• Both ischemic and reperfused rat myocardium can undergo apoptotic cell death, however the myocardium, which is subjected to ischemia followed by reperfusion, undergoes accelerated apoptosis [ 3 ]. (ac.ir)
  • In vivo rat hearts or isolated Langendorff-perfused mouse hearts were subjected to ischemia followed by reperfusion with intralipid (0.5%, 1% and 2% ex-vivo, and 20% in vivo), cyclosporine-A (0.2 μM, 0.8 μM, and 1.5 μM ex- vivo and 10 mg/kg in vivo), or vehicle. (silverchair.com)
  • Desflurane application at pharmacological concentrations efficiently upregulated aromatase expression in vivo and in vitro. (uni-wuerzburg.de)
  • We further provided evidence that IL-37 inhibited effectively tumor metastasis in vitro and in vivo . (nature.com)
  • In vitro, HL-1 cells (mouse cardiomyocytes) received chamber hypoxia-oxygenation reperfusion (H/R) for 24H4R with/without DLC1β plasmid, before collection for protein/mRNA analyses. (uwo.ca)
  • Area A will delineate the diagnostic potential of TSPO imaging by means of positron emission tomography (PET) in brain tumors in vivo and will enable the complementary characterization of brain tissue in vitro to delineate the neurobiological characteristics underlying TSPO PET labeling in the human brain. (uni-regensburg.de)
  • Finally, we made the intriguing observation in vitro that ERK1/2 activation reduces endothelial inflammation induced by LPS and TNFα, in contrast to its role in promoting leukocyte inflammation. (ucsf.edu)
  • In our early studies we found that bacterial lipoprotein TLR2 agonists are shed by bacteria into human serum in vitro and into the blood of septic mice and rats in vivo. (ucsf.edu)
  • We have characterized the effects of bacterial lipoproteins on monocytes, macrophages, and endothelial cells, and have done extensive work on the effects of TLR2 activation on coagulation and permeability in vitro and in vivo. (ucsf.edu)
  • We have found TLR2-dependent activation of endothelial inflammatory pathways, as well as pathways involved in coagulopathy and vascular leak in vitro and in vivo. (ucsf.edu)
  • The cardioprotective effect of CLU4A inhibition was detected by monitoring the cell viability, cell apoptosis, and LDH activity in vitro and in vivo , and examining the infarct size and cardiac function in vivo . (engreen.com.cn)
  • Thus, we attempt to investigated the possible regulation role of H2S on spinal cord I/R injury in vitro or in vivo. (biomedcentral.com)
  • We will investigate the effects of exenatide on vascular endothelial injury and nitrooxidative stress in hyperglycemia both in vivo and in vitro and explore the role of nitrooxidative stress in endothelium-protective action of exenatide. (hindawi.com)
  • Recent evidence has indicated that the vascular endothelial injury induced by hyperglycemia is associated with the enhanced nitrooxidative stress both in vivo and in vitro [ 3 - 6 ]. (hindawi.com)
  • In vitro, EUK-134 significantly reduced NO production by PTCs incubated with IFN-γ/LPS. (scienceopen.com)
  • Here, we tested the hypothesis that female sex hormones alter vasocontractile responses after experimental stroke in vivo or after organ culture in vitro, a model of vasocontractile receptor upregulation. (lu.se)
  • Interestingly, however, the HFD did not reduce infarct size in Epac1−/− deficient mice hearts (Epac1−/− HFD 65.1 ± 5.1% vs. Epac1−/− ND 56.1 ± 3.5%, ns. (uib.no)
  • The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. (uni-wuerzburg.de)
  • Aromatase metabolizes testosterone to 17b- estradiol (E2) and thereby significantly contributes The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. (uni-wuerzburg.de)
  • Anastrozole blocked DES induced preconditioning and increased infarct size compared to DES alone (37.94615.5% vs. 17.163.62%) without affecting area at risk and systemic hemodynamic parameters following ischemia/reperfusion. (uni-wuerzburg.de)
  • In lpr mice, a naturally occurring mutant deficient in Fas, there is marked reduction in infarct size and abundance of apoptotic cardiac myocytes following ischemia and reperfusion that also signifies the importance of Fas pathway in ischemia-reperfusion injury [ 5 ]. (ac.ir)
  • Reperfusion after cardiac ischemia increases cell death and infarct size (IS), called myocardial ischemia/reperfusion (I/R) injury, which is the main cause of myocardial injury during the cardiac surgery particularly in coronary artery bypass graft surgery ( 1 , 2 ). (spandidos-publications.com)
