The development of attenuation compensation models of fluorescence spectroscopy signals

This study examines the effect of blood absorption on the endogenous fluorescence signal intensity of biological tissues. Experimental studies were conducted to identify these effects. To register the fluorescence intensity, the fluorescence spectroscopy method was employed. The intensity of the blood flow was measured by laser Doppler flowmetry. We proposed one possible implementation of the Monte Carlo method for the theoretical analysis of the effect of blood on the fluorescence signals. The simulation is constructed as a four-layer skin optical model based on the known optical parameters of the skin with different levels of blood supply. With the help of the simulation, we demonstrate how the level of blood supply can affect the appearance of the fluorescence spectra. In addition, to describe the properties of biological tissue, which may affect the fluorescence spectra, we turned to the method of diffuse reflectance spectroscopy (DRS). Using the spectral data provided by the DRS, the tissue attenuation effect can be extracted and used to correct the fluorescence spectra

Detection of angiospastic disorders in the microcirculatory bed using laser diagnostics technologies

The evaluation of the microcirculatory bed functional state and the identification of angiospastic disorders with related complications, when the pathological changes are reversible, have an important role in medical practice. The aim of this study was to evaluate the possibility of using optical noninvasive methods and the cold pressor test to solve this problem. A total of 33 patients with rheumatological diseases and 32 healthy volunteers were included in the study. Laser Doppler flowmetry, tissue reflectance oximetry and pulse oximetry were used as optical noninvasive methods. The parameters were recorded before, immediately after and 20(Formula presented.)min after the cold pressor test. Based on the measured parameters, the complex parameters of the microcirculatory bed were calculated. A detailed statistical analysis of the parameter changes for each individual in the two groups displayed diverse microcirculatory bed parameter responses upon cold exposure, with differing recovery of parameters after CPT. New diagnostic criteria were proposed for the identification of angiospastic disorders. According to the proposed criteria, 27 people of the volunteers group were confirmed to not display any disorders. In the patient group, however, 18 people were observed to have a relatively normal functional state of the microcirculatory bed, while 15 people were observed to have a possible tendency to angiospasm. To highlight the differences between a relatively normal state and presence of angiospastic disorders, statistical analysis of experimental data was carried out, which revealed significant differences. Further analysis of data with angiospastic disorders identified a relationship between their diagnoses and the results of laboratory studies. Thus, the evaluation of combined noninvasive optical diagnostic method use, the cold pressor test and proposed diagnostic criteria showed a positive result. This approach can be used to detect the presence of possible angiospastic disorders and related complications, as well as microcirculatory bed disorders against the background of other diseases

Laser Doppler flowmetry in blood and lymph monitoring, technical aspects and analysis

The aim of this work was to study the possibilities of the laser Doppler flowmetry method for the joint study of microhaemo- and lymph circulation of human skin. Conducting a series of experimental studies allowed to trace the relationship of recorded signals of microcirculation of blood flow and lymph flow, as well as to study their oscillation nature by using wavelet analysis

The blood perfusion and NADH/FAD content combined analysis in patients with diabetes foot

Skin blood microcirculation and the metabolism activity of tissue were examined on the patients with type 2 diabetes. Laser Doppler flowmetry (LDF) with 1064 nm laser light source and fluorescence spectroscopy (FS) with excitation light of 365 nm and 450 nm have been used to monitor the blood perfusion and the content of coenzymes NADH and FAD. Concluding, the proposed combined LDF and tissue FS approach allows to identify the significant violations in the blood microcirculation and metabolic activity for type 2 diabetes patients

Multimodal optical measurement for study of lower limb tissue viability in patients with diabetes mellitus

