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Ahmad, F.

Publications and source records attributed to Ahmad, F..

At least 19 recordsLinked to original sources

Integrated in silico identification of fungal-derived dual-target inhibitors for anti-schistosomal drug discovery

Praziquantel, which has limited efficacy against young parasites and reduces susceptibility, is the principal therapy for schistosomiasis, a neglected tropical illness. This work identified fungal-derived compounds with potential dual inhibitory action against Schistosoma mansoni DHODH and cathepsin B1 using an integrated computational method. From 1,831 fungal metabolites, 120 were selected for molecular docking after structure standardisation, drug-likeness evaluation, ADMET, and toxicity screening. Ganoderlactone B (CID_122184973) and Spiroapplanatumine F (CID_132962217) strongly bound to DHODH and CB1, with docking affinities of -10.6 and -10.0 kcal/mol and -9.0 and -8.9, respectively. Docking validation showed good discrimination between active compounds and decoys with area-under-the-curve values of 0.98 for DHODH and 0.96 for CB1. The protein-ligand interaction study showed hydrogen bonding, hydrophobic interactions, and van der Waals contacts at the binding sites. In 100 ns molecular dynamics simulations, protein complexes exhibited modest backbone deviations and maintained compactness, although CID_132962217 showed sustained binding and a constrained conformation. MM-PBSA analysis identified CID_122184973 as the best common ligand for both targets. At the B3LYP/6-31G level, density functional theory calculations showed that CID_139584993 had the lowest HOMO-LUMO energy gap and hardness values of 3.552 and 1.776 eV, respectively, and the highest softness value of 0.282 eV-1, indicating greater electronic reactivity. Electrostatic potential mapping and QSAR predictions supported their interaction and antiparasitic potential. Overall, CID_122184973 and CID_132962217 are promising fungal scaffolds for dual-target anti-schistosomal drug development. Experimental enzyme inhibition, parasite viability, toxicity, and in vivo research are needed to confirm computational findings.

bioinformatics↗

From topography to connectome: Towards an integrated understanding of the resting brain

As the field expands from early research into the human connectome, there has been a fast expansion in the number of analytical approaches to study resting state functional MRI (rsfMRI) data. With increasing focus on individual differences, topographical brain maps of spatial organization have emerged in addition to traditional functional connectomes. Here, we developed a deep-learning model to embed maps of network topography and faithfully translate to individualized connectomes. Results confirmed the validity of the surface vision transformer based on reconstruction accuracy (0.73{+/-}0.09) and accurate topography-to-connectome translation (0.43{+/-}0.08). Importantly, translated connectomes retained identifiability and brain-cognition associations. These findings establish a direct mapping from spatial topography to connectomes that can be used to integrate scientific insights across rsfMRI sub-fields. This is an important step towards broadening our conceptualization of the connectome and supporting a broader integration of findings to inform a complete understanding of the human connectome. TeaserTranslating from spatial maps of brain organization to region-to-region connectomes retains shared individual differences.

bioinformatics↗

Profiles of Aging Based on Cognition, Affect, and Brain Reserve

The aging paradox describes improvements in emotional wellbeing as a function of aging, despite declines in cognition. Conversely, late life depression has been associated with increased cognitive decline in aging. We sought to understand these seemingly contradictory patterns of cognitive and mental health in older age. Building on cognitive reserve, affective reserve, and brain reserve models of aging, we developed three alternative algorithmic approaches to group N=22,686 participants from the UK Biobank into different profiles of aging. Our results revealed that aging profiles identified using our data-driven brain reserve model, which incorporated measures of cognition, neuroticism, and brain volume, achieved the highest validation results. Importantly, only two of the four aging profiles were characterized by the aging paradox (i.e., improved emotionality and decreased cognition with age). We identified one profile characterized by particularly low levels of neuroticism and relative resilience to cognitive decline. Another profile benefited from relatively preserved brain volumes, potentially driven by younger ages and/or higher socioeconomic status. Conversely, we identified two profiles with poorer health characteristics, including one profile with elevated cardiovascular risk. Taken together, these findings enrich our understanding of the emotion paradox and highlight the value of taking a nuanced and stratified approach when studying aging. In the future, aging profiles could be used to target preventative strategies to address modifiable risk factors and improve lifespan and healthspan.

