28 research outputs found
Screening of West Siberian patients with primary congenital glaucoma for CYP1B1 gene mutations
Primary congenital glaucoma (PΠ‘G) is a visual organ pathology that leads to progressive blindness and poor vision in children. Its main cause is an anomaly of the anterior chamber angle. Most cases of PΠ‘G are sporadic, but familial cases with an autosomal recessive (predominantly) and autosomal dominant (rare) type of inheritance have been described. Congenital glaucoma is a rare condition (1 case per 10,000β20,000 newborns), but its prevalence is substantially higher (up to 1 case per 250 newborns) in countries where consanguineous marriages are common. Mutations in the CYP1B1 gene, which encodes cytochrome P450 1B1, are the most common cause of autosomal recessive primary congenital glaucoma. This enzyme is known to be involved in retinoic acid metabolism and is necessary for normal eye development. The aim of this work was to assess the polymorphism of the CYP1B1Β gene among West Siberian patients with primary congenital glaucoma. Direct automatic Sanger sequencing of exons and adjacent splicing sites of the CYP1B1 gene was carried out in 28 people with the PCG phenotype from a West Siberian region. As a result, in the sample of the white population we examined, pathogenic variants previously described in other ethnic groups were revealed: E387K (rs55989760), R444* (rs377049098), R444Q (rs72549376), and P437L (rs56175199), as well as novel single-nucleotide deletion p.F114Lfs*38 in the CYP1B1 gene. The latter can cause a frame shift, changed amino acid composition, and a formation of truncated in the protein. None of the detected mutations were found in the control sample of ophthalmologically examined individuals without PCG (100Β people). Variants R444* (rs377049098) and R444Q (rs72549376) were not found in the general population sample either (576Β randomly selected West Siberia residents). All the detected mutations caused the development of the autosomal recessive form of primary congenital glaucoma. The most severe clinical phenotype was observed in carriers of mutations in codon 444 of the gene. Consequently, in children with signs of increased intraocular pressure, molecular genetic analysis of the CYP1B1 gene is advisable for early diagnosis and timely initiation of PCG therapy
ΠΠ°Π½Π΄ΠΈΠ΄Π΅ΠΌΠΈΡ Ρ ΠΎΠ½ΠΊΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ Π±ΠΎΠ»ΡΠ½ΡΡ : ΡΠ΅Π½ΠΎΡΠΈΠΏΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈ ΠΌΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΠΎ-Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ Ρ Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΡΡΠΈΠΊΠΈ ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΠΈ ΠΊ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ³ΡΠΈΠ±ΠΊΠΎΠ²ΡΠΌ Π»Π΅ΠΊΠ°ΡΡΡΠ²Π΅Π½Π½ΡΠΌ ΡΡΠ΅Π΄ΡΡΠ²Π°ΠΌ, Π³Π΅Π½Ρ ΡΠ°ΠΊΡΠΎΡΠΎΠ² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ Candida spp.
