Schistosoma mansoni and endocarditis: from egg to free DNA detection in Egyptian patients and infected BALB/c mice

2018 ◽  
Vol 93 (2) ◽  
pp. 139-148
Author(s):  
M.A. Hasby Saad ◽  
M.M. Watany
Keyword(s):  
Schistosoma Mansoni ◽  
Cardiac Tissue ◽  
Histopathological Examination ◽  
Inflammatory Cells ◽  
Cardiac Tissues ◽  
Genome Integration ◽  
Egyptian Patients ◽  
Stool Samples ◽  
Polymerase Chain ◽  
Low Incidence

AbstractWith the growing incidence of closed schistosomiasis and uncommon presentations, there is a risk of the infection rate being underestimated. A study in Japan reported an unexplained case of endocarditis that was finally diagnosed as a complex Schistosoma japonicum infection; in the absence of advanced techniques, the diagnosis was delayed. We therefore set out to explore the incidence of Schistosoma mansoni in endocarditis patients coming from areas of Egypt where S. mansoni is endemic. We also investigated histopathological changes in the cardiac valves and the presence of cell-free parasite DNA (CFPD) in cardiac tissues of laboratory mice infected with S. mansoni. The study included 186 patients with the manifestations of infective endocarditis. Eggs were detected in the stool samples of 5.91% of patients. Seropositivity was reported in 23.66% of patients and antigen was detected in the urine samples of 10.21%. Using real-time polymerase chain reaction (PCR), CFPD was detected in the blood of 6.98% of the endocarditis patients and 95% of the infected mice, while the cardiac samples of 45% of the mice tested positive for CFPD (means ± SD = 1390.2 ± 283.65, 2158.72 ± 1103.1 and 5.71 ± 2.91, respectively). Histopathological examination revealed abnormal collagen deposition, inflammatory cells and haemorrhagic pigmentation in the heart sections. Despite the low incidence of S. mansoni infection in the studied cohort, the presence of CFPD in the cardiac tissue of infected mice makes it necessary to: (1) investigate the hazards of CFPD deposition in endothelium-rich organs; and (2) test the potential of CFPD to trigger tissue inflammation, abnormal proliferation or genome integration.

Antioxidant properties of Rosa pisiformis and its protective effect against isoproterenol-induced oxidative stress in rats / Rosa pisiformis’in antioksidant özellikleri ve izoproterenol ile ratlarda oluşturulan okdidatif strese karşı koruyucu etkisi

2016 ◽  
Vol 41 (4) ◽  
Author(s):  
Mahire Bayramoğlu ◽  
Suat Ekin ◽  
Hatice Kızıltaş ◽  
Gökhan Oto ◽  
Ebru Altındal Susen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Tissue ◽  
Histopathological Examination ◽  
Antioxidant Properties ◽  
Albino Rats ◽  
Cardiac Tissues ◽  
Positive Effects ◽  
Icp Ms ◽  
Wistar Albino Rats ◽  
Method R

AbstractObjective: In this study, Rosa pisiformis was evaluated for its antioxidant activity, vitamin (A, E, C), trace element (Fe, Cu, Zn, Mn, Cr, Se) and mineral (Ca, K, Mg, Na) levels, in addition to its cardioprotective effects on cardiac tissue antioxidant enzymes (GSH-Px, SOD, CAT) during isoproterenol (ISO) - induced oxidative stress.Methods: In the study, vitamin and mineral analysis was carried out using HPLC and ICP-MS method, R. P. antioxidant and antiradical properties were determined using spectrophotometer. Forty wistar albino rats were divided into four groups: control (0.9% NaCl), ISO (100 mg/kg), ISO (100 mg/kg) + R. P. (300 mg/kg) and R. P. (300 mg/ kg). ISO was injected subcutaneously into rats twice at an interval of 24 h for two consecutive days (on 28Results: The results of the study indicated that R. P. fruit and leaves contain high levels of minerals and vitamins and possess antioxidant and antiradical activity and its fruits have positive effects on cardiac tissues. The results are supported with significant changes in antioxidant enzyme levels and histopathological examination.Conclusion: This study demonstrates that R. P. fruits in particular can be used to treat and prevent cardiac diseases.