neuroscience↗

Evolutionary divergence in sympatric populations of the fungal pathogen Alternaria alternata across wild tomato hosts

Alternaria alternata is a globally distributed fungal pathogen with a broad host range, increasingly affecting both tomato crops and wild tomato relatives. The genomic basis of this ecological breadth in A. alternata remains poorly understood. Here we leverage the opportunity of wild pathosystems to study pathogen evolution and diversity beyond agricultural settings. We sampled isolates from wild tomato species across a 2,500 km range in South America, producing highly contiguous genomes, to investigate population structure. Our comparative genomics analyses reveal that A. alternata sensu stricto consists of two divergent clades. Strikingly, this divergence is not linked to host species, geography, or habitat type. Transposable elements contribute to variation within clades but do not explain their separation. Although some signs of recombination are present, reproductive mode appears stable across clades. Notably, global reference isolates cluster with one clade, while the other, more diverse clade is only found in wild populations. We hypothesize that these wild populations may act as reservoirs of evolutionary potential. These findings challenge prevailing assumptions about the population structure of necrotrophic pathogens and raise new questions about how genetic divergence can persist without ecological or geographic isolation. Media summary (lay abstract)The fungus Alternaria alternata is an emerging threat on tomato and potato crops. In a previous study, we found that it also infects wild tomato plants over a large range in Chile and Peru. Here we sequenced and compared full genomes of the fungi. Surprisingly, they formed two distinct groups that do not reflect different host plant species, geographical locations, or environments. One of those groups is related more closely to global reference samples, while the other group is more diverse. This suggests wild plants may quietly harbour forms of the fungus that could affect crops in the future.

genomics↗

The neuroimaging correlates of depression established across six large-scale datasets

Neuroimaging data offers noninvasive insights into the structural and functional organization of the brain and is therefore commonly used to study the neuroimaging correlates of depression. To date, a substantial body of literature has suggested reduced size of subcortical regions and abnormal functional connectivity in frontal and default mode networks linked to depression. However, recent meta analyses have failed to identify significant converging correlates of depression across the literature such that a conclusive mapping of the neuroimaging correlates of depression remains elusive. Here we leveraged 23,417 participants across six datasets to comprehensively establish the neuroimaging correlates of depression. We found reductions in gray matter volume/ cortical surface area associated with depression in the frontal cortex, anterior cingulate, and insula, confirming prior studies showing the importance of prefrontal and default mode regions in depression. Our findings demonstrate multiple surprising results, including a lack of depression correlates in subcortical brain regions, significant depression correlates in somatomotor and visual regions, and limited functional connectivity findings. Overall, these results shed new light on key brain regions involved in the pathophysiology of depression, updating our understanding of the neuroimaging correlates of depression. We anticipate that these insights will inform further research into the role of sensorimotor and visual regions in depression and into the impact of heterogeneity on functional connectivity correlates of depression.

neuroscience↗

Application of spatial transcriptomics across organoids: a high-resolution spatial whole-transcriptome benchmarking dataset

Stem cell-derived organoids hold promise to model tissue-specific disease. To enable this, it is crucial to assess how transcriptional signatures, cellular organisation and composition of organoids compare to in vivo counterparts. However, technologies which elucidate regional molecular identity, like spatial transcriptomics, have been challenging to apply to organoids. This study presents the first systematic profiling of multiple stem cell derived organoid models (brain, heart muscle, heart valve, kidney, lung, cartilage, and haematopoietic) with Stereo-seq, a full transcriptome, spatial transcriptomics assay using on-chip in situ RNA capture at subcellular resolution. It describes optimisation of this assay to characterise organoids, use of multiple organoid samples on a single chip, assess differences in RNA capture efficiency compared to reference tissues and its limitations. This study introduces a bespoke analysis method that partitions samples into regions and further characterises them. These findings inform future works to characterise organoids using spatial transcriptomics, providing insights in optimising RNA capture of multiple organoids across a chip and novel methods for regional analysis.

bioinformatics↗

Methylsulfonylmethane: A Potential Dietary Supplement targeting sphingosine kinase 1 involved in Glioblastomamultiforme

