Publications by authors named "Rakesh S Dhanda"

Biofilms are assemblages of sessile microorganisms that form an extracellular matrix around themselves and mediate attachment to surfaces. The major component of the extracellular matrix of Uropathogenic E. coli and other Enterobacteriaceae are curli fibers, making biofilms robust and resistant to antimicrobials.

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Trichomonas vaginalis is the causative agent of Trichomoniasis (a sexually transmitted infection). Recent reports have shown that stimulation of cellular immunity can reduce trichomoniasis infection. Animal studies are essential to understanding the pathogenesis of infection and developing new potential drugs and vaccines to treat the infection.

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Urinary tract infections (UTI) are the most common infectious diseases in the world. It is becoming increasingly tough to treat because of emergence of antibiotic resistance. So, there is an exigency to develop novel anti-virulence therapeutics to combat multi-drug resistance pathogenic strains.

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RUNX1T1 has been found to be mutated in different cancers such as prostate, lung, colon, and breast cancer. A recent computational study involving the TCGA database of glioma patients found RUNX1T1 as one of the downregulated driver genes associated with poor overall survival of glioma patients. Hypoxia-inducible factor 1α (HIF1α) is upregulated in glioma and has been associated with the severity and drug resistance of glioma.

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is a parasitic protozoan that causes trichomoniasis. The involvement of NLRP3 inflammasome in trichomoniasis has been discussed in recent studies. The present study aimed to find out the involvement of , and in the BALB/c mouse model infected with symptomatic and asymptomatic isolates of by quantitative real-time PCR and immunohistochemistry.

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Hemolysin expressing UPEC strains have been associated with severe advanced kidney pathologies, such as cystitis and pyelonephritis, which are associated with an inflammatory response. Macrophages play an important role in regulating an inflammatory response during a urinary tract infection. We have studied the role of purified recombinant α-hemolysin in inducing inflammatory responses and cell death in macrophages.

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Trichomoniasis is caused by (a protozoan parasite). About 80% of the infected cases remain asymptomatic [1]. The differential response of showing symptoms or no symptoms is not yet explored.

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Background: Inflammatory response during urinary tract infection (UTI) is mediated by innate immune defense. Nod like receptors (NLRs) have been proposed to work simultaneously beside TLR pathways to mediate pro-inflammatory response and maintain tissue homeostasis. Some reports have showed the involvement of inflammasome during uropathogenic (UPEC) mediated UTI.

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Background: Hospital acquired infections (HAI) are principal threats to the patients of intensive care units. An increase in the antimicrobial resistance (AMR) observed in gram negative bacteria is a great challenge to deal with. HAI and AMR lead to prolonged hospitalization and additional doses of anti-microbial treatment affecting patient's fitness and finances.

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Urinary tract infections (UTI) are a major cause of morbidity, affecting at least four million women worldwide, 65-75% of these infections are caused by Uropathogenic (UPEC) (Foxman, 2010) [1]. Repertoire of virulence factors carried by UPEC provides the ability to precede urinary tract and additionally they provoke pro-inflammatory responses (Cirl et al., 2008; Verma et al.

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is one of the most frequently prevalent pathogens, causing infections in health care settings throughout the world. Here, we report the whole-genome sequence of MN067, a commensal bacterium with a pathogenic potential.

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Inflammasomes are multiprotein complexes present in the cytosol as pattern recognition receptors or as sensors of damage-associated molecular patterns. After recognition of microbe-associated molecular patterns or host-derived danger signals, nucleotide oligomerization domain-like receptors oligomerize to form inflammasomes. The activation of inflammasomes results in an alarm, which is raised to alert adjacent cells through the processing and release of a number of other substrates present in the cytosol.