scholarly journals Septicaemia due to a Proteus infection in a Humboldt penguin (Spheniscus humboldti)

2019 ◽  
Vol 64 (No. 12) ◽  
pp. 558-564
Author(s):  
SM Baek ◽  
SW Lee ◽  
AR Lee ◽  
JS Bang ◽  
MM Seo ◽  
...  
Keyword(s):  
Histopathological Examination ◽  
Abdominal Cavity ◽  
Inflammatory Cells ◽  
Bile Pigments ◽  
Fibrin Deposition ◽  
Severe Haemorrhage ◽  
Polymerase Chain ◽  
Gross Examination ◽  
Gallbladder Rupture ◽  
Humboldt Penguin

A 2-year-old male Humboldt penguin (Spheniscus humboldti) died after a very brief period of illness at a zoo aquarium; the penguin showed sudden depression, anorexia, dyspnoea, and had recurrent melena a day prior to death. The gross examination revealed an extensive bilious effusion in the abdominal cavity due to a gallbladder rupture. Moreover, abscess formation, purulent exudate, severe congestion, and haemorrhages were observed in the trachea and parenchymal organs such as the kidneys and the lungs. A histopathological examination revealed a fibrin deposition with a severe haemorrhage and secondary infiltration of chronic-active inflammatory cells in the parabronchi, atria, and air capillaries and blood vessels of the lungs as well as in most of the parenchymal organs. Moreover, Gram-negative bacilli were found in the lumen of the gastrointestinal tracts including the small and large intestines accompanied by severe epithelial necrosis and the capsule of the liver. Especially, bile pigments were microscopically observed in the whole liver, which indicated a gallbladder rupture. Samples collected from the trachea, lungs, and blood were cultured on a blood agar, and the pure colonies of Proteus genus were isolated. Proteus mirabilis, P.  penneri, P. vulgaris, and P. cibarius were identified with polymerase chain reaction (PCR). As a result, the diagnosis was confirmed as Proteus septicaemia. To our knowledge, this is the first report of concomitant infection by different Proteus species that eventually resulted in septicaemia in a Humboldt penguin, and it will provide valuable information for zoo veterinarians for its diagnosis as well, since Humboldt penguins are the most widely found penguins in zoos and Proteus septicaemia in the penguins has, to the best of our knowledge, not been reported as yet.

scholarly journals Cyclo-oxygenase 2, a putative mediator of vessel remodeling, is expressed in the brain AVM vessels and associates with inflammation

2021 ◽  
Author(s):  
Sara Keränen ◽  
Santeri Suutarinen ◽  
Rahul Mallick ◽  
Johanna P. Laakkonen ◽  
Diana Guo ◽  
...  
Keyword(s):  
Quantitative Polymerase Chain Reaction ◽  
Rank Correlation ◽  
Inflammatory Cells ◽  
Vessel Remodeling ◽  
Brain Avm ◽  
Inflammatory Drugs ◽  
Polymerase Chain ◽  
The Brain ◽  
Cox2 Expression