Methylsulfonylmethane (MSM) is a common dietary supplement mainly used for inflammatory disorders as well as MSM had shown anti-tumor effects on different types of cancers. However, the glioma cell line has not been tested against MSM, and we are reporting it in our study for the first time. This research used an in silico study in which sphingosine kinase 1(SphK1) is used as a therapeutic target which is associated with Glioblastoma multiforme(GBM) SphK1 is pivotal enzyme for sphingolipid metabolism whose high expression level is thought to be associated with cancer alongside other inflammatory diseases and it is a potential drug target for various types of cancer.First, in silico analysis was executed to evaluate the inhibitory effect of MSM on SphK1.Then we further observed the anti-tumor activities of MSM on the C6 glioma cell line. During in silico investigation at the initial stage, we performed molecular docking with Auto Dock Vina followed by molecular dynamics simulation at 100ns with Gromacs Software Package.MSM binds with SphK1 with a docked score of -2.1 kcal mol1. During molecular dynamics simulation complex maintain stability at 10ns but we ran simulation till 100ns to confirm the stability. We performed in depth analysis which includes post trajectory analysis like free energy landscape (FEL), principal constant analysis (PCA) with kernel density (KDE)estimation plots as well as probability distribution plots. Even molecular dynamics simulation shows stability, compactness and interaction of MSM with Sphk1, we calculated MMPBSA binding energy calculation is -13.922 +/- 19.518 kJ/mol- The viability and cellular metabolic activity of the C6 glioma in the presence of MSM showed 393.459 mM/ml of MSM reduced cell viability by 50% (CTC50) value in dose dependent manner. Further analysis like DNA fragmentation assay and Acridine orange and ethidium bromide (AO/EB) staining were carried out, which clearly depicts MSM inducing apoptosis in C6 gliomas. Based on in silico and in vitro results,for the first time we are reporting it in our study and we reach to conclusion that that MSM acts as a potential inhibitor for SphK1 as well as inhibits the growth of glioma cells and acts as a potential dietary supplement for the management of GBM which can cross blood brain barrier (BBB) and not toxic to cells even at high doze.

pharmacology and toxicology↗

GSK-3alpha-BNIP3 axis promotes mitophagy in human cardiomyocytes under hypoxia

Dysregulated autophagy/mitophagy is one of the major causes of cardiac injury in ischemic conditions. Glycogen synthase kinase-3alpha (GSK-3) has been shown to play a crucial role in the pathophysiology of cardiac diseases. However, the precise role of GSK-3 in cardiac mitophagy remains unknown. Herein, we investigated the role of GSK-3 in cardiac mitophagy by employing AC16 human cardiomyocytes under the condition of acute hypoxia. We observed that the gain-of-GSK-3 function profoundly induced mitophagy in the AC16 cardiomyocytes post-hypoxia. Moreover, GSK-3 overexpression led to increased ROS generation and mitochondrial dysfunction in cardiomyocytes, accompanied by enhanced mitophagy displayed by increased mt-mKeima intensity under hypoxia. Mechanistically, we identified that GSK-3 promotes mitophagy through upregulation of BNIP3, caused by GSK-3-mediated increase in expression of HIF-1 and FOXO3a in cardiomyocytes post-hypoxia. Moreover, GSK-3 displayed a physical interaction with BNIP3 and, inhibited PINK1 and Parkin recruitment to mitochondria was observed specifically under hypoxia. Taken together, we identified a novel mechanism of mitophagy in human cardiomyocytes. GSK-3 promotes mitochondrial dysfunction and regulates FOXO3a -mediated BNIP3 overexpression in cardiomyocytes to facilitate mitophagy following hypoxia. An interaction between GSK-3 and BNIP3 suggests a role of GSK-3 in BNIP3 recruitment to the mitochondrial membrane where it enhances mitophagy in stressed cardiomyocytes independent of the PINK1/Parkin.

