The absorption efficiency of any drug in blood is of prime importance. Compounds having the general formula: Kn[M(FO)2(H2O)2] · xH2O, where (M = Cu(II) or Fe(III), n = 2 or 1, FO = folate anion, x = 2 or 3 with respect), were prepared, and their absorption efficiency in rodent's blood was determined. The obtained compounds were characterized by elemental analysis, infrared as well as thermogravimetric analysis and polarization of light. The results suggest that the two folate complexes were formed in 1 : 2 molar ratio (metal : folic acid) which acted as a bidentate ligand through both carboxylic groups. Polarization of light proved that the folate complexes have symmetric geometry. Biological application proved that Cu(II) and Fe(III) complexes were absorbed more efficiently in rodent blood than folic acid itself.

Copper nanoparticles (nano‐Cu) were electrodeposited on the surface of glassy carbon electrode (GCE) potentiostatically at −0.6 V vs. Ag/AgCl for 60 s. The developed nano‐copper modified glassy carbon electrode (nano‐Cu/GCE) was optimized and utilized for electrochemical assay of chemical oxygen demand (COD) using glycine as a standard. The surface morphology and chemical composition of nano‐Cu/GCE were investigated using scanning electron microscope (SEM) and energy dispersive X‐ray spectrometer (EDX), respectively. The electrochemical behavior was investigated using linear sweep voltammetry (LSV) which is characterized by a remarkable anodic peak at ∼0.6 V, compared to bare GCE. This indicates that nano‐Cu enhances significantly the electrochemical oxidation of glycine. The effect of different deposition parameters, such as Cu2+ concentration, deposition potential, deposition time, pH, and scan rate on the response of the developed sensor were investigated. The optimized nano‐Cu/GCE based COD sensor exhibited a linear range of 15 to 629.3 ppm, and a lower limit of detection (LOD) of 1.7 ppm (S/N=3). This developed method exhibited high tolerance level to chloride ion (0.35 M chloride ion has minimal influence). The analytical utility of the prepared COD sensor was demonstrated by investigating the COD recovery (99.8±4.3) and the assay of COD in different water samples. The results obtained were verified using the standard dichromate method.

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Background:  Cranial neuropathy in rheumatoid arthritis (RA) is relatively rare compared to the frequently reported peripheral neuropathy. Methods:  We investigated the occurrence of subclinical cranial and peripheral nerve involvement in 55 patients with RA. Results:  Patients had a mean age of 43.1 years and a mean duration of illness of 6.4 years. All patients presented with electrophysiological findings suggestive of peripheral neuropathy. In addition, 69.1% of them had entrapment neuropathies, in which carpal tunnel syndrome was the most common (54.6%). Sensorimotor neuropathy at sites other than usual entrapment sites was diagnosed in 70.9%, while bilateral distal sensory neuropathy in lower limbs was identified in 29.1%. Among cranial nerves examined, optic and vestibulocochlear neuropathies were common (29.1% of eyes and 40% of ears examined). Spinal accessory neuropathy was reported in 21.8% of records. Neither facial nor trigeminal nerves were affected. Electrophysiological characteristics of neuropathies were indicative of axon loss. Significant association was identified between neuropathy and patients’ ages (P < 0.01), duration of the illness (P < 0.001), presence of rheumatoid nodules (P < 0.001) and disease stages (P < 0.001). Conclusions:  Our results indicate that cranial and non‐compressive neuropathies are not uncommon in RA. This extends the pathologic disease spectrum. We do not confirm, but suggest the contribution of chronic immune‐mediated vasculitis and/or neurotoxicity in RA neuropathies. Of clinical importance, subclinical neuropathy may never progress and/or be of clinical significance, which contradicts that of comparable diseases, such as systemic lupus erythematosus. Advances in genetics implicate a complex immune genetics which controls susceptibilities and adaptive molecular mechanisms as a culprit of phenotypical heterogenicity among related diseases.