Displaying publications 1 - 20 of 60 in total

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  1. Fulltext Mitochondrial Cardiomyopathy: Molecular Epidemiology, Diagnosis, Models, and Therapeutic Management
    Yang J, Chen S, Duan F, Wang X, Zhang X, Lian B, et al.
    Cells, 2022 Nov 06;11(21).
    PMID: 36359908 DOI: 10.3390/cells11213511
    Mitochondrial cardiomyopathy (MCM) is characterized by abnormal heart-muscle structure and function, caused by mutations in the nuclear genome or mitochondrial DNA. The heterogeneity of gene mutations and various clinical presentations in patients with cardiomyopathy make its diagnosis, molecular mechanism, and therapeutics great challenges. This review describes the molecular epidemiology of MCM and its clinical features, reviews the promising diagnostic tests applied for mitochondrial diseases and cardiomyopathies, and details the animal and cellular models used for modeling cardiomyopathy and to investigate disease pathogenesis in a controlled in vitro environment. It also discusses the emerging therapeutics tested in pre-clinical and clinical studies of cardiac regeneration.
    Matched MeSH terms: Myocardium/pathology
  2. The role of infarct transmural extent in infarct extension: A computational study
    Leong CN, Lim E, Andriyana A, Al Abed A, Lovell NH, Hayward C, et al.
    Int J Numer Method Biomed Eng, 2017 Feb;33(2).
    PMID: 27043925 DOI: 10.1002/cnm.2794
    Infarct extension, a process involving progressive extension of the infarct zone (IZ) into the normally perfused border zone (BZ), leads to continuous degradation of the myocardial function and adverse remodelling. Despite carrying a high risk of mortality, detailed understanding of the mechanisms leading to BZ hypoxia and infarct extension remains unexplored. In the present study, we developed a 3D truncated ellipsoidal left ventricular model incorporating realistic electromechanical properties and fibre orientation to examine the mechanical interaction among the remote, infarct and BZs in the presence of varying infarct transmural extent (TME). Localized highly abnormal systolic fibre stress was observed at the BZ, owing to the simultaneous presence of moderately increased stiffness and fibre strain at this region, caused by the mechanical tethering effect imposed by the overstretched IZ. Our simulations also demonstrated the greatest tethering effect and stress in BZ regions with fibre direction tangential to the BZ-remote zone boundary. This can be explained by the lower stiffness in the cross-fibre direction, which gave rise to a greater stretching of the IZ in this direction. The average fibre strain of the IZ, as well as the maximum stress in the sub-endocardial layer, increased steeply from 10% to 50% infarct TME, and slower thereafter. Based on our stress-strain loop analysis, we found impairment in the myocardial energy efficiency and elevated energy expenditure with increasing infarct TME, which we believe to place the BZ at further risk of hypoxia. Copyright © 2016 John Wiley & Sons, Ltd.
    Matched MeSH terms: Myocardium/pathology
  3. Fulltext Native T1 and T2 provide distinctive signatures in hypertrophic cardiac conditions - Comparison of uremic, hypertensive and hypertrophic cardiomyopathy
    Arcari L, Hinojar R, Engel J, Freiwald T, Platschek S, Zainal H, et al.
    Int J Cardiol, 2020 05 01;306:102-108.
    PMID: 32169347 DOI: 10.1016/j.ijcard.2020.03.002
    AIMS: Profound left ventricular (LV) hypertrophy with diastolic dysfunction and heart failure is the cardinal manifestation of heart remodelling in chronic kidney disease (CKD). Previous studies related increased T1 mapping values in CKD with diffuse fibrosis. Native T1 is a non-specific readout that may also relate to increased intramyocardial fluid. We examined concomitant T1 and T2 mapping signatures and undertook comparisons with other hypertrophic conditions.

    METHODS: In this prospective multicentre study, consecutive CKD patients (n = 154) undergoing routine clinical cardiac magnetic resonance (CMR) imaging were compared with patients with hypertensive (HTN, n = 163) and hypertrophic cardiomyopathy (HCM, n = 158), and normotensive controls (n = 133).

    RESULTS: Native T1 was significantly higher in all patient groups, whereas native T2 in CKD only (p 

    Matched MeSH terms: Myocardium/pathology
  4. Fulltext Non-infarcted myocardium bears the weight in CVD
    Zhou H, Zainal H, Puntmann VO
    Aging (Albany NY), 2019 03 25;11(6):1609-1610.
