14 research outputs found

    Microarray based comparative genome-wide expression profiling of major subtypes of leukemia

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    The uncontrolled proliferation of hematopoietic cells with no capacity to differentiate into mature blood cells leads to leukemia. Though considerable amount of work has been done in understanding the molecular basis and gene expression profiles of hematologic malignancies viz., chronic lymphocytic leukemia (CLL), chronic myelogenous leukemia (CML), acute lymphocytic leukemia (ALL) and acute myelogenous leukemia (AML), the role of various underlying genes and mechanisms predisposing the disease are poorly understood. To develop the early diagnosis, preventive and therapeutic strategies, identification of population specific novel mutations and candidate genes are required. Micro array based gene expression profiling was performed for total of 18 samples (4 from each subtype of leukemia that is, CLL, CML, ALL, AML and 2 controls) from Indian population using single color hybridization. The expression of all genes presented in terms of fold variation was subjected to F-test. The microarray data of genes showing differential regulation with respect to the control samples have been obtained from total 50, 238 probes covering 14,992 genes on Agilent’s Human 8X60K Array. The experiment was conducted with expectation to have similar patterns of result in terms of gene expression but it demonstrates statistically significant relationship only among CML and ALL which are of myeloid and lymphoid origin, respectively, in contrast to other combinations. Gene expression profiles of four subtypes of leukemia were compared to each other to ascertain the overall association and significance of genes for occurrence of different types of leukemiawhich would guide in the development of common probable biomarkers for leukemias followed by effective diagnosis, prognosis and treatment. Based on their geomean fold values, the highly upregulated genes found in this study are listed.Keywords: Leukemia, microarray, gene expression profiling, fold variation, lymphoid, myeloid, geomean foldAfrican Journal of Biotechnology, Vol. 13(10), pp. 1174-1181, 5 March, 201

    Home Automation on Android Using Arduino

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    Home automation system is obtaining fashionable and wide utilized in lots of homes worldwide. it's loads of blessings to users even additional to the disabled and/or aged users within which it'll build it easier for them to regulate their home appliances. Home automation systems will be tagged to 2 medium within which however it's connected and that they square measure either wired or wirelessly connected. The most distinction between these 2 types is that home appliances square measure joined wirelessly a central controller if it a wireless home automation system. On the opposite hand, the appliances square measure connected to a central controller if the medium use wired communication methodology. Wireless system had been introduced in order to dispose of wired communication among home appliances Arduino based. This project presents a web-based, flexible automation system, which is `basically android based home automation systems for wireless communication. The main concept of home automation through android mobile is that “physically challenged and disabled people” can also use his system to control their home appliances. However, end users, especially the disabled and old aged due to their complexity and cost, do not always accept these systems. And the mobile phone is the inseparable part of human lives today. With the help of mobile phones human can done many works related to their civil life. At today’s repaired technology the mobile phone is also become smart one. With the help of this smart gadget we can make our home smart one. Home automation Systems (HASs) represents a great research opportunity in creating new fields in engineering, architecture and computing HASs becoming popular now a day and enters quickly in this emerging market. The system is designed in user-friendly interface as well as easy of installation. In this device we will also implement one GSM module for when there will be more traffic of internet users and if we cannot get the internet connection with the help of GSM module we can control the appliances by sending message to the main circuit board of home

    The Effect of Socioeconomic Factors and Indoor Residual Spraying on Malaria in Mangaluru, India: A Case-Control Study

