Publications by authors named "Ashwini Rajasekaran"
Article Synopsis
- Recent research on mRNA therapeutics has increased due to COVID-19, with applications in vaccination, cancer therapy, and immune modulation, but they face challenges like instability and degradation.
- Traditional agarose gel electrophoresis has been the standard for analyzing RNA, but newer methods, like those using the Agilent 2100 Bioanalyzer, offer better quality assessment despite being more expensive and less accessible.
- The proposed full-lane quantification (FLQ) method integrates ImageJ with programming in Python and R to provide a quick and affordable way to evaluate mRNA degradation, yielding results comparable to those from more sophisticated systems.
Article Synopsis
- Type 1 diabetes (T1D) is caused by the destruction of pancreatic beta cells primarily by T cells, with dendritic cells (DCs) playing a key role in disease initiation and progression.
- Recent research highlights the function of DCs as antigen-presenting cells that influence T cell responses by integrating signals from tissue damage and presenting antigens to naïve T cells.
- Current therapeutic strategies aim to suppress the pro-inflammatory actions of DCs and enhance their ability to promote immune tolerance, focusing on both blocking T cell activation and promoting regulatory T cell populations to combat T1D.
Allergic rhinitis (AR) is characterized by an early-phase response (EPR), and in a subgroup of individuals, a late-phase response (LPR). We sought to investigate polymorphisms in cholinergic synapse pathway genes, previously associated with late-asthmatic responses, in the LPR. Twenty healthy participants and 74 participants with AR underwent allergen exposure using the Environmental Exposure Unit.
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- Research indicates Neuregulin-1 (NRG1) may play a significant role in the development of schizophrenia, particularly through genetic variants and environmental factors impacting brain development.
- Findings show that specific genetic variations (SNP8NRG221533) in NRG1 are linked to lower digit ratios and certain dermatoglyphic patterns in schizophrenia patients, suggesting a connection to neurodevelopmental issues.
- The study involved 221 schizophrenia patients and 200 healthy controls, highlighting how these genetic effects are more pronounced in individuals with schizophrenia.
Objective: Schizophrenia is a complex neuropsychiatric disorder with significant genetic predisposition. In a subset of schizophrenia patients, mitochondrial dysfunction could be explained by the genomic defects like mitochondrial DNA Copy Number Variations, which are considered as a sensitive index of cellular oxidative stress. Given the high energy demands for neuronal functions, altered Mitochondrial DNA copy number (mtDNAcn) and consequent impaired mitochondrial physiology would significantly influence schizophrenia pathogenesis.
View Article and Find Full Text PDFAccelerated ageing processes are postulated to underlie schizophrenia pathogenesis. This postulate is supported by observations of reduced telomere length in schizophrenia patients. Hippocampus, one of the most important brain regions implicated in schizophrenia, is shown to atrophy at a faster rate in aging.
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- Previous research has suggested a connection between the CHRNA7 gene, which codes for the α-7 nAChR receptor, and schizophrenia, yet the impact of CHRFAM7A gene expression on the severity of symptoms has not been thoroughly investigated.
- A study analyzed CHRFAM7A expression in lymphocytes of 90 schizophrenia patients who had not been treated with antipsychotics, revealing an inverse correlation between CHRFAM7A levels and negative symptoms, even when controlling for factors like age and smoking.
- Additionally, after a short-term treatment with antipsychotics, CHRFAM7A expression significantly increased, indicating its potential role as a marker for the severity of schizophrenia symptoms and its involvement in the
Article Synopsis
- Research indicates that the immuno-inflammatory pathway may influence the risk and progression of schizophrenia, particularly through prenatal infections leading to maternal immune activation and increased IL-6 levels in offspring.
- * The study focused on the link between a specific genetic variant (14 bp INDEL polymorphism) of the HLA-G gene and IL-6 gene expression in 56 schizophrenia patients versus 99 healthy controls.
- * Results showed that schizophrenia patients have lower IL-6 expression, especially those with the Del/Del genotype of HLA-G, suggesting that HLA-G may help reduce inflammation related to schizophrenia.
Early life immune aberrations have strongly been associated with the risk of schizophrenia. Amongst them, inflammation induced neurodevelopmental origin has emerged as one of the widely recognized underlying mechanisms. Interleukin-10 (IL-10) is an important anti-inflammatory and immunoregulatory cytokine.
View Article and Find Full Text PDFThe Major Histocompatibility Complex (MHC)/Human Leukocyte Antigen (HLA) is known to influence the pathogenesis of several complex human diseases resulting from gene-environmental interactions. Recently, it has emerged as one of the risk determinants of schizophrenia. The HLA-G protein (a non-classical MHC class I molecule), encoded by the HLA-G gene, is shown to play important role in embryonic development.
View Article and Find Full Text PDFBackground And Aim: Transcranial direct current stimulation (tDCS) is a non-invasive and well-tolerated brain stimulation technique with promising efficacy as an add-on treatment for schizophrenia and for several other psychiatric disorders. tDCS modulates neuroplasticity; psychiatric disorders are established to be associated with neuroplasticity abnormalities. This review presents the summary of research on potential genetic basis of neuroplasticity-modulation mechanism underlying tDCS and its implications for treating various psychiatric disorders.
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- * Impaired mitochondrial function can disrupt energy processes in the brain, potentially leading to neurodevelopmental issues such as schizophrenia, which has a neurodevelopmental origin influenced by inflammation.
- * Current research suggests that mitochondrial dysfunction may trigger inflammatory responses that contribute to the progression of schizophrenia, with evidence from various scientific studies supporting this connection.