Mitigation Effects of Selenium Nanoparticles on Depression-Like Behavior Induced by Fluoride in Mice via the JAK2-STAT3 Pathway.

Depression is a mental health problem with typically high levels of distress and dysfunction, and 150 mg/L fluoride (F) can induce depression-like behavior. The development of depression is correlated with neuronal atrophy, insufficient secretion of monoamine neurotransmitters, extreme deviations from the normal microglial activation status, and immune-inflammatory response. Studies found that Se supplementation was related to the improvement of depression. In this study, we applied selenium nanoparticles (SeNPs) for F-induced depression disease mitigation by regulating the histopathology, metabolic index, genes, and protein expression related to the JAK2-STAT3 signaling pathway in vivo. Results showed that F and 2 mg Se/kg BW/day SeNPs lowered the dopamine (DA) content (P < 0.05), altered the microglial morphology, ramification index as well as solidity, and triggered the microglial neuroinflammatory response by increasing the p-STAT3 nuclear translocation (P < 0.01). Furthermore, F reduced the cortical Se content and the number of surviving neurons (P < 0.05), increasing the protein expressions of p-JAK2/JAK2 and p-STAT3/STAT3 of the cortex (P < 0.01), accompanied by the depression-like behavior. Importantly, 1 mg Se/kg BW/day SeNPs alleviated the microglial ramification index as well as solidity changes and decreased the interleukin-1ß secretion induced by F by suppressing the p-STAT3 nuclear translocation (P < 0.01). Likewise, 1 mg Se/kg BW/day SeNPs restored the F-disturbed dopamine and noradrenaline secretion, increased the number of cortical surviving neurons, and reduced the vacuolation area, ultimately suppressing the occurrence of depression-like behavior through inhibiting the JAK2-STAT3 pathway activation. In conclusion, 1 mg Se/kg BW/day SeNPs have mitigation effects on the F-induced depression-like behavior. The mechanism of how SeNPs repair neural functions will benefit depression mitigation. This study also indicates that inhibiting the JAK/STAT pathway can be a promising novel treatment for depressive disorders.

Dietary Calcium Alleviates Fluorine-Induced Liver Injury in Rats by Mitochondrial Apoptosis Pathway.

Excessive fluoride (F) exposure can lead to liver damage; moreover, recent studies found that the addition of appropriate calcium (Ca) can alleviate the symptom of skeletal fluorosis. However, whether Ca can relieve F-induced liver damage through the mitochondrial apoptosis pathway has not been reported yet. Therefore, we assessed the liver morphology, serum transaminase content, liver oxidative stress-related enzymes, and apoptosis-related gene and protein expression in Sprague Dawley (SD) rats treated with 150 mg/L sodium fluoride (NaF) and different concentrations of calcium carbonate (CaCO3) for 120 days. Our results showed that NaF brought out pathological changes in liver morphology, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels increased, total antioxidant capacity (T-AOC), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) content decreased, and malondialdehyde (MDA) content increased, suggesting that NaF caused hepatotoxicity and oxidative stress. In addition, the results of quantitative real-time PCR (qRT-PCR) and immunohistochemistry showed that NaF exposure upregulated the expression of Bcl-2-associated x protein (Bax), rho-related coiled-coil kinase 1 (ROCK1), cytochrome C (Cyto-C) mRNA and protein (P < 0.01), and downregulated B cell lymphoma 2 (Bcl-2) protein and mRNA (P < 0.01), indicating that excessive F exposure activated mitochondrial-mediated apoptosis in the liver. However, the addition of 1% CaCO3 to the diet significantly increased the expression of anti-apoptotic gene Bcl-2 (P < 0.01), inhibited the activation of the mitochondrial apoptosis pathway, and reduced mitochondrial damage. In summary, supplementing 1% CaCO3 in the diet can alleviate the NaF-induced liver cell damage through the mitochondrial apoptosis pathway.

Theoretical insight into the electrocatalytic reduction of CO2 with different metal ratios and reaction mechanisms on palladium-copper alloys.

Environmental impacts of continued CO2 production have led to an increased need for new methods of CO2 removal and energy development. Electrochemical reduction of CO2 has been shown to be a good method through recent studies. Alloys are of special interest for these applications, because of their unique chemical and physical properties that allow for highly active surfaces. Here, PdnCum (m + n = 15 and n > m) bimetallic electrocatalysts were used for systematic studies to understand the effect of the composition of Pd and Cu on the electrochemical reduction of CO2 to CO. In particular, the Pd-Cu alloy with the Pd/Cu = 2/1 atomic ratio (i.e., Pd10Cu5) has the best catalytic effect, particularly true at the step of the hydrogenation of CO2 to COOH, and the Pd10Cu5 catalyst is better than most known electrodes. With the energetic analysis of the proposed reaction pathways over the Pd10Cu5 catalyst, the limiting voltages for CO2 reduction to CH3OH, CH4, and CH3CH2O have been compared. Most importantly, the kinetic model analysis showed that the rate constant values indicate that the probability of generating C2H5OH on the Pd10Cu5 catalyst is greater than that of CH3OH or CH4. The findings revealed in this study may shed some light on the design of cost-effective and efficient electrocatalysts for CO2 conversion to CO or to other useful hydrocarbons.

Atypical cystic adenoma of the parathyroid gland: case report and review of literature.

OBJECTIVE: To describe the clinical course of a patient with atypical cystic parathyroid adenoma manifesting as hypercalcemic parathyroid crisis. METHODS: We present a case report and review the relevant literature on parathyroid cysts and atypical cystic parathyroid adenomas. RESULTS: A 76-year-old woman was evaluated for weakness, weight loss, urinary incontinence, and memory disturbances. She had severe hypercalcemia (calcium level, 18.3 mg/dL) in conjunction with an elevated parathyroid hormone level of 1,472 pg/mL. She received aggressive hydration, pamidronate, and calcitonin. Ultrasonography revealed a large cystic structure (5.8 cm) at the lower pole of the left thyroid lobe. She underwent surgical exploration of the neck, total thyroidectomy for multinodular disease of the thyroid, and subtotal parathyroidectomy. Intraoperatively, 25 mL of fluid was aspirated from the cystic mass, and the parathyroid hormone level in the fluid was 7,400,000 pg/mL. The final pathologic diagnosis was an atypical cystic parathyroid adenoma. CONCLUSION: Parathyroid cysts are uncommon and should be considered in the differential diagnosis of a neck mass. Although most parathyroid cysts are nonfunctional, 10% to 15% of such cysts are functional and can rarely manifest as acute parathyroid crisis. Atypical cystic parathyroid adenomas are rare and have an unpredictable clinical course. They exhibit some features of carcinoma but lack the indisputable evidence of malignant disease, such as angioinvasion or metastatic involvement. Treatment options for parathyroid cysts include aspiration, injection of sclerosing agents, and surgical excision.