Biology subjects

Tarek, M.

Publications and source records attributed to Tarek, M..

5 recordsLinked to original sources

bioRxiv2026

A Comprehensive epidemiological and molecular study of gastrointestinal helminths of Companion Animals in Northeastern Bangladesh: A neglected zoonotic threat

BackgroundGastrointestinal helminths of companion animals are neglected sources of zoonotic infection in low and middle-income countries. In Bangladesh, close humananimal contact and large free-roaming dog and cat populations may facilitate parasite transmission, yet region-specific data remain limited. This study assessed the prevalence, species diversity, and zoonotic potential of gastrointestinal helminths in companion animals in northeastern Bangladesh. MethodsA cross-sectional study was conducted between January and December 2025 across urban and rural areas of the Sylhet Division. Fecal samples from 900 animals (600 dogs and 300 cats; owned and stray) were examined using standard coproscopic techniques. Molecular confirmation of selected positive samples was performed using PCR targeting ITS-2, 18S rRNA, and mitochondrial cox1 genes, followed by sequencing. Risk factors associated with infection were evaluated using multivariable logistic regression. ResultsOverall, 45.9% (95% CI: 42.6-49.2) of animals were infected with at least one gastrointestinal helminth, with mixed infections detected in 18.4%. Prevalence was similar in dogs (45.7%) and cats (46.3%) but significantly higher in stray animals (65.7%) than in owned animals (36.6%). Predominant zoonotic helminths included Ancylostoma spp., Toxocara canis, Toxocara cati, Dipylidium caninum, and Taenia/Echinococcus spp. Molecular analysis confirmed 93% of morphologically identified infections and revealed high genetic similarity to zoonotic reference strains. Stray status, lack of deworming, young age, and outdoor roaming were significant risk factors for infection (p < 0.05). ConclusionsCompanion dogs and cats in northeastern Bangladesh harbor a high burden of zoonotic gastrointestinal helminths and represent important reservoirs for human exposure. Strengthening One Health-based surveillance, routine deworming, and stray animal management is essential to reduce zoonotic transmission.

microbiology↗

bioRxiv2021

Modulation of the IKS channel by PIP2 requires two binding sites per monomer

The phosphatidyl-inositol-4,5-bisphosphate (PIP2) lipid has been shown to be crucial for the coupling between the voltage sensor and the pore of the potassium voltage-gated KV7 channel family, especially the KV7.1 channel. The latter, expressed in the myocardium membrane is complexed with its auxiliary subunits, KCNE1 to generate the so-called IKS current. We present here molecular models of transmembrane domain of this complex in its three known states, namely the Resting/Closed (RC), the Intermediate/Closed (IC), and the Activated/Open (AO), robustness of which is assessed by agreement with a range of biophysical data. Molecular Dynamics (MD) simulations of these models embedded in a lipid bilayer including phosphatidyl-inositol-4,5-bisphosphate (PIP2) lipids show that in presence of KCNE1, two PIP2 lipids are necessary to stabilize each state. The simulations also show that KCNE1 interacts with both PIP2 binding sites, forming a tourniquet around the pore and preventing its opening. The present investigation provides therefore key molecular elements that govern the role of PIP2 in KCNE1 modulation of IKS channels, possibly a common mechanism by which auxiliary KCNE subunits might modulate a variety of other ion channels.

biophysics↗

bioRxiv2020

Glycolysis downregulation is a hallmark of HIV-1 latency and sensitizes infected cells to oxidative stress

HIV-1 infects lymphoid and myeloid cells, which can harbor a latent proviral reservoir responsible for maintaining lifelong infection. Glycolytic metabolism has been identified as a determinant of susceptibility to HIV-1 infection, but its role in the development and maintenance of HIV-1 latency has not been elucidated. By combining transcriptomic, proteomic and metabolomic analysis, we here show that transition to latent HIV-1 infection downregulates glycolysis, while viral reactivation by conventional stimuli reverts this effect. Decreased glycolytic output in latently infected cells is associated with downregulation of NAD+/NADH. Consequently, infected cells rely on the parallel pentose phosphate pathway and its main product, the antioxidant NADPH, fueling antioxidant pathways maintaining HIV-1 latency. Of note, blocking NADPH downstream effectors, thioredoxin and glutathione, favors HIV-1 reactivation from latency in lymphoid and myeloid cellular models. This provides a "shock and kill effect" decreasing proviral DNA in cells from people-living-with-HIV/AIDS. Overall, our data show that downmodulation of glycolysis is a metabolic signature of HIV-1 latency that can be exploited to target latently infected cells with eradication strategies.

