BeSO4 Research Articles

Differences in Cytokine Expression at Baseline and in Response to Mineral Stimulation by Peripheral Blood Mononuclear Cells from Podoconiosis Cases and Healthy Control Individuals

Epidemiological, histological, and immunogenetic studies suggest that podoconiosis (a non-infectious tropical lymphoedema affecting approximately 4 million people globally) is an HLA class II-associated inflammatory condition that develops in response to an unknown trigger found in volcanic red clay soils. Silicate particles of the kaolinite and aluminum types have been identified in femoral lymph node biopsy samples from endemic area residents, suggesting a possible role in the pathogenesis of podoconiosis. We measured in vitro peripheral blood mononuclear cell cytokine responses (TNF-α, IL-1β, and IFN-γ) to stimulation with the minerals kaolinite, chlorite, and beryllium sulfate (all at 100 µM) using ELISA. Real time PCR was used to measure gene expression of signature cytokines in fresh whole blood, comparing podoconiosis patients and endemic healthy controls. Our results showed that the levels of TNF-α and IL-1β from in vitro cell cultures were significantly higher in unstimulated samples from patients compared to controls (p = 0.04 and p = 0.005, respectively). The minerals kaolinite and chlorite induced two and three-fold higher levels of IL-1β following 24 h of stimulation in healthy controls compared to patients, respectively. We did not find significant differences in mRNA expression of the cytokine genes assayed, though a slight fold increment in IL-1β and TGF-β was observed. In conclusion, our data suggest that the immune system is in a state of persistent activation in vivo in podoconiosis patients, and additional studies of immune regulation and exhaustion are needed to further characterize immune dysfunction in the pathogenesis of the disease. A better understanding of the underlying processes could lead to the development of a ‘biosignature’ detectable in the early reversible stages that could ultimately contribute to the elimination of this preventable, disabling, neglected tropical disease.

MtDNA amplifies beryllium sulfate-induced inflammatory responses via the cGAS-STING pathway in 16HBE cells.

Beryllium sulfate (BeSO4) can cause inflammation through the mechanism, which has not been elucidated. Mitochondrial DNA (mtDNA) is a key contributor of inflammation. With mitochondrial damage, released mtDNA can bind to specific receptors (e.g., cGAS) and then activate related pathway to promote inflammatory responses. To investigate the mechanism of mtDNA in BeSO4-induced inflammatory response in 16HBE cells, we established the BeSO4-induced 16HBE cell inflammation model and the ethidium bromide (EB)-induced ρ016HBE cell model to detect the mtDNA content, oxidative stress-related markers, mitochondrial membrane potential, the expression of the cGAS-STING pathway, and inflammation-related factors. Our results showed that BeSO4 caused oxidative stress, decline of mitochondrial membrane potential, and the release of mtDNA into the cytoplasm of 16HBE cells. In addition, BeSO4 induced inflammation in 16HBE cells by activating the cGAS-STING pathway. Furthermore, mtDNA deletion inhibited the expression of cGAS-STING pathway, IL-10, TNF-α, and IFN-β. This study revealed a novel mechanism of BeSO4-induced inflammation in 16HBE cells, which contributes to the understanding of the molecular mechanism of beryllium and its compounds-induced toxicity.

Hsa_circ_0004214 involved in the epithelial-mesenchymal transition induced by beryllium sulfate through modulating JAK-STAT signaling pathway.

