The causative agent of Tuberculosis meningitis is Mycobacterium tuberculosis, which is the bacteria that causes pulmonary tuberculosis. Proliferating into the central nervous system occurs from other sites of infection within the body. Brain damage can result from the infection that may lead to abnormal behavior, mental impairments, motor type paralysis, and seizures. Tuberculosis infections of the central nervous system are a serious and often fatal disease predominantly impacting young children, and is thought to be the most devastating form of the disease. Isoniazid is the only first line bactericidal agent that easily crosses the blood-brain barrier and achieves concentrations in cerebrospinal fluid similar to those in serum. Rifampicin, ethambutol, and streptomycin all penetrate into the cerebrospinal fluid poorly, and even in the setting of meningeal inflammation. As much as one-third of the current world's population may be infected with tuberculosis. Tuberculosis infection of the central nervous system is a serious type of extrapulmonary proliferation of this disease . In developing countries, it has high predominance in children. Pathological manifestations of cerebral tuberculosis occur, of which the most common is tuberculous meningitis, followed by tuberculoma, tuberculous abscess, cerebral miliary tuberculosis, tuberculous encephalopathy, tuberculous encephalitis, and tuberculous arteritis. Brain abscesses of Mycobacterium tuberculosis can induce seizures and coma leading to death and complicated due to multiorgan failure. Rapid diagnosis and early intervention is vital for successful outcome for patients. Further studies are required to understand the proliferation of tuberculosis meningitis in addition to the elucidation of new therapeutic drugs for the successful clinical treatment of this deadly disease.

The effects of the application of potassium ferrate to remove possible toxic compounds are presented. Potassium ferrate (K2FeO4) is shown in this work to be an effective means to remove toxic metals and nonmetals from aqueous solution. The toxic material present in water is precipitated from aqueous solution and readily removed. Potassium ferrate removes itself from solution. Discolored contaminated water may be made clear by utilizing potassium ferrate. In addition, turbidities of solutions induced by dissolved substances are eliminated by the action of potassium ferrate. The efficacy of potassium ferrate in cleaning contaminated water shows great potential in application to municipal and industrial waste water.

One conjugative pathway for the inactivation of endogenous and exogenous hydroxylated aromatic compounds is catalyzed by phenol (aryl) sulfotransferases (PSTs), which esterify phenolic acceptors with sulfate. The tracheobronchial epithelium is commonly exposed to phenolic drugs and pollutants, and metabolic sulfation and PST activity in this tissue have been previously demonstrated. To determine what factors may control PST expression, extracts of serum-free, growth factor-supplemented cultures of bovine bronchial epithelial cells were assayed for PST activity and PST antigen. The most significant finding was dose-dependent, apparent stimulated expression by hydrocortisone (EC50 = 4 nM, maximal stimulation at 20 nM). Time-course experiments, however, revealed progressive loss of PST in the absence of corticosteroid. After decay of extant PST in steroid-free medium, hydrocortisone reinduced the expression of PST three to fivefold. Western blots using mouse anti-bovine PST revealed corresponding increases in 32 kDa PST protein levels in response to hydrocortisone. Steady state kinetic analyses indicated apparent Km values of 1-3 microM for 2-naphthol regardless of culture conditions. These results suggest that detoxification of phenolic compounds by sulfation may be regulated by corticosteroids.

No abstract

The detection and assay of vitamin B-2 (riboflavin) was accomplished under aqueous conditions using sodium borate buffering at pH 7.52 conditions. The absorbance spectrum of riboflavin was determined at different pH values utilizing several buffers. The buffer at pH at 7.52 is followed by accurate and sensitive assay of riboflavin by spectrophotometer at 440 nm wavelength. Where indicated an origin solution (stock) was employed by dissolving sufficient vitamin to make a stock solution of 1.403 × 10−4 molar concentrations. Measurements of various aqueous solutions containing riboflavin were accomplished that included aqueous test samples, vitamin capsules/tablets, and water vitamin mixtures. A standard curve extended from 7.97 × 10−7 molar to 1.23 × 10−4 molar (a 154x folds spread in concentration). The equation of the line was y = 12545x (intercept at origin) with Pearson r correlation of 1.000 (R 2 = 1.000). Concentration of riboflavin assayed ranged from 3.00 × 10−4 gram per liter (0.30 ppm) to 0.0463 gram per liter (46.35 ppm). The B vitamin riboflavin can be assayed by UV/VIS spectrophotometer at 440 nm in aqueous media and using sodium borate buffer at pH 7.52. The assay can reach as low as 0.30 parts per million with high levels of accuracy and sensitivity.