Abstract Background Brain arteriovenous malformations (bAVM) may rupture causing disability or death. BAVM vessels are characterized by abnormally high flow that in general triggers expansive vessel remodeling mediated by cyclo-oxygenase-2 (COX2), the target of non-steroidal anti-inflammatory drugs. We investigated whether COX2 is expressed in bAVMs and whether it associates with inflammation and haemorrhage in these lesions. Methods Tissue was obtained from surgery of 139 bAVMs and 21 normal Circle of Willis samples. The samples were studied with immunohistochemistry and real-time quantitative polymerase chain reaction (RT-PCR). Clinical data was collected from patient records. Results COX2 expression was found in 78% (109/139) of the bAVMs and localized to the vessels’ lumen or medial layer in 70% (95/135) of the bAVMs. Receptors for prostaglandin E2, a COX2-derived mediator of vascular remodeling, were found in the endothelial and smooth muscle cells and perivascular inflammatory cells of bAVMs. COX2 was expressed by infiltrating inflammatory cells and correlated with the extent of inflammation (r = .231, p = .007, Spearman rank correlation). COX2 expression did not associate with haemorrhage. Conclusion COX2 is induced in bAVMs, and possibly participates in the regulation of vessel wall remodelling and ongoing inflammation. Role of COX2 signalling in the pathobiology and clinical course of bAVMs merits further studies.

scholarly journals Seasonal Differences in Cyclospora cayetanensis Prevalence in Colombian Indigenous People

2021 ◽  
Vol 9 (3) ◽  
pp. 627
Author(s):  
Hagen Frickmann ◽  
Juliane Alker ◽  
Jessica Hansen ◽  
Juan Carlos Dib ◽  
Andrés Aristizabal ◽  
...  
Keyword(s):  
Indigenous People ◽  
Rainy Season ◽  
Gastrointestinal Symptoms ◽  
Dry Season ◽  
Seasonal Effects ◽  
Chain Reaction ◽  
Resource Limited Settings ◽  
Resource Limited ◽  
Stool Samples ◽  
Polymerase Chain

Fecal-orally transmitted cyclosporiasis is frequent in remote resource-limited settings in Central and South America with poor hygiene conditions. In this study, we aimed at assessing seasonal effects on the epidemiology of colonization or infection with C. cayetanensis in Colombian indigenous people living under very restricted conditions. In the rainy season between July and November and in the dry season between January and April, stool samples from indigenous people with and without gastrointestinal symptoms were collected and screened for C. cayetanensis applying in-house real-time polymerase chain reaction (PCR). In the rainy season and in the dry season, positive PCR results were observed for 11.8% (16/136) and 5.1% (15/292), respectively, with cycle threshold (Ct) values of 30.6 (±3.4) and 34.4 (±1.6), respectively. Despite higher parasite loads in the rainy season, fewer individuals (2/16, 12.5%) reported gastrointestinal symptoms compared to the dry season (6/15, 40%). In conclusion, considerable prevalence of C. cayetanensis in Colombian indigenous people persists in the dry season. Low proportions of gastrointestinal symptoms along with higher parasite loads make colonization likely rather than infection.

scholarly journals A double-edged sword of immuno-microenvironment in cardiac homeostasis and injury repair

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Kang Sun ◽  
Yi-yuan Li ◽  
Jin Jin
Keyword(s):  
Nk Cells ◽  
Cardiac Remodeling ◽  
Cardiac Fibrosis ◽  
Cardiac Tissue ◽  
Early Stage ◽  
Cardiac Injury ◽  
Inflammatory Cells ◽  
Treg Cells ◽  
Scar Formation

AbstractThe response of immune cells in cardiac injury is divided into three continuous phases: inflammation, proliferation and maturation. The kinetics of the inflammatory and proliferation phases directly influence the tissue repair. In cardiac homeostasis, cardiac tissue resident macrophages (cTMs) phagocytose bacteria and apoptotic cells. Meanwhile, NK cells prevent the maturation and transport of inflammatory cells. After cardiac injury, cTMs phagocytose the dead cardiomyocytes (CMs), regulate the proliferation and angiogenesis of cardiac progenitor cells. NK cells prevent the cardiac fibrosis, and promote vascularization and angiogenesis. Type 1 macrophages trigger the cardioprotective responses and promote tissue fibrosis in the early stage. Reversely, type 2 macrophages promote cardiac remodeling and angiogenesis in the late stage. Circulating macrophages and neutrophils firstly lead to chronic inflammation by secreting proinflammatory cytokines, and then release anti-inflammatory cytokines and growth factors, which regulate cardiac remodeling. In this process, dendritic cells (DCs) mediate the regulation of monocyte and macrophage recruitment. Recruited eosinophils and Mast cells (MCs) release some mediators which contribute to coronary vasoconstriction, leukocyte recruitment, formation of new blood vessels, scar formation. In adaptive immunity, effector T cells, especially Th17 cells, lead to the pathogenesis of cardiac fibrosis, including the distal fibrosis and scar formation. CMs protectors, Treg cells, inhibit reduce the inflammatory response, then directly trigger the regeneration of local progenitor cell via IL-10. B cells reduce myocardial injury by preserving cardiac function during the resolution of inflammation.

