Sodium fluoride suppresses spleen development through MAPK/ERK signaling pathway in mice.

Numerous studies have documented that excessive fluoride intake could cause pathological damage and functional disorder in organisms. Nevertheless, the systemic mechanism of fluorosis inhibiting the proliferation and development of splenic cell is still scarce. The preliminary studies have confirmed that high-dose NaF could inhibit splenic lymphocytes proliferation in vitro and cause toxic effects on spleen development in vivo.

Voltage-Gated Sodium Channels Are Involved in Cognitive Impairments in Parkinson's Disease- like Rats.

Cognitive impairment is one of the common non-motor symptoms in Parkinson's disease (PD). The hippocampus is a critical structure for learning and memory processes. The abnormal synaptic plasticity in the hippocampus is suggested to be associated with cognitive dysfunction in PD.

Sodium fluoride impairs splenic innate immunity via inactivation of TLR2/MyD88 signaling pathway in mice.

Fluoride is known to affect the inflammatory process and autoregulation of immune responses, but the molecular mechanism by which fluoride causes innate immune injury remain largely unknown. Also, studies on sodium fluoride (NaF)-caused alteration of TLR signaling are still lacking. In the present study, we examined the effects of NaF on the mRNA and protein expression levels of TLR2/MyD88 signaling pathway molecules in the mouse spleen by using the methods of qRT-PCR and Western blotting.

Sodium Fluoride Arrests Renal G2/M Phase Cell-Cycle Progression by Activating ATM-Chk2-P53/Cdc25C Signaling Pathway in Mice.

Background/aims: Excessive fluoride intake can induce cytotoxicity, DNA damage and cell-cycle changes in many tissues and organs, including the kidney. However, the underlying molecular mechanisms of fluoride-induced renal cell-cycle changes are not well understood at present. In this study, we used a mouse model to investigate how sodium fluoride (NaF) induces cell-cycle changes in renal cells.

Re-expression of voltage-gated sodium channel subtype Nav1.3 in the substantia nigra after dopamine depletion.

Abnormal synchronized oscillatory bursts occurring in the basal ganglia (BG) are suggested to be correlated with motor symptoms in Parkinson's disease (PD) patients and animal models of PD. Voltage-gated sodium channels (VGSCs) have been demonstrated to play an important role in the abnormal electrical activity of neurons in the BG. Nav1.

Sodium Fluoride (NaF) Induces Inflammatory Responses Via Activating MAPKs/NF-κB Signaling Pathway and Reducing Anti-inflammatory Cytokine Expression in the Mouse Liver.

At present, no reports are focused on fluoride-induced hepatic inflammatory responses in human beings and animals. This study aimed to investigate the mRNA and protein levels of inflammatory cytokines and signaling molecules for evaluating the effect of different doses (0, 12, 24, and 48 mg/kg) of sodium fluoride (NaF) on inflammatory reaction in the mouse liver by using methods of experimental pathology, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot analysis. We found that NaF in excess of 12 mg/kg caused the hepatic inflammatory responses, and the results showed that NaF activated the mitogen-activated protein kinases (MAPKs) signaling pathway by markedly increasing (p < 0.

Sodium fluoride induces splenocyte autophagy via the mammalian targets of rapamycin (mTOR) signaling pathway in growing mice.

Fluoride is known to impair organism's development and function via adverse effects, and autophagy plays a regulation role in human or animal health and disease. At present, there are no reports focused on fluoride-induced autophagy in the animal and human spleen. The objective of this study was to investigate sodium fluoride (NaF)-induced splenocyte autophagy and the potential mechanism via regulation of p-mTOR in growing mice by using the methods of transmission electron microscopy (TEM), immunohistochemistry (IHC), quantitative real-time polymerase chain reaction (qRT-PCR) and western blot.

Sodium fluoride causes hepatocellular S-phase arrest by activating ATM-p53-p21 and ATR-Chk1-Cdc25A pathways in mice.

In this study, experimental pathology, flow cytometry (FCM), quantitative real-time polymerase chain reaction (qRT-PCR), and western blot (WB) were used to evaluate the effects of sodium fluoride (NaF) on hepatocellular cell cycle progression in mice. A total of 240 ICR mice were divided equally into four groups; the experimental groups received 12, 24, or 48 mg/kg NaF intragastrically for 42 days, while the control group received distilled water. Doses of NaF above 12 mg/kg increased the percentage of cells in S phase (S-phase arrest), reduced percentages of cells in G0/G1 or G2/M phase, and activated the ATM-p53-p21 and ATR-Chk1-Cdc25A pathways.