cell biology↗

Natural compound screening predicts novel GSK-3 isoform-specific inhibitors

Glycogen synthase kinase-3 (GSK-3) plays important roles in the pathogenesis of cardiovascular, metabolic, neurological disorders and cancer. Isoform-specific loss of either GSK-3 or GSK-3{beta} often provides cytoprotective effects under such clinical conditions. However, available synthetic small molecule inhibitors are relatively non-specific, and their chronic use may lead to adverse effects. Therefore, screening for natural compound inhibitors to identify the isoform-specific inhibitors may provide improved clinical utility. Here, we screened 70 natural compounds to identify novel natural GSK-3 inhibitors employing comprehensive in silico and biochemical approaches. Molecular docking and pharmacokinetics analysis identified two natural compounds Psoralidin and Rosmarinic acid as potential GSK-3 inhibitors. Specifically, Psoralidin and Rosmarinic acid exhibited the highest binding affinities for GSK-3 and GSK-3{beta}, respectively. Consistent with in silico findings, the kinase assay-driven IC50 revealed superior inhibitory effects of Psoralidin against GSK-3 (IC50=2.26 {micro}M) vs. GSK-3{beta} (IC50=4.23 {micro}M) while Rosmarinic acid was found to be more potent against GSK-3{beta} (IC50=2.24 {micro}M) than GSK-3 (IC50=5.14 {micro}M). Taken together, these studies show that the identified natural compounds may serve as GSK-3 inhibitors with Psoralidin serving as a better inhibitor for GSK-3 and Rosmarinic for GSK-3{beta} isoform, respectively. Further characterization employing in vitro and preclinical models will be required to test the utility of these compounds as GSK-3 inhibitors for cardiometabolic and neurological disorders and cancers. HighlightsO_LICurrent GSK-3 inhibitors lack specificity and cause side effects. C_LIO_LIThis study identifies potential GSK-3 isoform-specific natural compounds. C_LIO_LIPsoralidin is likely a better inhibitor for GSK-3 while Rosmarinic for GSK-3{beta}. C_LIO_LIThese natural compounds may be promising future treatments. C_LI

biochemistry↗

Metabolic and imaging phenotypes associated with RB1 loss in castrate resistant prostate cancer

Advanced prostate cancer is treated with androgen receptor (AR) signaling inhibitors, which are initially effective, but most patients eventually develop resistance and progress to castrate-resistant prostate cancer (CRPC). Loss of RB1 in CRPC tumors is correlated with rapid progression and poor patient survival and, in combination with TP53 loss, predisposes patients to the development of transitional neuroendocrine prostate cancer (NEPC). Although progressive CRPC is clinically associated with higher 18FDG-PET SUVmax values, it is unknown whether inactivation of RB1 and/or TP53 is a driver of increased glucose import. Using a cohort of patient-derived xenograft (PDX)-derived CRPC organoids, we found that NEPC could not be conclusively distinguished from adenocarcinoma by 18FDG uptake alone, and PSMA protein levels did not correlate with cancer phenotype or 18FDG uptake. Castration-resistant models showed higher 18FDG uptake, but lower pyruvate-to-lactate conversion compared to their castration-sensitive counterparts. In parallel studies using castration-sensitive prostate cancer models, RB1/TP53 knockdown did not affect 18FDG uptake, but increased basal respiration and glycolytic activity, with combined depletion leading to glucose diversion into glycogenesis. These metabolic changes were reflected in increased lactate dehydrogenase flux detected by 13C-hyperpolarized magnetic resonance spectroscopy upon RB1 loss, but not in 18FDG uptake. The metabolic heterogeneity revealed here suggests that a multimodal molecular imaging approach can improve tumor characterization, potentially leading to a better prognosis in cancer treatment.