scholarly journals Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats

Biomolecules ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 498
Author(s):  
Mojdeh Khajehlandi ◽  
Lotfali Bolboli ◽  
Marefat Siahkuhian ◽  
Mohammad Rami ◽  
Mohammadreza Tabandeh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endurance Training ◽  
Molecular Mechanisms ◽  
Cardiac Tissue ◽  
Critical Role ◽  
Diabetic Rats ◽  
Moderate Intensity ◽  
Pcr Analysis ◽  
Cardiac Tissues ◽  
The Impact

Exercise can ameliorate cardiovascular dysfunctions in the diabetes condition, but its precise molecular mechanisms have not been entirely understood. The aim of the present study was to determine the impact of endurance training on expression of angiogenesis-related genes in cardiac tissue of diabetic rats. Thirty adults male Wistar rats were randomly divided into three groups (N = 10) including diabetic training (DT), sedentary diabetes (SD), and sedentary healthy (SH), in which diabetes was induced by a single dose of streptozotocin (50 mg/kg). Endurance training (ET) with moderate-intensity was performed on a motorized treadmill for six weeks. Training duration and treadmill speed were increased during five weeks, but they were kept constant at the final week, and slope was zero at all stages. Real-time polymerase chain reaction (RT-PCR) analysis was used to measure the expression of myocyte enhancer factor-2C (MEF2C), histone deacetylase-4 (HDAC4) and Calmodulin-dependent protein kinase II (CaMKII) in cardiac tissues of the rats. Our results demonstrated that six weeks of ET increased gene expression of MEF2C significantly (p < 0.05), and caused a significant reduction in HDAC4 and CaMKII gene expression in the DT rats compared to the SD rats (p < 0.05). We concluded that moderate-intensity ET could play a critical role in ameliorating cardiovascular dysfunction in a diabetes condition by regulating the expression of some angiogenesis-related genes in cardiac tissues.

scholarly journals High Frequency of Cryptosporidium hominis Infecting Infants Points to A Potential Anthroponotic Transmission in Maputo, Mozambique

Pathogens ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 293
Author(s):  
Idalécia Cossa-Moiane ◽  
Hermínio Cossa ◽  
Adilson Fernando Loforte Bauhofer ◽  
Jorfélia Chilaúle ◽  
Esperança Lourenço Guimarães ◽  
...  
Keyword(s):  
Public Hospitals ◽  
Diagnostic Methods ◽  
Molecular Diagnostic ◽  
P Value ◽  
Cryptosporidium Hominis ◽  
Cryptosporidium Spp ◽  
Pcr Rflp ◽  
Maputo City ◽  
Stool Samples ◽  
Polymerase Chain

