Superior removal of dyes by mesoporous MgO/g-C3N4 fabricated through ultrasound method: Adsorption mechanism and process modeling.

The present research concerns the synthesis of a mesoporous composite characterized with high surface area and superior adsorption capacity in order to investigate its efficacity in removing hazardous and harmful dyes molecules from water. The synthesized mesoporous composite, MgO/g-C3N4 (MGCN), was successfully prepared through the sonication method in a methanolic solution followed by an evaporation and a calcination process. The configuration, crystalline phase, surface properties, chemical bonding, and morphological study of the fabricated nanomaterials were investigated via XRD, BET, FESEM, HRTEM, XPS, and FTIR instrumentation. The obtained nanomaterials were used as sorbents of Congo Red (CR) and Basic Fuchsin (BF) dyes from aqueous solutions. Batch elimination experimental studies reveal that the elimination of CR and BF dyes from an aqueous solution onto the MGCN surface was pH-dependent. The highest removal of CR and BF pollutants occurs, respectively, at pH 5 and 7. The absorptive elimination of CR and BF dyes into the MGCN surface was well-fitted with a pseudo-second-order kinetics and Langmuir model. In this concern, the maximum nanocomposite elimination capacity for CR and BF was observed to be 1250 and 1791 mg g-1, respectively. This investigation confirms that MGCN composite is an obvious and efficient adsorbent of CR, BF, and other organic dyes from wastewater.

Nano selenium protects against deltamethrin-induced reproductive toxicity in male rats.

Greater understanding of the efficiency of nanoparticles will assist future research related to male reproductive performance. The current study was performed to assess the potency of selenium nanoparticles (SeNPs) in alleviating deltamethrin (DLM)-induced detrimental effects on sperm characteristics, oxidative status, sexual behavior, and the histological structure of the testes and epididymis in male rats. Thirty-two male Wister rats were divided into four groups according to treatment received orally by gavage 3 times/week for 60 days; control, DLM (0.6 mg/kg bwt), SeNPs (0.5 mg/kg bwt), and DLM-SeNPs groups. DLM caused a significant reduction in sperm count, motility, and viability percent, as well as in body weight and serum testosterone level, blood total antioxidant capacity (TAC), and glutathione peroxidase (GPx) activity. The DLM-treated group showed a significant increase in blood malondialdehyde (MDA) concentration and sperm abnormalities (%), as well as a significant reduction in sexual activity, manifested as an increase in mount, intromission, or ejaculation latency and a reduction in mount or intromission frequency. These toxic effects were confirmed by histological alterations, represented by a significant reduction in the diameter of the seminiferous tubules and spermatogenesis. Conversely, treatment with SeNPs improved DLM-induced negative effects on sperm characteristics, testosterone, and antioxidant biomarkers, as well as behavioral and histopathological alterations. The SeNPs treated group showed improved semen parameters, antioxidant status, and sexual performance. In conclusion, SeNPs may represent an effective treatment for reducing the detrimental effects of DLM on male fertility, and lead to enhanced male reproductive performance.

Pharmacokinetics of cefquinome in healthy and Pasteurella multocida-infected rabbits.

The pharmacokinetics of cefquinome were studied in healthy and Pasteurella multocida-infected rabbits after a single intramuscular (IM) injection at 2 mg/kg of its sulfate salt. Twelve female New Zealand white rabbits (2.0-2.5 kg) were used; six of them served as controls, and the other six had been infected with P. multocida; the experiments were conducted 1-2 days after nasal inoculation of P. multocida when rabbits showed the signs of respiratory infection. Plasma concentrations of cefquinome were determined using high-performance liquid chromatography. The values of elimination half-life, area under the curve, area under the first moment curve, and mean residence time were significantly lower in infected rabbits (0.48 hr, 4.54 hr*µg/ml, 3.63 hr* hr*µg/ml and 0.8 hr, respectively) than healthy rabbits (0.72 hr, 9.11 hr*µg/ml, 9.85 hr* hr*µg/ml and 1.1 hr, respectively), whereas total body clearance was significantly higher in infected than healthy rabbits. Therefore, P. multocida infection caused significant changes in some of the pharmacokinetic parameters of cefquinome in rabbits. These pharmacokinetic changes may affect dose regimen when used in P. multocida-infected rabbits.