cancer biology↗

Technique for rapidly forming networks of microvessel-like structures

Modelling organ-blood barriers through the inclusion of microvessel networks within in vitro tissue models could lead to more physiologically accurate results, especially since organ-blood barriers are crucial to the normal function, drug transport, and disease states of vascularized organs. Microvessel networks are difficult to form, since they push the practical limit of most fabrication methods, and it is difficult to coax vascular cells to self-assemble into structures larger than capillaries. Here we present a method for rapidly forming networks of microvessel-like structures using sacrificial, alginate structures. Specifically, we encapsulated endothelial cells within short alginate threads, then embedded them in collagen gel. Following enzymatic degradation of the alginate, the collagen gel contained a network of hollow channels seeded with cells, all surrounding a perfusable central channel. This method uses a 3D printed coaxial extruder and syringe pumps to generate short threads in a way that is repeatable and easily transferrable to other labs. The cell-laden, sacrificial alginate threads can be frozen after fabrication and thawed before embedding without significant loss of cell viability. The ability to freeze the threads enables future scale up and ease of use. Within millifluidic devices that restrict access to media, the threads enhance cell survival under static conditions. These results indicate the potential for use of this method in a range of tissue engineering applications. Impact StatementGenerating microvascular networks is a challenge in tissue engineering. Popular 3D bioprinting techniques use sacrificial structures to generate vascular networks, but those approaches can require expensive equipment and extensive troubleshooting. In this article, a method is presented for easy and rapid generation of centimeter-scale microvascular networks using endothelial cells frozen within sacrificial structures. The method for fabricating and freezing the sacrificial threads of alginate containing cells using a 3D printed coaxial extruder is also described. Experimental results indicate that these microstructures have the potential to enhance cell survival in environments with restricted access to media.

bioengineering↗

Mathematical Modeling of PCR with Variable Concentrations of DNA and Taq Polymerase

Polymerase Chain Reaction (PCR) is one of the important techniques in molecular biology for many diagnostics and research applications. In this current theoretical PCR optimization research, out of its seven recipe reagents, two of the important constituents e.g., DNA which might be very rare in forensic cases and polymerase enzyme due to its high cost were mathematically modeled and computationally simulated using MATLAB programming platform. Chemical equations of PCR stages were established using the law of mass action followed by differential equations derivations from each of the DNA amplification phases. Firstly, a mathematical model of Taq polymerase enzyme with its variable concentrations ranging from 0.05-0.35 IU/L was formulated which showed the best PCR product of 0.61 ng/L obtained with 0.2 IU/L of polymerase. Similarly, by fixing the optimal polymerase concentration obtained in the previous simulation, the prime-DNA variable concentrations ranging from 0.5-3.5 ng/L were further simulated which showed the best PCR product of 0.94 ng/L at 2.0 ng/L of DNA. PCR wet-lab experimentation and gel-electrophoresis visualization validated mathematically simulated optimized concentrations of the aforementioned two reagents which vary the PCR product considerably. Current findings indicate that mathematically optimized concentrations of Taq-polymerase and template-DNA may reduce the PCR cost, time and energy, but other factors of target-sequence specificity, purity/concentrations of the other reagents, working hygiene, technical intricacies, biosafety and biosecurity factors may also contribute the desired yield of the amplicon.

bioengineering↗

Nicotinamide riboside kinase-2 inhibits JNK pathway and limits dilated cardiomyopathy in mice with chronic pressure overload

Nicotinamide riboside kinase-2 (NRK-2) has recently emerged as a critical regulator of cardiac remodeling however, underlying molecular mechanisms is largely unknown. To explore the same, NRK2 knockout (KO) and littermate control mice were subjected to trans-aortic constriction (TAC) or sham surgeries and cardiac function was assessed by serial M-mode echocardiography. A mild cardiac contractile dysfunction was observed in the KOs at the early adaptive phase of remodeling followed by a significant deterioration during the maladaptive cardiac remodeling phase. Consistently, NRK2 KO hearts displayed increased cardiac hypertrophy and heart failure reflected by morphometric parameters as well as increased fetal genes ANP and BNP expressions. Histological assessment revealed an extensive left ventricular (LV) chamber dilatation accompanied by elevated cardiomyopathy and fibrosis in the KO hearts post-TAC. In a gain-of-function model, NRK-2 overexpressing in AC16 cardiomyocytes displayed significantly attenuated fetal genes ANP and BNP expression. Consistently, NRK-2 overexpression attenuated angiotensin II-induced cardiomyocyte death. Mechanistically, we identified NRK-2 as a regulator of JNK MAP kinase and mitochondrial function where NRK-2 overexpression in human cardiomyocytes markedly suppressed the angiotensin II-induced JNK activation and mitochondrial depolarization. Thus, our results demonstrate that NRK-2 plays protective roles in pressure overload-induced dilatative cardiac remodeling and, genetic ablation exacerbates dilated cardiomyopathy, interstitial collagen deposition, and cardiac dysfunction post-TAC due, in part, to increased JNK activation and mitochondrial dysfunction.