Chronic beryllium disease is characterized by granulomas and pulmonary fibrosis. Recent studies have shown that microRNAs (miRNAs) and circular RNAs (circRNAs) play critical roles in the pathogenesis and development of many diseases. However, the role of miRNAs and circRNAs in pulmonary fibrosis induced by beryllium sulfate (BeSO4) has not been elucidated. Previous studies demonstrated hsa-miR-663b was down-regulated in the 150 μmol/L BeSO4-treated 16HBE cells, while hsa_circ_ 0004214 was up-regulated. Here we found epithelial-mesenchymal transition (EMT) involved in pulmonary fibrosis induced by BeSO4 (4, 8, and 12 mg/kg·BW) in SD rats. Elevated expression of hsa-miR-663b blocked the EMT progression of 16HBE cells induced by 150 μmol/L BeSO4. Notably, the overexpression of hsa-miR-663b decreased the expression of leukemia inhibitory factor (LIF), which was predicted as a target gene of hsa-miR-663b by bioinformatics tools. Furthermore, elevated miR-663b inhibited the activation of the downstream Janus kinase-signal transducers and activators of transcription (JAK-STAT) signaling pathway induced by BeSO4 in 16HBE cells. Previous study suggested that hsa_circ_0004214 had binding sites for hsa-miR-663b. The results indicated hsa_circ_0004214 alleviated the BeSO4-induced EMT via JAK-STAT pathway in 16HBE cells. Collectively, the overexpression of hsa-miR-663b and knockdown of hsa_circ_0004214 attenuated the EMT induced by BeSO4 through the inhibition of JAK-STAT signaling pathway. The aberrant expressed hsa-miR-663b and hsa_circ_0004214 stimulated by BeSO4 may exert an important function in the toxic mechanism of beryllium exposure to 16HBE cells, providing the potential therapeutic targets in chronic beryllium disease.

Hydrogen sulfide alleviates beryllium sulfate-induced ferroptosis and ferritinophagy in 16HBE cells.

Beryllium sulfate (BeSO4 ) can result to lung injuries, such as leading to lipid peroxidation and autophagy, and the treatment of beryllium disease has not been well improved. Ferroptosis is a regulated cell death process driven by iron-dependent and lipid peroxidation, while ferritinophagy is a process mediated by nuclear receptor coactivator 4 (NCOA4), combined with ferritin heavy chain 1 (FTH1) degradation and release Fe2+ , which regulated intracellular iron metabolism and ferroptosis. Hydrogen sulfide (H2 S) has the effects of antioxidant, antiautophagy, and antiferroptosis. This study aimed to investigate the effect of H2 S on BeSO4 -induced ferroptosis and ferritinophagy in 16HBE cells and the underlying mechanism. In this study, BeSO4 -induced 16HBE cell injury model was established based on cellular level and pretreated with deferoxamine (DFO, a ferroptosis inhibitor), sodium hydrosulfide (NaHS, a H2 S donor), or NCOA4 siRNA and, subsequently, performed to detect the levels of lipid peroxidation and Fe2+ and the biomarkers of ferroptosis and ferritinophagy. More importantly, our research found that DFO, NaHS, or NCOA4 siRNA alleviated BeSO4 -induced ferroptosis and ferritinophagy by decreasing the accumulation of Fe2+ and lipid peroxides. Furthermore, the relationship between ferroptosis, ferritinophagy, H2 S, and beryllium disease is not well defined; therefore, our research is innovative. Overall, our results provided a new theoretical basis for the prevention and treatment of beryllium disease and suggested that the application of H2 S, blocking ferroptosis, and ferritinophagy may be a potential therapeutic direction for the prevention and treatment of beryllium disease.

Formation of beryllium oxide nanofibers by polyvinyl alcohol/beryllium sulfate/polyethyleneimine composite precursors

Polyvinyl alcohol (PVA)/beryllium sulfate (BeSO4) precursor nanofibers are fabricated by electrospinning technique, mixing PVA aqueous solution with BeSO4 salt. The productivity is increased by adding polyethyleneimine (PEI) with PVA/BeSO4 spinning solution. The beryllium oxide (BeO) nanofibers are obtained by calcinating the PVA/BeSO4/PEI precursor nanofiber heated at 1000 °C or above. The crystallographic structure of BeO nanofibers is examined by X-ray diffraction. The thermal behaviors of the pure PVA nanofibers, BeSO4 salt, and PVA/BeSO4/PEI precursor nanofibers are studied by thermogravimetry analysis. The BeO nanofiber diameters are reduced with the increase in calcination temperatures. The specific surface area of the PVA/BeSO4/PEI precursor nanofibers is around 36.9 m2 g−1, and that of the BeO nanofibers calcined at 1200 °C is about 11.9 m2 g−1. The pore properties deteriorate due to sintering and blockage as the calcination temperature increases. This work introduces mesoporous BeO nanofibers for the very first time.

