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Begum, R.

Publications and source records attributed to Begum, R..

10 recordsLinked to original sources

Focused Ultrasound Neuromodulation of the Central Lateral Thalamus in a Non-Human Primate Model of Disorders of Consciousness

Objectives: Disorders of consciousness (DOC) affect an estimated 200,000 patients in the United States. Effective treatment options have remained elusive. Focused ultrasound neuromodulation (FUS) of brain regions controlling consciousness, such as the central lateral thalamus (CLT), has emerged as a promising non-invasive treatment. However, prior studies have been limited by broad effective stimulation volumes, missing control conditions, and limited target validation. This study investigated the effects of FUS of the CLT in a non-human primate model of DOC with robust control conditions and more robust targeting than previous experiments. Materials and Methods: Two male rhesus macaques underwent 1-hour propofol anesthesia sessions as a model of DOC. Bilateral CLT targets were sonicated using a stereotactically mounted 256-element phased-array focused ultrasound system. Focused and unfocused (random phases) paradigms were tested in both animals, and a spotlighting (sonicating multiple targets) paradigm was tested in one animal. Arousal was monitored via EEG beta power, pulse oximetry, breathing rate, and movement, and compared between sonication and control sessions for each paradigm. Results: Paired Wilcoxon signed-rank tests showed no significant differences for any of the four measures across the three paradigms (all pFDR [≥] 0.30). The largest observed effect was increased body movement under the unfocused paradigm (rrb = +0.58), though this did not reach statistical significance. Animals remained physiologically stable throughout sessions and recovery periods, with no clinically significant changes in heart rate, breathing rate, blood oxygen saturation, or other safety concerns. Conclusions: Under the tested parameters, FUS of the CLT did not produce measurable changes in arousal. The absence of adverse physiological effects supports the safety of this FUS paradigm. The largest effect occurring under spatially distributed sonication, consistent with prior evidence that broader stimulation volumes produce stronger arousal responses, suggests that distributed network stimulation may warrant investigation as an alternative to focal targeting. Future studies should investigate this possibility and should include robust control conditions to properly quantify effects.

neuroscience↗

Melatonin and GABA monotherapies are as efficacious as combination therapy in managing T1D and T2D: In-vivo studies on experimental diabetic models

BackgroundLoss of functional {beta}-cell mass is a critical factor in the ontogenesis of type 1 (T1D) and type 2 diabetes (T2D) marked by chronic hyperglycemia. Melatonin (M) and {gamma}-aminobutyric acid (GABA/G) have immunoregulatory properties and have shown potential to increase {beta}-cell mass in experimental diabetic models. Thus, we aimed to investigate the therapeutic potential of melatonin combined with GABA on {beta}-cell regeneration in streptozotocin (STZ)-induced T1D and on a high-fat diet (HFD)-induced T2D mouse models. MethodsThe BALB/c mice were injected with 50 mg/kg body weight STZ on five consecutive days to induce T1D and were subjected to six weeks of monotherapy with melatonin or GABA and combination therapy (M+G). HFD was fed to C57BL/6J mice for 30 weeks to induce insulin resistance and T2D, followed by six weeks of mono or combination therapy exposure. ResultsOur studies on monotherapies and combination therapy reduced fasting blood glucose levels, increased plasma insulin levels and glucose tolerance, and promoted {beta}-cell proliferation and transdifferentiation, with a simultaneous decrease in {beta}-cell apoptosis in T1D mice. It also improved metabolic parameters and glycolipid metabolism in the liver and adipose tissue, respectively, and increased mitochondrial function in the skeletal muscle. Moreover, it restored peripheral insulin sensitivity and {beta}-cell mass in T2D mice. ConclusionOur studies suggest that monotherapies are as effective as combination therapy since melatonin and GABA sub-additively ameliorates T1D and T2D manifestations.

biochemistry↗

Genetic and immune landscape evolution defines subtypes of MMR deficient colorectal cancer