According to the International Diabetes Federation, the challenge of early stage diagnosis and treatment effectiveness monitoring in diabetes is currently one of the highest priorities in modern healthcare. The potential of combined measurements of skin fluorescence and blood perfusion by the laser Doppler flowmetry method in diagnostics of low limb diabetes complications was evaluated. Using Monte Carlo probabilistic modeling, the diagnostic volume and depth of the diagnosis were evaluated. The experimental study involved 76 patients with type 2 diabetes mellitus. These patients were divided into two groups depending on the degree of complications. The control group consisted of 48 healthy volunteers. The local thermal stimulation was selected as a stimulus on the blood microcirculation system. The experimental studies have shown that diabetic patients have elevated values of normalized fluorescence amplitudes, as well as a lower perfusion response to local heating. In the group of people with diabetes with trophic ulcers, these parameters also significantly differ from the control and diabetes only groups. Thus, the intensity of skin fluorescence and level of tissue blood perfusion can act as markers for various degrees of complications from the beginning of diabetes to the formation of trophic ulcers

The Cytotoxin-Associated Gene A (CagA) of Helicobacter pylori: the Paradigm of an Oncogenic Virulence Factor

Helicobacter pylori is a microaerophilic, spiral-shaped and gram-negative microorganism that produces various virulence factors such as CagA, VacA, urease, and host cells adhesins, which in a synchronous concert, allow H. pylori to colonize and infect the host gastric epithelium. H. pylori infection is associated with some severe side effects in human, such as gastritis, peptic ulcer, non-Hodgkin’s lymphoma and adenocarcinoma. CagA is the most notorious virulence factor of H. pylori. It is known as the first bacterial oncoprotein. The gene encoding CagA is localized on the cag pathogenicity island (cagPAI), a 40kbp DNA segment which also carries genes for the type four secretion system (T4SS) of H. pylori. The interaction of CagA with intracellular partner proteins leads to some irreversible alteration of host cells by increasing cell size, elevating motility, phenomena known as the “hummingbird phenotype”. CagA also disrupts the epithelium apical junctions and thereby destroys the normal epithelial architecture. A tyrosine phosphorylation site, named EPIYA motif, helps CagA to bind to cytosolic proteins in a phosphorylation-dependent manner. CagA is also interacts with host proteins in a phosphorylation-independent fashion, which altogether will assist to develop adenocarcinoma in infected cells. This review summarizes the core data on the structure and function of CagA and its role in conferring the main pathophysiologic effects of H. pylori infection as well as suggesting a therapeutic option for treatment of H. pylori infection based on CagA virulence

The Cytotoxin-Associated Gene A (CagA) of Helicobacter pylori: the Paradigm of an Oncogenic Virulence Factor

Helicobacter pylori is a microaerophilic, spiral-shaped and gram-negative microorganism that produces various virulence factors such as CagA, VacA, urease, and host cells adhesins, which in a synchronous concert, allow H. pylori to colonize and infect the host gastric epithelium. H. pylori infection is associated with some severe side effects in human, such as gastritis, peptic ulcer, non-Hodgkin’s lymphoma and adenocarcinoma. CagA is the most notorious virulence factor of H. pylori. It is known as the first bacterial oncoprotein. The gene encoding CagA is localized on the cag pathogenicity island (cagPAI), a 40kbp DNA segment which also carries genes for the type four secretion system (T4SS) of H. pylori. The interaction of CagA with intracellular partner proteins leads to some irreversible alteration of host cells by increasing cell size, elevating motility, phenomena known as the “hummingbird phenotype”. CagA also disrupts the epithelium apical junctions and thereby destroys the normal epithelial architecture. A tyrosine phosphorylation site, named EPIYA motif, helps CagA to bind to cytosolic proteins in a phosphorylation-dependent manner. CagA is also interacts with host proteins in a phosphorylation-independent fashion, which altogether will assist to develop adenocarcinoma in infected cells. This review summarizes the core data on the structure and function of CagA and its role in conferring the main pathophysiologic effects of H. pylori infection as well as suggesting a therapeutic option for treatment of H. pylori infection based on CagA virulence

Цитотоксин-ассоциированный ген А (CagA) Helicobacter pylori: парадигма онкогенного фактора вирулентности