Relevance. The global trend of rapid increase in resistance to antifungal drugs due to multiple factors, dictates the need for continuous monitoring of taxonomic structure and susceptibility of nosocomial pathogens, causing invasive fungal infections, for permanent correction of the optimal prevention and treatment strategies.Purpose: to determine antifungal susceptibility of the main yeast pathogens in candidemia in cancer patients, as well as to determine resistance genes and pathogenic factor genes.Material and Methods. Eighty-two strains of Candida spp. isolated from blood of cancer patients from 2015 to 2021 were analyzed. Minimum inhibitory concentrations of fuconazole, voriconazole, posaconazole, anidulafungin and micafungin were determined by a gradient method (E-test, BioMerieux, France). The EUCAST and CLSI criteria were used for MIC value assessment. The genes, associated with pathogenicity factors, and resistance to antifungal drugs were identifed.Results. Our study results based on EUCAST 2020, v.10.0 criteria showed that triazoles, especially fuconazole, were the least effective drugs in empirical therapy for invasive candidiasis (including candidemia). Resistance of Candida spp. fuconazole was superior to that of voriconazole (47.2 % vs 23.2 %, respectively, p<0.01) and posaconazole (47.2 % vs 30.4 %, respectively, p><0.05). The highest in vitro activity was observed in echinocandins, and anidulafungin was 2 times more active than micafungin (4.1 % of resistant strains vs 11.4 %, respectively), with no statistically signifcant difference (p>0.05). The ERG11 and FKS1 genes associated with resistance to antifungal drugs were detected in 28.6 % of Candida spp. strains. The ERG11 gene was detected in 8.6 % of cases, exclusively in Candida albicans strains. The FKS1 gene was identifed in 20.0 % of strains (85.7 % of them were C. parapsilosis, 7.1 % each were C. tropicalis and C. glabrata). Pathogenic factor genes were identifed in 78.6 % of C. albicans and in 79.1 % of C. parapsilosis strains.Conclusion. Molecular genetic methods for the detection of Candida spp strains carrying resistance genes to antifungal drugs, and the determination of pathogenicity factors are promising trends in searching for biomarkers. They facilitate interpretation of results of microbiological study to assess the ability of Candida spp. strains to develop invasive mycoses.ΠΠΊΡΡΠ°Π»ΡΠ½ΠΎΡΡΡ. ΠΠΈΡΠΎΠ²Π°Ρ ΡΠ΅Π½Π΄Π΅Π½ΡΠΈΡ ΡΡΡΠ΅ΠΌΠΈΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΡ ΡΡΠΎΠ²Π½Ρ ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΠΈ ΠΊ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ³ΡΠΈΠ±ΠΊΠΎΠ²ΡΠΌ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°ΠΌ, ΠΊΠΎΡΠΎΡΠ°Ρ ΡΠ²ΡΠ·Π°Π½Π° ΡΠΎ ΠΌΠ½ΠΎΠ³ΠΈΠΌΠΈ ΡΠ°ΠΊΡΠΎΡΠ°ΠΌΠΈ, Π΄ΠΈΠΊΡΡΠ΅Ρ Π½Π΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΠΎΡΡΡ ΠΏΠΎΡΡΠΎΡΠ½Π½ΠΎΠ³ΠΎ ΠΌΠΎΠ½ΠΈΡΠΎΡΠΈΠ½Π³Π° ΡΠ°ΠΊΡΠΎΠ½ΠΎΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΡΡΡΠΊΡΡΡΡ Π½ΠΎΠ·ΠΎΠΊΠΎΠΌΠΈΠ°Π»ΡΠ½ΡΡ