  • Although intralipid inhibits the opening of the mitochondrial permeability transition pore as efficiently as cyclosporine-A, intralipid is more effective in reducing the infarct size and improving the cardiac functional recovery. (silverchair.com)
  • Consistently, knockdown of CLU4A reduced the myocardial infarct size and improved cardiac function in vivo . (engreen.com.cn)
  • An IL-36R antagonist (IL-36Ra) decreased neutrophil recruitment, improved blood flow, and reduced infarct size in both adult and aged mice. (jci.org)
  • Compared to I/R injury groups, H 2 S pretreatment had reduced spinal cord infarct zone, improved hind motor function in rats. (biomedcentral.com)
  • Rosuvastatin (80 mg) is shows to decrease infarct size and improve cardiac mechanical function after ischemia/reperfusion in animal model. (bioservuk.com)
  • These findings were further confirmed when HIF-1 stabilization in the rat and murine heart resulted in smaller myocardial infarct sizes (both in vivo and ex vivo), decreased mitochondrial oxidative stress, and inhibited MPTP opening following IRI, effects which were also found to be dependent on HKII. (ox.ac.uk)
  • Acute administration of cannabidiol in vivo suppresses ischaemia- induced cardiac arrhythmias and reduces infarct size when given at reperfusion. (myoptivida.com)
  • APC reduces the pulmonary endothelial cell injury and hypotension in rats administered endotoxin (ET) by inhibiting TNF-α production through inhibition of its transcription. (eurekaselect.com)
  • One of the primary causes of ARF is ischemia/reperfusion (I/R). Inflammatory process and oxidative stress are thought to be the major mechanisms causing I/R. MK-886 is a potent inhibitor of leukotrienes biosynthesis which may have anti-inflammatory and antioxidant effects through inhibition of polymorphonuclear leukocytes (PMNs) infiltration into renal tissues. (biomedcentral.com)
  • X-ray analysis was used to validate the design concept, and biological evaluation revealed selective cellular inhibition of CypD and the permeability transition pore with reduced cellular toxicity compared with cyclosporine. (rcsb.org)
  • These findings suggest that selective CypD inhibition may represent a viable therapeutic strategy for MS and identify quinolinium as a mitochondrial targeting group for in vivo use. (rcsb.org)
  • Consequently, inhibition of endocannabinoids may be a tool in reducing the prevalence of metabolic syndrome and augmenting the benefits of physical exercise. (medscape.com)
  • However, harmful stimuli (such as ischemia-reperfusion, oxidative stress, and toxic chemicals) can change the direction and efficiency of intercellular mitochondrial transfer. (frontiersin.org)
  • Livers treated with NMP combined with BMMSCs showed better liver function, relieved histopathological damage, reduced oxidative stress injury and ferroptosis, and the mechanism of reduction was associated with downregulation of intracellular reactive oxygen species (ROS) and free Fe²⁺ levels. (medscimonit.com)
  • We propose that EUK-134 reduces renal I/R injury not only via reduction of oxidative stress, but also by reducing nitrosative stress caused by renal I/R. (scienceopen.com)
  • A total of 24 Adult males of Swiss albino mice were randomized to four groups: I/R group (n = 6), mice underwent 30 minute bilateral renal ischemia and 48 hr reperfusion. (biomedcentral.com)
  • Rats, subjected to bilateral renal ischemia (45 min) followed by reperfusion (6 h), were administered EUK-134 (0.3 and 3 mg/kg, i.v.) prior to and during reperfusion, after which biochemical and histological indicators of renal dysfunction and injury were measured. (scienceopen.com)
  • Furthermore, APC reduces the ischemia / reperfusion-induced renal injury and the stress-induced gastric mucosal injury in rats. (eurekaselect.com)
  • Furthermore, APC reduced the spinal cord injury induced by compression-trauma or ischemia / reperfusion by inhibiting TNF-α production in rats, suggesting that APC may be a potential therapeutic agent for spinal cord injury in which only limited therapeutic measures are currently available. (eurekaselect.com)
  • Thirty Wistar rats were selected and divided into three groups (n = 10): acute ischemia-reperfusion (I/R) group, acute ischemia-reperfusion and treated with atorvastatin group and sham-operated group. (ac.ir)
  • Pretreating the rats with simvastatin 18 hour prior to the induction of ischemiareperfusion has been shown to reduce cardiac dysfunction and improve coronary flow [ 7 ]. (ac.ir)
