Textural properties and adsorption behavior of Zn-Mg-Al layered double hydroxide upon crystal violet dye removal as a low cost, effective, and recyclable adsorbent.

The preparation of adsorbents plays a vital role in the adsorption method. In particular, many adsorbents with high specific surface areas and unique shapes are essential for the adsorption strategy. A Zn-Mg-Al/layer double hydroxide (LDH) was designed in this study using a simple co-precipitation process. Adsorbent based on Zn-Mg-Al/LDH was used to remove crystal violet (CV) from the wastewater. The impacts of the initial dye concentration, pH, and temperature on CV adsorption performance were systematically examined. The adsorbents were analyzed both before and after adsorption using FTIR, XRD, and SEM. The roughness parameters and surface morphologies of the produced LDH were estimated using 3D SEM images. Under the best conditions (dose of adsorbent = 0.07 g and pH = 9), the maximum adsorption capacity has been achieved. Adsorption kinetics studies revealed that the reaction that led to the adsorption of CV dye onto Zn-Mg-Al/LDH was a pseudo-second-order model. Additionally, intraparticle diffusion suggests that Zn-Mg-Al/LDH has a fast diffusion constant for CV molecules (0.251 mg/(g min1/2)). Furthermore, as predicted by the Langmuir model, the maximal Zn-Mg-Al/LDH adsorption capacity of CV was 64.80 mg/g. The CV dimensionless separation factor (RL) onto Zn-Mg-Al/LDH was 0.769, indicating that adsorption was favorable. The effect of temperature was performed at 25, 35, and 45 °C in order to establish the thermodynamic parameters ∆Ho, ∆So, and ∆Go. The computed values indicated exothermic and spontaneous adsorption processes. The study presented here might be used to develop new adsorbents with enhanced adsorption capabilities for the purpose of protecting the water environment.

Genome-wide analysis of the emerging infection with Mycobacterium avium subspecies paratuberculosis in the Arabian camels (Camelus dromedarius).

Mycobacterium avium subspecies paratuberculosis (M. ap) is the causative agent of paratuberculosis or Johne's disease (JD) in herbivores with potential involvement in cases of Crohn's disease in humans. JD is spread worldwide and is economically important for both beef and dairy industries. Generally, pathogenic ovine strains (M. ap-S) are mainly found in sheep while bovine strains (M. ap-C) infect other ruminants (e.g. cattle, goat, deer), as well as sheep. In an effort to characterize this emerging infection in dromedary/Arabian camels, we successfully cultured M. ap from several samples collected from infected camels suffering from chronic, intermittent diarrhea suggestive of JD. Gene-based typing of isolates indicated that all isolates belong to sheep lineage of strains of M. ap (M. ap-S), suggesting a putative transmission from infected sheep herds. Screening sheep and goat herds associated with camels identified the circulation of this type in sheep but not goats. The current genome-wide analysis recognizes these camel isolates as a sub-lineage of the sheep strain with a significant number of single nucleotide polymorphisms (SNPs) between sheep and camel isolates (∼1000 SNPs). Such polymorphism could represent geographical differences among isolates or host adaptation of M. ap during camel infection. To our knowledge, this is the first attempt to examine the genomic basis of this emerging infection in camels with implications on the evolution of this important pathogen. The sequenced genomes of M. ap isolates from camels will further assist our efforts to understand JD pathogenesis and the dynamic of disease transmission across animal species.

Pathology and molecular diagnosis of paratuberculosis of camels.

Camels are the prime source of meat and milk in many desert regions of the world including Saudi Arabia. Paratuberculosis of camels, locally called Silag, is a serious and invariably fatal disease in the Arabian camel. Six camels were used in this study. Five camels with clinical paratuberculosis were used to study the pathology of the disease and confirm its aetiology. The sixth camel was clinically healthy and used as a control. The camels were examined clinically and bled for haematological and blood chemistry analysis. They were then humanely killed with a high intravenous dose of thiopental sodium (10 mg/kg) for pathological studies as well as obtaining tissues for microbiological and molecular studies. The clinical signs of the disease were emaciation, diarrhoea, alopecia, wry neck and pale mucous membranes. Laboratory diagnosis showed reduced haemoglobin concentration, low haematocrit and high activity of the serum enzyme alanine aminotransferase. Serum creatinine concentration was normal. These results indicated the infected camels were anaemic and the function of their livers was affected. Postmortem examination showed thickened and corrugated intestinal mucosa, enlarged granulomatous mesenteric lymph nodes, miliary and diffuse granulomas in the liver (in four camels), generalized lymph node granulomas (in one camel), splenic granuloma (in one camel) and mediastinal lymph node granuloma (in two camels). Histopathological examination showed diffuse infiltration of macrophages in all organs showing lesions. Ziehl-Neelsen staining of tissue scraping and tissue sections showed masses of acid fast bacilli, except for the spleen. Infection with Mycobacterium avium subsp. paratuberculosis was confirmed by PCR by targeting the IS900 gene.

Influence of spironolactone treatment on gentamicin-induced nephrotoxicity in rats.

The effect of treatment of rats with gentamicin (80 mg/kg/day for 6 days), oral doses of spironolacatone (20 mg/kg/day for 6 days), and the combined treatment (spironolactone + gentamicin) on renal histology and reduced glutathione (GSH) concentration, and some serum constituents indicative of kidney function were studied. The serum concentrations of creatinine and urea were not significantly affected by spironolactone treatment, but were significantly elevated (P<0.05) by gentamicin administration. The antibiotic treatment also reduced GSH concentration and caused a moderate renal cortical necrosis. However, rats exposed to spironolactone + gentamicin revealed drastic increases in the serum urea and creatinine concentrations amounting to about 1.8 and 2.1 times those of rats treated with gentamicin alone, respectively. The histological examination of slides of the renal cortex of rats exposed to the combined drugs exhibited more extensive necrosis in the tubules when compared to those treated with gentamicin alone. The reduction in GSH induced by gentamicin was unaffected by the concomitant treatment of gentamicin and spironolactone. The concentration of gentamicin accumulated in the renal cortex was significantly larger (twofold) in rats treated concomitantly with spironolactone + gentamicin than in rats treated with gentamicin alone. The present results indicate that spironolactone aggravates gentamicin-induced nephrotoxicity in the rat.