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    India faces 0.5 million malaria cases annually, including half of all Plasmodium vivax malaria cases worldwide. This case–control study assessed socioeconomic determinants of urban malaria in coastal Mangaluru, Karnataka, southwestern India. Between June and December 2015, we recruited 859 malaria patients presenting at the governmental Wenlock Hospital and 2190 asymptomatic community controls. We assessed clinical, parasitological, and socioeconomic data. Among patients, p. vivax mono-infection (70.1%) predominated. Most patients were male (93%), adult (median, 27 years), had no or low-level education (70.3%), and 57.1% were daily labourers or construction workers. In controls (59.3% male; median age, 32 years; no/low-level education, 54.5%; daily labourers/construction workers, 41.3%), 4.1% showed asymptomatic Plasmodium infection. The odds of malaria was reduced among those who had completed 10th school grade (aOR, 0.3; 95% CI, 0.26–0.42), lived in a building with a tiled roof (aOR, 0.71; 95% CI, 0.53–0.95), and reported recent indoor residual spraying (aOR, 0.02; 95% CI, 0.01–0.04). In contrast, migrant status was a risk factor for malaria (aOR, 2.43; 95% CI, 1.60–3.67). Malaria in Mangaluru is influenced by education, housing condition, and migration. Indoor residual spraying greatly contributes to reducing malaria in this community and should be promoted, especially among its marginalised members.Peer Reviewe

    Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

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    In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

    Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

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    Summary Background Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. Methods We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung’s disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. Findings We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung’s disease) from 264 hospitals (89 in high-income countries, 166 in middleincome countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in lowincome countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≀0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. Interpretation Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between lowincome, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

    A study on the ayurveda intervention (Virechana - therapeutic purgation and Rasayana - rejuvenation) on molecular gene expression profiling in familial breast cancer patients

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    Background: The study was conducted to assess the ayurvedic intervention Virechana - therapeutic purgation and Rasayana - rejuvenation on predisposed familial breast cancer expression profiling of BRCA1 and BRCA2 genes. Materials and Methods: The total RNA was extracted from blood of five subjects of familial breast cancer predisposition patients using PAX Gene Blood RNA Kit who had undergone the ayurvedic intervention Virechana - therapeutic purgation and Rasayana - rejuvenation therapy. BRCA1 and BRCA2 gene expression was assessed by reverse transcription polymerase chain reaction and quantitative polymerase chain reaction (qPCR). The qPCR-based BRCA1 gene expression results were analyzed for fold variation based on Ct values using the following formula: 2 (−ΔΔCt), where ΔCt is the Ct (GOI) − avg.(Ct (HKG)), GOI is the gene of interest, and HKG is the housekeeping gene. Results: In one subject (S1), the upregulation (61.82) showed further increase (843.36) by therapeutic purgation and then decreased below the baseline level (11.3) in the rejuvenation phase. In three subjects (S2, S3, and S5), the upregulated genes (1488.87, 15825.9, and 19.16) showed down trend continuously till rejuvenation phase (1.92, 4.17, and 3.97) but not to downregulation. Another subject (S4) showed reversal of genetic expression, i.e., downregulated gene (−1) showed upregulation (237,900.70) continuously throughout the therapy, which is in conformity of the proposed hypothesis, i.e., biopurification (therapeutic purgation) followed by rejuvenation leads to upregulation of gene. Conclusion: With the available limited and diversified data, it may be concluded that therapeutic purgation followed by rejuvenation (Narasimha Rasayana) therapy exerted effect on gene expression, but further study needs to be conducted with more number of samples

    SNAP SHOT OF EPIDEMIOLOGICAL PATTERN OF CERVICAL CANCER PATIENTS REPORTING TO A TERTIARY CANCER CARE CENTER IN NORTH KARNATAKA, INDIA

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    ABSTRACT Cervical Cancer (CC) has declined in the developed countries but the same has not been observed in the developing countries. India has 1,34,000 cases and the mortality is about 73,000. This retrospective study was carried out to understand the sociodemographic and clinico-pathologic results that would aid in identifying possible risk factors involved in cervical cancer patients attending to the tertiary cancer care hospital from the year 2001 to 2011 located in North Karnataka in the southern part of India. A total of 22,049 of cancer cases were reported and out of these 5,035 i.e., 41.52% were cervical cancer patients. The average age was 45 years and the median age was 50 years. Maximum number of patients was in the age group of 40-49 years. Majority of the patients were from the rural background with lower socio-economic status. This epidemiological study throws some light to the incidence of cervical cancer in this region and also the most likely risk factors involved. The increasing burden of CC among women requires immediate epidemiological investigations among the rural and urban population. This hospital based study gives an insight into the pattern and possible risk factors and to identify the high risk groups for CC