  • In cynomolgus monkeys, Rosuvastatin decreases plasma cholesterol levels by 22% [2] Rosuvastatin (20 mg/kg/day) administration for 2 weeks, significantly reduces very low-density lipoproteins (VLDL) in diabetes mellitus rats induced by Streptozocin. (bioservuk.com)
  • 5] Rosuvastatin (20 mg/kg) inhibits ROS production, normalizes NO-dependent endothelial function and reduces platelet activation in diabetic rats induced by Streptozocin. (bioservuk.com)
  • However, EUK-134 also reduced nitrosative stress caused by I/R in vivo (reduction of iNOS expression and nitrotyrosine formation), which was reflected by a significant reduction in serum NO levels in rats subjected to renal I/R. Specifically, serum NO levels were reduced from 57 ± 12 (n = 12, I/R only) to 23 ± 3 m M (n = 12, I/R +3 mg/kg EUK-134). (scienceopen.com)
  • Ischemia-reperfusion injured rat model was induced by middle cerebral artery occlusion and reperfusion (MCAO/R). EA treatment at the DU 20 and DU 24 acupoints treatment were conducted to rats from the 12 h after MCAO/R injury for consecutive 7 days. (biomedcentral.com)
  • Female rats with intact ovaries and ovariectomized (OVX) females treated with 17β-estradiol, progesterone, or placebo were subjected to transient, unilateral middle cerebral artery occlusion followed by reperfusion (I/R). The maximum contractile response, measured my wire myography, in response to the endothelin B receptor agonist sarafotoxin 6c was increased in female arteries after I/R, but the maximum response was significantly lower in arteries from OVX females. (lu.se)
  • Therefore, the aim of this study was to use the novel technique of hyperpolarized magnetic resonance to investigate the in vivo effects of treatment with meldonium on cardiac metabolism and function in control and diabetic rats. (ox.ac.uk)
  • We therefore investigated the impact of global brain hypoxia-ischemia on the thalamic circuit function in the somatosensory system of young rats. (cdc.gov)
  • Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. (frontiersin.org)
  • We conclude that desflurane efficiently regulates aromatase expression and activity which might lead to increased local estrogen synthesis and thus preserve cellular integrity and reduce cardiac damage in an acute myocardial infarction model. (uni-wuerzburg.de)
  • Before ischemia, acute troglitazone treatment had no effect on LV function, electrocardiogram, or substrate utilization. (diabetesjournals.org)
  • Acute treatment with troglitazone increases susceptibility to ventricular fibrillation during myocardial ischemia and reperfusion. (diabetesjournals.org)
  • Therefore, we designed this study to see the influence of atorvastatin on cardiomyocyte apoptosis and Fas expression following acute I/R in vivo. (ac.ir)
  • AIMS: Hypoxia-inducible factor-1 (HIF-1) has been reported to promote tolerance against acute myocardial ischaemia-reperfusion injury (IRI). (ox.ac.uk)
  • Upregulation of Fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting Fas expression. (ac.ir)
  • Apoptosis of the cardiomyocytes has been demonstrated in animal models with coronary artery occlusion [ 1 ], and experimental evidence suggests that myocardial cells are able to undergo apoptosis during ischemia followed by reperfusion [ 2 ]. (ac.ir)
  • HPC protected neonatal rat cardiomyocytes against H/R injury by increasing cell viability, while reducing LDH release and cell apoptosis. (spandidos-publications.com)
  • Isolated ex vivo mice hearts were perfused in a constant pressure Langendorff mode, and exposed to 30min of global ischemia (GI) and 60min of reperfusion. (uib.no)
  • In vivo, C57/BL6 mice received heterotopic HTx with/without DLC1β-OE plasmid tail-vein injections. (uwo.ca)
  • Sham group (n = 6), mice underwent same anesthetic and surgical procedures except for ischemia induction. (biomedcentral.com)
  • After the end of reperfusion phase mice were sacrificed, blood samples were collected directly from the heart for determination of serum TNF-a, IL-6, urea and Creatinine. (biomedcentral.com)
  • These data identify distinct electrophysiologic abnormalities in FHC mice with a specific alpha-myosin mutation, and also validate a novel method to explore in vivo the relationship between specific genotypes and their electrophysiologic phenotypes. (jci.org)
  • Furthermore, we observed that treatment with ERK5 inhibitor reduces inflammation, coagulopathy, and mortality in LPS-treated mice, but conversely increases mortality and bacteremia in a cecal ligation and puncture model of sepsis. (ucsf.edu)