    PMID: 30908271 DOI: 10.18632/aging.101890
    Matched MeSH terms: Myocardium/pathology*
  5. Fulltext Pirfenidone improves early cardiac function following myocardial infarction by enhancing the elastin/collagen ratio
    Yu Y, Xu Y, Chen J, Yao Y, Liu Y, Chen Y, et al.
    Biomed Pharmacother, 2024 Sep;178:117254.
    PMID: 39142250 DOI: 10.1016/j.biopha.2024.117254
    BACKGROUND: Acute myocardial infarction (AMI) is a leading cause of mortality worldwide, with reduced elastin/collagen ratios exacerbating cardiac dysfunction due to collagen-rich scar tissue replacing necrotic myocardial cells. This study aims to evaluate pirfenidone's therapeutic effect on early cardiac function post-AMI and elucidate its impact on the elastin/collagen ratio.

    METHODS: Sprague-Dawley rats were divided into four groups: Sham, AMI, AMI treated with PBS (AMI-PBS), and AMI treated with pirfenidone (AMI-PFD) (n=12 each). AMI was induced via coronary artery ligation. The AMI-PFD and AMI-PBS groups received pirfenidone and PBS for 14 days, respectively. Cardiac function, fibrosis, serum cytokines, collagen and elastin content, and their ratios were assessed. Cardiac fibroblasts (CFs) from neonatal rats were categorized into control, hypoxia-induced (LO), LO+PBS, and LO+PFD groups. ELISA measured inflammatory factors, and RT-PCR analyzed collagen and elastin gene expression.

    RESULTS: The AMI-PFD group showed improved cardiac function and reduced serum interleukin-1β (IL-1β), IL-6, and transforming growth factor-β (TGF-β). Type I and III collagen decreased by 22.6 % (P=0.0441) and 34.4 % (P=0.0427), respectively, while elastin content increased by 79.4 % (P=0.0126). E/COLI and E/COLIII ratios rose by 81.1 % (P=0.0026) and 88.1 % (P=0.0006). CFs in the LO+PFD group exhibited decreased IL-1β, IL-6, TGF-β, type I and III collagen, with increased elastin mRNA, enhancing the elastin/collagen ratio.

    CONCLUSION: Pirfenidone enhances cardiac function by augmenting the early elastin/collagen ratio post-AMI.

    Matched MeSH terms: Myocardium/pathology
  6. Leave methamphetamine to be alive--Part II
    Islam MN, Khan J, Jaafar H
    Leg Med (Tokyo), 2009 Apr;11 Suppl 1:S143-6.
    PMID: 19345604 DOI: 10.1016/j.legalmed.2009.02.045
    Series of experiments have been completed with Methamphetamine (MA). Some were with the higher, medium or lower duration of MA administration and some were with acute or chronic doses. Whatever may be the dose or duration the ultimate result came out with the further establishment of cardio-toxic effect of this drug. Cardiovascular symptoms related to MA toxicity include chest pain, palpitations, dyspnoea, hypertension, tachycardia, atrial and ventricular arrhythmias, and myocardial ischemia. MA abusers often go through a repeated pattern of frequent drug administrations followed by a period of abstinence. Previous studies have focused largely upon the chronic effect of MA intake to major organs, such as the brains and the heart, by using animal experiments. However, there is a lack of research into the effects of acute dose of MA, especially pertaining to the heart. To clarify the effect of MA on myocardium, 22 male Wister rats aged six weeks were divided into MA, Placebo (P) and Control (C) group were examined following single intraperitoneal administration of MA at a dose of 50 mg/kg body weight. Normal saline was similarly injected in P group. Light microscopic changes was seen in the myocardium of MA treated group including cellular infiltration, with clusters of macrophage-like cells having large nuclei and little cytoplasm evident in the sub-endocardium region. There were presence of few macrophages, leucocytes, and spindle-like fibroblasts. Bringing in to account of cardiac changes by a single dose of MA, slogan should be voiced out to leave methamphetamine.
    Matched MeSH terms: Myocardium/pathology*
  7. Lightning fatality with blast, flame, heat and current effects: a macroscopic and microscopic view
    Murty OP
    J Forensic Leg Med, 2009 Apr;16(3):162-7.
    PMID: 19239970 DOI: 10.1016/j.jflm.2008.07.009
    A case is presented of a fatal environmental accidental injuries of lightning. A pedestrian was struck by lightning. The macroscopic and microscopic lightning injuries are reviewed.
    Matched MeSH terms: Myocardium/pathology
  8. Silent bony calcification of coronaries in an adolescent--an unusual case
    Murty OP, Mun KS, Hussin H
    J Forensic Leg Med, 2008 Jan;15(1):37-41.