Sodium fluoride induces apoptosis in mouse splenocytes by activating ROS-dependent NF-κB signaling.

In this study, we investigated the roles of reactive oxygen species (ROS) and nuclear factor-κB (NF-κB) signaling in sodium fluoride-induced DNA damage and apoptosis in mouse splenocytes. Intragastric administration of 12, 24 or 48 mg/kg sodium fluoride resulted in a time- and dose-dependent increase in DNA fragmentation and apoptosis in mouse splenocytes on days 21 and 42. High ROS levels correlated with increased levels of phosphorylated IκB kinase and NF-κB p65 and decreased levels of inhibitory kappa B protein in splenocytes from mice treated with sodium fluoride.

Effects of sodium fluoride on blood cellular and humoral immunity in mice.

Exposure to high fluorine can cause toxicity in human and animals. Currently, there are no systematic studies on effects of high fluorine on blood cellular immunity and humoral immunity in mice. We evaluated the alterations of blood cellular immunity and humoral immunity in mice by using flow cytometry and ELISA.

Sodium fluoride induces renal inflammatory responses by activating NF-κB signaling pathway and reducing anti-inflammatory cytokine expression in mice.

Fluoride is widely distributed in the environment and often results in adverse health effects on animals and human beings. It has been proved that fluoride can induce inflammatory responses . However, very limited reports are focused on fluoride-induced inflammatory responses .

Anticonvulsant effect of gentamicin on the seizures induced by kainic acid.

Objective:  Epilepsy is a chronic neurological disorder affecting approximately 0.5-2% of the population worldwide. Gentamicin (GM) is an aminoglycoside antibiotic used to treat several types of bacterial infections.

Histopathological findings of renal tissue induced by oxidative stress due to different concentrations of fluoride.

It has been reported that excessive intake of fluoride can induce renal lesions. However, its pathogenesis is still less understood. Therefore, this study was conducted to investigate oxidative damage and the relationships between the oxidative damage and renal lesions in fluoride-treated mice by using the methods of histopathology, biochemistry, flow cytometry and quantitative real-time polymerase chain reaction (qRT-PCR).

Sodium fluoride causes oxidative stress and apoptosis in the mouse liver.

The current study was conducted to investigate the effect of sodium fluoride (NaF) on the oxidative stress and apoptosis as well as their relationship in the mouse liver by using methods of flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR), western blot, biochemistry and experimental pathology. 240 four-week-old ICR mice were randomly divided into 4 groups and exposed to different concentration of NaF (0 mg/kg, 12 mg/kg, 24 mg/kg and 48 mg/kg) for a period of 42 days. The results showed that NaF caused oxidative stress and apoptosis.

Effectively infinite optical path-length created using a simple cubic photonic crystal for extreme light trapping.

A 900 nm thick TiO simple cubic photonic crystal with lattice constant 450 nm was fabricated and used to experimentally validate a newly-discovered mechanism for extreme light-bending. Absorption enhancement was observed extending 1-2 orders of magnitude over that of a reference TiO film. Several enhancement peaks in the region from 600-950 nm were identified, which far exceed both the ergodic fundamental limit and the limit based on surface-gratings, with some peaks exceeding 100 times enhancement.

Transient upregulation of Nav1.6 expression in the genu of corpus callosum following middle cerebral artery occlusion in the rats.

Focal ischemic stroke can lead to brain damage and cause human disability and death. Increased excitatory transmission and reduced neuronal inhibition are important pathological alterations in the cerebral ischemia, which can induce abnormal brain excitability. Nav1.

Sodium fluoride (NaF) induces the splenic apoptosis via endoplasmic reticulum (ER) stress pathway and .

At present, there are no reports on the relationship between fluoride-induced apoptosis and endoplasmic reticulum (ER) stress (ER stress) in the spleen of human and animals and . Therefore, the aim of this study was to define sodium fluoride (NaF)-induced apoptosis mediated by ER stress in the spleen of mice and . Apoptosis and expression levels of the ER stress-related proteins were detected by flow cytometry and western blot, respectively.