    Clinical profile of hemophilia B patients from Karnataka

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    Background: The most prevalent severe inherited hemorrhagic condition is hemophilia, which means “love of blood.” Hemophilia A and B are caused by a lack or malfunction of the factor VIII and factor IX proteins. Objective: The present study is to determine the prevalence and clinical profile of hereditary coagulation disorder, particularly hemophilia B, in Karnataka. Methods: The study comprised 150 HB patients with a mean age of 25, nmale = 148 and nfemale = 2. The samples were collected from hemophilia societies across Karnataka. The detailed history of HB patients was recorded in a predesigned Performa regarding family history, age, time of first bleed, site of the bleed, and bleeding history. Result: In our study cohort, the majority of the 58 (38.7%) cases belong to 21–30 years of age. The mean age of onset was 2.0 ± 1.0 years in severe, 7.5 ± 2.8 0 years in moderate, and 10.0 ± 3.5 years in mild HB patients. Out of 150 HB cases, 102 (68%) cases were diagnosed as severe, 30 (20%) as moderate, and 18 (12%) as mild. Mean factor IX levels were 0.6 ± 0.2, 2.5 ± 1.3, and 8.0 ± 2.6 in the severe, moderate, and mild group, respectively. A family history of bleeding was observed in 97 [64.7%] HB patients. Forty-seven (32.3%) HB patients had a history of consanguinity. The most common initial site of bleed was in joints in 86 [57.3%]. Conclusion: The present study is one of the fewer studies from Karnataka studying the demographic and clinicopathological features of hemophilia B. Early diagnosis can be only helpful with knowledge of spectral presentation of hemophilia B in a local population

    Mutation analysis of the LDL receptor gene in Indian families with familial hypercholesterolemia

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    Objective: Familial Hypercholesterolemia (FH) is a metabolic disorder inherited as an autosomal dominant trait characterized by an increased plasma Low-density Lipoprotein (LDL) level. The disease is caused by several different mutations in the LDL Receptor (LDLR) gene. Several mutations have been reported in this gene in patients from several ethnic groups. Early identification of individuals carrying the defective gene could be useful in reducing the risk of atherosclerosis and myocardial infraction by the available therapeutic methods. The techniques available for determining the number of the functional LDLR molecules are difficult to carry out and expensive. Our study presents mutation analysis of the LDLR gene in 24 Indian families with FH. Material &#38; Methods: Peripheral blood samples were obtained form individuals after taking informed consent on the condition that each of these individuals had at least one first-degree relative affected with FH. Genomic DNA was isolated, exon-specific intronic primers were designed and used to amplify DNA samples from individuals. PCR products were directly subjected to automated DNA sequencing to detect the mutations. Along with the affected individuals, ten ethnically matched controls were also analyzed to determine the presence of the same mutations. Patients with Nephrotic Syndrome admitted to hospital were excluded from the study. Results: All the 24 patients had total cholesterol level above 300 mg/dl and LDL cholesterol level above 200mg/dl. Sequence analysis of the LDL Receptor (LDLR) gene showed 3 novel mutations which have never been reported elsewhere. In exon 10 we reported g.29372_29373insC, which was found in all the 24 patients and was missence mutation coding for C (cysteine) instead of V (valine). Conclusion: Our study reported 3 novel mutations in 24 Indian families. These novel mutations are predicted to produce change in the amino acid and thus leading to the conformational changes in the structure of LDLR protein. Change in the LDLR protein makes the LDL receptor unable to transport the cholesterol in to the cell and hence cholesterol starts accumulating in the blood stream and leads to FH
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