Π²ΠΎΠ·Π±ΡΠ΄ΠΈΡΠ΅Π»Π΅ΠΉ ΠΈΠ½Π²Π°Π·ΠΈΠ²Π½ΡΡ
Π³ΡΠΈΠ±ΠΊΠΎΠ²ΡΡ
ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΉ ΠΈ ΠΈΡ
ΡΡΠ²ΡΡΠ²ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΠΈ ΠΊ Π°Π½ΡΠΈΡΡΠ½Π³Π°Π»ΡΠ½ΡΠΌ Π»Π΅ΠΊΠ°ΡΡΡΠ²Π΅Π½Π½ΡΠΌ ΡΡΠ΅Π΄ΡΡΠ²Π°ΠΌ Ρ ΡΠ΅Π»ΡΡ ΠΏΠΎΡΡΠΎΡΠ½Π½ΠΎΠΉ ΠΊΠΎΡΡΠ΅ΠΊΡΠΈΠΈ Π½Π°ΠΈΠ±ΠΎΠ»Π΅Π΅ ΠΎΠΏΡΠΈΠΌΠ°Π»ΡΠ½ΠΎΠΉ ΡΠ°ΠΊΡΠΈΠΊΠΈ ΠΏΡΠΎΡΠΈΠ»Π°ΠΊΡΠΈΠΊΠΈ ΠΈ Π»Π΅ΡΠ΅Π½ΠΈΡ ΠΈΠ½Π²Π°Π·ΠΈΠ²Π½ΡΡ
Π³ΡΠΈΠ±ΠΊΠΎΠ²ΡΡ
ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΉ.Π¦Π΅Π»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ β ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅ ΡΡΠ²ΡΡΠ²ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΠΈ ΠΊ Π°Π½ΡΠΈΡΡΠ½Π³Π°Π»ΡΠ½ΡΠΌ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°ΠΌ ΠΎΡΠ½ΠΎΠ²Π½ΡΡ
Π²ΠΎΠ·Π±ΡΠ΄ΠΈΡΠ΅Π»Π΅ΠΉ ΠΏΡΠΈ ΠΊΠ°Π½Π΄ΠΈΠ΄Π΅ΠΌΠΈΠΈ Ρ ΠΎΠ½ΠΊΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
Π±ΠΎΠ»ΡΠ½ΡΡ
, Π° ΡΠ°ΠΊΠΆΠ΅ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅ Π³Π΅Π½ΠΎΠ² ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΠΈ ΠΈ ΡΠ°ΠΊΡΠΎΡΠΎΠ² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ.ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. ΠΡΠΎΠ°Π½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π½ΠΎ 82 ΡΡΠ°ΠΌΠΌΠ° Candida spp., Π²ΡΠ΄Π΅Π»Π΅Π½Π½ΡΡ
ΠΈΠ· ΠΊΡΠΎΠ²ΠΈ ΠΎΠ½ΠΊΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
Π±ΠΎΠ»ΡΠ½ΡΡ
Π² ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ 2015β21 Π³Π³. ΠΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅ ΠΌΠΈΠ½ΠΈΠΌΠ°Π»ΡΠ½ΡΡ
ΠΈΠ½Π³ΠΈΠ±ΠΈΡΡΡΡΠΈΡ
ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠΉ ΡΠ»ΡΠΊΠΎΠ½Π°Π·ΠΎΠ»Π°, Π²ΠΎΡΠΈΠΊΠΎΠ½Π°Π·ΠΎΠ»Π°, ΠΏΠΎΠ·Π°ΠΊΠΎΠ½Π°Π·ΠΎΠ»Π°, Π°Π½ΠΈΠ΄ΡΠ»Π°ΡΡΠ½Π³ΠΈΠ½Π° ΠΈ ΠΌΠΈΠΊΠ°ΡΡΠ½Π³ΠΈΠ½Π° Π²ΡΠΏΠΎΠ»Π½ΡΠ»ΠΈ Π³ΡΠ°Π΄ΠΈΠ΅Π½ΡΠ½ΡΠΌ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ (Π-ΡΠ΅ΡΡ, BioMerieux, France). ΠΠ»Ρ ΠΎΡΠ΅Π½ΠΊΠΈ Π·Π½Π°ΡΠ΅Π½ΠΈΠΉ ΠΠΠ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π»ΠΈ ΠΊΡΠΈΡΠ΅ΡΠΈΠΈ EUCAST ΠΈ CLSI. ΠΠΏΡΠ΅Π΄Π΅Π»Π΅Π½Ρ Π³Π΅Π½Ρ, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΠ΅ Ρ ΡΠ°ΠΊΡΠΎΡΠ°ΠΌΠΈ ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ ΠΈ ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΠΈ ΠΊ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ³ΡΠΈΠ±ΠΊΠΎΠ²ΡΠΌ Π»Π΅ΠΊΠ°ΡΡΡΠ²Π΅Π½Π½ΡΠΌ ΡΡΠ΅Π΄ΡΡΠ²Π°ΠΌ.Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. ΠΠΎ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ°ΠΌ Π½Π°ΡΠ΅Π³ΠΎ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ (ΠΊΡΠΈΡΠ΅ΡΠΈΠΈ EUCAST) Π² ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ ΡΠΌΠΏΠΈΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ ΠΈΠ½Π²Π°Π·ΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΊΠ°Π½Π΄ΠΈΠ΄ΠΎΠ·Π° (Π² Ρ. Ρ. ΠΊΠ°Π½Π΄ΠΈΠ΄Π΅ΠΌΠΈΠΈ) Π½Π°ΠΈΠΌΠ΅Π½Π΅Π΅ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΡΠΌΠΈ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°ΠΌΠΈ ΡΠ²Π»ΡΡΡΡΡ ΡΡΠΈΠ°Π·ΠΎΠ»Ρ, ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎ ΡΠ»ΡΠΊΠΎΠ½Π°Π·ΠΎΠ», ΠΊ ΠΊΠΎΡΠΎΡΠΎΠΌΡ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΠΎ ΡΠ°ΡΠ΅ ΡΡΠ°ΠΌΠΌΡ Candida spp. ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½Ρ ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ Π²ΠΎΡΠΈΠΊΠΎΠ½Π°Π·ΠΎΠ»ΠΎΠΌ (47,2 % ΠΏΡΠΎΡΠΈΠ² 23,2 %, p<0,01) ΠΈ ΠΏΠΎΠ·Π°ΠΊΠΎΠ½Π°Π·ΠΎΠ»ΠΎΠΌ (47,2 % ΠΏΡΠΎΡΠΈΠ² 30,4 %, p><0,05). ΠΠ°ΠΈΠ±ΠΎΠ»ΡΡΠ°Ρ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ in vitro ΠΎΡΠΌΠ΅ΡΠ°Π΅ΡΡΡ Ρ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠΎΠ² Π³ΡΡΠΏΠΏΡ ΡΡ
ΠΈΠ½ΠΎΠΊΠ°Π½Π΄ΠΈΠ½ΠΎΠ², ΠΏΡΠΈΡΠ΅ΠΌ Π°Π½ΠΈΠ΄ΡΠ»Π°ΡΡΠ½Π³ΠΈΠ½ Π² 2 ΡΠ°Π·Π° Π°ΠΊΡΠΈΠ²Π½Π΅Π΅ ΠΌΠΈΠΊΠ°ΡΡΠ½Π³ΠΈΠ½Π° (4,1 % ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΡΡ
ΡΡΠ°ΠΌΠΌΠΎΠ² ΠΏΡΠΎΡΠΈΠ² 11,4 %), Π½ΠΎ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΠΎΠΉ ΡΠ°Π·Π½ΠΈΡΡ ΠΏΡΠΈ ΡΡΠΎΠΌ Π½Π΅ Π²ΡΡΠ²Π»Π΅Π½ΠΎ. ΠΠ΅Π½Ρ ERG11 ΠΈ FKS1, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΠ΅ Ρ ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΡΡ ΠΊ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ³ΡΠΈΠ±ΠΊΠΎΠ²ΡΠΌ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°ΠΌ, Π±ΡΠ»ΠΈ Π²ΡΡΠ²Π»Π΅Π½Ρ Ρ 28,6 % ΡΡΠ°ΠΌΠΌΠΎΠ² Candida spp.. ΠΠ΅Π½ ERG11 Π΄Π΅ΡΠ΅ΠΊΡΠΈΡΠΎΠ²Π°Π½ Π² 8,6 % ΡΠ»ΡΡΠ°Π΅Π², ΠΏΡΠΈΡΠ΅ΠΌ ΡΠΎΠ»ΡΠΊΠΎ Ρ ΡΡΠ°ΠΌΠΌΠΎΠ² Candida albicans. ΠΠ΅Π½ FKS1 ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ Ρ 20,0 % ΡΡΠ°ΠΌΠΌΠΎΠ² (85,7 % β C. parapsilosis, ΠΏΠΎ 7,1 % β C. tropicalis ΠΈ C. glabrata). ΠΠ΅Π½Ρ ΡΠ°ΠΊΡΠΎΡΠΎΠ² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½Ρ Ρ 78,6 % ΡΡΠ°ΠΌΠΌΠΎΠ² C. albicans ΠΈ Ρ 79,1 % ΠΈΠ·ΠΎΠ»ΡΡΠΎΠ² C. parapsilosis. ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΠΎ-Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΌΠ΅ΡΠΎΠ΄Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ ΡΡΠ°ΠΌΠΌΠΎΠ² Candida spp., Π½Π΅ΡΡΡΠΈΡ
Π³Π΅Π½Ρ ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΠΈ ΠΊ Π°Π½ΡΠΈΡΡΠ½Π³Π°Π»ΡΠ½ΡΠΌ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°ΠΌ, ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅ ΡΠ°ΠΊΡΠΎΡΠΎΠ² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ β><Β 0,01) ΠΈ ΠΏΠΎΠ·Π°ΠΊΠΎΠ½Π°Π·ΠΎΠ»ΠΎΠΌ (47,2 % ΠΏΡΠΎΡΠΈΠ² 30,4 %, p<0,05). ΠΠ°ΠΈΠ±ΠΎΠ»ΡΡΠ°Ρ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ in vitro ΠΎΡΠΌΠ΅ΡΠ°Π΅ΡΡΡ Ρ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠΎΠ² Π³ΡΡΠΏΠΏΡ ΡΡ
ΠΈΠ½ΠΎΠΊΠ°Π½Π΄ΠΈΠ½ΠΎΠ², ΠΏΡΠΈΡΠ΅ΠΌ Π°Π½ΠΈΠ΄ΡΠ»Π°ΡΡΠ½Π³ΠΈΠ½ Π² 2 ΡΠ°Π·Π° Π°ΠΊΡΠΈΠ²Π½Π΅Π΅ ΠΌΠΈΠΊΠ°ΡΡΠ½Π³ΠΈΠ½Π° (4,1 % ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΡΡ
ΡΡΠ°ΠΌΠΌΠΎΠ² ΠΏΡΠΎΡΠΈΠ² 11,4 %), Π½ΠΎ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΠΎΠΉ ΡΠ°Π·Π½ΠΈΡΡ ΠΏΡΠΈ ΡΡΠΎΠΌ Π½Π΅ Π²ΡΡΠ²Π»Π΅Π½ΠΎ. ΠΠ΅Π½Ρ ERG11 ΠΈ FKS1, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΠ΅ Ρ ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΡΡ ΠΊ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ³ΡΠΈΠ±ΠΊΠΎΠ²ΡΠΌ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°ΠΌ, Π±ΡΠ»ΠΈ Π²ΡΡΠ²Π»Π΅Π½Ρ Ρ 28,6 % ΡΡΠ°ΠΌΠΌΠΎΠ² Candida spp.. ΠΠ΅Π½ ERG11 Π΄Π΅ΡΠ΅ΠΊΡΠΈΡΠΎΠ²Π°Π½ Π² 8,6 % ΡΠ»ΡΡΠ°Π΅Π², ΠΏΡΠΈΡΠ΅ΠΌ ΡΠΎΠ»ΡΠΊΠΎ Ρ ΡΡΠ°ΠΌΠΌΠΎΠ² Candida albicans. ΠΠ΅Π½ FKS1 ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ Ρ 20,0 % ΡΡΠ°ΠΌΠΌΠΎΠ² (85,7 % β C. parapsilosis, ΠΏΠΎ 7,1 % β C. tropicalis ΠΈ C. glabrata). ΠΠ΅Π½Ρ ΡΠ°ΠΊΡΠΎΡΠΎΠ² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½Ρ Ρ 78,6 % ΡΡΠ°ΠΌΠΌΠΎΠ² C. albicans ΠΈ Ρ 79,1 % ΠΈΠ·ΠΎΠ»ΡΡΠΎΠ² C. parapsilosis. ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΠΎ-Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΌΠ΅ΡΠΎΠ΄Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ ΡΡΠ°ΠΌΠΌΠΎΠ² Candida spp., Π½Π΅ΡΡΡΠΈΡ
Π³Π΅Π½Ρ ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΠΈ ΠΊ Π°Π½ΡΠΈΡΡΠ½Π³Π°Π»ΡΠ½ΡΠΌ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°ΠΌ, ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅ ΡΠ°ΠΊΡΠΎΡΠΎΠ² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ β>< 0,05). ΠΠ°ΠΈΠ±ΠΎΠ»ΡΡΠ°Ρ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ in vitro ΠΎΡΠΌΠ΅ΡΠ°Π΅ΡΡΡ Ρ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠΎΠ² Π³ΡΡΠΏΠΏΡ ΡΡ
ΠΈΠ½ΠΎΠΊΠ°Π½Π΄ΠΈΠ½ΠΎΠ², ΠΏΡΠΈΡΠ΅ΠΌ Π°Π½ΠΈΠ΄ΡΠ»Π°ΡΡΠ½Π³ΠΈΠ½ Π² 2 ΡΠ°Π·Π° Π°ΠΊΡΠΈΠ²Π½Π΅Π΅ ΠΌΠΈΠΊΠ°ΡΡΠ½Π³ΠΈΠ½Π° (4,1 % ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΡΡ
ΡΡΠ°ΠΌΠΌΠΎΠ² ΠΏΡΠΎΡΠΈΠ² 11,4 %), Π½ΠΎ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΠΎΠΉ ΡΠ°Π·Π½ΠΈΡΡ ΠΏΡΠΈ ΡΡΠΎΠΌ Π½Π΅ Π²ΡΡΠ²Π»Π΅Π½ΠΎ. ΠΠ΅Π½Ρ ERG11 ΠΈ FKS1, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΠ΅ Ρ ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΡΡ ΠΊ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ³ΡΠΈΠ±ΠΊΠΎΠ²ΡΠΌ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°ΠΌ, Π±ΡΠ»ΠΈ Π²ΡΡΠ²Π»Π΅Π½Ρ Ρ 28,6 % ΡΡΠ°ΠΌΠΌΠΎΠ² Candida spp.. ΠΠ΅Π½ ERG11 Π΄Π΅ΡΠ΅ΠΊΡΠΈΡΠΎΠ²Π°Π½ Π² 8,6 % ΡΠ»ΡΡΠ°Π΅Π², ΠΏΡΠΈΡΠ΅ΠΌ ΡΠΎΠ»ΡΠΊΠΎ Ρ ΡΡΠ°ΠΌΠΌΠΎΠ² Candida albicans. ΠΠ΅Π½ FKS1 ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ Ρ 20,0 % ΡΡΠ°ΠΌΠΌΠΎΠ² (85,7 % β C. parapsilosis, ΠΏΠΎ 7,1 % β C. tropicalis ΠΈ C. glabrata). ΠΠ΅Π½Ρ ΡΠ°ΠΊΡΠΎΡΠΎΠ² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½Ρ Ρ 78,6 % ΡΡΠ°ΠΌΠΌΠΎΠ² C. albicans ΠΈ Ρ 79,1 % ΠΈΠ·ΠΎΠ»ΡΡΠΎΠ² C. parapsilosis.ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΠΎ-Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΌΠ΅ΡΠΎΠ΄Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ ΡΡΠ°ΠΌΠΌΠΎΠ² Candida spp., Π½Π΅ΡΡΡΠΈΡ