Cyclic adenosine monophosphate and hypertension in rats.

Aortas from spontaneously hypertensive and stress hypertensive rats contained significantly lower intracellular concentrations of cyclic adenosine monophosphate than did their respective controls. Adenylate cyclase activity was normal but was less responsive to stimulation, while phosphodiesterase activity (especially the low Michaelis-Menten constant form) was significantly elevated. Human aortas contained two forms of phosphodiesterase that were similar to those in rat aortas.

Stereo-selective inhibition of transient receptor potential TRPC5 cation channels by neuroactive steroids.

BACKGROUND AND PURPOSE: Transient receptor potential canonical 5 (TRPC5) channels are widely expressed, including in the CNS, where they potentiate fear responses. They also contribute to other non-selective cation channels that are stimulated by G-protein-coupled receptor agonists and lipid and redox factors. Steroids are known to modulate fear and anxiety states, and we therefore investigated whether TRPC5 exhibited sensitivity to steroids. EXPERIMENTAL APPROACH: Human TRPC5 channels were conditionally expressed in HEK293 cells and studied using intracellular Ca2+ measurement, whole-cell voltage-clamp and excised patch techniques. For comparison, control experiments were performed with cells lacking TRPC5 channels or expressing another TRP channel, TRPM2. Native TRPC channel activity was recorded from vascular smooth muscle cells. KEY RESULTS: Extracellular application of pregnenolone sulphate, pregnanolone sulphate, pregnanolone, progesterone or dihydrotestosterone inhibited TRPC5 activity within 1-2min. Dehydroepiandrosterone sulphate or 17ß-oestradiol had weak inhibitory effects. Pregnenolone, and allopregnanolone, a progesterone metabolite and stereo-isomer of pregnanolone, all had no effects. Progesterone was the most potent of the steroids, especially against TRPC5 channel activity evoked by sphingosine-1-phosphate. In outside-out patch recordings, bath-applied progesterone and dihydrotestosterone had strong and reversible effects, suggesting relatively direct mechanisms of action. Progesterone inhibited native TRPC5-containing channel activity, evoked by oxidized phospholipid. CONCLUSIONS AND IMPLICATIONS: Our data suggest that TRPC5 channels are susceptible to relatively direct and rapid stereo-selective steroid modulation, leading to channel inhibition. The study adds to growing appreciation of TRP channels as non-genomic steroid sensors.

Lanthanum inhibition of Vibrio cholerae and Escherichia coli enterotoxin-induced enterosorption and its effects on intestinal mucosa cyclic adenosine 3',5'-monophosphate and cyclic guanosine 3',5'-monophosphate levels.

Several trivalent cations, including lanthanum (La3+), inhibited the secretion (enterosorption) induced by the enterotoxins of Vibrio cholerae and Escherichia coli in the rabbit ileum in vivo. High concentrations (greater than 10 mM) of La3+ were required to inhibit cholera enterotoxin (CE)-induced enterosorption, probably because of the adsorption of the La3+ often potentiated the CE-induced enterosorption. If luminal La3+ exposure followed CE exposure, some recovery of the enterosorptive response was observed. The longer the lag between the CE exposure and the La3+ exposure, the greater was the recovery of the enterosorptive response. Lanthanum inhibited HCO3- secretion more than Cl- secretion. By altering the luminal fluid pH at the time of La3+ exposure, it was found that La3+ was adsorbed to negatively charged luminal sites, having an apparent pK between 2.5 and 3.0. Although La3+ antagonized the enterosorptive response to CE, it mimicked rather than antagonized the cyclic adenosine 3',5'-monophosphate elevation and cyclic guanosine 3',5'-monophosphate depression induced by the toxin. It is therefore concluded that the La3+ inhibition of the CE-induced enterosorption must have occurred at a site following the generation of the cyclic nucleotides. Cholera enterotoxin caused complex time-dependent changes in the mucosal cyclic adenosine 3',5'-monophosphate and cyclic guanosine 3',5'-monophosphate levels, as revealed by studying tissue cyclic adenosine 3',5'-monophosphate/cyclic guanosine 3',5'-monophosphate ratios. The possible roles these two cyclic nucleotides may play in the pathogenesis of the cholera diarrhea are discussed.

