8 research outputs found
Synthesis, crystal structure, thermal and nonlinear optical properties of new metal-organic single crystal: Tetrabromo (piperazinium) zincate (II) (TBPZ)
No full textDataset of natural antisense transcripts in P. vivax clinical isolates derived using custom designed strand-specific microarray
No full textAbstractNatural antisense transcripts (NATs) have been detected in many organisms and shown to regulate gene expression. Similarly, NATs have also been observed in malaria parasites with most studies focused on Plasmodium falciparum. There were no reports on the presence of NATs in Plasmodium vivax, which has also been shown to cause severe malaria like P. falciparum, until a recent study published by us. To identify in vivo prevalence of antisense transcripts in P. vivax clinical isolates, we performed whole genome expression profiling using a custom designed strand-specific microarray that contains probes for both sense and antisense strands. Here we describe the experimental methods and analysis of the microarray data available in Gene Expression Omnibus (GEO) under GSE45165. Our data provides a resource for exploring the presence of antisense transcripts in P. vivax isolated from patients showing varying clinical symptoms. Related information about the description and interpretation of the data can be found in a recent publication by Boopathi and colleagues in Infection, Genetics and Evolution 2013
Surface modification of CZTS nanoparticles using reflux method for effective utilizing absorber material
No full textSCIENTOMETRIC ANALYSIS OF DIABETES RESEARCH OUTPUT DURING THE YEAR 2014-2018: Indexed by Web of Science
No full textTo assess diabetes research productivity in India and analysis to various parameters in the view of the scientometric analytical study. Collections include (Articles, Reviews, Meeting Abstracts, Letters and book chapter), etc. published 8016 diabetes journals in 2014 – 2018 were screened with the Web of Science database (Clarivate Analytics). The study mainly focused on the Author and journal wise distribution, Year and country wise output and Institution wise collaboration are discussed in this paper. Most of the research articles published from India, between 2016 and 2017 has been published more journals. All India Institute of Medical Science has published highest journals compare with the other institutions
A cross strain Plasmodium falciparum microarray optimized for the transcriptome analysis of Plasmodium falciparum patient derived isolates
No full textAbstractMalarial parasite P. falciparum, an apicomplexan protozoan has a 23.3MB nuclear genome and encodes ~5600 transcripts. The genetic diversity of the parasite within and across geographical zones is a challenge to gene expression studies which are essential for understanding of disease process, outcome and developing markers for diagnostics and prognostics. Here, we describe the strategy involved in designing a custom P. falciparum 15K array using the Agilent platform and Genotypic's Right Design methodology to study the transcriptome of Indian field isolates for which genome sequence information is limited. The array contains probes representing genome sequences of two distinct geographical isolates (i.e. 3D7 and HB3) and sub-telomeric var gene sequences of a third isolate (IT4) known to adhere in culture condition. Probes in the array have been selected based on their efficiency to detect transcripts through a 244K array experimentation. Array performance for the 15K array, was evaluated and validated using RNA materials from P. falciparum clinical isolates. A large percentage (91%) of the represented transcripts was detected from Indian P. falciparum patient isolates. Replicated probes and multiple probes representing the same gene showed perfect correlation between them suggesting good probe performance. Additional transcripts could be detected due to inclusion of unique probes representing HB3 strain transcripts. Variant surface antigen (VSA) transcripts were detected by optimized probes representing the VSA genes of three geographically distinct strains. The 15K cross strain P. falciparum array has shown good efficiency in detecting transcripts from P. falciparum parasite samples isolated from patients. The low parasite loads and presence of host RNA makes arrays a preferred platform for gene expression studies over RNA-Seq
An in vivo transcriptome data set of natural antisense transcripts from Plasmodium falciparum clinical isolates
