Publications by authors named "Mohsin Ahmed"

10 Publications

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Pre hospital delay and its associated factors in acute myocardial infarction in a developing country.

PLoS One 2021 24;16(11):e0259979. Epub 2021 Nov 24.

Department of Cardiology, Ibrahim Cardiac Hospital and Research Institute, Dhaka, Bangladesh.

Background: Early revascularization and treatment is key to improving clinical outcomes and reducing mortality in acute myocardial infarction (AMI). In low- and middle-income countries such as Bangladesh, timely management of AMI is challenging, with pre-hospital delays playing a significant role. This study was designed to investigate pre-hospital delay and its associated factors among patients presenting with AMI in the capital city of Dhaka.

Methods: This retrospective cohort study was conducted on 333 patients presenting with AMI over a 3-month period at two of the largest primary reperfusion-capable tertiary cardiac care centres in Dhaka. Of the total patients, 239(71.8%) were admitted in the National Institute of Cardiovascular Diseases, Dhaka and 94(28.2%) at Ibrahim Cardiac Hospital & Research Institute, Dhaka Data were collected from patients by semi-structured interview and hospital medical records. Pre-hospital delay (median and inter-quartile range) was calculated. Statistical significance was determined by Chi-square test. Multivariate logistic regression analysis was done to determine the independent predictors of pre-hospital delay.

Results: The mean age of the respondents was 53.8±11.2 years. Two-thirds (67.6%) of the respondents were males. Median total pre-hospital delay was 11.5 (IQR-18.3) hours with median decision time from symptom onset to seeking medical care being 3.0 (IQR: 11.0) hours. Nearly half (48.9%) of patients presented to the hospital more than 12 hours after symptom onset. On multivariate logistic regression analysis, AMI patients with absence of typical chest pain [OR 5.21; (95% CI: 2.5-9.9)], diabetes [OR: 1.7 (95% CI: 1.0-2.9)], residing/staying > 30 km away from nearest hospital at the time of onset [OR: 4.3(95% CI = 2.3-7.2)] and belonged to lower and middle class [OR: 1.9(95% CI = 1.0-3.5)] were significantly associated with pre-hospital delays.

Conclusion: Acute myocardial infarction (AMI) patients with atypical chest pain, diabetes, staying far away from nearest hospital and belonged to lower and middle socioeconomic strata were significantly associated with pre-hospital delays. The findings could have immense implications for improvements about timely reaching of AMI patients to the hospital within the context of their sociodemographic status and geographic barriers of the city.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0259979PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8612565PMC
November 2021

Overview of deep learning models for identification Covid-19.

Mater Today Proc 2021 Jun 11. Epub 2021 Jun 11.

Computer Science Department, University of Technology, 10066 Baghdad, Iraq.

The well-being and health of global population is continuously and badly affected by COVID-19 pandemic. Thus, to prevent the spread the pandemic between individuals, there is high importance in implementing automatic detection systems as rapid alternative diagnosis. The virus is affecting the person's respiratory system as well as creating white patchy shadows in the X-ray images of the lungs of individuals experiencing COVID-19. Also, deep learning can be defined as a useful and efficient AI technique used for analyzing chest X-ray images for reliable and effective screening of COVID-19; therefore, distinguishing people infected with COVID-19 and normal persons, and after that the infected individuals will be isolated for mitigating the virus spread. This study provides an overview regarding a few of the modern deep learning-based COVID-19, with design steps and types, also it compares the diagnostic method of COVID-19 with other methods of deep learning created with the use of radiology images. After a comparison between the most recent methods used in the previous works, it was found that RestNet50 pre-trained and DCNN model gives accuracy of 98%, which is the highest reported so far from among other proposed models were discussed in this paper.
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http://dx.doi.org/10.1016/j.matpr.2021.05.553DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8192882PMC
June 2021

Hippocampal Network Reorganization Underlies the Formation of a Temporal Association Memory.

Neuron 2020 07 8;107(2):283-291.e6. Epub 2020 May 8.

