Determination Of IgG Concentrations Research Articles

Determination of the Immunoglobulin G Spectrum by Surface-Enhanced Raman Spectroscopy Using Quasispherical Gold Nanoparticles

Background. Immunoglobulins (Ig) are glycoprotein molecules produced by plasma cells in response to antigenic stimuli involved in various physiological and pathological conditions. Intravenous immunoglobulin (IVIG) is a compound whose composition corresponds to Ig concentrations in human plasma, predominantly IgG. It is used as a replacement treatment in immunodeficiencies and as an immunomodulator in inflammatory and autoimmune diseases. The determination of IgG concentrations is useful in the diagnosis of these immunodeficiencies. Surface-enhanced Raman spectroscopy (SERS) is a technique that allows protein quantification in a fast and straightforward way. Objective. This study is aimed at determining the Raman spectrum of IgG at physiological concentrations using quasispherical gold nanoparticles as a SERS substrate. Methods. We initially determined the Raman spectrum of IVIG at 5%. Subsequently, for SERS’ characterization, decreasing dilutions of the protein were made by adding deionized water and an equal volume of the 5 nm gold quasispherical nanoparticle colloid. For each protein concentration, the Raman spectrum was determined using a 10x objective; we focused the 532 and 785 nm laser on the sample surface, in a range of 500-1800 cm-1, with five acquisitions and an acquisition time of 30 seconds. Results. We obtained the IVIG spectrum using SERS up to a concentration of 75 mg/dl. The Raman bands correspond to aromatic amino acid side chains and the characteristic beta-sheet structure of IgG. Conclusion. The use of 5 nm quasispherical gold nanoparticles as a SERS substrate allows for detecting the Raman spectrum of IVIG at physiological concentrations.

Toxoplasmosis and mental disorders in the Russian Federation (with special reference to schizophrenia).

The association of latent toxoplasmosis with mental disorders in general and with schizophrenia in particular was noticed in the mid-1950s. In subsequent years, the role of Toxoplasma gondii was established based on its ability to survive for long periods of time in the nerve cells of the brain. The acute manifestations of the infection include psychopathic symptoms resembling those of schizophrenia. In the former USSR, and in other parts of the world, a number of studies were performed with respect to the association of latent toxoplasmosis and schizophrenia. However, with the dissolution of the USSR at the beginning of the 1990s, studies on the subject were halted due to financial problems and have resumed only recently. The reasons for the resumption of such studies in contemporary Russia are related to the progressively increasing incidence of schizophrenia over the last 25–30 years in the country. According to official data, approximately 550 000 persons reported suffering from the disease in 2014. There are reasons to believe that this is only a fraction of the real burden of the disease. Economically, it cost the state no less than approximately US $10 billion. The purpose of the study was to identify the level of toxoplasmosis seroprevalence in patients with verified diagnoses of schizophrenia in comparison to healthy people in Moscow City and in the Moscow region. A total of 155 persons constituted the patients group and 152 healthy people were in the control group. An integrated approach to the diagnosis and comparison of data from the entire spectrum of serological markers of infection was used, including the detection of specific IgM and the determination of IgG concentrations. It was found that among persons with neuropsychiatric disorders, the incidence of cases with latent toxoplasmosis was higher than in the control group. The effect of toxoplasmosis was significant and similar for men and women. Further statistical analyses revealed that among patients with a diagnosis of schizophrenia, the incidence of latent toxoplasmosis was significantly higher than in the control group. These data are in agreement with the results of similar studies in other countries.

Transcytosis of IgG anti-D by human term trophoblast cells in culture.

Placental trophoblast cells were cultured on filters that allow access to medium bathing the apical and basal surfaces of cells. Purified human IgG was added to either the apical or the basal chambers and sampled at intervals of up to 100min for determination of IgG concentration by ELISA. Using this experimental system, transport of IgG1 and IgG3 monoclonal anti-D, affinity-purified polyclonal anti-D and human polyclonal IgG were shown to occur primarily in the apical to basal (i.e. maternal to fetal) direction. The overall transport of monoclonal and polyclonal anti-D was less than 10% in 45 min, several times lower than that of IgG. There was no difference in the rate or percentage of transport between IgG1 (BRAD-5) and IgG3 (BRAD-3) monoclonal anti-D. The possibility that the Fc receptor mediating transcytosis of IgG anti-D through human trophoblast cells in culture is the placental hFcRn is proposed.

Immunoglobulin G in serum and cerebrospinal fluid from epileptic patients treated with phenytoin.

Concentrations of IgG and titres of IgG antibodies to rabbit erythrocytes were studied in serum and cerebrospinal fluid (CSF) from 21 phenytoin-treated patients; 11 of these had reduced serum IgA. The CSF IgG concentration was not reduced in any patient. A reduction of CSF IgG has been found earlier in phenytoin-treated patients, when other antisera to IgG were used for the determination of IgG concentration. The present findings therefore indicate that an alteration of the composition or quality of the CSF IgG is present in phenytoin-treated patients. 1 patient had a phenytoin-induced low serum concentration of IgG and IgA. In this patient the ratios CSF:serum were normal both for IgG concentration and for IgG antibodies to rabbit erythrocytes.