Cyclic nucleotides as mediators of drug action.

PIP: Literature on the influence of cyclic nucleotides on the mechanism o f action of various drugs is reviewed. Cyclic nucleotides seem to participate in all aspects of nervous activity and thus mediate the effects of drugs acting on the central nervous system. They also seem to have a role in the actions of drugs on the cardiovascular system, the gastrointestinal tract, smooth muscle activity, and the immune response. The drugs which are discussed whose effects may be mediated by cyclic nucleotides include morphine, apomorphine, ethanol, local anesthetics, drugs affecting cardiac contractility, antihypertensive agents, drugs that reduce intraocular pressure, diuretics, anticancer and antiproliferation drugs, antiinflammatory agents, oral antidiabetic agents, muscle relaxants, carcinogenic agents, and contraceptive agents.^ieng

Changes in cyclic nucleotide metabolism in aorta and heart of neurogenically hypertensive rats: possible trigger mechanism of hypertension.

Changes in cyclic nucleotide metabolism similar to those characteristic of the chronic forms of hypertension were observed in an acute neurogenic form of hypertension in rats produced by electrolytic lesions of the nucleus tractus solitarii. These changes that were evident 2 hr after the lesions were made included decreased cyclic AMP levels in the heart, increased cGMP:cAMP ratio, cAMP phosphodiesterase (3':5'-cAMP 5'-nucleotidohydrolase, EC 3.1.4.17) and guanylyl cyclase (GTP pyrophosphate-lyase (cyclizing), EC 4.6.1.2) activities in the aorta and decreased snesitivity of adenylyl cyclase (ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1) in both the aorta and heart to stimulation by the beta-adrenergic stimulant isoproterenol. These changes appear to depend on catecholamine release and are not due to mechanical distortion secondary to the increased arterial pressure. These studies provide biochemical support to the concept that the sympathetic nervous system may play a critical role in the initiation of the hypertensive syndrome and that chronic hypertension could result from the fixation of the biochemical effects of increased sympathetic activity.

Study of C-reactive protein in bilharziasis and malignancy as causes of ascites.

C-reactive protein titre was estimated in serum and ascitic fluid in 23 patients, 12 with cancer stomach accompanied by liver metastatases and 11 with bilharzial liver fibrosis. The results showed no statistically significant differences between the titre in serum and ascitic fluid in the group of cancer with mean of serum/ascitic level ratio 1.3, while in bilharzial group there was significant difference with ratio mean 6.3.

Studies with tryptophan metabolites in vitro. Kynurenine metabolism in liver homogenates of normal and Schistosoma mansoni-infested mice.

The conversion of kynurenine into kynurenic acid and anthranilic acid in both normal and Schistosoma mansoni-infested mouse liver was investigated. It was found that in the S. mansoni-infested mouse liver there is probably a deficiency of pyridoxal phosphate that resulted in an inhibition of kynurenine transaminase and a low production of kynurenic acid. Deoxypyridoxine and its phosphorylated derivative inhibited kynurenine transaminase in the normal liver in a pattern qualitatively similar to that observed with infested liver. The lowered concentration of pyridoxal phosphate in the infested liver is discussed in view of the possibility of two combined mechanisms: (a) an antimetabolite being secreted by the infesting worms or present in its eggs that partially inhibited the phosphorylation of pyridoxal, and (b) concentration of pyridoxal phosphate by the worms, resulting in a lowered concentration of the cofactor in the host tissue.

Studies with tryptophan metabolites in vitro. Kynurenine metabolism in kidneys of mice infested with Schistosoma mansoni.

The conversion in vitro of kynurenine into kynurenic acid and anthranilic acid in both normal kidneys and those obtained from mice infested with Schistosoma mansoni was investigated. Normal mouse kidneys seem to possess an excess of functional pyridoxal phosphate over those obtained from infested mice. Kynureninase and kynurenine transaminase in the latter kidneys are more easily inhibited by deoxypyridoxal phosphate and tartar emetic, indicating low stores of active pyridoxal phosphate. The possible implication of these findings in relation to the role of the kidneys in producing abnormal patterns of tryptophan metabolism and possibly contributing to the production of bladder tumours in bilharzial patients is discussed.