LncRNA SNHG11 promotes the malignant transformation of human bronchial epithelial cells induced by beryllium sulfate.

Beryllium and its compounds are carcinogenicity, but the mechanisms through which this occurs have yet to be clarified. Accumulating evidence exists that long noncoding RNAs (lncRNAs) play an important role in occurrence and development of cancer. To explore the carcinogenic mechanism of beryllium, human bronchial epithelial cells (16HBE) were treated with 50 μM beryllium sulfate (BeSO4) for 45 passages (~23weeks). The expression levels of lncRNA SNHG7, SNHG11, SNHG15, MIR22HG, GMPS, and SIK1 were detected at passage 0 (P0), 15 (P15), 25 (P25), 35 (P35), and 45 (P45). The results indicated that enhanced cell proliferation, extensive clones in soft agar, protein expressions of up-regulated matrix metalloproteinase 9 (MMP9), matrix metalloproteinase 2 (MMP2), proliferating cell nuclear antigen (PCNA), cyclin D1, and down-regulated p53 were all observed at the 45th passage in 16HBE cells. Thus, BeSO4-transformed 16HBE cells (T-16HBE) were established. Meanwhile, the study found that the expression of lncRNA SNHG11 was elevated during malignant transformation. Knockdown of SNHG11 in T-16HBE cells blocked cell proliferation, invasion, and migration, and decreased the protein levels of MMP9, MMP2, PCNA, cyclin D1, but increased p53. The studies revealed that SNHG11 acts as an oncogene in the malignant transformation of 16HBE cells induced by BeSO4, which signifies progress in the study of the carcinogenic mechanism of beryllium.

Whole transcriptome analysis of long noncoding RNA in beryllium sulfate-treated 16HBE cells

Beryllium and its compounds can cause pulmonary interstitial fibrosis through mechanisms that are not yet clear. Long non-coding RNA (lncRNA) is implicated in various diseases. The molecular toxicity of beryllium sulfate (BeSO4) was investigated through the RNA-seq analysis of the lncRNA and mRNA whole-transcriptome of BeSO4-treated 16HBE cells. A total of 1014 lncRNAs (535 upregulated and 479 downregulated) and 4035 mRNAs (2224 upregulated and 1811 downregulated) were found to be significantly dysregulated (|logFC| ≥> 2.0, p < 0.05) in the BeSO4-treated groups when compared with the control group. Five differentially expressed lncRNAs and mRNAs were verified by qRT-PCR. KEGG analysis showed that lncRNA regulates the ECM receiver interaction and PI3K/AKT signaling pathways, etc. In addition, H19:17, lnc-C5orf13–1:1, lnc-CRYAA-17:1, lnc-VSTM5–1:11, and lnc-THSD7A-7:1 may regulate BeSO4-induced 16HBE cytotoxicity through ceRNA mechanism. The results of this study will provide some theoretical support for the study of the toxic mechanism of beryllium and its compounds.

Serum-derived exosomes from SD rats induce inflammation in macrophages through the mTOR pathway.

Inhalation of beryllium and its compounds can cause lung injuries, resulting from inflammation and oxidative stress. Multivesicular bodies (MVB), such as exosomes, are membrane vesicles produced by early and late endosomes that mediate intercellular communications. However, the role of exosomes in beryllium toxicity has not been elucidated. This current study aimed to investigate the functional role of exosomes in lung injury resulting from beryllium sulfate (BeSO4 ). Here, Sprague-Dawley (SD) rats were exposed to 4, 8, and 12 mg/kg BeSO4 by nonexposed intratracheal instillation. Murine macrophage (RAW 264.7) cells were pretreated with 50 nmol/L rapamycin (an mTOR signaling pathway inhibitor) for 30 min and then cultured for 24 h with 100 μg/mL exosomes, which had been previously isolated from the serum of 12 mg/kg BeSO4 -treated SD rats. Compared with those of the controls, exposure to BeSO4 in vivo increased LDH activity, elevated levels of inflammatory cytokines (IL-10, TNF-α, and IFN-γ) alongside inflammation-related proteins expression (COX-2 and iNOS), and enhanced secretion of exosomes from the SD rat's serum. Moreover, the BeSO4 -Exos-induced upregulation of LDH activity and inflammatory responses in RAW 264.7 cells can be alleviated following pretreatment with rapamycin. Collectively, these results suggest that serum exosomes play an important role in pulmonary inflammation induced by BeSO4 in RAW 264.7 cells via the mTOR pathway.