Cryptosporidium is one of the most important causes of diarrhea in children less than 2 years of age. In this study, we report the frequency, risk factors and species of Cryptosporidium detected by molecular diagnostic methods in children admitted to two public hospitals in Maputo City, Mozambique. We studied 319 patients under the age of five years who were admitted due to diarrhea between April 2015 and February 2016. Single stool samples were examined for the presence of Cryptosporidium spp. oocysts, microscopically by using a Modified Ziehl–Neelsen (mZN) staining method and by using Polymerase Chain Reaction and Restriction Fragment Length Polymorphism (PCR-RFLP) technique using 18S ribosomal RNA gene as a target. Overall, 57.7% (184/319) were males, the median age (Interquartile range, IQR) was 11.0 (7–15) months. Cryptosporidium spp. oocysts were detected in 11.0% (35/319) by microscopy and in 35.4% (68/192) using PCR-RFLP. The most affected age group were children older than two years, [adjusted odds ratio (aOR): 5.861; 95% confidence interval (CI): 1.532–22.417; p-value < 0.05]. Children with illiterate caregivers had higher risk of infection (aOR: 1.688; 95% CI: 1.001–2.845; p-value < 0.05). An anthroponotic species C. hominis was found in 93.0% (27/29) of samples. Our findings demonstrated that cryptosporidiosis in children with diarrhea might be caused by anthroponomic transmission.

scholarly journals 781. C.difficile PCR+/ Toxin EIA- treat or not treat? A clinician survey

2020 ◽  
Vol 7 (Supplement_1) ◽  
pp. S435-S436
Author(s):  
Sarath G Nath ◽  
Francesca Lee ◽  
Anjali Bararia ◽  
Ank E Nijhawan
Keyword(s):  
Clinical Judgment ◽  
Clinical Care ◽  
Cost Effective ◽  
False Positive Diagnosis ◽  
Missed Diagnosis ◽  
Stool Samples ◽  
Polymerase Chain ◽  
Low Sensitivity ◽  
Survey Responses ◽  
And Training

Abstract Background C.difficile Toxin Polymerase Chain Reaction (C.diff PCR) and C.difficile Toxin Enzyme Immunoassays (toxin EIA) are commonly used tests to diagnose Clostridoides difficile infection (CDI). C.diff PCR cannot differentiate between colonization and infection, leading to a higher false-positive diagnosis of CDI. Toxin EIA has low sensitivity leading to a missed diagnosis of CDI. In patients with C.diff PCR positive(+) and Toxin EIA negative(-), clinical judgment is often needed regarding the decision to treat or not to treat. C.diff cytotoxic assay (CCA), is a more sensitive method to detect the toxin but is time-consuming and not readily available. Methods Between 6/2019 and 12/2019, 83 patients who were admitted to the hospital, met our inclusion criteria (C.diff PCR+/EIA-). Clinicians who cared for these patients were contacted and surveyed with a predesigned questionnaire evaluating the rationale of treatment. Also, a simultaneous medical records review was done to ensure consistency. Along with this C.diff PCR+/EIA- stool samples were sent to ARUP laboratories for CCA. The CCA results were not available for clinicians and did not impact clinical care. Average cost for a CCA assay was $29 Results Demographics of the clinicians were variable (Table 1). Several parameters were considered when making decisions regarding treatment and GI/ID were frequently involved (figure 1). Among the 83 patients, 41(49%) were CCA (+) and 42(51%) were CCA (-). 48 of 83 (58%) patients received treatment for CDI. 25 of 48 (52%) patients who were treated were CCA positive while 23 of 48 (48%) patients were CCA negative. Among the untreated patients, 16/35 (46%) were CCA+ while 19/35(54%) were CCA-. There was no statistically significant correlation between clinical judgment and CCA assay results (p: 0.56 on the Chi test). Demographics of the clinicians Clinician survey responses CDI Treatment and by CCA positivity Conclusion Clinicians regardless of their background and training face challenges with the treatment of C.diff PCR+/EIA- patients. Patient outcomes based on the incorporation of CCA assay into an algorithm for C.diff PCR+/EIA- patients, need to be evaluated. But it has a potential role in stopping unnecessary CDI treatment as well as avoidance of missed treatment opportunities while possibly also being cost-effective. Disclosures Ank E. Nijhawan, MD, MPH, Gilead (Grant/Research Support, Scientific Research Study Investigator, Research Grant or Support)

Molecular Detection and Phylogenetic Analysis of Chicken Astrovirus Associated with Poultry Enteritis

