Displaying publications 1 - 20 of 114 in total

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  1. Bhattacharjee M, Venugopal B, Wong KT, Goto YI, Bhattacharjee MB
    Ultrastruct Pathol, 2006 Nov-Dec;30(6):481-7.
    PMID: 17183762
    The authors describe the case of a 50-year-old man with chronic progressive external ophthalmoplegia (CPEO), diabetes mellitus (DM), and coronary artery disease. The patient had no cardiac conduction abnormalities. During coronary artery bypass surgery, his heart and two skeletal muscles were biopsied. All three muscles showed ragged red fibers. The heart muscle showed significant glycogen accumulation. Analysis of mitochondrial DNA (mtDNA) showed a 5019-base-pair deletion, with no duplications. There were morphologically abnormal mitochondria in all 3 muscles, with clinically apparent difference in preservation of function. The combination of diabetes mellitus and mtDNA deletion is fortuitous, as they can be causally linked. The cardiac pathology allows speculation about the possible adaptive processes that may occur in the heart in DM. There are few reported cases with CPEO and excess glycogen in the heart. Most show deposition of fat and poorer clinical outcomes as compared to those with glycogen deposition. This observation may lend support to the hypothesis that in the myocardium, adaptive responses are mediated via changes in glucose handling, whereas alterations in fat metabolism likely represent maladaptation.
    Matched MeSH terms: Myocardium/ultrastructure*
  2. Fung SY, Tan NH, Liew SH, Sim SM, Aguiyi JC
    Trop Biomed, 2009 Apr;26(1):80-4.
    PMID: 19696731
    Seed of Mucuna pruriens (Velvet beans) has been prescribed by traditional medicine practitioners in Nigeria as a prophylactic oral antisnake remedy. In the present studies, we investigated the protective effects of M. pruriens seed extract (MPE) against histopathological changes induced by intravenous injection of Naja sputatrix (Malayan cobra) venom in rats pretreated with the seed extract. Examination by light microscope revealed that the venom induced histopathological changes in heart and blood vessels in liver, but no effect on brain, lung, kidney and spleen. The induced changes were prevented by pretreatment of the rats with MPE. Our results suggest that MPE pretreatment protects rat heart and liver blood vessels against cobra venom-induced damages.
    Matched MeSH terms: Myocardium/pathology*
  3. Toulah FH, El-Aswad BEW, Harba NM, Naguib YM
    Trop Biomed, 2018 Dec 01;35(4):893-907.
    PMID: 33601839
    High-fat diet (HFD) can cause hyperlipidemia, fatty liver and cardiovascular disorders. Herein, we evaluated therapeutic effects and possible underlying mechanisms of actions of Schistosoma mansoni soluble egg antigen (SEA) against experimental HFD induced dyslipidemia, hepatic and cardiovascular pathology. Forty Swiss albino mice were divided into four groups (10 each); mice fed standard diet (SD), mice fed HFD, mice fed HFD for 8 weeks then infected by S. mansoni cercaria (HFD+I) and mice fed HFD for 8 weeks then treated with SEA (HFD+SEA), all mice were euthanized 16 weeks after starting the experiment. HFD+SEA mice showed significantly (p<0.001) reduced total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG), and significantly (p<0.05) increased high-density lipoprotein cholesterol (HDL-C) comparing to HFD mice with non-significant difference with HFD+I mice group. Doppler flowmetry showed significantly (p<0.01) lower arterial resistance and significantly (p<0.05) higher blood flow velocity in HFD+SEA and HFD+I mice groups than HFD mice. HFD+SEA mice revealed improving in liver and aortic pathology and these were better than HFD+I mice group. HFD+SEA and HFD+I mice groups had less myocardium lipid deposits, but still showing some congested blood vessels. HFD myocardium revealed strong CD34+ expression on immunohistochemistry study, while that of HFD+SEA showed weak and HFD+I mice had moderate expressions. HFD+SEA mice had significantly (p<0.01) lower serum IL-1β and vascular endothelial growth factor (VEGF) and significantly (p<0.001) higher serum transforming growth factor beta 1 (TGF-β1) and IL-10 than HFD mice with non-significant difference with HFD+I mice. In conclusion, SEA lowered serum lipids, improved aortic function, decreased liver and cardiovascular pathology in HFD mice, so, it is recommended to purify active molecules from SEA to develop anti-dyslipidemic treatment.