Mismatch repair deficient colorectal cancers have high mutation loads and many respond to immune checkpoint-inhibitors. We investigated how genetic and immune landscapes co-evolve in these tumors. All cases had high truncal mutation loads. Driver aberrations showed a clear hierarchy despite pervasive intratumor heterogeneity: Those in WNT/{beta}Catenin, mitogen-activated protein kinase and TGF{beta} receptor family genes were almost always truncal. Immune evasion drivers were predominantly subclonal and showed parallel evolution. Pan-tumor evolution, subclonal evolution, and evolutionary stasis of genetic immune evasion drivers defined three MMRd CRC subtypes with distinct T-cell infiltrates. These immune evasion drivers have been implicated in checkpoint-inhibitor resistance. Clonality and subtype assessments are hence critical for predictive immunotherapy biomarker development. Cancer cell PD-L1 expression was conditional on loss of the intestinal homeobox transcription factor CDX2. This explains infrequent PD-L1 expression by cancer cells and likely contributes to the high recurrence risk of MMRd CRCs with impaired CDX2 expression.

cancer biology↗

Calorie Restriction in combination with GABA: improved glycaemic control in type 2 diabetes mouse model

AimDysfunctional adipocytes and {beta}-cells are crucial in the advancement of obesity-induced type 2 diabetes (T2D). Calorie restriction (CR) improves insulin sensitivity and fasting blood glucose (FBG) levels, while {gamma}-aminobutyric acid (GABA), a neurotransmitter secreted by {beta}-cells, exerts regenerative effects. MethodsHigh-fat diet (HFD) and streptozotocin (STZ) induced T2D mouse model was used to assess the effect of CR and GABA combination therapy. The mice were fed with CR diet (30% reduction of HFD) and treated with GABA (2.5 mg/kg i.p) daily for 5 weeks. Assessment of FBG, body weight (BW), insulin sensitivity, glucose tolerance, and estimation of plasma insulin and lipid profile were carried out by standard methods. The mRNA expression of target genes [liver (glucoregulatory enzymes), adipose tissue (lipid metabolism markers) and skeletal muscle (mitochondrial biogenesis markers)] was assessed by SYBR Green-qPCR. Oxygen consumption rate for mitochondrial complex I, II and III was measured in skeletal muscle using Oxytherm Clark-type oxygen electrode. The effect of monotherapies and combination treatment on pancreatic {beta}-cell regeneration and apoptosis was analysed by IHC. ResultsCR+GABA group showed significant reduction in FBG levels, improved lipid profile and whole-body insulin responsiveness as indicated by increased insulin levels, insulin sensitivity and glucose tolerance compared to the monotherapies. The transcript expression profile of glucoregulatory enzymes in the liver showed significant reduction in G6Pase, PEPCK, Glycogen Phosphorylase and increased GCK expression in CR+GABA group as compared to the monotherapies The ACC and ATG expression was up-regulated in adipose tissue; and significant increase in SIRT-1, PGC-1 and TFAM expression with up-regulated mitochondrial complex I and III activities was observed in CR+GABA group as compared to the monotherapies. Percentage of BrdU/Insulin and PDX1/Ngn3/Insulin co-positive cells was significantly higher in CR+GABA treated group than the monotherapy and HFD+STZ groups. Finally, there was a significant reduction in TUNEL/Insulin co-positive cells suggesting reduced apoptosis in CR+GABA treated group. ConclusionOur results suggest that CR in combination with GABA ameliorates T2D in HFD+STZ treated mice, by GABA induced {beta}-cell regeneration and CR mediated insulin sensitivity.

physiology↗

Repurposing statin and L-glutamine: replenishing β-cells in hyperlipidemic T2D mouse model