    PMID: 18309549
    This is a case report of 16-year-old adolescent school boy who died due to unusual calcification of coronary arteries. He died while cycling with his friends. While cycling fast he fell. He was brought dead to hospital. At times unsuspected cardiac lesions cause sudden death during extraneous physical activities in healthy persons. Sudden death in adolescents is not very common. It is an unusual case as apparently healthy adolescent boy actively participating in sports had stony hard coronary arteries. The coronaries showed advanced calcification and early bone formation. The myocardial septum had extensive fibrosis. The pathogenesis and other possible similar conditions are also discussed in the report.
    Matched MeSH terms: Myocardium/pathology
  9. Pulmonary edema of enterovirus 71 encephalomyelitis is associated with left ventricular failure: implications for treatment
    Fu YC, Chi CS, Jan SL, Wang TM, Chen PY, Chang Y, et al.
    Pediatr Pulmonol, 2003 Apr;35(4):263-8.
    PMID: 12629622
    Epidemics of enterovirus 71 infections caused the rapid death of many children in Malaysia in 1997 and in Taiwan in 1998. Pulmonary edema occurred in most of the fatal cases and was considered to be neurogenic. The role of the heart was rarely investigated before. Between January 1998-January 2001, 34 consecutive patients who were admitted to the intensive care unit due to enterovirus infection were studied prospectively. Patients were divided into two groups: group I with pulmonary edema, and group II without pulmonary edema. Comparisons were made between the two groups based upon demographic, neurological, and cardiovascular manifestations. Group I consisted of 11 patients (5 boys, 6 girls; mean age, 22.8 months), and group II of 23 patients (12 boys, 11 girls; mean age, 28.8 months). There were no significant differences between the two groups in comparing sex, age, body weight, neurological severity, intracranial pressure, cell count, protein and glucose levels in cerebral spinal fluid, and blood pressure. All group I patients had left ventricular dysfunction, and their ejection fractions were significantly lower than those of patients in group II (37 +/- 11% vs. 75 +/- 6%, P < 0.001). Group I heart rates were higher than those of group II (175 +/- 24 vs. 137 +/- 25, P < 0.001). In group I, 9 patients who received conventional treatment died, and the only two survivors received left ventricular assist devices. In conclusion, the pulmonary edema of fulminant enterovirus 71 infection is associated with left ventricular failure. Left ventricular function is the major determinant of outcome. Early recognition of heart failure and aggressive cardiac intervention are life-saving. Pediatr Pulmonol. 2003; 35:263-268.
    Matched MeSH terms: Myocardium/pathology
  10. Fulltext Mechanoregulation of cardiac myofibroblast differentiation: implications for cardiac fibrosis and therapy
    Yong KW, Li Y, Huang G, Lu TJ, Safwani WK, Pingguan-Murphy B, et al.
    Am J Physiol Heart Circ Physiol, 2015 Aug 15;309(4):H532-42.
    PMID: 26092987 DOI: 10.1152/ajpheart.00299.2015
    Cardiac myofibroblast differentiation, as one of the most important cellular responses to heart injury, plays a critical role in cardiac remodeling and failure. While biochemical cues for this have been extensively investigated, the role of mechanical cues, e.g., extracellular matrix stiffness and mechanical strain, has also been found to mediate cardiac myofibroblast differentiation. Cardiac fibroblasts in vivo are typically subjected to a specific spatiotemporally changed mechanical microenvironment. When exposed to abnormal mechanical conditions (e.g., increased extracellular matrix stiffness or strain), cardiac fibroblasts can undergo myofibroblast differentiation. To date, the impact of mechanical cues on cardiac myofibroblast differentiation has been studied both in vitro and in vivo. Most of the related in vitro research into this has been mainly undertaken in two-dimensional cell culture systems, although a few three-dimensional studies that exist revealed an important role of dimensionality. However, despite remarkable advances, the comprehensive mechanisms for mechanoregulation of cardiac myofibroblast differentiation remain elusive. In this review, we introduce important parameters for evaluating cardiac myofibroblast differentiation and then discuss the development of both in vitro (two and three dimensional) and in vivo studies on mechanoregulation of cardiac myofibroblast differentiation. An understanding of the development of cardiac myofibroblast differentiation in response to changing mechanical microenvironment will underlie potential targets for future therapy of cardiac fibrosis and failure.
    Matched MeSH terms: Myocardium/pathology
  11. Heated palm oil causes rise in blood pressure and cardiac changes in heart muscle in experimental rats
    Leong XF, Aishah A, Nor Aini U, Das S, Jaarin K
    Arch Med Res, 2008 Aug;39(6):567-72.