immunology↗

bioRxiv2019

Two-stage electro-mechanical coupling of a Kv channel in voltage-dependent activation

In voltage-gated potassium (KV) channels, the voltage-sensing domain (VSD) undergoes sequential activation from the resting state to the intermediate state and activated state to trigger pore opening via electro-mechanical (E-M) coupling. However, the spatial and temporal details underlying E-M coupling remain elusive. Here, we leverage KV7.1s unique two open states associated with the VSD adopting the intermediate and activated conformations to report a two-stage E-M coupling mechanism in voltage-dependent gating of KV7.1 as triggered by VSD activations to the intermediate and then activated state. When the S4 segment transitions to the intermediate state, the hand-like C-terminus of the VSD-pore linker (S4-S5L) interacts with the pore in the same subunit. When S4 then proceeds on to the fully-activated state, the elbow-like hinge between S4 and S4-S5L engages with the pore to activate conductance. This two-stage \"hand-and-elbow\" gating mechanism elucidates distinct tissue-specific modulations, pharmacology, and disease pathogenesis of KV7.1, and likely applies to numerous KV channels.

biophysics↗

bioRxiv2018

Competing endogenous RNA network: Potential entrants to gene editing in Hepatocellular Carcinoma

BackgroundHepatocellular Carcinoma (HCC) is the leading cause of cancer deaths worldwide as well as in Egypt. We aimed to use Clustered Regulatory Interspaced Short Palindromic Repeats (CRISPR) gene editing technique to induce forced down-regulation of the circRNA which consequently modified miRNA expression in HepG2 cell line to prove the regulatory relationship between the RNA parts of an in silico-detected competing endogenous RNA network in HCC\n\nMethodWe first retrieved hsa_circ_0000064-miR-1285-TRIM2 mRNA from public microarray databases followed by in silico modelling to mimic the regulation kinetics of cirRNA associated ceRNA network. Secondly, we performed polymerase chain reaction (PCR)-based amplification of synthetic fragments, Gibson assembly of both CRISPR and non CRISPR based circuits, E-coli transformation, plasmid purification, HePG2 cell line transfection. Finally Expression levels of the chosen RNAs in hepatocellular carcinoma (HCC) cell line, HepG2, were examined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and the cytotoxic effect was validated by viability assay.TRIM2 protein expression was proved by immunohistochemistry and flowcytometry.\n\nResultsInduction of hsa_circ_0000064 into HepG2 cell line via CRISPR-and non-CRISPR mediated synthetic circuit resulted in statistically significant decrease in cell number and, then, cellular viability with marked increase in hsa_circ_0000064 and TRIM2 mRNA levels and concomitant decrease in miR-1285 expression in HepG2 cell line compared with control (p<0.0). Moreover exogenous expression of hsa_circ_0000064 in HepG2 cell line showed increased expression of the tumor suppressor protein, TRIM2.\n\nConclusionsOur integrative approach, including in silico data analysis and experimental validation proved that CRISPR-mediated synthetic circuit-based overexpression of hsa_circ_0000064 was more efficient than conventional transient transfection, representing a promising therapeutic strategy for HCC.\n\nData AvailabilityOur Data was made available online on the IGEM wiki of team AFCM-EGYPT: http://2017.igem.org/Team:AFCM-Egypt. Synthetic parts have been submitted to IGEM Parts Registry.\n\nFinancial DisclosureThe project was funded by Armed Forces College of Medicine AFCM, Zewail City of Science and Technology, National Research Center NRC, VitaBiotics, PHARCO Pharmaceuticals, Sim Era and DANUB Paintings. IDT provided 20 kb of DNA synthesis. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

bioengineering↗