    Matched MeSH terms: Myocardium
  4. Chaisakul J, Khow O, Wiwatwarayos K, Rusmili MRA, Prasert W, Othman I, et al.
    Toxins (Basel), 2021 Jul 26;13(8).
    PMID: 34437392 DOI: 10.3390/toxins13080521
    Acute kidney injury (AKI) following Eastern Russell's viper (Daboia siamensis) envenoming is a significant symptom in systemically envenomed victims. A number of venom components have been identified as causing the nephrotoxicity which leads to AKI. However, the precise mechanism of nephrotoxicity caused by these toxins is still unclear. In the present study, we purified two proteins from D. siamensis venom, namely RvPLA2 and RvMP. Protein identification using LCMS/MS confirmed the identity of RvPLA2 to be snake venom phospholipase A2 (SVPLA2) from Thai D. siamensis venom, whereas RvMP exhibited the presence of a factor X activator with two subunits. In vitro and in vivo pharmacological studies demonstrated myotoxicity and histopathological changes of kidney, heart, and spleen. RvPLA2 (3-10 µg/mL) caused inhibition of direct twitches of the chick biventer cervicis muscle preparation. After administration of RvPLA2 or RvMP (300 µg/kg, i.p.) for 24 h, diffuse glomerular congestion and tubular injury with minor loss of brush border were detected in envenomed mice. RvPLA2 and RvMP (300 µg/kg; i.p.) also induced congestion and tissue inflammation of heart muscle as well as diffuse congestion of mouse spleen. This study showed the significant roles of PLA2 and SVMP in snake bite envenoming caused by Thai D. siamensis and their similarities with observed clinical manifestations in envenomed victims. This study also indicated that there is a need to reevaluate the current treatment strategies for Thai D. siamensis envenoming, given the potential for irreversible nephrotoxicity.
    Matched MeSH terms: Myocardium/pathology
  5. Ait Abderrahim L, Taïbi K, Abderrahim NA, Alomery AM, Abdellah F, Alhazmi AS, et al.
    Toxicon, 2019 Aug 26;169:38-44.
    PMID: 31465783 DOI: 10.1016/j.toxicon.2019.08.005
    Microcystin Leucine-Arginine (MC-LR) is a toxin produced by the cyanobacteria Microcystis aeruginosa. It is the most encountered and toxic type of cyanotoxins. Oxidative stress was shown to play a role in the pathogenesis of microcystin LR by the induction of intracellular reactive oxygen species (ROS) formation that oxidize and damage cellular macromolecules. In the present study we examined the effect of acute MC-LR dose on the cardiac muscle of BALB/c mice. Afterwards, melatonin and N-acetyl cysteine (NAC) were assayed and evaluated as potential protective and antioxidant agents against damages generated by MC-LR. For this purpose, thirty mice were assigned into six groups of five mice each. The effect of MC-LR was first compared to the control group supplied with distilled water, then compared to the other groups supplied with melatonin and NAC. The experiment lasted 10 days after which animals were euthanized. Biomarkers of toxicity such as alkaline phosphatase activity, lipid peroxidation, protein carbonyl content, reduced glutathione content, serum lactate dehydrogenase and serum sorbitol dehydrogenase were assayed. Results showed that toxin treated mice have experienced significant oxidative damage in their myocardial tissue as revealed by noticeable levels of oxidative stress biomarkers and by the reduction in alkaline phosphatase activity. Whereas, melatonin and NAC treated mice manifested lesser oxidative damages. Our findings suggest a potential therapeutic use of melatonin and N-acetyl cysteine as antioxidant protective agents against oxidative damage induced by MC-LR.