    PMID: 18662587 DOI: 10.1016/j.arcmed.2008.04.009
    Palm oil used worldwide contains considerable amounts of antioxidants, namely, vitamin E and carotenes. The purpose of the study was to observe the effect of heated palm oil on blood pressure and observe the cardiac histological changes in rats.
    Matched MeSH terms: Myocardium/pathology
  12. Echocardiographic and electrocardiographic presentations of patients with endomyocardial biopsy-proven cardiac amyloidosis
    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
  13. The role of end-diastolic myocardial fibre stretch on infarct extension
    Leong CN, Dokos S, Andriyana A, Liew YM, Chan BT, Abdul Aziz YF, et al.
    Int J Numer Method Biomed Eng, 2020 01;36(1):e3291.
    PMID: 31799767 DOI: 10.1002/cnm.3291
    Myocardial infarct extension, a process involving the enlargement of infarct and border zone, leads to progressive degeneration of left ventricular (LV) function and eventually gives rise to heart failure. Despite carrying a high risk, the causation of infarct extension is still a subject of much speculation. In this study, patient-specific LV models were developed to investigate the correlation between infarct extension and impaired regional mechanics. Subsequently, sensitivity analysis was performed to examine the causal factors responsible for the impaired regional mechanics observed in regions surrounding the infarct and border zone. From our simulations, fibre strain, fibre stress and fibre stress-strain loop (FSSL) were the key biomechanical variables affected in these regions. Among these variables, only FSSL was correlated with infarct extension, as reflected in its work density dissipation (WDD) index value, with high WDD indices recorded at regions with infarct extension. Impaired FSSL is caused by inadequate contraction force generation during the isovolumic contraction and ejection phases. Our further analysis revealed that the inadequacy in contraction force generation is not necessarily due to impaired myocardial intrinsic contractility, but at least in part, due to inadequate muscle fibre stretch at end-diastole, which depresses the ability of myocardium to generate adequate contraction force in the subsequent systole (according to the Frank-Starling law). Moreover, an excessively stiff infarct may cause its neighbouring myocardium to be understretched at end-diastole, subsequently depressing the systolic contractile force of the neighbouring myocardium, which was found to be correlated with infarct extension.
    Matched MeSH terms: Myocardium/pathology*
  14. Acute myocarditis mimicking ST-elevation myocardial infarction: A diagnostic challenge for frontline clinicians
    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*
  15. Fulltext Cardiac magnetic resonance assessment of diastolic dysfunction in acute coronary syndrome
    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*
  16. Dancing to death: A case of heat stroke
    Nadesan K, Kumari C, Afiq M
    J Forensic Leg Med, 2017 Aug;50:1-5.
    PMID: 28651196 DOI: 10.1016/j.jflm.2017.05.008
    Heat stroke is a medical emergency which may lead to mortality unless diagnosed early and treated effectively. Heat stroke may manifest rapidly, hence making it difficult to differentiate it from other clinical causes in a collapsed victim.(1) We are presenting a case report of twelve patients who were admitted to our emergency department from a music festival held on 13-15th of March 2014. They developed complications arising from a combination of severe adverse weather condition, prolonged outdoor physical exertion due to long hours of dancing and drug-use, resulting in heat stroke. Three of them died while the remaining patients survived. Their condition was initially misdiagnosed as a classical illicit drug overdose. This was based on the history of drug ingestion by some of the patients who attended the music festival on that day. The information in this case report aims, to create awareness amongst members of the medical team on duty in outdoor events, pre hospital responders and ED physicians when treating and managing similar cases in the future. In addition it is intended to warn the organizers of such events to take adequate precautions to avoid such tragedies in the future.
    Matched MeSH terms: Myocardium/pathology
  17. Fulltext Metformin and Dapagliflozin Attenuate Doxorubicin-Induced Acute Cardiotoxicity in Wistar Rats: An Electrocardiographic, Biochemical, and Histopathological Approach
    Satyam SM, Bairy LK, Shetty P, Sainath P, Bharati S, Ahmed AZ, et al.
    Cardiovasc Toxicol, 2023 Feb;23(2):107-119.