molecular biology↗

Cardiomyocyte GSK-3β deficiency induces cardiac progenitor cell proliferation in the ischemic heart through paracrine mechanisms

Cardiomyopathy is an irreparable loss and novel strategies are needed to induce resident cardiac progenitor cell (CPC) proliferation in situ to enhance the possibility of cardiac regeneration. Here we sought to identify the potential roles of glycogen synthase kinase-3{beta} (GSK-3{beta}), a critical regulator of cell proliferation and differentiation, in CPC proliferation post-myocardial infarction (MI). Cardiomyocyte-specific conditional GSK-3{beta} knockout (cKO) and littermate control mice were employed and challenged with MI. Though cardiac left ventricular chamber dimension (LVID) and contractile functions were comparable at two-week post-MI, cKO mice displayed significantly preserved LV chamber and contractile function vs. control mice at four-weeks post-MI. Consistent with protective phenotypes, an increased percentage of c-kit-positive cells (KPCs) were observed in the cKO hearts at four and six-weeks post-MI which was accompanied by increased levels of cardiomyocyte proliferation. Further analysis revealed that the observed increased number of KPCs in the ischemic cKO hearts was mainly from a cardiac lineage as the majority of identified KPCs were negative for the hematopoietic lineage marker, CD45. Mechanistically, cardiomyocyte-GSK-3{beta} profoundly suppresses the expression and secretion of growth factors, including basic-FGF angiopoietin-2, erythropoietin, stem cell factor (SCF), PDGF-BB, G-CSF, and VEGF, post-hypoxia. In conclusion, our findings strongly suggest that loss of cardiomyocyte-GSK-3{beta} promotes cardiomyocyte and resident CPC proliferation post-MI. The induction of cardiomyocyte and CPC proliferation in the ischemic cKO hearts is potentially regulated by autocrine and paracrine signaling governed by dysregulated growth factors post-MI. A strategy to inhibit cardiomyocyte GSK-3{beta} could be helpful for the promotion of in situ cardiac regeneration post-ischemic injury.

molecular biology↗

Induction of soluble platelet activation markers and FXIII deficiency promote COVID-19 severity

IntroductionCoagulation dysfunction and thromboembolism emerge as strong comorbidity factors in severe COVID-19. However, it is unclear when particularly platelet activation markers and coagulation factors dysregulated during the pathogenesis of COVID-19. Here, we sought to assess the levels of coagulation and platelet activation markers at moderate and severe stages of COVID-19 to understand the pathogenesis. MethodsTo understand this, hospitalized COVID-19 patients with (severe cases that required intensive care) or without pneumonia (moderate cases) were recruited. Phenotypic and molecular characterizations were performed employing basic coagulation tests including PT, APTT, D-Dimer and TFPI. The flow cytometry-based multiplex assays were performed to assess FXI, anti-thrombin, prothrombin, fibrinogen, FXIII, P-selectin, sCD40L, plasminogen, tissue-plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1) and D-Dimer. ResultsThe investigations revealed induction of plasma P-selectin and CD40 ligand (sCD40L) in moderate COVID-19 cases which were significantly abolished with the progression of COVID-19 severity. Moreover, a profound reduction in plasma tissue factor pathway inhibitor (TFPI) and FXIII were identified particularly in the severe COVID-19. Further analysis revealed fibrinogen induction in both moderate and severe patients. Interestingly, an elevated PAI-1 more prominently in moderate, and tPA particularly in severe COVID-19 cases were observed. Particularly, the levels of fibrinogen and tPA directly correlated with the severity of the disease. ConclusionsIn summary, induction of soluble P-selectin, sCD40L, fibrinogen and PAI-1 in moderate COVID-19 cases suggests the activation of platelets and coagulation system before patients require intensive care. These findings would help in designing better thromboprophylaxis to limit the COVID-19 severity.

pathology↗

BCL-XL blockage in TNBC models confers vulnerability to inhibition of specific cell cycle regulators