Helicobacter pylori is a microaerophilic, spiral-shaped and gram-negative microorganism that produces various virulence factors such as CagA, VacA, urease, and host cells adhesins, which in a synchronous concert, allow H. pylori to colonize and infect the host gastric epithelium. H. pylori infection is associated with some severe side effects in human, such as gastritis, peptic ulcer, non-Hodgkin’s lymphoma and adenocarcinoma. CagA is the most notorious virulence factor of H. pylori. It is known as the first bacterial oncoprotein. The gene encoding CagA is localized on the cag pathogenicity island (cagPAI), a 40kbp DNA segment which also carries genes for the type four secretion system (T4SS) of H. pylori. The interaction of CagA with intracellular partner proteins leads to some irreversible alteration of host cells by increasing cell size, elevating motility, phenomena known as the “hummingbird phenotype”. CagA also disrupts the epithelium apical junctions and thereby destroys the normal epithelial architecture. A tyrosine phosphorylation site, named EPIYA motif, helps CagA to bind to cytosolic proteins in a phosphorylation-dependent manner. CagA is also interacts with host proteins in a phosphorylation-independent fashion, which altogether will assist to develop adenocarcinoma in infected cells. This review summarizes the core data on the structure and function of CagA and its role in conferring the main pathophysiologic effects of H. pylori infection as well as suggesting a therapeutic option for treatment of H. pylori infection based on CagA virulenceHelicobacter pylori – это микроаэрофильная, спиралевидная, грамотрицательная бактерия, которая производит различные факторы вирулентности, такие как CagA, VacA, уреаза, а также адгезины, которые обеспечивают адгезию к клетке-хозяину. Синхронизированное взаимодействие факторов вирулентности позволяет H. pylori колонизировать и инфицировать эпителий желудка хозяина. Инфицирование организма человека H. pylori вызывает ряд побочных эффектов, таких как гастрит, язвенная болезнь желудка и двенадцатиперстной кишки, неходжкинская лимфома и аденокарцинома. CagA является наиболее печально известным фактором вирулентности H. pylori и признан первым бактериальным онкогеном. Он расположен на островке патогенности cag (cagPAI) – сегменте ДНК размером 40 т.п.н., который также содержит гены системы секреции четвертого типа (T4SS) H. pylori. Взаимодействие CagA с внутриклеточными белками-партнерами приводит к некоторым необратимым изменениям в клетках хозяина (увеличение их размера, повышение подвижности клеток), а также возникновению в клетках феномена, известного под названием «фенотип колибри». CagA также разрушает соединения в апикальном полюсе эпителиальных клеток, и тем самым разрушает нормальную архитектуру эпителия. Сайт фосфорилирования тирозина, называемый EPIYA мотивы, помогает CagA связываться с цитозольными белками фосфорилированно-зависимым образом. Также CagA может взаимодействовать с белками хозяина фосфорилированно-независимым способом, что в совокупности способствует развитию аденокарциномы в инфицированных клетках. В данном обзоре обобщены основные данные о структуре и функциях CagA, его роли в развитии основных патофизиологических эффектов в результате инфицирования H. pylori, а также о терапевтическом варианте лечения инфекции, вызываемой H. pylori, содержащей CagA фактор вирулентност

Цитотоксин-ассоциированный ген А (CagA) Helicobacter pylori: парадигма онкогенного фактора вирулентности