Identification of molecular signatures and pathways common to blood cells and brain tissue based RNA-Seq datasets of bipolar disorder: Insights from comprehensive bioinformatics approach

Bipolar disorder (BD), also referred to as manic depression, is a mental illness marked by significant mood fluctuations as well as changes in sleep, energy, thinking, and behavior. About 1% of the world's population is affected by BD. In the United States, roughly 3% of people are thought to be impacted at some point in their lives; female and male percentages appear to be similar. The most prevalent age for the onset of symptoms is 20 years old; early-onset is connected with a worse prognosis. The primary molecular markers for identification and therapeutic target screening have now become a worldwide concern. We looked at gene expression data from brain tissue (RNA-seq) in this work. Transcriptomic analysis of GSE53239 and GSE81396 was implemented to figure out the DEGs. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses were used to perform functional annotation and pathway enrichment analysis of DEGs, respectively. In addition, a protein-protein interaction network was built to find hub proteins (HSPA1A, GNL1, FOSL1, DDX39B, BAG3, ARHGAP11A, MDC1, PRRC2A, VPS52, and DHX16). Subsequently, TFs-DEGs interaction, miRNAs-DEGs interaction, and correlated diseases were also identified. In the brain tissues of BD patients, we discovered possible new linkages between pathogenic processes. Beryllium sulfate exhibited the most negative correlation and ability to reverse BD. As a result, this research provides molecular biomarkers at the RNA and protein levels that may aid in the better understanding of molecular processes, as well as potential pharmacological targets and therapies for the treatment of BD patients.

Circular RNA expression profiles in human bronchial epithelial cells treated with beryllium sulfate.

Circular RNAs (circRNAs), is a novel type of endogenous non-coding RNAs (ncRNAs) participated in the pathogenesis of many diseases. Beryllium is one of the carcinogenesis elements. However, the mechanism and function of circRNAs in human bronchial epithelial cells (16HBE) induced by beryllium sulfate (BeSO4) was rarely reported. Therefore, the high-throughput RNA sequencing analysis was performed to detect the circRNA profiles between control groups and BeSO4-induced groups. Furthermore, circRNA-miRNA-mRNA network, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and PPI network analysis were used for bioinformatics analysis. CircRNA sequencing analysis revealed that 36 circRNAs were up-regulated and 35 circRNAs were down-regulated in the BeSO4-exposed groups. The selected circRNAs were verified by real-time fluorescent quantitative PCR (qRT-PCR). Hsa_circ_0004214 and hsa_circ_0003586 were validated to be up-regulated, hsa_circ_0047958, hsa_circ_0001944, and hsa_circ_0008982 were down-regulated. The circRNA-miRNA-mRNA network annotated the key signaling pathway including cellular senescence, TNF signaling pathway, NF-kappa B signaling pathway, HIF-1 signaling pathway, and Hippo signaling pathway. The PPI network indicated the most circRNAs might participate in the BeSO4 toxicity by acting as a sponge for the miR-663b through JAK-STAT signaling pathway. In summary, our study suggests that circRNAs may play roles in the mechanism of beryllium toxicity.

Proteomic characteristics of beryllium sulfate-induced differentially expressed proteins in rats.