Department of Neuroscience, Columbia University, New York, NY 10027, USA; Kavli Institute for Brain Sciences, Columbia University, New York, NY 10027, USA; Mortimer B. Zuckerman Mind Brain Behavior Institute, Columbia University, New York, NY 10027, USA. Electronic address:

Episodic memory requires linking events in time, a function dependent on the hippocampus. In "trace" fear conditioning, animals learn to associate a neutral cue with an aversive stimulus despite their separation in time by a delay period on the order of tens of seconds. But how this temporal association forms remains unclear. Here we use two-photon calcium imaging of neural population dynamics throughout the course of learning and show that, in contrast to previous theories, hippocampal CA1 does not generate persistent activity to bridge the delay. Instead, learning is concomitant with broad changes in the active neural population. Although neural responses were stochastic in time, cue identity could be read out from population activity over longer timescales after learning. These results question the ubiquity of seconds-long neural sequences during temporal association learning and suggest that trace fear conditioning relies on mechanisms that differ from persistent activity accounts of working memory.
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http://dx.doi.org/10.1016/j.neuron.2020.04.013DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643350PMC
July 2020

Endoplasmic reticulum stress-induced complex I defect: Central role of calcium overload.

Arch Biochem Biophys 2020 04 12;683:108299. Epub 2020 Feb 12.

Pauley Heart Center, Division of Cardiology, Department of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA. Electronic address:

Background: ER (endoplasmic reticulum) stress leads to decreased complex I activity in cardiac mitochondria. The aim of the current study is to explore the potential mechanisms by which ER stress leads to the complex I defect. ER stress contributes to intracellular calcium overload and oxidative stress that are two key factors to induce mitochondrial dysfunction. Since oxidative stress is often accompanied by intracellular calcium overload during ER stress in vivo, the role of oxidative stress and calcium overload in mitochondrial dysfunction was studied using in vitro models. ER stress results in intracellular calcium overload that favors activation of calcium-dependent calpains. The contribution of mitochondrial calpain activation in ER stress-mediated complex I damage was studied.

Methods: Thapsigargin (THAP) was used to induce acute ER stress in H9c2 cells and C57BL/6 mice. Exogenous calcium (25 μM) and HO (100 μM) were used to induce modest calcium overload and oxidative stress in isolated mitochondria. Calpain small subunit 1 (CAPNS1) is essential to maintain calpain 1 and calpain 2 (CPN1/2) activities. Deletion of CAPNS1 eliminates the activities of CPN1/2. Wild type and cardiac-specific CAPNS1 deletion mice were used to explore the role of CPN1/2 activation in calcium-induced mitochondrial damage.

Results: In isolated mitochondria, exogenous calcium but not HO treatment led to decreased oxidative phosphorylation, supporting that calcium overload contributes a key role in the mitochondrial damage. THAP treatment of H9c2 cells decreased respiration selectively with complex I substrates. THAP treatment activated cytosolic and mitochondrial CPN1/2 in C57BL/6 mice and led to degradation of complex I subunits including NDUFS7. Calcium treatment decreased NDUFS7 content in wild type but not in CAPNS1 knockout mice.

Conclusion: ER stress-mediated activation of mitochondria-localized CPN1/2 contributes to complex I damage by cleaving component subunits.
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http://dx.doi.org/10.1016/j.abb.2020.108299DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7092715PMC
April 2020

Automatic control of Hypothalamus-Pituitary-Adrenal axis dynamics.

Comput Methods Programs Biomed 2019 Sep 13;178:59-75. Epub 2019 Jun 13.

Atilim University, Department of Electrical and Electronic Engineering, Incek, Golbasi, Ankara, 06836, Turkey. Electronic address:

Background And Objective: In this study, a presentation is made for the automatic control of the hypothalamus-pituitary-adrenal axis which plays an important role in the immune stress responses and the circadian rhythms of mammalian organisms.

Methods: Control approaches are implemented on a novel second order nonlinear system which accepts adrenocorticotropin hormone as an input and models the variation of plasma concentrations of adrenocorticotropin and cortisol respectively. The control methods are based on back-stepping and input-output feedback linearization techniques. The controllers adjust the adrenocorticotropin injection to maintain the daily rhythm of the cortisol concentration. In accordance with the periodicity of biological clock mechanism, we provide a sinusoidally varying cortisol reference to the controllers.