Π³Π΅Π½Ρ ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΠΈ ΠΊ Π°Π½ΡΠΈΡΡΠ½Π³Π°Π»ΡΠ½ΡΠΌ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°ΠΌ, ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅ ΡΠ°ΠΊΡΠΎΡΠΎΠ² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ β ΡΡΠΎ ΠΏΠ΅ΡΡΠΏΠ΅ΠΊΡΠΈΠ²Π½ΡΠ΅ Π½Π°ΠΏΡΠ°Π²Π»Π΅Π½ΠΈΡ Π΄Π»Ρ ΠΏΠΎΠΈΡΠΊΠ° Π±ΠΈΠΎΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ², ΠΎΠ±Π»Π΅Π³ΡΠ°ΡΡΠΈΡ
ΡΠ»ΠΎΠΆΠ½ΡΡ Π·Π°Π΄Π°ΡΡ ΡΡΠ°ΠΊΡΠΎΠ²ΠΊΠΈ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠΎΠ² ΠΌΠΈΠΊΡΠΎΠ±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ ΠΏΠΎ ΠΎΡΠ΅Π½ΠΊΠ΅ ΡΠΏΠΎΡΠΎΠ±Π½ΠΎΡΡΠΈ ΡΡΠ°ΠΌΠΌΠΎΠ² Candida spp. ΠΊ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΈΠ½Π²Π°Π·ΠΈΠ²Π½ΡΡ
ΠΌΠΈΠΊΠΎΠ·ΠΎΠ²
Genes of susceptibility to early neurodegenerative changes in the rat retina and brain: analysis by means of congenic strains
Chilling acclimation provides immunity to stress by altering regulatory networks and inducing genes with protective functions in Cassava
AGE- MACULAR DEGENERATION AND GLAUCOMA. EPIDEMIOLOGICAL AND CLINIC-PATHOGENETIC ASPECTS
Nowadays age-related macular degeneration (AMD) and glaucoma are the main causes of the irreversible loss of sight in the developed countries. The analysis of 5000 of out-patient records of senior patients (over 50 years) has revealed glaucoma in 30.3 %, AMD in 37.94 %, and their combination in 20.3 % cases. In AMD, the structure signs of the dry form of the disease are diagnosed in 74 % of the cases, the geographical atrophy in 12 % and the wet atrophy - in 14 %. Primary open-angle glaucoma reduces risk of the wet AMD development while the tendency of early formation of the geographical atrophy of the retina increases and the share of the patients with the wet form goes down to 7 %. The article is intended to scrutinize the main pathogenetic mechanisms of the development of the diseases. Distinctions in the quantitative and qualitative components of biomarkers of the oxidative stress, endothelial dysfunction and inflammation are analysed as predictors of the start and development of comorbid pathology. This allows to identify the risk groups and therapy prospects. The vascular theory of pathogenesis related to the reduction of the perfusion of the head of the optic nerve, retina and chorioidea defines the diagnostic importance of the layer thickness parameters of the peripapillar nervous fibers and ganglion cell in differential diagnostics of this pathology. Application of anti-VEGF to patients with AMD and glaucoma is harmless and does not significantly influence the level of intraocular pressure and intraocular blood circulation. However, it requires careful monitoring of dynamics of the visual-functional and structural changes of the retina and optic nerve, as well as timely therapy correction. A combined course of the diseases with neurodegenerative nature of lesion leads to decrease of not only visual, but also cognitive functions, significantly influences of the senior age group patientsβ quality of life and their adaptation in society