While cases of obesity-induced type 2 diabetes (T2D) are on the upswing, current therapies help only manage the symptoms. Of late, L-glutamine has been implicated in the amelioration of T2D by virtue of its glucagon like peptide-1 (GLP-1) secretagogue property. Alongside, there are mixed reports on adiponectin (insulin sensitizer) potentiating property of statins. We aimed to investigate the effect of pitavastatin (P) and L-glutamine (LG) combination on glycemic control and pancreatic {beta}-cell regeneration in a high-fat diet (HFD)+Streptozotocin (STZ) induced T2D mouse model. C57BL6/J mice treated with HFD+STZ were randomly assigned into four groups: Diabetic control, L-glutamine, Pitavastatin and P+LG. Control group was fed with the chow diet. Significant amelioration in insulin resistance along with plasma glucose, lipid profile, adiponectin levels, and mitochondrial complexes I, II, III activities were observed in P+LG group as compared to HFD+STZ treated group. Phosphoenolpyruvate carboxykinase, glucose 6-phophatase, glycogen phosphorylase, and GLUT2 transcript levels were reduced with increased glycogen synthase transcript levels in liver. Further, the protein levels of Insulin receptor 1-{beta}, pAkt/Akt, and AdipoR1 were restored in the skeletal muscle and a significant increase in islet number as a result of {beta}-cell regeneration and reduced {beta}-cell death were also observed in the combination drug treated group. Thus, L-glutamine and pitavastatin in combination can induce {beta}-cell regeneration and regulate glucose homeostasis to bring about amelioration of HFD+STZ induced T2D.

biochemistry↗

Antimicrobial Resistance Profile and mcr-1 gene Detection in Salmonella Isolates from Poultry in Bangladesh: Molecular and Bioinformatics Characterization

Antimicrobial resistance gene mcr-1 has been disseminated globally since its first discovery in Southern China in late 2015. However, the mcr-1 gene had not been identified previously in Salmonella isolates from poultry in Bangladesh. Here, we aimed to explore antimicrobial resistance gene mcr-1 in Salmonella isolates. Eighty two Salmonella isolates were isolated and characterized from suspected poultry specimens received from different zones of the country. A phenotypic disc diffusion assay with 15 antimicrobial agents was performed following CLSI standard. The disk diffusion assay showed that, all of the isolates presented high resistance to colistin (92.68%), oxytetracycline (86.59%), co-trimoxazole (76.83%), ciprofloxacin (73.17%) and enrofloxacin (65.85%). Further, randomly selected 10 Salmonella isolates were analyzed by polymerase chain reaction (PCR) targeting genus-specific invA and antimicrobial (colistin) resistance mcr-1 genes. Five were confirmed for the presence of the mcr-1 gene belonging to Salmonella spp. Further, sequencing followed by phylogenetic analysis revealed divergent evolutionary relation between the LptA and MCR proteins rendering them resistant to colistin. Three-dimensional homology structures of MCR-1 proteins were constructed and verified using different bioinformatics tools. Moreover, molecular docking interactions suggested that, MCR-1 and LptA share a similar substrate binding cavity which could be validated for the functional analysis. The results represent here is the first molecular and in silico analysis of colistin resistance mcr-1 gene of Salmonella in poultry in Bangladesh, which may emphasize the importance of the study on antibiotic resistance genes requiring for national monitoring and strategic surveillance in the country.

microbiology↗

Genomic and transcriptomic determinants of therapy resistance and immune landscape evolution during anti-EGFR treatment in colorectal cancer

Anti-epidermal growth factor receptor (EGFR) antibodies (anti-EGFR-Ab) are effective in a subgroup of patients with metastatic colorectal cancer (CRC). We applied genomic and transcriptomic analyses to biopsies from 35 RAS wild-type CRCs treated with the anti-EGFR-Ab cetuximab in a prospective trial to interrogate the molecular resistance landscape. This validated transcriptomic CRC-subtypes as predictors of cetuximab benefit; identified novel associations of NF1-inactivation and non-canonical RAS/RAF-aberrations with primary progression; and of FGF10- and non-canonical BRAF-aberrations with AR. No genetic resistance drivers were detected in 64% of AR biopsies. The majority of these had switched from the cetuximab-sensitive CMS2-subtype pretreatment to the fibroblast- and growth factor-rich CMS4-subtype at progression. Fibroblast supernatant conferred cetuximab resistance in vitro, together supporting subtype-switching as a novel mechanism of AR. Cytotoxic immune infiltrates and immune-checkpoint expression increased following cetuximab responses, potentially providing opportunities to treat CRCs with molecularly heterogeneous AR with immunotherapy.

