments were undertaken to assess the potential effect of porewater advection and dissolved inorganic phosphorus (DIP) concentration on benthic DIP dynamics in permeable sediments collected from the Weizhou Island, northern South China Sea. The flux of DIP ranged from -0.13 to 0.05 mmol m-2 h-1, and the reversal from DIP efflux to influx occurred when the DIP concentration reached a threshold. DIP release from the sediment into the seawater peaked at intermediate advection rate, which perhaps provide optimum conditions for DIP release related to CaCO3 dissolution. Phosphorus limitation in seawater could be relieved by DIP release from the sediment, and CaCO3-bound P in carbonate sands may play a major role in benthic DIP release and decrease in the molar nitrogen/phosphorus ratio in seawater around the Weizhou Island.

Formononetin attenuates atherosclerosis via regulating interaction between KLF4 and SRA in apoE-/- mice.

Background and Purpose: Atherosclerosis is an underlying cause of coronary heart disease. Foam cell, a hallmark of atherosclerosis, is prominently derived from monocyte-differentiated macrophage, and vascular smooth muscle cells (VSMCs) through unlimitedly phagocytizing oxidized low-density lipoprotein (oxLDL). Therefore, the inhibition of monocyte adhesion to endothelium and uptake of oxLDL might be a breakthrough point for retarding atherosclerosis. Formononetin, an isoflavone extracted from Astragalus membranaceus, has exhibited multiple inhibitory effects on proatherogenic factors, such as obesity, dyslipidemia, and inflammation in different animal models. However, its effect on atherosclerosis remains unknown. In this study, we determined if formononetin can inhibit atherosclerosis and elucidated the underlying molecular mechanisms. Methods: ApoE deficient mice were treated with formononetin contained in high-fat diet for 16 weeks. After treatment, mouse aorta, macrophage and serum samples were collected to determine lesions, immune cell profile, lipid profile and expression of related molecules. Concurrently, we investigated the effect of formononetin on monocyte adhesion, foam cell formation, endothelial activation, and macrophage polarization in vitro and in vivo. Results: Formononetin reduced en face and aortic root sinus lesions size. Formononetin enhanced lesion stability by changing the composition of plaque. VSMC- and macrophage-derived foam cell formation and its accumulation in arterial wall were attenuated by formononetin, which might be attributed to decreased SRA expression and reduced monocyte adhesion. Formononetin inhibited atherogenic monocyte adhesion and inflammation. KLF4 negatively regulated the expression of SRA at transcriptional and translational level. Conclusions: Our study demonstrate that formononetin can substantially attenuate the development of atherosclerosis via regulation of interplay between KLF4 and SRA, which suggests the formononetin might be a novel therapeutic approach for inhibition of atherosclerosis.

Formononetin ameliorates cholestasis by regulating hepatic SIRT1 and PPARα.

Cholestasis, which is characterized by bile acid (BA) overload within the hepatocytes, is a major contributor to liver injury. The dysregulation of bile acid homeostasis, such as excessive bile acid synthesis and defected secretion, leads to intracellular retention of hydrophobic bile acid which undermines the physiological function of hepatocytes. Cholestasis can further develop into hepatic fibrosis and cirrhosis, and eventually life-threating liver failure. In the liver, BA-activated FXR can reduce hepatic BA concentration by negative feedback regulation. Clinically, FXR and PPARα are the pharmacological targets of obeticholic acid and fenofibrate for the treatment of primary biliary cirrhosis, respectively. Formononetin, a natural isoflavone compound, exerts beneficial effects in various biological processes, such as anti-inflammation, anti-tumor. However, the role of formononetin in bile acid metabolism remains unclear. Herein, we show that formononetin improves hepatic/systemic bile acid metabolism and protects against ANIT-induced liver injury. Mechanistically, formononetin improves the genes profile orchestrating bile acid homeostasis through modulating SIRT1-FXR signaling pathway. Moreover, formononetin attenuated ANIT-induced inflammatory response by inactivating JNK inflammation pathway in PPARα dependent manner. Taken together, our study demonstrates that formononetin ameliorates hepatic cholestasis by upregulating expression of SIRT1 and activating PPARα, which is an important anti-cholestatic mechanism of formononetin.