Results: Numerical simulations are performed (on MATLAB) to demonstrate the closed loop performance of the controllers. Major concerns in the selection of the control gains are chattering and negative concentration in responses. The simulation results showed that one can successfully find gain levels which do not lead to those issues. However, the gains lie in different ranges for back-stepping and feedback linearization based controllers.

Conclusion: The results showed that, both back-stepping and feedback linearization based controllers fulfilled their duty of synchronization of the cortisol concentration to a reference daily periodic rhythm. In addition to that, the risk of negative valued adrenocorticotropin injection can be eliminated by properly choosing the controller gains.
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http://dx.doi.org/10.1016/j.cmpb.2019.06.012DOI Listing
September 2019

Mitochondrial Complex I Inhibition by Metformin Limits Reperfusion Injury.

J Pharmacol Exp Ther 2019 05 7;369(2):282-290. Epub 2019 Mar 7.

Department of Biochemistry and Molecular Biology (A.A.M., M.W.M., E.J.L.) and Pauley Heart Center, Division of Cardiology, Department of Internal Medicine (Q.C., A.S., J.T., Y.H., E.J.L.), Virginia Commonwealth University, Richmond, Virginia; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi (N.Q., T.R., J.L.); and Cardiology Section Medical Service, McGuire Veterans Affairs Medical Center, Richmond, Virginia (E.J.L.)

Transient, reversible blockade of complex I during early reperfusion after ischemia limits cardiac injury. We studied the cardioprotection of high dose of metformin in cultured cells and mouse hearts via the novel mechanism of acute downregulation of complex I. The effect of high dose of metformin on complex I activity was studied in isolated heart mitochondria and cultured H9c2 cells. Protection with metformin was evaluated in H9c2 cells at reoxygenation and at early reperfusion in isolated perfused mouse hearts and in vivo regional ischemia reperfusion. Acute, high-dose metformin treatment inhibited complex I in ischemia-damaged mitochondria and in H9c2 cells following hypoxia. Accompanying the complex I modulation, high-dose metformin at reoxygenation decreased death in H9c2 cells. Acute treatment with high-dose metformin at the end of ischemia reduced infarct size following ischemia reperfusion in vitro and in vivo, including in the AMP kinase-dead mouse. Metformin treatment during early reperfusion improved mitochondrial calcium retention capacity, indicating decreased permeability transition pore (MPTP) opening. Acute, high-dose metformin therapy decreased cardiac injury through inhibition of complex I accompanied by attenuation of MPTP opening. Moreover, in contrast to chronic metformin treatment, protection by acute, high-dose metformin is independent of AMP-activated protein kinase activation. Thus, a single, high-dose metformin treatment at reperfusion reduces cardiac injury via modulation of complex I.
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http://dx.doi.org/10.1124/jpet.118.254300DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6474909PMC
May 2019

The lignan manassantin is a potent and specific inhibitor of mitochondrial complex I and bioenergetic activity in mammals.

J Biol Chem 2017 12 18;292(51):20989-20997. Epub 2017 Oct 18.

From the Departments of Biochemistry and Molecular Biology,

Dineolignans manassantin A and B from the plant are used in traditional medicine to manage a wide range of ailments such as edema, jaundice, and gonorrhea. Cell-based studies have identified several molecular target candidates of manassantin including NF-κB, MAPK, STAT3, and hypoxia-inducible factor 1α (HIF-1α). It is unclear whether or how these structurally diverse proteins or pathways mediate any of the medical benefits of manassantin Moreover, it has recently been reported that manassantin causes developmental arrest in zebrafish by inhibiting the mitochondrial complex I, but it is unknown whether manassantin inhibits mitochondrial respiration in intact mammalian cells and live animals. Here, we present direct evidence that manassantin potently and specifically inhibits the mitochondrial complex I and bioenergetic activity in mammalian systems. Manassantin had no effect on complex II- or complex IV-mediated respiration. Of note, it decreased NADH-ubiquinone reductase activity but not the activity of NADH-ferricyanide reductase. Treatment with manassantin reduced cellular ATP levels and concomitantly stimulated AMP-activated protein kinase and As an adaptive response to manassantin-induced bioenergetic deficiency, mammalian cells up-regulated aerobic glycolysis, a process mediated by AMP-activated protein kinase (AMPK) independently of HIF-1α. Together these results demonstrate a biologically important activity of manassantin in the control of complex I-mediated respiration and its profound effects on oxygen utilization, energy homeostasis, and glucose metabolism in mammalian cells.
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http://dx.doi.org/10.1074/jbc.M117.812925DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743073PMC
December 2017

