Molecular identification of adenoviruses associated with respiratory infection in Egypt from 2003 to 2010.

BACKGROUND: Human adenoviruses of species B, C, and E (HAdV-B, -C, -E) are frequent causative agents of acute respiratory infections worldwide. As part of a surveillance program aimed at identifying the etiology of influenza-like illness (ILI) in Egypt, we characterized 105 adenovirus isolates from clinical samples collected between 2003 and 2010. METHODS: Identification of the isolates as HAdV was accomplished by an immunofluorescence assay (IFA) and confirmed by a set of species and type specific polymerase chain reactions (PCR). RESULTS: Of the 105 isolates, 42% were identified as belonging to HAdV-B, 60% as HAdV-C, and 1% as HAdV-E. We identified a total of six co-infections by PCR, of which five were HAdV-B/HAdV-C co-infections, and one was a co-infection of two HAdV-C types: HAdV-5/HAdV-6. Molecular typing by PCR enabled the identification of eight genotypes of human adenoviruses; HAdV-3 (n = 22), HAdV-7 (n = 14), HAdV-11 (n = 8), HAdV-1 (n = 22), HAdV-2 (20), HAdV-5 (n = 15), HAdV-6 (n = 3) and HAdV-4 (n = 1). The most abundant species in the characterized collection of isolates was HAdV-C, which is concordant with existing data for worldwide epidemiology of HAdV respiratory infections. CONCLUSIONS: We identified three species, HAdV-B, -C and -E, among patients with ILI over the course of 7 years in Egypt, with at least eight diverse types circulating

Investigating mitochondrial metabolism in contracting HL-1 cardiomyocytes following hypoxia and pharmacological HIF activation identifies HIF-dependent and independent mechanisms of regulation.

Hypoxia is a consequence of cardiac disease and downregulates mitochondrial metabolism, yet the molecular mechanisms through which this occurs in the heart are incompletely characterized. Therefore, we aimed to use a contracting HL-1 cardiomyocyte model to investigate the effects of hypoxia on mitochondrial metabolism. Cells were exposed to hypoxia (2% O2) for 6, 12, 24, and 48 hours to characterize the metabolic response. Cells were subsequently treated with the hypoxia inducible factor (HIF)-activating compound, dimethyloxalylglycine (DMOG), to determine whether hypoxia-induced mitochondrial changes were HIF dependent or independent, and to assess the suitability of this cultured cardiac cell line for cardiovascular pharmacological studies. Hypoxic cells had increased glycolysis after 24 hours, with glucose transporter 1 and lactate levels increased 5-fold and 15-fold, respectively. After 24 hours of hypoxia, mitochondrial networks were more fragmented but there was no change in citrate synthase activity, indicating that mitochondrial content was unchanged. Cellular oxygen consumption was 30% lower, accompanied by decreases in the enzymatic activities of electron transport chain (ETC) complexes I and IV, and aconitase by 81%, 96%, and 72%, relative to controls. Pharmacological HIF activation with DMOG decreased cellular oxygen consumption by 43%, coincident with decreases in the activities of aconitase and complex I by 26% and 30%, indicating that these adaptations were HIF mediated. In contrast, the hypoxia-mediated decrease in complex IV activity was not replicated by DMOG treatment, suggesting HIF-independent regulation of this complex. In conclusion, 24 hours of hypoxia increased anaerobic glycolysis and decreased mitochondrial respiration, which was associated with changes in ETC and tricarboxylic acid cycle enzyme activities in contracting HL-1 cells. Pharmacological HIF activation in this cardiac cell line allowed both HIF-dependent and independent mitochondrial metabolic changes to be identified

Metabolic adaptation to chronic hypoxia in cardiac mitochondria.

Chronic hypoxia decreases cardiomyocyte respiration, yet the mitochondrial mechanisms remain largely unknown. We investigated the mitochondrial metabolic pathways and enzymes that were decreased following in vivo hypoxia, and questioned whether hypoxic adaptation was protective for the mitochondria. Wistar rats were housed in hypoxia (7 days acclimatisation and 14 days at 11% oxygen), while control rats were housed in normoxia. Chronic exposure to physiological hypoxia increased haematocrit and cardiac vascular endothelial growth factor, in the absence of weight loss and changes in cardiac mass. In both subsarcolemmal (SSM) and interfibrillar (IFM) mitochondria isolated from hypoxic hearts, state 3 respiration rates with fatty acid were decreased by 17-18%, and with pyruvate were decreased by 29-15%, respectively. State 3 respiration rates with electron transport chain (ETC) substrates were decreased only in hypoxic SSM, not in hypoxic IFM. SSM from hypoxic hearts had decreased activities of ETC complexes I, II and IV, which were associated with decreased reactive oxygen species generation and protection against mitochondrial permeability transition pore (MPTP) opening. In contrast, IFM from hypoxic hearts had decreased activity of the Krebs cycle enzyme, aconitase, which did not modify ROS production or MPTP opening. In conclusion, cardiac mitochondrial respiration was decreased following chronic hypoxia, associated with downregulation of different pathways in the two mitochondrial populations, determined by their subcellular location. Hypoxic adaptation was not deleterious for the mitochondria, in fact, SSM acquired increased protection against oxidative damage under the oxygen-limited conditions

Paras selenium, zink dan kromium dalam kalangan pesawah yang terdedah pestisid di MADA, Perlis dan komuniti nelayan di Mersing, Johor

Pendedahan terhadap pestisid dapat menyebabkan penurunan paras unsur surih di dalam badan manusia. Unsur surih memainkan peranan penting dalam metabolisma tubuh. Kajian ini dijalankan untuk mengkaji paras unsur surih selenium, zink dan kromium dalam kalangan pesawah yang terdedah kepada pestisid di Wilayah I, MADA, Perlis. Kajian keratan rentas ini melibatkan 70 orang pesawah dan 57 orang yang tinggal di perkampungan nelayan sebagai kumpulan kawalan yang berumur di antara 21 hingga 80 tahun. Maklumat sosiodemografi pesawah dilakukan melalui temuduga borang soal selidik yang telah divalidasi. Pemeriksaan tekanan darah dan glukosa darah pesawah dilakukan. Paras selenium, zink dan kromium sampel kuku dan rambut dianalisis dengan menggunakan kaedah penghadaman asid dan mesin Inductively Coupled Plasma-Mass Spectrometry (ICP-MS). Hasil kajian mendapati bahawa paras selenium pada rambut (5.11 ± 17.05 µg/L) dan kuku (4.92 ± 2.17 µg/L) adalah lebih rendah secara signifikannya (p < 0.05) berbanding paras selenium pada rambut (15.67 ± 10.59 µg/L) dan kuku (6.67 ± 2.81 µg/L) kumpulan kawalan. Paras kromium pada rambut (31.83 ± 15.17 µg/L) dan kuku (87.64 ± 23.30 µg/L) kumpulan pesawah juga didapati lebih rendah secara signifikannya (p < 0.05) berbanding paras kromium pada rambut (85.19 ± 56.90 µg/L) dan kuku (99.36 ± 56.89 µg/L) pada kumpulan kawalan. Walau bagaimanapun, tiada perbezaan paras unsur surih yang signifikan (p > 0.05) menurut tempoh pendedahan pestisid. Kesimpulannya, paras selenium dan kromium pada kuku dan rambut pesawah yang terdedah kepada pestisid adalah lebih rendah berbanding kumpulan komuniti nelayan