Sprague Dawley rats were exposed to beryllium sulfate (BeSO4), and proteomic and bioinformatic techniques were applied to screen for differentially expressed proteins in their lung tissue and serum. A total of 12 coexpression modules were constructed for 18 samples with 2333 proteins. Four modules were found to have significant differences in the regulation of protein coexpression modules in the serum following exposure to BeSO4. A further three modules had significant differences in the regulation of protein coexpression modules in the lung tissues. Five modules with good correlation were obtained by calculating the gene significance and module membership values, whereas these module Hub proteins included: Hspbp1, Rps15a, Srsf2, Hadhb, Elmo3, Armt1, Rpl18, Afap1L1, Eif3d, Eif3c, and Rps3. The five proteins correlating highest with the Hub proteins in the lung tissue and serum samples were obtained using string analysis. KEGG and GO enrichment analyses showed that these proteins are mainly involved in ribosome formation, apoptosis, cell cycle regulation, and tumor necrosis factor regulation. By analyzing the biological functions of these proteins, proteins that can be used as biomarkers, such as Akt1, Prpf19, Cct2, and Rpl18, are finally obtained.

Hydrogen sulfide alleviates apoptosis and autophagy induced by beryllium sulfate in 16HBE cells.

Beryllium and its compounds are systemic toxicants that are widely applied in many industries. Hydrogen sulfide has been found to protect cells. The present study aimed to determine the protective mechanisms involved in hydrogen sulfide treatment of 16HBE cells following beryllium sulfate-induced injury. 16HBE cells were treated with beryllium sulfate doses ranging between 0 and 300 μM BeSO4 . Additionally, 16HBE cells were subjected to pretreatment with either a 300 μM dose of sodium hydrosulfide (a hydrogen sulfide donor) or 10 mM DL-propargylglycine (a cystathionine-γ-lyase inhibitor) for 6 hr before then being treated with 150 μM beryllium sulfate for 48 hr. This study illustrates that beryllium sulfate induces a reduction in cell viability, increases lactate dehydrogenase (LDH) release, and increases cellular apoptosis and autophagy in 16HBE cells. Interestingly, pretreating 16HBE cells with sodium hydrosulfide significantly reduced the beryllium sulfate-induced apoptosis and autophagy. Moreover, it increased the mitochondrial membrane potential and alleviated the G2/M-phase cell cycle arrest. However, pretreatment with 10 mM DL-propargylglycine promoted the opposite effects. PI3K/Akt/mTOR and Nrf2/ARE signaling pathways are also activated following pretreatment with sodium hydrosulfide. These results indicate the protection provided by hydrogen sulfide in 16HBE cells against beryllium sulfate-induced injury is associated with the inhibition of apoptosis and autophagy through the activation of the PI3K/Akt/mTOR and Nrf2/ARE signaling pathways. Therefore, hydrogen sulfide has the potential to be a promising candidate in the treatment against beryllium disease.

Geochemistry and mineralogy of the sebkha Oum El Khialate evaporites mixtures, southeastern Tunisia

AbstractThis work is meant to study the variation of geochemistry and mineralogy of three salts recuperated from brines of the sebkha Oum El Khialate based on XRF, X‐ray diffraction (XRD), and Fourier transform infrared (FTIR) analyses. Elemental analyses indicate enrichment with major element having an economic interest such as potassium. Compared to standards, minor elements analyses yield high concentrations of hazardous elements such as Cd and Cr, and represent a threat for human consumption. XRD and FTIR analyses display a variable mineralogy along the evaporation path including minerals that are specific for this sebkha, such as vaterite (CaCO3), potassium pentasulphate (K2S5O16), thenardite (Na2SO4), beryllium sulfate (BeSO4), brucite (Mg(OH)2), and mirabilite (Na2SO4·10 H2O). The geochemistry and mineralogy of recuperated salts prove the relevance of the sebkha Oum Khialete as a potential ore resource to be used in industry and agriculture.

Geoeconomic Interest Versus Environmental and Health Issues of the Mineralogical Assemblage of Sebkha Oum El Khialate, Southeastern Tunisia