A thin film approach for SiC-derived graphene as an on-chip electrode for supercapacitors.

Nanotechnology 2015 Oct 8;26(43):434005. Epub 2015 Oct 8.

Queensland Micro- and Nanotechnology Centre, Griffith University, Nathan, QLD, Australia.

We designed a nickel-assisted process to obtain graphene with sheet resistance as low as 80 Ω square(-1) from silicon carbide films on Si wafers with highly enhanced surface area. The silicon carbide film acts as both a template and source of graphitic carbon, while, simultaneously, the nickel induces porosity on the surface of the film by forming silicides during the annealing process which are subsequently removed. As stand-alone electrodes in supercapacitors, these transfer-free graphene-on-chip samples show a typical double-layer supercapacitive behaviour with gravimetric capacitance of up to 65 F g(-1). This work is the first attempt to produce graphene with high surface area from silicon carbide thin films for energy storage at the wafer-level and may open numerous opportunities for on-chip integrated energy storage applications.
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http://dx.doi.org/10.1088/0957-4484/26/43/434005DOI Listing
October 2015

Graphitized silicon carbide microbeams: wafer-level, self-aligned graphene on silicon wafers.

Nanotechnology 2014 Aug 23;25(32):325301. Epub 2014 Jul 23.

Queensland Micro- and Nanotechnology Centre, Griffith University, Nathan 4111, Queensland, Australia.

Currently proven methods that are used to obtain devices with high-quality graphene on silicon wafers involve the transfer of graphene flakes from a growth substrate, resulting in fundamental limitations for large-scale device fabrication. Moreover, the complex three-dimensional structures of interest for microelectromechanical and nanoelectromechanical systems are hardly compatible with such transfer processes. Here, we introduce a methodology for obtaining thousands of microbeams, made of graphitized silicon carbide on silicon, through a site-selective and wafer-scale approach. A Ni-Cu alloy catalyst mediates a self-aligned graphitization on prepatterned SiC microstructures at a temperature that is compatible with silicon technologies. The graphene nanocoating leads to a dramatically enhanced electrical conductivity, which elevates this approach to an ideal method for the replacement of conductive metal films in silicon carbide-based MEMS and NEMS devices.
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http://dx.doi.org/10.1088/0957-4484/25/32/325301DOI Listing
August 2014

Recruitment of N-Type Ca(2+) channels during LTP enhances low release efficacy of hippocampal CA1 perforant path synapses.

Neuron 2009 Aug;63(3):372-85

Department of Neuroscience, Columbia University, New York, NY 10032, USA.

The entorhinal cortex provides both direct and indirect inputs to hippocampal CA1 neurons through the perforant path and Schaffer collateral synapses, respectively. Using both two-photon imaging of synaptic vesicle cycling and electrophysiological recordings, we found that the efficacy of transmitter release at perforant path synapses is lower than at Schaffer collateral inputs. This difference is due to the greater contribution to release by presynaptic N-type voltage-gated Ca(2+) channels at the Schaffer collateral than perforant path synapses. Induction of long-term potentiation that depends on activation of NMDA receptors and L-type voltage-gated Ca(2+) channels enhances the low efficacy of release at perforant path synapses by increasing the contribution of N-type channels to exocytosis. This represents a previously uncharacterized presynaptic mechanism for fine-tuning release properties of distinct classes of synapses onto a common postsynaptic neuron and for regulating synaptic function during long-term synaptic plasticity.
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http://dx.doi.org/10.1016/j.neuron.2009.07.013DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746441PMC
August 2009
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