Purpose: To evaluate serum 25(OH) vitamin D levels in patients with low-energy hip fractures. Materials and Methods: Among 983 patients who underwent hip fracture surgery between August 2013 and March 2019, 732 patients were evaluated. The remaining patients were excluded due to the presence of one or more of the following: metastatic bone tumor, metabolic bone disease other than osteoporosis, fracture due to high-energy injury, atypical femoral fracture, and no blood test. We collected patient’s data about age, sex male female, date of injury, a place of residence, fracture type, preinjury ambulation ability according to their Koval score, and their serum level of 25(OH) vitamin D. The mean age was 79.3 years (60-104 years). The sample was comprised of 530 female and 202 male, of which 342 had femoral neck fractures and 390 had trochanteric fractures. Results: Of the total 732 patients, 346 patients (47.3%) had a 25(OH) vitamin D level of less than 10 ng/mL, 264 patients (36.1%) had scores of 10-19.9 ng/mL, 87 patients (11.9%) had scores of 20-29.9 ng/mL, and 35 patients (4.8%) had a level higher than 30 ng/mL. Vitamin D deficiency (less than 20 ng/mL) was present in 610 patients (83.3%), insufficiency (20-29.9 ng/mL) was found in 87 patients (11.9%), and 35 patients (4.8%) had normal vitamin D levels. The differences in vitamin D concentration based on season and fracture type were statistically significant. Conclusion Vitamin D deficiency and inadequacy were high in patients with low-energy hip fractures, with only 4.9% of patients had normal vitamin D levels. These findings suggest that efforts should be made to maintain proper vitamin D concentration.

Bladder dysfunction is a common complication of diabetes mellitus (DM). However, there have been a few studies evaluating bladder smooth muscle contraction in DM in the presence of pharmacological inhibitors. In the present study, we compared the contractility of bladder smooth muscle from normal rats and DM rats. Furthermore, we utilized pharmacological inhibitors to delineate the mechanisms underlying bladder muscle differences between normal and DM rats. DM was established in 14 days after using a single injection of streptozotocin (65 mg/kg, intraperitoneal) in Sprague-Dawley rats. Bladder smooth muscle contraction was induced electrically using electrical field stimulation consisting of pulse trains at an amplitude of 40 V and pulse duration of 1 ms at frequencies of 2–10 Hz. In this study, the pharmacological inhibitors atropine (muscarinic receptor antagonist), U73122 (phospholipase C inhibitor), DPCPX (adenosine A₁ receptor antagonist), udenafil (PDE5 inhibitor), prazosin (α₁-receptor antagonist), verapamil (calcium channel blocker), and chelerythrine (protein kinase C inhibitor) were used to pretreat bladder smooth muscles. It was found that the contractility of bladder smooth muscles from DM rats was lower than that of normal rats. In addition, there were significant differences in percent change of contractility between normal and DM rats following pretreatment with prazosin, udenafil, verapamil, and U73122. In conclusion, we suggest that the decreased bladder muscle contractility in DM rats was a result of perturbations in PLC/IP₃-mediated intracellular Ca²⁺ release and PDE5 activity.
Animals ; Atropine ; Diabetes Mellitus ; Muscle, Smooth ; Phosphotransferases ; Prazosin ; Rats* ; Rats, Sprague-Dawley ; Streptozocin ; Type C Phospholipases ; Urinary Bladder* ; Verapamil

Aripiprazole (ARI) is a commonly prescribed medication used to treat schizophrenia and bipolar disorder. To date, there have been no studies regarding the molecular pathological and immunotoxicological profiling of aripiprazole. Thus, in the present study, we prepared two different formulas of aripiprazole [Free base crystal of aripiprazole (ARPGCB) and cocrystal of aripiprazole (GCB3004)], and explored their effects on the patterns of survival and apoptosis-regulatory proteins under acute toxicity and cytotoxicity test conditions. Furthermore, we also evaluated the modulatory activity of the different formulations on the immunological responses in macrophages primed by various stimulators such as lipopolysaccharide (LPS), pam3CSK, and poly(I:C) via toll-like receptor 4 (TLR4), TLR2, and TLR3 pathways, respectively. In liver, both ARPGCB and GCB3004 produced similar toxicity profiles. In particular, these two formulas exhibited similar phospho-protein profiling of p65/nuclear factor (NF)-kappaB, c-Jun/activator protein (AP)-1, ERK, JNK, p38, caspase 3, and bcl-2 in brain. In contrast, the patterns of these phospho-proteins were variable in other tissues. Moreover, these two formulas did not exhibit any cytotoxicity in C6 glioma cells. Finally, the two formulations at available in vivo concentrations did not block nitric oxide (NO) production from activated macrophage-like RAW264.7 cells stimulated with LPS, pam3CSK, or poly(I:C), nor did they alter the morphological changes of the activated macrophages. Taken together, our present work, as a comparative study of two different formulas of aripiprazole, suggests that these two formulas can be used to achieve similar functional activation of brain proteins related to cell survival and apoptosis and immunotoxicological activities of macrophages.
Aripiprazole ; Apoptosis ; Bipolar Disorder ; Brain ; Caspase 3 ; Cell Survival ; Glioma ; Liver ; Macrophages ; Nitric Oxide ; Schizophrenia ; Toll-Like Receptor 4