cancer biology↗

Electrospun Cellulose-Silk Composite Nanofibres Direct Mesenchymal Stem Cell Chondrogenesis in the Absence of Biological Stimulation

Smart biomaterials with an inherent stimulating capacity that elicit specific behaviours in lieu of biological prompts would prove advantageous for regenerative medicine applications. Specific blends of the natural polymers cellulose and silk cast as films can drive the chondrogenic differentiation of human bone marrow mesenchymal stem cells (hMSCs) upon in vitro culture. However, the true potential of such biomaterials for cartilage tissue engineering can be realised upon its three-dimensional fabrication. In this work we employ an electrospinning technique to model the in vivo nanofibrous extracellular matrix (ECM). Cellulose and silk polymers at a mass ratio of 75:25 were regenerated using a trifluoroacetic acid and acetic acid cosolvent system. This natural polymer composite was directly electrospun for the first time, into nanofibers without post-spun treatment. The presence and size of fibre beading was influenced by environmental humidity. The regenerated composite retained the key chemical functionalities of its respective components. Biocompatibility of the natural polymer composite with hMSCs was demonstrated and its inherent capacity to direct chondrogenic stem cell differentiation, in the absence of stimulating growth factors, was confirmed. This physical chondrogenic stimulation was countered biochemically using fibroblast growth factor-2 (FGF-2), a growth factor used to enhance the proliferation of hMSCs. The newly fabricated scaffold provides the foundation for designing a robust, self-inductive, and cost-effective biomimetic biomaterial for cartilage tissue engineering.

bioengineering↗

Mesenchymal Stem Cell Chondroinduction on Cellulose-Silk Composites is Driven by Substrate Elasticity

Biomaterials that can physically control the fate of stem cells are critical for the application of in situ tissue engineering. However, the mechanisms underlying this phenomenon remain unclear. In this study, cellulose and silk composite substrates, known to induce physically the chondrogenic differentiation of human mesenchymal stem cells (MSCs), were regenerated to fabricate two-dimensional film surfaces. MSCs were grown on these surfaces in the presence of chemicals that interfere with the biochemical and mechanical signalling pathwys of MSCs. The data shows that preventing substrate surface elasticity transmission results in significant downregulation of chondrogenic gene expression. Interference with the classical, chondrogenic Smad2/3 Phosphorylation pathway does not impact the chondrogenic capacity of the substrates. The results highlight the importance of the substrate mechanical elasticity on chondrogenic MSCs and its independence of known chondrogenic biochemical pathways.

bioengineering↗

Ultra-sensitive mutation detection and genome-wide DNA copy number reconstruction by error corrected circulating tumour DNA sequencing

Minimally invasive circulating free DNA (cfDNA) analysis can portray cancer genome landscapes but highly sensitive and specific genetic approaches are necessary to accurately detect mutations with often low variant frequencies. We developed a targeted cfDNA sequencing technology using novel off-the-shelf molecular barcodes for error correction, in combination with custom solution hybrid capture enrichment. Modelling based on cfDNA yields from 58 patients shows that our assay, which requires 25ng of cfDNA input, should be applicable to >95% of patients with metastatic colorectal cancer. Sequencing of a 163.3 kb target region including 32 genes detected 100% of single nucleotide variants with 0.15% variant frequency in cfDNA spike-in experiments. Molecular barcode error correction reduced false positive mutation calls by 98.6%. In a series of 28 patients with metastatic colorectal cancers, 80 out of 91 (88%) mutations previously detected by tumour tissue sequencing were called in the cfDNA. Call rates were similar for single nucleotide variants and small insertions/deletions. Mutations only called in cfDNA but not detectable in matched tumour tissue included, among others, a subclonal resistance driver mutation to anti-EGFR antibodies in the KRAS gene, multiple activating PIK3CA mutations in each of two patients (indicative of parallel evolution), and TP53 mutations originating from clonal haematopoiesis. Furthermore, we demonstrate that cfDNA off-target read analysis allows the reconstruction of genome wide copy number aberration profiles from 71% of these 28 cases. This error-corrected ultra-deep cfDNA sequencing assay with a target region that can be readily customized enables broad insights into cancer genomes and evolution.

genomics↗