Cell cycle regulators are frequently altered in Triple-Negative Breast Cancer (TNBC). Emerging agents targeting these signals offer the possibility to design new combinatorial therapies. However, preclinical models that recapitulate TNBC primary resistance and heterogeneity are essential to evaluate the potency of these combined treatments. MethodsBioinformatic processing of human breast cancer datasets was used to analyse correlations between expression levels of cell cycle regulators and patient survival outcome. The MMTV-R26Met mouse model of TNBC resistance and heterogeneity was employed to analyse expression and targeting vulnerability of cell cycle regulators in the presence of BCL-XL blockage. Robustness of outcomes and selectivity was further explored using a panel of human breast cancer cells. Alterations of protein expression, phosphorylation, and/or cellular localisation were analysed by western blots, reverse phase protein array, and immunocytochemistry. Bioinformatics was performed to highlight drugs mechanisms of action. ResultsWe report that high expression levels of BCL-XL and specific cell cycle regulators correlate with poor survival outcomes of TNBC patients. Blockage of BCL-XL confers vulnerability to drugs targeting CDK1/2/4, but not FOXM1, CDK4/6, Aurora A and Aurora B, to all MMTV-R26Met and human TNBC cell lines tested. Mechanistically, we show that, co-targeting of BCL-XL and CDK1/2/4 synergistically inhibited cell growth by combinatorial depletion of survival and RTK/AKT signals, and concomitantly restoring FOXO3a tumour suppression actions. This was accompanied by an accumulation of DNA damage and consequently apoptosis. ConclusionsOur studies illustrate the possibility to exploit the vulnerability of TNBC cells to CDK1/2/4 inhibition by targeting BCL-XL. Moreover, they underline that specificity matters in targeting cell cycle regulators for combinatorial anticancer therapies.

cancer biology↗

Effect of pesticides and metals on zebrafish embryo development and larval locomotor activity

The zebrafish has been widely used as a predictive model in safety and toxicology. Low cost high-throughput screening can be achieved with this model, and the genome contains orthologues of the majority of human disease genes. However, previous studies indicate that the predictivity of the zebrafish model in toxicology varies between compound and compound class. We examined this issue by screening 24 compounds from two different compound classes, metals and biocides (pesticides/insecticides) for toxicity in the zebrafish model and looked at the effects on hatching, morphology and predictivity for mammalian toxicity. Wild-type zebrafish embryos were exposed to test compounds in 96-well plates for 96 hours starting at 24 hours post fertilization. Hatching was either delayed or accelerated depending on the compound. Three types of alteration in behavioural responses were noted: (i) hypoactivity; (ii) hyperactivity; and (iii) biphasic response (a dose-dependent shift between hypo- and hyperactivity). LC50 of compounds was calculated and compared to published LD50 values in rodents. The zebrafish-rodent values were poorly correlated for both metals and biocides. We conclude that, although the zebrafish is a good model for some aspects of toxicology, its predictivity for mammalian toxicity needs to be determined per compound class.

pharmacology and toxicology↗

Causality Mapping Using Resting-State fMRI reveals Suppressed Functional Connectivity in Schizophrenia Patients

Schizophrenia is a psychotic brain disorder in which patients exhibit aberrant connectivity between different regions of the brain. Neuroimaging is a state-of-the-art technique that is now increasingly been employed in clinical investigation of Schizophrenia. In the present study, we have used resting-state functional magnetic resonance neuroimaging (rsfMRI) to elucidate the cause-and-effect relationships among four regions of the brain including occipital, temporal, and frontal lobes and hippocampus in Schizophrenia. For that, we have employed independent component analysis, a seed-based temporal correlation analysis, and Granger causality analysis for measuring causal relationships amongst four regions of the brain in schizophrenia patients. Eighteen subjects with nine patients and nine controls were evaluated in the study. Our results show that Schizophrenia patients exhibit significantly different activation patterns across the selected regions of the brain in comparison with the control. In addition to that, we also observed an aberrant causal relationship between these four regions of the brain. In particular, the temporal and frontal lobes of patients with schizophrenia had a significantly lowered causal relationship with the other areas of the brain. Taken together, the study elucidates the dysregulated brain activity in Schizophrenia patients, decodes its causal mapping and provides novel insights towards employment in clinical evaluation of Schizophrenia.

neuroscience↗