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Objective. Genetic factors substantially contribute to the development and duration of arterial hypertension. The study of the A1166C polymorphism of the angiotensin II type 1 receptor gene (AGTR1) in arterial hypertension is an auspicious area for assessing the relationship between heredity, hypertension development, and adipokines, but it still remains debatable. The purpose of the current study was to investigate serum adipokines levels depending on the AGTR1 A1166C polymorphism. Methods. A total of 86 patients with arterial hypertension were examined, who underwent the evaluation of the allelic A1166C polymorphism of AGTR1 by polymerase chain reaction with electrophoretic detection and determination of serum adipokines levels using enzyme-linked immunosorbent assay. Results. In the group of patients with arterial hypertension, a significant increase in serum adipokines (resistin, adiponectin, and leptin) levels was found against the background of a decrease in the antianorexic hormone ghrelin with a predominance of CC genotype carriers compared with AA genotype carriers of the AGTR1. A statistically significant decrease in ghrelin and an increase in serum adipokines (resistin, adiponectin, and leptin) in CC genotype carriers compared with AA genotype carriers of the AGTR1 were found suggesting that CC genotype carriers may be predictors of the development of arterial hypertension in our patients. Conclusions. Statistically significant decrease in ghrelin and increase in serum adipokines (resistin, adiponectin, and leptin) were found in CC genotype carriers compared with AA genotype carriers of the AGTR1, which suggests that carriers of the CC genotype are predictors of the arterial hypertension development in our patients.
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Adipoquinas , Hipertensión , Receptor de Angiotensina Tipo 1 , Humanos , Receptor de Angiotensina Tipo 1/genética , Femenino , Masculino , Hipertensión/genética , Hipertensión/sangre , Persona de Mediana Edad , Adipoquinas/sangre , Adipoquinas/genética , Adulto , Leptina/sangre , Leptina/genética , Polimorfismo de Nucleótido Simple , Adiponectina/sangre , Adiponectina/genética , Anciano , Ghrelina/genética , Ghrelina/sangre , Genotipo , Predisposición Genética a la Enfermedad , Resistina/genética , Resistina/sangreRESUMEN
Objective. Polymorphism investigation of T786C gene promoter of endothelial nitric oxide synthase (eNOS/NOS3) in the arterial hypertension is a promising field for determining the relationship between heredity, hypertension, and dyslipidemia, which still remains controversial. The purpose of the study was to investigate the lipid profile, which depends on the NOS3 T786C gene promotor region polymorphism in patients with arterial hypertension. Methods. The study involved 86 patients with arterial hypertension. The control group consisted of 30 basically healthy individuals. The lipid profile in the blood serum of the studied patients was measured by commercially available kits using Biochem FC-200 analyzer (HTI, USA). The allelic polymorphism of NOS3 T786C gene promoter was studied using a polymerase chain reaction technique with electrophoretic detection of the results. Results. An increase at the level of all atherogenic fractions in the blood was found in the group of patients carrying the CC genotype compared with carriers of the TT genotype of the NOS3 gene. The total cholesterol serum level in the group of carriers of the CC genotype of NOS3 T786C gene promoter increased by 33.3% compared with carriers of the TT genotype and it was almost twice as high as the control values. In the group of carriers in the CC genotype of the NOS3 gene, the serum level of triglycerides was statistically significantly higher (2.9 times) than in the group of carriers of the TT genotype. The low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) serum levels significantly increased in patients with arterial hypertension with the CC genotype by 1.6 and 4.6 times, respectively, compared with the TT genotype carriers. The high-density lipoprotein (HDL) serum level, as an antiatherogenic factor, was statistically significantly lower (by 45.8%) in the group of the CC genotype carriers of the NOS3 gene than in the group with carriers of the TT genotype (0.58±0.06 vs. 1.07±0.03 mmol/l.) Conclusions. The increase in all atherogenic and decrease in antiatherogenic lipid parameters of the lipidogram of patients with arterial hypertension and the deepening of dyslipidemia in carriers of the CC genotype compared with carriers of the TT genotype of the NOS3 T786C gene promoter is crucial in the development of dyslipidemia.