This work focuses on the formation of evaporite minerals through a progressive evaporation of water of Sebkha Oum El Khialate. The precipitated salt is variable along the evaporation path. Weights of evaporite before each phase of precipitation indicate a heterogeneous evaporation process with a final cumulative amount of 294 g L−1. With an increasing evaporation of Oum El Khialate brine, the number of precipitated mineral species is increased. The cumulative number of species along the evaporation process reaches eight in the following depositional sequence: calcite (CaCO3) (29%), Vaterite (CaCO3) (10%), Potassium Pentasulphate (K2S5O16) (9%), thenardite (Na2SO4) (33%), beryllium sulfate (BeSO4) (10%), brucite (Mg(OH)2) (4%), gypsum (CaSO4·2H2O) (2%) and mirabilite (Na2SO4·10 H2O) (3%). The sebkha can provide 86 kt of evaporite deposits per year at 100% evaporation. These evaporite minerals have variable industrial, medical and military uses. However, beryllium sulfate may cause a health risk to the population including lung cancer. The study shows that the use of a fractional crystallization may decrease the cost of salt extraction and the environmental risks by localizing the crystallization domains of valuable and hazardous minerals.

The expression profile and bioinformatics analysis of microRNAs in human bronchial epithelial cells treated by beryllium sulfate.

Beryllium and its compounds are systemic toxicants that mainly accumulate in the lungs. As a regulator of gene expression, microRNAs (miRNAs) were involved in some lung diseases. This study aimed to analyze the levels of some inflammatory cytokine and the differential expressions of miRNAs in human bronchial epithelial cells (16HBE) induced by berylliumsulfate (BeSO4 ) and to further explore the biological functions of differentially expressed miRNAs. The profile of miRNAs in 16HBE cells was detected using the high-throughput sequencing between the control groups (n=3) and the 150μmol/L of BeSO4 -treated groups (n=3). Bioinformatics analysis of differentially expressed miRNAs was performed, including the prediction of target genes, Gene Ontology (GO) analysis, and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to verify some damage-related miRNAs. We found that BeSO4 can increase the levels of some inflammatory cytokine such as interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), interferon-γ (IFN-γ), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). And BeSO4 altered miRNAs expression of 16HBE cells and a total of 179 differentially expressed miRNAs were identified, including 88 upregulated miRNAs and 91 downregulated miRNAs. The target genes predicted by 28 dysregulated miRNAs were mainly involved in the transcription regulation, signal transduction, MAPK, and VEGF signaling pathway. The qRT-PCR verification results were consistent with the sequencing results. miRNA expression profiling in 16HBE cells exposed to BeSO4 provides new insights into the toxicity mechanism of beryllium exposure.

Features of recording the analytical signal of beryllium using APESI mass-spectrometry and different procedures of sample preparation

The significance of the problem of determining the concentration of beryllium in solutions is substantiated. A method of APESI mass-spectrometry (atmospheric pressure electrospray ionization with in-source atomization) is compared with a number of other common procedures used for solving the aforementioned problem and a number of advantages of APESI mass spectrometry are highlighted. The possibility of measuring the beryllium concentration in various chemical forms using APESI mass-spectrometry is studied. We used sulfate, nitric acid and chloride salts of beryllium. The measurements were carried out on a specialized small-sized mass spectrometer MI-20 «LowMass» developed at MS-Bio Company, Russia. A schematic diagram of the device designed to determine the concentration of beryllium in solutions is presented and described. A technique of solution preparation and measurement procedure are proposed. Presented ass spectra obtained on the samples containing beryllium and lithium isotopes were used as an internal standard. It is shown that beryllium can be detected from the salts of chloride and nitric acids with close relative sensitivity coefficients. The obtained detection limit for beryllium chloride in those measurements was ~1 – 2 × 10–8 M. At the same time, the analytical signal of beryllium cannot be detected during electrospray of the solution of beryllium sulfate under any experimental conditions. It has been suggested that this effect may be attributed to the features of dissolution of beryllium sulfate, in particular, to hydrolysis and formation of complex compounds with sulfate, including complex polymer and colloidal forms.