No full textAbstractAntisense transcription is pervasive among biological systems and one of the products of antisense transcription is natural antisense transcripts (NATs). Emerging evidences suggest that they are key regulators of gene expression. With the discovery of NATs in Plasmodium falciparum, it has been suggested that these might also be playing regulatory roles in this parasite. However, all the reports describing the diversity of NATs have come from parasites in culture condition except for a recent study published by us. In order to explore the in vivo diversity of NATs in P. falciparum clinical isolates, we performed a whole genome expression profiling using a strand-specific 244K microarray that contains probes for both sense and antisense transcripts. In this report, we describe the experimental procedure and analysis thereof of the microarray data published recently in Gene Expression Omnibus (GEO) under accession number GSE44921. This published data provide a wealth of information about the prevalence of NATs in P. falciparum clinical isolates from patients with diverse malaria related disease conditions. Supplementary information about the description and interpretation of the data can be found in a recent publication by Subudhi et al. in Experimental Parasitology (2014)
Thrombocytopenia in<i>Plasmodium falciparum</i>,<i>Plasmodium vivax</i>and mixed infection malaria: A study from Bikaner (Northwestern India)
No full textСигнальный механизм рецептора андрогена при раке предстательной железы: резистентность к антиандрогенной терапии и связь с генами репарации повреждений ДНК
No full textBackground. Metastatic castration-resistant prostate cancer remains a complex problem due to patients' previous treatments and limited selection of subsequent therapies. While 2nd generation antiandrogens are initially effective, resistance to them is not an exceptional event. Mechanisms depending on androgen receptor and independent of it have been described. A special focus is on mutations in DNA repair genes, particularly genes involved in homologous recombination repair (HRR) as a possible cause of somatic genetic abnormalities specifically in progressive metastatic disease. However, data on the effect of the HRR defect on the effectiveness of antiandrogen therapy for prostate cancer are very limited, which requires additional clinical studies.Aim. To evaluate the effect of clinical, morphological, molecular and genetic factors on the effectiveness of enzalutamide antiandrogen therapy in patients with prostate cancer and known mutations in DNA repair genes involved in HRR and mismatch repair.Materials and methods. The study was performed at the Clinical Oncological Dispensary No. 1 (Krasnodar). Retrospective analysis of clinical and morphological parameters of 54 patients with prostate cancer who received enzalutamide antiandrogen therapy and with known status of germ line and somatic mutations of HRR DNA repair genes (BRCA1, BRCA2, ATM, BARD, BRIP1, CDK12, CHEK1, CHEK2, PALB2, RAD51B, RAD51C, RAD54L, FANCL) and microsatellite instability in immunohistochemical determination of mismatch repair deficit was performed. Statistical analysis was performed using IBM SPSS Statistics v.22 software.Results and conclusion. In 17 of 54 patients, pathogenic germline and somatic mutations of HRR genes were detected: 7 mutations in BRCA2 gene, 4 - in CHEK2, 2 - in BRCA1, 2 - in CDK12, 1 - in BRIP1 and 1 - in ATM. It was shown that in the group of patients with metastatic castration-resistant prostate cancer, histological grade per the International Society of Urological Pathology (ISUP) G2 (total Gleason score 7 (3 + 4)) is significantly associated with the absence of HRR mutation, and grade G3 (total Gleason score 7 (4 + 3)) was associated with HRR mutations (р <0.05). Increase in prostate-specific antigen (PSA) level/biochemical progression 12-16 weeks after enzalutamide therapy start was significantly associated with metastatic castration-resistant prostate cancer without HRR mutations (р <0.05). In case of tumor response to enzalutamide therapy, decrease in PSA level did not depend on the age of disease onset, differentiation grade, primary advancement, previous docetaxel treatment, and presence of HRR mutation. Cox multivariate regression test showed that prescription of docetaxel before enzalutamide increased the risk of PSA-progression (hazard ratio (HR) 5.160; 95 % confidence interval (CI) 1.549-17.189; р = 0.008) and radiographic progression (HR 5.161; 95 % CI 1.550-17.187; р = 0.008). Progression risk decreased with increased level of PSA decrease 12-16 weeks after enzalutamide therapy start: for PSA decrease >30 % HR 0.150; 95 % CI 0.040-0.570; р = 0.005; for PSA decrease >50 % HR 0.039; 95 % CI 0.006-0.280; р = 0.001; for PSA decrease >90 % HR 0.116; 95 % CI 0.036-0.375; р = 0.000. Presence of HRR mutation, age <58 years, primary metastatic disease and poorly differentiated morphology did not affect duration without PSA-progression (p >0.05). Kaplan-Meier curves showed a trend towards increased time to development of castration resistance in the group of primary early cancer (Breslow р = 0.06; Tarone-Ware р = 0.062). Subgroup analysis showed that in the cohort of patients with castration-resistant prostate cancer (n = 48), absence of HRR mutation in patients who previously received docetaxel therapy increases time to PSA-progression compared to patients with mutations (log-rank р <0.05).