Sodium fluoride (NaF) causes toxic effects on splenic development in mice.

At present, very limited studies focus on the toxic effect of sodium fluoride (NaF) on splenic development of human and animals in vivo. This study was firstly designed to evaluate the toxic effects of NaF on the splenic development of mice in vivo by observing histopathological lesions, changes of splenic growth index (GI), T and B cells, immunoglobulin A (IgA), immunoglobulin G (IgG) and immunoglobulin M (IgM) contents, cytokine protein expression levels, and cell cycle and cyclins/cdks protein expression levels using the methods of pathology, flow cytometry (FCM), western blot (WB), and enzyme-linked immunosorbent assay (ELISA). A total of 240 ICR mice were equally allocated into four groups with intragastric administration of distilled water in the control group and 12, 24, 48 mg/kg NaF solution in the experimental groups for 42 days.

Sodium fluoride induces apoptosis in cultured splenic lymphocytes from mice.

Though fluorine has been shown to induce apoptosis in immune organs in vivo, there has no report on fluoride-induced apoptosis in the cultured lymphocytes. Therefore, this study was conducted with objective of investigating apoptosis induced by sodium fluoride (NaF) and the mechanism behind that in the cultured splenic lymphocytes by flow cytometry, western blot and Hoechst 33258 staining. The splenic lymphocytes were isolated from 3 weeks old male ICR mice and exposed to NaF (0, 100, 200, and 400 μmol/L) in vitro for 24 and 48 h.

Suppressive effects of sodium fluoride on cultured splenic lymphocyte proliferation in mice.

Fluoride-induced immunotoxicity has been documented in vivo, but limited reports have focused on the effects of fluoride on lymphocytes in vitro. Therefore, we have examined the suppressive effects of sodium fluoride on cultured splenic lymphocytes in mice. CD3+ T lymphocytes, CD19+ B lymphocytes, cytokines, and cell-cycle markers were analyzed through the use of a cell-counting kit, western blot, and flow cytometery.

Glutamine deprivation plus BPTES alters etoposide- and cisplatin-induced apoptosis in triple negative breast cancer cells.

Glutamine provides cancer cells with the energy required to synthesize macromolecules. Methods which block glutamine metabolism in treatment of breast cancer inhibit oncogenic transformation and tumor growth. We investigated whether inhibiting glutamine metabolism produces effects that are synergistic with those produced by drugs which damage DNA in triple-negative breast cancer cells.

Achieving an Accurate Surface Profile of a Photonic Crystal for Near-Unity Solar Absorption in a Super Thin-Film Architecture.

In this work, a teepee-like photonic crystal (PC) structure on crystalline silicon (c-Si) is experimentally demonstrated, which fulfills two critical criteria in solar energy harvesting by (i) its Gaussian-type gradient-index profile for excellent antireflection and (ii) near-orthogonal energy flow and vortex-like field concentration via the parallel-to-interface refraction effect inside the structure for enhanced light trapping. For the PC structure on 500-μm-thick c-Si, the average reflection is only ∼0.7% for λ = 400-1000 nm.

Multitarget, quantitative nanoplasmonic electrical field-enhanced resonating device (NE2RD) for diagnostics.

Recent advances in biosensing technologies present great potential for medical diagnostics, thus improving clinical decisions. However, creating a label-free general sensing platform capable of detecting multiple biotargets in various clinical specimens over a wide dynamic range, without lengthy sample-processing steps, remains a considerable challenge. In practice, these barriers prevent broad applications in clinics and at patients' homes.

Light trapping and near-unity solar absorption in a three-dimensional photonic-crystal.

We report what is to our knowledge the first observation of the effect of parallel-to-interface-refraction (PIR) in a three-dimensional, simple-cubic photonic-crystal. PIR is an acutely negative refraction of light inside a photonic-crystal, leading to light-bending by nearly 90 deg over broad wavelengths (λ). The consequence is a longer path length of light in the medium and an improved light absorption beyond the Lambertian limit.

Metal-nanowall grating transparent electrodes: achieving high optical transmittance at high incident angles with minimal diffraction.

A novel architecture has been employed to fabricate transparent electrodes with high conductivity and high optical transmittance at high incident angles. Soft lithography is used to fabricate polymer grating patterns onto which thin metallic films are deposited. Etching removes excess metal leaving tall walls of metal.