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Hipertensión , Lípidos , Óxido Nítrico Sintasa de Tipo III , Regiones Promotoras Genéticas , Humanos , Óxido Nítrico Sintasa de Tipo III/genética , Óxido Nítrico Sintasa de Tipo III/sangre , Hipertensión/genética , Hipertensión/sangre , Regiones Promotoras Genéticas/genética , Masculino , Femenino , Persona de Mediana Edad , Adulto , Lípidos/sangre , Polimorfismo Genético , Estudios de Casos y Controles , Polimorfismo de Nucleótido Simple , Predisposición Genética a la Enfermedad , Dislipidemias/genética , Dislipidemias/sangreRESUMEN
Bronchial asthma (BA) is among the most prevalent chronic inflammatory disorders of the lung airways, and it has become clear that a mixture of genetic predisposition and environmental factors plays a critical role in its pathogenesis. The aim of presented review is to analyze the published data on the possible role of ACE gene polymorphism in BA development. The article is based on available literature found in Pubmed, Elsevier, Scopus, and Google scholar databases. We have found that ACE I/D polymorphism may contribute to an important molecular mechanisms of BA development (specially D/D genotype), and may become a useful tool in risk assessment and in designing effective treatment approaches. The difference in the literature on the role of ACE alleles and genotypes can be explained by minor influence of the investigated genetic component and contributions of other genetic variations, as well as other environmental factors, considering multifactorial causes of BA.
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Asma , Peptidil-Dipeptidasa A/genética , Polimorfismo Genético , Asma/genética , Humanos , Mutación INDELRESUMEN
OBJECTIVE: The study was performed with an aim to investigate the efficiency of two treatment options in experimental nickel-induced contact dermatitis (CT), with either betamethasone or chitosan cross-linked nano-encapsulated betamethasone lanoline solutions (nano-betamethasone). METHODS: Male Wistar rats were used. The differences were compared based on lesion visual appearance, skinfold thickness, white blood cell count (WBC), erythrocyte sedimentation rate (ESR), blood serum prooxidant-antioxidant balance (thiobarbituric acid reactive substances, TBARS; supersoxide dismutase, SOD; catalase, KAT), blood cytokine profile (TNF-α, IL-1ß, IL-10, and IL-4), and histological examination of affected skin. RESULTS: All animals treated with nickel sulfate developed CT and systemic inflammatory response on day 12, which only slightly lessened, if left untreated, on day 20. The therapeutic effectiveness of nano-betamethasone was significantly far superior (p < 0.01) compared to betamethasone. Specifically, the visual appearance of lesion severity of betamethasone vs. nano-betamethasone ± SD was 1.82 ± 0.18 vs. 1.17 ± 0.24 points, skinfold thickness-2.68 ± 0.12 vs. 2.12 ± 0.10 mm, ESR-6.38 ± 0.27 vs. 5.12 ± 0.20 mm/h, WBC-8.47 ± 0.28 vs. 7.17 ± 0.24 109/L, TBARS-1.09 ± 0.04 vs. 0.94 ± 0.02 µmol/L, SOD-3.38 ± 0.26 vs. 4.12 ± 0.18 r.u./L, KAT-11.54 ± 0.14 vs. 10.02 ± 0.19 mkatal/L, respectively. The nano-betamethasone formulation was also more effective (p < 0.01) in increasing anti-inflammatory cytokines level, IL-10 (8.96 ± 0.32 vs. 7.54 ± 0.52 pg/mL) and IL-4 (13.16 ± 0.45 vs. 11.43 ± 0.58 pg/mL); and decreasing in pro-inflammatory TNF-α (20.94 ± 2.30 vs. 26.98 ± 1.16 pg/mL) and IL-1ß (19.35 ± 1.28 vs. 24.77 ± 1.75 pg/mL), respectively. These findings were also supported with histological examination. CONCLUSIONS: Nano-betamethasone may be considered as a more successful transcutaneous therapy for managing contact dermatitis compared to ointments consisting of betamethasone in traditional form.