    Matched MeSH terms: Myocardium
  6. Roslan A, Kamsani SH, Nay TW, Tan KL, Hakim N, Tan AM, et al.
    Med J Malaysia, 2018 12;73(6):388-392.
    PMID: 30647209
    OBJECTIVE: Cardiac amyloidosis is under diagnosed and its prevalence is unknown. This is a retrospective, nonrandomised, single centre study of patients with endomyocardial biopsy-proven cardiac amyloidosis focusing on their echocardiographic and electrocardiogram (ECG) presentations. This is the first case series in Malaysia on this subject.

    METHODS: We identified all of our endomyocardial biopsyproven cardiac amyloidosis patients from January 2010 to January 2018 and reviewed their medical records. All patients echocardiographic and ECG findings reviewed and analysed comparing to basic mean population value.

    RESULTS: In total there are 13 biopsy-proven cardiac amyloidosis patients. All of the biopsies shows light chain (AL) amyloid. Majority of the patients (8, 61.5%) is male, and most of our patients (8, 61.5%) is Chinese. All seven patients on whom we performed deformation imaging have apical sparing pattern on longitudinal strain echocardiogram. Mean ejection fraction is 49.3%, (SD=7.9). All patients have concentric left ventricular hypertrophy and right ventricular hypertrophy. Diastolic dysfunction was present in all of our patients with nine out of 13 patients (69.2%) having restrictive filling patterns (E/A ≥2.0 E/e' ≥15). On electrocardiogram, 12 (92%) patients have prolonged PR interval (median 200ms, IQR 76.50ms) and 9 (69.2%) patients have pseudoinfarct pattern.

    CONCLUSION: Echocardiography plays an important role in diagnosing cardiac amyloidosis. The findings of concentric left ventricular hypertrophy with preserved ejection fraction without increased in loading condition should alert the clinician towards its possibility. This is further supported by right ventricular hypertrophy and particularly longitudinal strain imaging showing apical sparing pattern.

    Matched MeSH terms: Myocardium/pathology
  7. Buttery JE
    Med J Malaysia, 1974 Mar;28(3):180-4.
    PMID: 4278233
    Matched MeSH terms: Myocardium/enzymology
  8. Ang KP, Quek ZQ, Lee CY, Lu HT
    Med J Malaysia, 2019 12;74(6):561-563.
    PMID: 31929492
    The clinical presentation of acute myocarditis is highly variable ranging from no symptoms to cardiogenic shock. Despite considerable progress, it remains a challenge for frontline physicians to discriminate between acute myocarditis and myocardial infarction, especially in the early phase. Our case serves as a reminder that acute presentation of myocarditis could resemble ST elevation myocardial infarction potentially misdirecting the therapeutic decision. The clinical presentation, electrocardiographic and laboratory findings of the patient are not specific enough to distinguish acute myocarditis from myocardial infarction. The gold standard tests such coronary angiography and cardiovascular magnetic resonance (CMR) can reliably differentiate the two entities.
    Matched MeSH terms: Myocardium/pathology*
  9. Wan Muhaizan WM, Swaminathan M, Daud MS
    Malays J Pathol, 2004 Jun;26(1):59-63.
    PMID: 16196153
    Cardiac sarcoidosis is a disease of young adults. In most cases it presents with sudden death, arrhythmias, conduction disorders, heart failure or cardiomyopathy. The authors describe two cases of myocardial involvement by sarcoidosis that lead to death of the patients. Case one was a 26-year-old Indian man who was previously well and presented with sudden death. Autopsy showed nodules of sarcoid granuloma involving the heart, lungs and lymph nodes. Case two was a 47-year-old Indian lady who complained of reduced effort tolerance. Echocardiography showed that she had restrictive hypertrophic cardiomyopathy with heart failure. Seven months after initial presentation, she developed worsening of heart failure and died. Autopsy revealed involvement of the heart, lungs and liver by sarcoidosis.
