The results suggest that inflammation does not play a significant role in the remote stages of schizophrenia, in contrast to earlier stages of the disease, and the activity of the pathological process decreased in the late stages. These characteristics can reflect the body reactivity in elderly patients.

The objective: of the study was to present the main provisions of a new clinical and biological model of schizophrenia, which establishes links between disorders in the field of biological processes and the formation of positive and negative in the general psychopathological space of schizophrenia on the basis of the analysis of long-term results of clinical and biological research of the Mental Health Research Centre.Material and method: by keywords “schizophrenia”, “biological hypotheses of schizophrenia”, “neuroinflammation”, “neurodegeneration”; “positive disorders”, “negative disorders”, “neuroimmune relationships”, “catabolismof tryptophan”, “activation of microglia”, publications from PubMed/MEDLINE databases, RSCI and other sources were analyzedover the past 10 years in comparison with the results of clinical and biological studies of schizophrenia at the Mental Health Science Center.Results: comparison and analysis of current biological hypotheses of schizophrenia indicates that immunological studies are the most promising for solving the problem of establishing links between disorders of  neurobiological processes and psychopathological specificities of  schizophrenia. Within the framework of the new clinical and biological  model, a key role is assigned to the process of neuroinflammation, which determines the pathogenesis of both negative and positive disorders by various, albeit interrelated, molecular mechanisms. One of these mechanisms,  associated with the development of reversible positive symptom complexes, is based on an imbalance in the neurotransmitter  systems, which is formed as a result of the effect of proinflammatory  cytokines on tryptophan catabolism. Another mechanism that determines the  development of negative symptom complexes is associated with the influence of cytotoxic metabolites on the processes of neurodegeneration. Conclusion:  a new clinical and biological model of schizophrenia establishes a paradigm of the relationship between disorders in the sphere of biological processes determined by neuroinflammation/inflammation and the  formation of the main procedural dimensions — positive and negative disorders in the general psychopathological space of schizophrenia. This model makes it possible to clarify some general provisions related to the pharmacotherapy of schizophrenia and the relief of negative disorders, and also serves as the basis for the development of new approaches to early diagnosis, clinical and social prognosis.

A leukocyte-inhibitory index (LII) is the ratio of the proteolytic enzyme leukocyte elastase (LE) to its inhibitor, an α1- proteinase inhibitor (α1-PI). LII characterizes the activity of the proteolytic system and can be considered as a potential objective criterion that determines both the course and the outcome of the disease. The changes of LII in schizophrenia patients with clinically diagnosed asthenia (schizoasthenia) and patients with schizophrenia without clinical signs of this syndrome were revealed. The objective: to study the possibility of the 95% confidence intervals for a comparative assessment of LII in patients with schizoasthenia and patients with schizophrenia without clinical signs of asthenic syndrome to obtain correct statistical conclusions. Patients and methods: Overall, 95 patients aged 20–55 years with paroxysmal-progressive (F20.x1) and paranoid (F20.00) schizophrenia were examined: 61 patients in the total sample were clinically diagnosed with asthenic symptom-complex. The enzymatic activity of LE and the functional activity of α1-PI were determined in blood serum. LII was calculated according to the formula. The confidence intervals were built using 4 different methods: Fieller’s theorem, delta method, regression methods and bootstrap method. Results: the statistical analysis indicates that the 95% confidence intervals of these indicators for the examined patient groups do not overlap. Therefore, these indicators relate to different populations, which mean the examined groups are characterized by different variants of the ratio of the proteolytic system components. Conclusion: the assessment of LII can serve as an objective statistically correct criterion for presence or absence of asthenic disorder in patients with schizophrenia in addition to clinical examination.

Резюме. В настоящее время моноциты крови разделяют по крайней мере на две фенотипически различные субпопуляции: «классические» моноциты с фенотипом CD14 ++ /CD16и «неклассические» (провоспалительные) с фенотипом CD14 + /CD16 +. Установлено, что моноциты CD14 + /CD16 + , наряду с нейтрофилами крови и микроглиальными клетками мозга, которые являются аналогом моноцит/ макрофагальной системы в мозге, участвуют в развитии скрытого, или так называемого системного, воспаления рассматривают как одно из звеньев нейродегенеративного процесса неинфекционного воспаления в организме человека, нарушения функций моноцитов, лежащего в основе нейровоспалительной гипотезы развития шизофрении. В связи с этим целью настоящего исследования было изучение количества провоспалительных моноцитов у больных юношескими депрессиями по уровню экспрессии рецепторов CD14 + /CD16 + , а также активности лейкоцитарной эластазы и α1-протеиназного ингибитора. Представлялось также интересным определить механизмы их взаимодействия в патогенезе иммуновоспаления, в частности, выявить возможную связь моноцитов CD14 + СD16 + с активностью лейкоцитарной эластазы и α1-протеиназного ингибитора у больных юношескими депрессиями на ранней стадии заболевания. Было обследовано 27 больных мужского пола в возрасте 17-23 лет. Диагностическая оценка заболевания проводилась в соответствии с критериями МКБ-10, согласно которой у всех больных в структуре психопатологических расстройств выявлялаcь депрессия с синдромом аттенуированных психотических симптомов (Attenuated Psychotic Syndrome). В качестве контроля обследовали 12 психически здоровых мужчин соответствующего возраста. Моноциты получали общепринятым способом адгезии к пластиковой поверхности из мононуклеарных клеток, выделенных из периферической венозной крови больных и здоровых центрифугированием в градиенте плотности фиколл-урографина (ρ = 1,077). Изучали в крови больных и здоровых уровень моноцитов с фенотипом CD14 + /CD16 + , энзиматическую активность лейкоцитарной эластазы и функциональную активность α1-протеиназного ингибитора эластазы. В ходе проведенного клинико-лабораторного исследования выявлено повышение более чем в два раза уровня провоспалительной субпопуляции моноцитов CD14 + /CD16 + у больных по сравнению с его уровнем у здоровых индивидуумов, которое сопровождалось увеличением активности лейкоцитарной эластазы и α1-протеиназного ингибитора. Выявлена положительная корреляционная связь между повышением экспрессии поверхностных рецепторов CD14 + /CD16 + на моноцитах и увеличением активности лейкоцитарной эластазы. Эти результаты подтверждают участие моноцитов СD14 + /СD16 + в развитии скрытого или неинфекционного иммунного воспаления, а также определяют механизмы возможного взаимодействия Адрес для переписки:

The purpose of this was to study the dynamics of markers of inflammation and apoptosis in the serum of patients with ischemic stroke in the early post-stroke period. Materials and methods. The study involved 22 patients (mean age 60 ± 5.5 years) with different dynamics of neurological symptoms in the acute post-stroke period. Patients were examined twice: on the 1st and 10th day of observation. Quantitative assessment of the severity of neurological deficit using ESS and NIHSS scales was carried. Enzymatic activity of leukocyte elastase, functional activity of a1-proteinase inhibitor, level of autoantibodies to MBP (inflammatory markers), as well as the content of p53 and Bcl-2 proteins (markers of apoptosis) were determined in serum. The control group consisted of 35 somatically healthy people of the appropriate age and sex. Results. Identified the different features of the spectrum of the analyzed markers of inflammation and apoptosis in patients with positive and negative dynamics of neurological symptoms in the acute period of ischemic stroke assessed according to the ESS and NIHSS scales. The observed clinical and biological relationships reflect the features of the course of the early post-stroke period and can be considered as possible predictors of the development trajectory of acute brain ischemia.