Helicobacter pylori is a microaerophilic, spiral-shaped and gram-negative microorganism that produces various virulence factors such as CagA, VacA, urease, and host cells adhesins, which in a synchronous concert, allow H. pylori to colonize and infect the host gastric epithelium. H. pylori infection is associated with some severe side effects in human, such as gastritis, peptic ulcer, non-Hodgkin’s lymphoma and adenocarcinoma. CagA is the most notorious virulence factor of H. pylori. It is known as the first bacterial oncoprotein. The gene encoding CagA is localized on the cag pathogenicity island (cagPAI), a 40kbp DNA segment which also carries genes for the type four secretion system (T4SS) of H. pylori. The interaction of CagA with intracellular partner proteins leads to some irreversible alteration of host cells by increasing cell size, elevating motility, phenomena known as the “hummingbird phenotype”. CagA also disrupts the epithelium apical junctions and thereby destroys the normal epithelial architecture. A tyrosine phosphorylation site, named EPIYA motif, helps CagA to bind to cytosolic proteins in a phosphorylation-dependent manner. CagA is also interacts with host proteins in a phosphorylation-independent fashion, which altogether will assist to develop adenocarcinoma in infected cells. This review summarizes the core data on the structure and function of CagA and its role in conferring the main pathophysiologic effects of H. pylori infection as well as suggesting a therapeutic option for treatment of H. pylori infection based on CagA virulenceHelicobacter pylori – это микроаэрофильная, спиралевидная, грамотрицательная бактерия, которая производит различные факторы вирулентности, такие как CagA, VacA, уреаза, а также адгезины, которые обеспечивают адгезию к клетке-хозяину. Синхронизированное взаимодействие факторов вирулентности позволяет H. pylori колонизировать и инфицировать эпителий желудка хозяина. Инфицирование организма человека H. pylori вызывает ряд побочных эффектов, таких как гастрит, язвенная болезнь желудка и двенадцатиперстной кишки, неходжкинская лимфома и аденокарцинома. CagA является наиболее печально известным фактором вирулентности H. pylori и признан первым бактериальным онкогеном. Он расположен на островке патогенности cag (cagPAI) – сегменте ДНК размером 40 т.п.н., который также содержит гены системы секреции четвертого типа (T4SS) H. pylori. Взаимодействие CagA с внутриклеточными белками-партнерами приводит к некоторым необратимым изменениям в клетках хозяина (увеличение их размера, повышение подвижности клеток), а также возникновению в клетках феномена, известного под названием «фенотип колибри». CagA также разрушает соединения в апикальном полюсе эпителиальных клеток, и тем самым разрушает нормальную архитектуру эпителия. Сайт фосфорилирования тирозина, называемый EPIYA мотивы, помогает CagA связываться с цитозольными белками фосфорилированно-зависимым образом. Также CagA может взаимодействовать с белками хозяина фосфорилированно-независимым способом, что в совокупности способствует развитию аденокарциномы в инфицированных клетках. В данном обзоре обобщены основные данные о структуре и функциях CagA, его роли в развитии основных патофизиологических эффектов в результате инфицирования H. pylori, а также о терапевтическом варианте лечения инфекции, вызываемой H. pylori, содержащей CagA фактор вирулентност

The study of galectin-3, Ki-67, ubiquitin, HMGA-2 by polymerase chain reaction in real time (RT-PCR) in the puncture specimens of nodular goiter

Actuality. The differential diagnosis of follicular adenoma, follicular variant of papillary thyroid cancer and follicular thyroid cancer (TC) is one of the main topics of research. For this purpose several molecular markers were approbated, however their diagnostic effectiveness differs. Aim. Quantification of candidate mRNA markers for differentiated thyroid cancer (galectin-3, Ki-67, ubiquitin, HMGA2) using polymerase chain reaction in real time (RT-PCR) of thyroid nodules pre-operative material. To evaluate the efficiency of this method for thyroid malignancy diagnostics. Materials and methods. The study included 55 patients with a clinical diagnosis of nodular / multinodular goiter. A quantitative analysis of mRNA of galectin-3, Ki-67, ubiquitin, HMGA2 was performed on material puncture by reverse transcription and RT-PCR. The Second Derivative Maximum Method was used to analyze the results. Results. The study included 46 women (83.6%) and 8 men (14.5%). The average age of the patients was 52.1 (from 23 to 82) years old. According to the results of histological examination, there were 35 (63.6%) benign tumors, 20 (36.4%) – cancer tumors (papillary carcinoma). There were no cases of follicular cancer in the histological findings. We found significant differences in the expression of mRNA of the ubiquitin gene between malignant and benign thyroid nodules. Conclusion. The method of ubiquitin gene 8.24 mRNA estimation has a sensitivity of 68.4% and a specificity of 68.6% in the well-differentiated cancer diagnostics. The estimation of mRNA of gene Ki-67, galectin-3, HMGA by RT-PCR did not show itself as a reliable method for the differential diagnosis of thyroid nodules in the preoperative stage