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The oncogenic potential of Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G (APOBEC3G) was recently appreciated by the finding that revealed its ability to downregulate Kruppel-like factor 4 (KLF4) gene translation through its affinity for 3'UTR of KLF4 mRNA. Keeping in view the fact that KLF4 is known to repress apoptosis antagonizing transcription factor (AATF) gene expression, the present study employed stem cells as archetype model to explore the effect of APOBEC3G over-expression upon AATF gene expression within these cells as well as on the genes involved in oncogenic transformation. Such a study revealed that APOBEC3G had the ability to bind AATF mRNA within its third exon to facilitate the generation of truncated 23 kDa AATF translation product which, in turn, had the inherent capacity to be the crucial mediator of APOBEC3G induced oncogenic transformation within such cells.

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The infection of epithelial cells is a necessary step for Mycobacterium bovis BCG dissemination, but the mechanism of mycobacterial epithelial interactions is not completely understood. Similarly, Streptococcus pyogenes is a strictly human pathogen that favorably colonizes the skin and the pharynx. Effective cytokine secretion is essential in order to fabricate a suitable inflammatory response against an infection.

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Bacterial virulence factors (VFs) influence the site and severity of urinary tract infections (UTI) and further leading to sepsis infection. Phenotypic characterisation of VFs specific to sepsis strains has not been characterized in Indian population till date. In this data article, we have described important VFs of uropathogenic (UPEC) that is P fim, Type-1 fim, cell surface hydrophobicity, mannose resistant haemagglutination/mannose sensitive haemagglutination (MRHA/MSHA) expression and α-haemolysin production.

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Purpose: We evaluated the status of autophagy in different grades of urothelial carcinoma and explored autophagy modulators as a potential adjunctive therapeutic agent for urothelial carcinoma.

Materials And Methods: The study was performed in tumor tissue from patients with low and high grade urothelial carcinoma, in normal urothelial tissue and in the T24 cell line. Autophagic vesicles and the expression of various autophagic proteins were studied in tissue samples by transmission electron microscopy and Western blot, respectively.

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Background: MTG16, MTGR1 and ETO are nuclear transcriptional corepressors of the human ETO protein family. MTG16 is implicated in hematopoietic development and in controlling erythropoiesis/megakaryopoiesis. Furthermore, ETO homologue genes are 3'participants in leukemia fusions generated by chromosomal translocations responsible of hematopoietic dysregulation.

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Background: The in vivo clinical significance of malignant stem cells remains unclear.

Methods: Patients who have the 5q deletion (del[5q]) myelodysplastic syndrome (interstitial deletions involving the long arm of chromosome 5) have complete clinical and cytogenetic remissions in response to lenalidomide treatment, but they often have relapse. To determine whether the persistence of rare but distinct malignant stem cells accounts for such relapses, we examined bone marrow specimens obtained from seven patients with the del(5q) myelodysplastic syndrome who became transfusion-independent while receiving lenalidomide treatment and entered cytogenetic remission.

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Background: The Eight-Twenty-One (ETO) nuclear co-repressor gene belongs to the ETO homologue family also containing Myeloid Translocation Gene on chromosome 16 (MTG16) and myeloid translocation Gene-Related protein 1 (MTGR1). By chromosomal translocations ETO and MTG16 become parts of fusion proteins characteristic of morphological variants of acute myeloid leukemia. Normal functions of ETO homologues have as yet not been examined.

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Article Synopsis
  • ETO, MTG16, and MTGR1 are transcriptional repressors that interact with corepressors like SIN3 and N-CoR, often involved in acute myeloid leukaemia (AML) through fusion proteins.
  • Researchers studied how ETO and MTG16 repress transcription, focusing on specific regions of these proteins and their interactions with corepressors, using a luciferase reporter system in a cell line.
  • Findings showed that while certain regions of ETO and MTG16 are important for repression, the presence of corepressors hSIN3B and N-CoR did not significantly enhance this repression, suggesting that their roles in transcription regulation might be more complex than previously thought.
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Background: SIN3 (SWI-Independent) is part of a transcriptional deacetylase complex, which generally mediates the formation of repressive chromatin. The purpose of this work was to study possible interactions between corepressors human SIN3B (hSIN3B) and the ETO homologues - ETO (eight twenty-one), MTG16 (myeloid-transforming gene 16) and MTGR1 (MTG-related protein 1). In addition, the subnuclear localization of the hSIN3B and the ETO homologues was also examined.

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