Введение. Метастатический кастрационно-резистентный рак предстательной железы остается сложной проблемой ввиду предлеченности пациентов и ограниченного выбора методов последующей терапии. При первоначальной эффективности антиандрогенов 2-го поколения резистентность к ним не является исключительным событием. Описаны механизмы, зависящие от рецептора андрогена и не зависящие от него. При этом пристальное внимание уделено мутациям в генах репарации повреждений ДНК, в частности путем гомологичной рекомбинации (homologous recombination repair, HRR), как возможной причине соматических генетических нарушений именно при прогрессирующем метастатическом течении. Однако данные о влиянии дефекта HRR на эффективность антиандрогенной терапии РПЖ весьма ограниченны, что требует проведения дополнительных клинических исследований.Цель исследования - оценка влияния клинико-морфологических и молекулярно-генетических факторов на эффективность антиандрогенной терапии энзалутамидом у больных раком предстательной железы с известным статусом мутаций генов репарации ДНК путем HRR и механизма репарации некомплементарных пар нуклеотидов.Материалы и методы. Исследование выполнено на базе Клинического онкологического диспансера № 1 (Краснодар). Ретроспективно проанализированы клинико-морфологические параметры 54 больных раком предстательной железы, получивших антиандрогенную терапию энзалутамидом, с известным статусом герминальных и соматических мутаций генов репарации повреждений ДНК путем HRR (BRCA1, BRCA2, ATM, BARD, BRIP1, CDK12, CHEK1, CHEK2, PALB2, RAD51B, RAD51C, RAD54L, FANCL) и микросателлитной нестабильности при иммуногистохимическом определении дефицита репарации некомплементарных пар нуклеотидов. Статистический анализ выполнен с использованием пакета IBM SPSS Statistics v.22.Результаты и заключение. У 17 из 54 пациентов выявлены патогенные герминальные и соматические мутации генов HRR: 7 мутаций в гене BRCA2, 4 - в CHEK2, 2 - в BRCA1, 2 - в CDK12, 1 - в BRIP1 и 1 - в ATM. Показано, что в группе больных метастатическим кастрационно-резистентным раком предстательной железы гистологическая градация по классификации Международного общества урологических патологов (ISUP) G2 (сумма баллов по шкале Глисона 7 (3 + 4)) статистически значимо связана с отсутствием мутации генов HRR, при этом градация G3 (сумма баллов по шкале Глисона 7 (4 + 3)) ассоциирована с наличием мутаций генов HRR (р <0,05). Рост уровня простатического специфического антигена (ПСА)/биохимическое прогрессирование в сроки 12-16 нед от начала терапии энзалутамидом был статистически значимо связан с метастатическим кастрационно-резистентным раком предстательной железы без мутаций генов HRR (р <0,05). В случае ответа опухоли на лечение энзалутамидом снижение уровня ПСА не зависело от возраста манифестации заболевания, степени дифференцировки, первичной распространенности, предшествующего назначения доцетаксела и наличия мутации генов HRR. В многофакторном регрессионном анализе Кокса назначение доцетаксела до энзалутамида повышало риск ПСА-прогрессирования (отношение рисков (ОР) 5,160; 95 % доверительный интервал (ДИ) 1,549-17,189; р = 0,008) и рентгенологического прогрессирования (ОР 5,161; 95 % ДИ 1,550-17,187; р = 0,008). Риск прогрессирования уменьшался при увеличении степени снижения уровня ПСА после 12-16 нед терапии энзалутамидом: при снижении уровня ПСА >30 % ОР 0,150; 95 % ДИ 0,040-0,570; р = 0,005; при снижении уровня ПСА >50 % ОР 0,039; 95 % ДИ 0,006-0,280; р = 0,001; при снижении уровня ПСА >90 % ОР 0,116; 95 % ДИ 0,036-0,375; р = 0,000. Наличие мутации генов HRR, возраст <58 лет, первично-метастатическое заболевание и низкодифференцированная морфология не влияли на время без ПСА-прогрессирования (p >0,05). При построении кривых Каплана-Майера имелась тенденция к увеличению времени до развития кастрационной резистентности в группе первичного раннего рака (Breslow р = 0,06; Tarone-Ware р = 0,062). При подгрупповом анализе в когорте больных метастатическим кастрационно-резистентным раком предстательной железы (n = 48) наличие мутации генов HRR у пациентов, предлеченных доцетакселом, было связано с уменьшением времени до ПСА-прогрессирования по сравнению с больными без мутации (log-rank р <0,05)