    Matched MeSH terms: Myocardium/pathology
  10. Azarisman SM, Teo KS, Worthley MI, Worthley SG
    J Int Med Res, 2017 Dec;45(6):1680-1692.
    PMID: 29239257 DOI: 10.1177/0300060517698265
    Chest pain is an important presenting symptom. However, few cases of chest pain are diagnosed as acute coronary syndrome (ACS) in the acute setting. This results in frequent inappropriate discharge and major delay in treatment for patients with underlying ACS. The conventional methods of assessing ACS, which include electrocardiography and serological markers of infarct, can take time to manifest. Recent studies have investigated more sensitive and specific imaging modalities that can be used. Diastolic dysfunction occurs early following coronary artery occlusion and its detection is useful in confirming the diagnosis, risk stratification, and prognosis post-ACS. Cardiac magnetic resonance provides a single imaging modality for comprehensive evaluation of chest pain in the acute setting. In particular, cardiac magnetic resonance has many imaging techniques that assess diastolic dysfunction post-coronary artery occlusion. Techniques such as measurement of left atrial size, mitral inflow, and mitral annular and pulmonary vein flow velocities with phase-contrast imaging enable general assessment of ventricular diastolic function. More novel imaging techniques, such as T2-weighted imaging for oedema, T1 mapping, and myocardial tagging, allow early determination of regional diastolic dysfunction and oedema. These findings may correspond to specific infarcted arteries that may be used to tailor eventual percutaneous coronary artery intervention.
    Matched MeSH terms: Myocardium/pathology*
  11. Zainudin H, Caszo BA, Knight VF, Gnanou JV
    Eurasian J Med, 2019 Jun;51(2):116-120.
    PMID: 31258349 DOI: 10.5152/eurasianjmed.2019.18106
    Objective: Regular moderate-intensity exercise has beneficial health effects, whereas regular strenuous exercise increases the production of oxidants that may lead to DNA, skeletal, and cardiac muscle damages. Triathletes experience strenuous muscular activity both during competition and training, being at risk of developing these tissue damages. The objective of the present study was to estimate DNA, skeletal, and cardiac muscle damages using blood biomarkers, 8-hydroxy-2'-deoxyguanosine (8-OHdG), myoglobin, and cardiac troponin I (cTnI) among young triathletes.

    Materials and Methods: Age-matched seven male and seven female triathletes were recruited for the study. They were on a standardized training regimen and on average competed in at least one endurance event every month for the past 3-4 years. Serum biomarkers were measured using enzyme-linked immunosorbent assay at the start and at end of the racing season.

    Results: Both male and female triathletes showed a statistically significant increase in 8-OHdG. A similar pattern of increase was seen with serum myoglobin, which was not statistically significant in both male and female triathletes. cTnI levels did not show any change in both sexes.

    Conclusion: Our study shows that there could be an increased evidence of DNA damage among triathletes. However, similar effects were not observed with skeletal and cardiac muscle biomarkers.

    Matched MeSH terms: Myocardium
  12. Git KA, Fioravante LA, Fernandes JL
    Br J Radiol, 2015 Sep;88(1053):20150269.
    PMID: 26118302 DOI: 10.1259/bjr.20150269
    To assess whether an online open-source tool would provide accurate calculations of T2(*) values for iron concentrations in the liver and heart compared with a standard reference software.
    Matched MeSH terms: Myocardium/metabolism; Myocardium/chemistry*
  13. Dayapala A, Kumar V
    Am J Forensic Med Pathol, 2009 Jun;30(2):171-4.