    PMID: 36790727 DOI: 10.1007/s12012-023-09784-8
    Doxorubicin is a widely used anticancer drug whose efficacy is limited due to its cardiotoxicity. There is no ideal cardioprotection available against doxorubicin-induced cardiotoxicity. This study aimed to investigate the anticipated cardioprotective potential of metformin and dapagliflozin against doxorubicin-induced acute cardiotoxicity in Wistar rats. At the beginning of the experiment, cardiac screening of experimental animals was done by recording an electrocardiogram (ECG) before allocating them into the groups. Thereafter, a total of thirty healthy adult Wistar rats (150-200 g) were randomly divided into five groups (n = 6) and treated for eight days as follows: group I (normal control), group II (doxorubicin control), group III (metformin 250 mg/kg/day), group IV (metformin 180 mg/kg/day), and group V (dapagliflozin 0.9 mg/kg/day). On the 7th day of the treatment phase, doxorubicin 20 mg/kg was administered intraperitoneal to groups II, III, IV, and V. On the 9th day (immediately after 48 h of doxorubicin administration), blood was collected from anesthetized animals for glucose, lipid profile, CK-MB & AST estimation, and ECG was recorded. Later, animals were sacrificed, and the heart was dissected for histopathological examination. We found that compared to normal control rats, CK-MB, AST, and glucose were significantly increased in doxorubicin control rats. There was a significant reversal of doxorubicin-induced hyperglycemia in the rats treated with metformin 250 mg/kg compared to doxorubicin control rats. Both metformin (180 mg/kg and 250 mg/kg) and dapagliflozin (0.9 mg/kg) significantly altered doxorubicin-induced ECG changes and reduced the levels of cardiac injury biomarkers CK-MB and AST compared to doxorubicin control rats. Metformin and dapagliflozin protected the cellular architecture of the myocardium from doxorubicin-induced myocardial injury. Current study revealed that both metformin and dapagliflozin at the FDA-recommended antidiabetic doses mitigated doxorubicin-induced acute cardiotoxicity in Wistar rats. The obtained data have opened the perspective to perform chronic studies and then to clinical studies to precisely consider metformin and dapagliflozin as potential chemoprotection in the combination of chemotherapy with doxorubicin to limit its cardiotoxicity, especially in patients with comorbid conditions like type II diabetes mellitus.
    Matched MeSH terms: Myocardium/pathology
  18. Intrapericardial Administration of Human Pericardial Fluid Cells Improves Cardiac Functions in Rats with Heart Failure
    Xu Y, Zhang X, Fu Z, Dong Y, Yu Y, Liu Y, et al.
    Stem Cells Dev, 2024 Nov;33(21-22):616-629.
    PMID: 39155804 DOI: 10.1089/scd.2024.0072
    Heart failure (HF) is still the main cause of mortality worldwide. This study investigated the characteristics of human pericardial fluid-derived cells (hPFCs) and their effects in treating doxorubicin (DOX)-induced HF rats through intrapericardial injection. hPFCs were isolated from patients who underwent heart transplantation (N = 5). These cells that primarily expressed SCA-1, NANOG, and mesenchymal markers, CD90, CD105, and CD73, were able to form adipocytes, osteoblasts, and cardiomyocytes in vitro. Passage 3 hPFCs (2.5 × 105 cells/heart) were injected into the pericardial cavity of the DOX-injured rat hearts, significantly improving cardiac functions after 4 weeks. The tracked and engrafted red fluorescent protein-tagged hPFCs coexpressed cardiac troponin T and connexin 43 after 4 weeks in the host myocardium. This observation was also coupled with a significant reduction in cardiac fibrosis following hPFC treatment (P < 0.0001 vs. untreated). The elevated inflammatory cytokines interleukin (IL)-6, IL-10, and tumor necrosis factor-α in the DOX-treated hearts were found to be significantly reduced (P < 0.001 vs. untreated), while the regional proangiogenic vascular endothelial growth factor A (VEGFA) level was increased in the hPFC-treated group after 4 weeks (P < 0.05 vs. untreated). hPFCs possess stem cell characteristics and can improve the cardiac functions of DOX-induced HF rats after 4 weeks through pericardial administration. The improvements were attributed to a significant reduction in cardiac fibrosis, inflammation, and elevated regional proangiogenesis factor VEGFA, with evidence of cellular engraftment and differentiation in the host myocardium.
    Matched MeSH terms: Myocardium/pathology
  19. Angiostrongylus malaysiensis (Nematoda: Metastrongylidae), a new species of rat lung-worm from Malaysia
    Bhaibulaya M, Cross JH
    Southeast Asian J Trop Med Public Health, 1971 Dec;2(4):527-33.
    PMID: 5144154
    Matched MeSH terms: Myocardium/pathology
  20. The prevalence of Angiostrongylus cantonensis larvae collected from the giant African snail, Achatina fulica in west Malaysia and Singapore
    Bisseru B
    Southeast Asian J Trop Med Public Health, 1971 Dec;2(4):523-6.
    PMID: 5144153
    Matched MeSH terms: Myocardium/pathology
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