A simplification of gas clathrate hydrate thermochemistry using the Thermodynamic Difference Rule (TDR). Part 4. Further extension of the TDR to temperatures other than 298 K and validation of the similarity found between inorganic hydrate and clathrate hydrate TDR equations

Abstract This paper continues the investigation of the role of TDR equations as they apply to heat capacity data. A TDR equation is proposed and investigated using heat capacity data for CH4·6H2O, C2H6·7.67H2O, C3H8·17.0H2O, Xe·5.90H2O, Xe·6.29H2O and Kr·6.10H2O Variation of Θ C p ( H 2 O,s - g ) / J K - 1 mol - 1 is examined as a function of temperature, T/K by fitting a linear regression line. The main conclusion of the paper is that the equation: [ C p ( M p X q . n H 2 O,s,T ) - C p ( M p X q ,g,T ) ] = [ 0.1378 T / K + 0.7972 ] n represents a TDR equation capable of yielding an estimate of heat capacity, C p ( M p X q . n H 2 O,s,T ) for any general hydrate (gas hydrate or conventional inorganic hydrate) in the temperature, T/K, range 100–300 K, with errors not usually greater than 10% and often considerably less than this. So vast are the capabilities of the TDR that a proposal is made for the creation of a vast database of entirely self-consistent thermodynamic data for hydrates and their parents without use of further experimental calorimetry. The TDR is used to determine an improved value for the heat capacity of the tetrahydrate of beryllium sulfate: C p ( BeSO 4 · 4 H 2 O,s ) / J K - 1 mol - 1 = 247.1 .

Characterization of α-MoO3 anode with aqueous beryllium sulfate for supercapacitors

α-MoO3 is a well-investigated layer-structured material for intercalation of different ions. Here, for the first time, we utilized Be2+ electrolyte for electrochemical characterization of α-MoO3 for supercapacitor applications. Our studies revealed a minimized detrimental effect of proton (H+) co-intercalation at a high current density 25 Ag−1 resulting in excellent cyclability with a specific capacitance of 169 Fg−1 and a retention of 81% capacitance after 2000 cycles. The electrochemical impedance and ionic diffusion measurements reflected a reduced intercalation of H+ and higher diffusion coefficient of Be2+ as the contributing factors for unusually high and stable capacitance of MoO3 at high current density.

Spectral luminescent properties of 5-(2-hydroxyphenyl)-3-ethyl-1-(pyridin-2-yl)-1Н-1,2,4-triazole and its Be(II) complex

The interaction of 4-oxo-1,3-benzoxazinium perchlorate with 2-pyridylhydrazine has given 5-(2-hydroxyphenyl)-3-ethyl-1-(pyridin-2-yl)-1Н-1,2,4-triazole (L). Boiling of the latter in methanol with 0.5 equiv of beryllium sulfate tetrahydrate has afforded the L2Be metal complex. In contrast to the starting triazole, its beryllium complex exhibits strong violet luminescence (λmaxfl = 431–434 nm, φ = 0.56–0.64).

P53-dependent up-regulation of CDKN1A and down-regulation of CCNE2 in response to beryllium.

Beryllium salts (here, beryllium sulphate) can produce a cytostatic effect in some cell types. The basis for this effect may include increased expression of proliferation inhibitors, reduced expression of proliferation promoters, or both. This study sought to determine the role of p53, the tumour-suppressing transcription factor, in mediating beryllium-induced cytostasis. Human A172 glioma cells express wild-type TP53 gene. Activity of p53 was experimentally manipulated using siRNA and related approaches. Key elements of the beryllium-response were compared in normal and p53-knockdown A172 cells using RT-PCR and Western blotting. In A172 cells, 10μm BeSO4 caused 300% increase in CDKN1A (cyclin-dependent kinase inhibitor p21) mRNA and 90% reduction of CCNE2 (cyclin E2) mRNA. The increased p21 mRNA and reduced cyclin E2 mRNA were each dependent on presence of functional p53. For p21, increased mRNA led to commensurately increased protein levels. In contrast, reduction in cyclin E2 mRNA levels did not lead to corresponding reductions in cyclin E2 protein. The proteasomal inhibitor MG-132 caused p53 protein to increase, but it had no effect on cyclin E2 protein levels. Cycloheximide time course studies indicated that the cyclin E2 protein half-life was more than 12hours in these cells. Beryllium elicited p53-dependent changes in mRNA levels of key determinants of cell proliferation such as p21 and cyclin E2. However, cyclin E2 protein appeared to be aberrantly regulated in this cell type, as its turnover was unexpectedly slow.