    PMID: 19465810 DOI: 10.1097/PAF.0b013e3181875a79
    Sudden deaths because of congenital heart diseases are infrequently referred to the forensic pathologist for autopsy. Many of such deaths, if already diagnosed are released directly from the hospital without autopsy. Even forensic pathologists face a few difficulties in performing the autopsy on such infrequent cases, as they are not always updated with the anatomy of anomalies. While dealing with such cases, the concerned forensic pathologist is compelled to refer literature and textbooks again to understand the nature of developmental defects. This is especially so when dealing with cases of situs inversus accompanied by transposition of great arteries and other congenital cardiac abnormalities and variants such as single ventricle, double outlet right ventricle, Taussig-Bing variety etc. In the present case also, situs inversus with transposition of great vessels and other anomalies have been noted and studied.
    Matched MeSH terms: Myocardium/pathology*
  14. Murty OP
    Am J Forensic Med Pathol, 2008 Sep;29(3):245-8.
    PMID: 18725781 DOI: 10.1097/PAF.0b013e318183d55f
    Giant cell myocarditis (GCM) is a rare but fatal disease of idiopathic origin. It results in focal necrosis of myocardium. This is a case report of middle aged Malaysian Indian female who died due to cardiac tamponade due to rupture myocardium and tear in the root of aorta. On naked eye examination, it simply resembled as recent as well as old fibrotic areas of myocardial infarction. She was clinically diagnosed as a case of obstructive cardiomyopathy with atrioventricular block, and was on pace maker. There was subendocardial fibrosis and left ventricular transmural infarction in the left ventricle. On histopathology, this was diagnosed as GCM, there were widespread areas of inflammatory cellular infiltration within the myocardium with multinucleated giant cells and granulomas interspersed with lymphocytes. Microscopic field showed up to 10 multinucleated giant cells. In this case, there were focal areas at multiple locations and caused uneven thickness in the left ventricle wall. Idiopathic GCM is very rare and causation of hemopericardium is the unique feature of this case. In this case the direct link of GCM with aortitis and rupture of left ventricle wall resulting in hemopericardium is shown. This case is documented through macroscopic as well as microscopic photographs in H&E, Ziel-Nelson, and GMS staining.
    Matched MeSH terms: Myocardium/pathology
  15. Wee Ling JL, Khan A, Saad B, Ab Ghani S
    Talanta, 2012 Jan 15;88:477-83.
    PMID: 22265529 DOI: 10.1016/j.talanta.2011.11.018
    A new poly(4-vinyl pyridine) (P4VP) based cadmium (Cd)-ion selective electrode (ISE) was developed. The 4-vinyl pyridine (4VP) was first polymerized electrochemically on the surface of graphite, later characterized by FTIR, SEM/EDX and then optimized as ISE for Cd. At optimal pH 6.4, slope of 27.7±0.8mVdecade(-1), linear concentration range of 1×10(-7) to 1.0×10(-1)M Cd(2+) and limit of detection (S/N=3) of 2.51×10(-8)M were obtained. The ISE was very selective towards Cd(2+), with K(pot)<1×10(-2) in the presence of the usual cations and anions in water samples. Response time and shelf life of less than 1min and 90 days, respectively, were observed. Its application was tested in various types of samples.
    Matched MeSH terms: Myocardium/chemistry
  16. Rasdi Z, Kamaludin R, Ab Rahim S, Syed Ahmad Fuad SB, Othman MHD, Siran R, et al.
    Sci Rep, 2020 Apr 03;10(1):5882.