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Quitosano , Dermatitis por Contacto , Nanopartículas , Animales , Betametasona , Interleucina-10 , Interleucina-4 , Masculino , Ratas , Ratas Wistar , Superóxido Dismutasa , Sustancias Reactivas al Ácido Tiobarbitúrico , Factor de Necrosis Tumoral alfaRESUMEN
Coronavirus disease 2019 (COVID-19), caused by the novel coronavirus, Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2), led to the ongoing global public health crisis. Existing clinical data suggest that COVID-19 patients with acute respiratory distress syndrome (ARDS) have worse outcomes and increased risk of intensive care unit (ICU) admission. The rapid increase in the numbers of patients requiring ICU care may imply a sudden and major challenge for affected health care systems. In this narrative review, we aim to summarize current knowledge of pathophysiology, clinical and morphological characteristics of COVID-19-associated ARDS and ARDS caused by other factors (classical ARDS) as defined by Berlin criteria, and therefore to elucidate the differences, which can affect clinical management of COVID-19-associated ARDS. Fully understanding the characteristics of COVID-19-associated ARDS will help identify its early progression and tailor the treatment, leading to improved prognosis in severe cases and reduced mortality. The notable mechanisms of COVID-19-associated ARDS include severe pulmonary infiltration/edema and inflammation, leading to impaired alveolar homeostasis, alteration of pulmonary physiology resulting in pulmonary fibrosis, endothelial inflammation and vascular thrombosis. Despite some distinct differences between COVID-19-associated ARDS and classical ARDS as defined by Berlin criteria, general treatment principles, such as lung-protective ventilation and rehabilitation concepts should be applied whenever possible. At the same time, ventilatory settings for COVID-19-associated ARDS require to be adapted in individual cases, depending on respiratory mechanics, recruitability and presentation timing.
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Previous short-duration depuration studies with the eastern oyster ( Crassostrea virginica) demonstrated difficulty in achieving significant naturally incurred Vibrio vulnificus population count reductions. The present study used long-duration depuration (14 days) at controlled temperatures (10 or 22°C) and salinities (12, 16, or 20 mg/g). All depuration temperature-salinity combinations significantly reduced V. vulnificus counts, with greatest reductions seen in 12 mg/g, 10°C seawater (2.7-log CFU/g reduction) and in 20 mg/g, 22°C seawater (2.8-log reduction). Mesophilic vibrios dominated the overall microflora of freshly harvested oysters, whereas refrigerated storage selected for psychrotrophic bacteria ( Pseudomonas spp., Aeromonas spp., Shewanella spp., Psychrobacter spp.) as well as did depuration at 10°C ( Pseudoalteromonas spp., Shewanella spp., Vibrio spp.). Depuration at 22°C retained dominance of mesophilic vibrios, including pathogenic species, followed by Shewanella spp., Pseudoalteromonas spp., and Photobacterium spp. Although aerobic plate counts were lower in 22°C depurated oysters (5.0 log versus 6.0 log) compared with 10°C, depuration at 10°C offered greater V. vulnificus population reductions than depuration at 22°C. This advantage was only seen at 12 mg/g salinity, with no impact at 16 and 20 mg/g salinities. No depuration treatment reduced V. vulnificus counts to nondetectable levels. Use of prolonged depuration may be a helpful intervention to control V. vulnificus populations in oysters.
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Crassostrea , Contaminación de Alimentos/análisis , Vibrio vulnificus , Animales , Crassostrea/microbiología , Microbiología de Alimentos , Ostreidae , Salinidad , Temperatura , Vibrio vulnificus/aislamiento & purificaciónRESUMEN
The combined lactic acid, monolaurin, and nisin effects on time-to-detection (optical density at 600 nm) extension were greater (P < 0.05) than any single or paired combination effect, which demonstrates a synergistic interaction among the antimicrobials. Monolaurin exposure caused C12:0 cell membrane incorporation. Lactic acid caused increased monolaurin C12:0 membrane incorporation, while nisin had no influence. We postulate that lactic acid-enhanced monolaurin C12:0 incorporation into the cell membrane increased membrane fluidity resulting in increased nisin activity.
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Antibacterianos/farmacología , Ácido Láctico/farmacología , Lauratos/farmacología , Listeria monocytogenes/efectos de los fármacos , Listeria monocytogenes/crecimiento & desarrollo , Monoglicéridos/farmacología , Nisina/farmacología , Membrana Celular/química , Sinergismo Farmacológico , Ácidos Grasos/análisis , Listeria monocytogenes/química , Fluidez de la MembranaRESUMEN
This review critically evaluates different types of immunosensors proposed for rapid identification of Escherichia coli O157:H7. The methods are compared with approved USDA-FSIS standard procedures for determination of this pathogen in raw or ready-to-eat meat products. Major advantages and disadvantages for each method are highlighted. Our analysis suggests that application of immunosensors in the meat-processing industry may be limited to identification of uncontaminated samples after conventional selective enrichment in broth. Use for detection appears limited at the present time.