2021 ◽  
Author(s):  
C. Patidar ◽  
D.K. Sharma ◽  
R. Singathia ◽  
P. Suthar ◽  
A. Saraswat ◽  
...  
Keyword(s):  
Phylogenetic Analysis ◽  
Molecular Characterization ◽  
Histopathological Examination ◽  
Villous Atrophy ◽  
Inflammatory Cells ◽  
Liver Parenchyma ◽  
Amino Acid Sequences ◽  
Poultry Birds ◽  
Commercial Poultry ◽  
Liver Specimen

Background: Poultry enteritis is an important multifactorial disease. Chicken Astrovirus (CAstV) usually associated with enteritis. The aim of this study was to investigate the occurrence of CAstV in poultry enteritis cases, its molecular characterization, phylogenetic analysis and gross and microscopic examination of intestine and liver specimen affected with CAstV. Methods: Total 604 dead poultry birds from commercial poultry farms affected with enteritis were examined for presence of CAstV. Intestinal samples of four birds were pooled to make one biological sample. CAstV was detected by reverse transcriptase PCR (RT-PCR) using ORF-1b gene specific primers. Molecular characterization was carried out by partial gene sequencing. Result: CAstV was detected in 20.52% (31/151) of samples. Highest prevalence (49.29%) was observed in 0-1 week old chicks. The partial molecular characterization revealed high similarity of the nucleotide sequence from India (97% to 93%) and from USA, Brazil, Poland and Korea (94 to 92%). Further similarity of amino acid sequences of CAstV from India (100% to 98%) and from USA, Brazil, Poland and Korea (98 to 97%) was observed. Histopathological examination revealed villous atrophy, congestion and atrophic cystic glands in sub-mucosa of intestine. Further severe congestion and hemorrhages along with infiltration of inflammatory cells in liver parenchyma was observed.

Pygo1 regulates pathological cardiac hypertrophy via a β-catenin-dependent mechanism

2021 ◽  
Author(s):  
Li Lin ◽  
Wei Xu ◽  
Yongqing Li ◽  
Ping Zhu ◽  
Wuzhou Yuan ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Tissue ◽  
Heart Weight ◽  
Dependent Manner ◽  
Tissue Specific ◽  
Cardiac Tissues ◽  
Pathological Cardiac Hypertrophy ◽  
Interaction Factor ◽  
Myocardial Remodelling

Wnt/β-catenin signalling plays a key role in pathological cardiac remodelling in adults. The identification of a tissue-specific Wnt/β-catenin interaction factor may realise a tissue-specific clinical targeting strategy. Drosophila Pygo codes for the core interaction factor of Wnt/β-catenin. Two Pygo homologs, Pygo1 and Pygo2, have been identified in mammals. Different from the ubiquitous expression profile of Pygo2, Pygo1is enriched in cardiac tissue. However, the role of Pygo1 in mammalian cardiac disease remains unelucidated. Here, we found that Pygo1 was upregulated in human cardiac tissues with pathological hypertrophy. Cardiac-specific overexpression of Pygo1 in mice spontaneously led to cardiac hypertrophy accompanied by declined cardiac function, increased heart weight/body weight and heart weight/tibial length ratios and increased cell size. The canonical β-catenin/T-cell transcription factor 4 complex was abundant in Pygo1-overexpressingtransgenic(Pygo1-TG) cardiac tissue,and the downstream genes of Wnt signaling, i.e., Axin2, Ephb3, and C-myc, were upregulated. A tail vein injection of β-catenin inhibitor effectively rescued the phenotype of cardiac failure and pathological myocardial remodelling in Pygo1-TG mice. Furthermore, in vivo downregulated pygo1 during cardiac hypertrophic condition antagonized agonist-induced cardiac hypertrophy. Therefore, our study is the first to present in vivo evidence demonstrating that Pygo1 regulates pathological cardiac hypertrophy in a canonical Wnt/β-catenin-dependent manner, which may provide new clues for a tissue-specific clinical treatment targeting this pathway.

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