    PMID: 32246001 DOI: 10.1038/s41598-020-62420-1
    This study aimed to examine the impact of BPA exposure on pregnancy and foetuses on cardiac tissues and the expression of cardiac microRNAs (miRNAs) related to heart development and diseases. Pregnancy is known to be the "critical windows" in determining the offspring physical and cells development in their life after birth. The increment of the risk of cardiovascular disease (CVD) in a later stage of life has been reported by few studies demonstrated from prenatal exposure of BPA. BPA has been shown to alter miRNAs expression profiles for organ development, regeneration and metabolic functions. These alterations have been associated with the risk of CVDs. However, the associations between pregnancy outcomes and miRNAs expression in cardiac of mother- and foetuses-exposed to BPA are still not entirely explored. In BPA-exposed pregnant rat groups, a significant weight gained was observed in comparison to control (p 
    Matched MeSH terms: Myocardium/pathology
  17. Dong Y, Kang Z, Zhang Z, Zhang Y, Zhou H, Liu Y, et al.
    Sci Bull (Beijing), 2024 Apr 15;69(7):949-967.
    PMID: 38395651 DOI: 10.1016/j.scib.2024.02.003
    Myocardial ischemia-reperfusion injury (MIRI) is a major hindrance to the success of cardiac reperfusion therapy. Although increased neutrophil infiltration is a hallmark of MIRI, the subtypes and alterations of neutrophils in this process remain unclear. Here, we performed single-cell sequencing of cardiac CD45+ cells isolated from the murine myocardium subjected to MIRI at six-time points. We identified diverse types of infiltrating immune cells and their dynamic changes during MIRI. Cardiac neutrophils showed the most immediate response and largest changes and featured with functionally heterogeneous subpopulations, including Ccl3hi Neu and Ym-1hi Neu, which were increased at 6 h and 1 d after reperfusion, respectively. Ym-1hi Neu selectively expressed genes with protective effects and was, therefore, identified as a novel specific type of cardiac cell in the injured heart. Further analysis indicated that neutrophils and their subtypes orchestrated subsequent immune responses in the cardiac tissues, especially instructing the response of macrophages. The abundance of Ym-1hi Neu was closely correlated with the therapeutic efficacy of MIRI when neutrophils were specifically targeted by anti-Lymphocyte antigen 6 complex locus G6D (Ly6G) or anti-Intercellular cell adhesion molecule-1 (ICAM-1) neutralizing antibodies. In addition, a neutrophil subtype with the same phenotype as Ym-1hi Neu was detected in clinical samples and correlated with prognosis. Ym-1 inhibition exacerbated myocardial injury, whereas Ym-1 supplementation significantly ameliorated injury in MIRI mice, which was attributed to the tilt of Ym-1 on the polarization of macrophages toward the repair phenotype in myocardial tissue. Overall, our findings reveal the anti-inflammatory phenotype of Ym-1hi Neu and highlight its critical role in myocardial protection during the early stages of MIRI.
    Matched MeSH terms: Myocardium
  18. Mawad D, Mansfield C, Lauto A, Perbellini F, Nelson GW, Tonkin J, et al.
    Sci Adv, 2016 Nov;2(11):e1601007.
    PMID: 28138526 DOI: 10.1126/sciadv.1601007
    Electrically active constructs can have a beneficial effect on electroresponsive tissues, such as the brain, heart, and nervous system. Conducting polymers (CPs) are being considered as components of these constructs because of their intrinsic electroactive and flexible nature. However, their clinical application has been largely hampered by their short operational time due to a decrease in their electronic properties. We show that, by immobilizing the dopant in the conductive scaffold, we can prevent its electric deterioration. We grew polyaniline (PANI) doped with phytic acid on the surface of a chitosan film. The strong chelation between phytic acid and chitosan led to a conductive patch with retained electroactivity, low surface resistivity (35.85 ± 9.40 kilohms per square), and oxidized form after 2 weeks of incubation in physiological medium. Ex vivo experiments revealed that the conductive nature of the patch has an immediate effect on the electrophysiology of the heart. Preliminary in vivo experiments showed that the conductive patch does not induce proarrhythmogenic activities in the heart. Our findings set the foundation for the design of electronically stable CP-based scaffolds. This provides a robust conductive system that could be used at the interface with electroresponsive tissue to better understand the interaction and effect of these materials on the electrophysiology of these tissues.
    Matched MeSH terms: Myocardium*
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