  • CLU4A expression was measured after myocardial ischemia/reperfusion in mice and in H9C2 cells with hypoxia/reoxygenation treatment by q-PCR and western blotting. (engreen.com.cn)
  • Using a 90-min lobar warm ischemia model, wild type (WT), TLR4 KO/mutant and TLR2 KO mice were first assessed for the severity of hepatocellular damage at 6 h postreperfusion. (houstonmethodist.org)
  • Unlike in WT or TLR2-deficient mice, disruption/absence of TLR4 pathway reduced IRI, as manifested by liver function (serum alanine aminotransferase levels), histology (Suzuki's scores), neutrophil infiltration (myeloperoxidase activity) and local/systemic TNF-α production (mRNA/protein levels). (houstonmethodist.org)
  • 1994. Gas uptake studies of deuterium isotope effects on dichloromethane metabolism in female B6C3F1 mice in vivo . (cdc.gov)
  • Matrix-metalloproteinase upregulation in ischemia reperfusion can be imaged acutely in-vivo with NIRF using MMPSense750. (biomedcentral.com)
  • A deleterious consequence of cerebral ischemia is upregulation of vasoconstrictor receptors in cerebral arteries that exacerbate stroke injury. (lu.se)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)
  • 6] Rosuvastatin displays cardioprotective effects in vivo. (bioservuk.com)
  • In our studies, the feasibility of using PAI for estimating the spatial distribution of oxygen saturation is examined, in models of occlusion reperfusion and adrenalin-dependent vasoconstriction in humans. (lu.se)
  • It is well-documented that extracellular ATP triggers surrounding glial purinergic receptors signaling pathway and pro-inflammatory cytokines release to aggravate neural injury in cerebral ischemia [ 8 , 9 ]. (biomedcentral.com)
  • Hyperpolarized magnetic resonance shows that the anti-ischemic drug meldonium leads to increased flux through pyruvate dehydrogenase in vivo resulting in improved post-ischemic function in the diabetic heart. (ox.ac.uk)
  • Isolated perfused hearts were challenged with low-flow ischemia/reperfusion to assess the impact of meldonium on post-ischemic recovery. (ox.ac.uk)
  • The increase in pyruvate dehydrogenase flux in vivo was accompanied by an improvement in post-ischemic function ex vivo, as meldonium elevated the rate pressure product by 1.3-fold and 1.5-fold in the control and diabetic animals, respectively. (ox.ac.uk)
  • We tested the hypothesis that 8-Br is also protective under clinically relevant conditions (regional ischaemia) when applied either before ischemia or at the beginning of reperfusion, and this effect is associated with the mitochondrial permeability transition pore (MPTP). (mdpi.com)
  • Intralipid was as efficient as cyclosporine-A in inhibiting the mitochondrial permeability transition pore opening (calcium retention capacity = 280 ± 8.2 vs. 260.3 ± 2.9 nmol/mg mitochondria protein in cyclosporine-A, P = 0.454, n = 6) and in reducing cardiac mitochondrial superoxide production. (silverchair.com)
  • HIF-1 reduces ischaemia-reperfusion injury in the heart by targeting the mitochondrial permeability transition pore. (ox.ac.uk)
  • The mitochondrial permeability transition pore is a recognized drug target for neurodegenerative conditions such as multiple sclerosis and for ischemia-reperfusion injury in the brain and heart. (rcsb.org)
  • The anti- inflammatory and immune-modulating abilities of Hemp Extract, as well as its antioxidant protection, reduces damage to heart tissue. (myoptivida.com)
  • Therefore, we speculate that purinergic receptors might play dualistic roles in response to EA effects treating inflammatory injury induced by ischemia. (biomedcentral.com)
  • Our previous studies have demonstrated that EA protects cerebral neural cells against inflammatory injury after cerebral ischemia, which appears at 24 h to 14 days after treatment. (biomedcentral.com)
  • The microvascular and parenchymal organ damage induced upon ischemia tissue reperfusion is mainly attributed to the reactive oxygen-free radicals, and it has been demonstrated in many organs. (frontiersin.org)
  • Specifically, the gelatinases MMP-2 and MMP-9 have previously been considered to specifically injure the important components of the basal lamina around the cerebral blood vessels that precede microvascular damage in cerebral ischemia [ 1 ]. (biomedcentral.com)
  • An intravital model for imaging the adult and aged IR-injured beating heart in real time in vivo was used to demonstrate heightened basal and injury-induced neutrophil recruitment, and poorer blood flow, in the aged coronary microcirculation when compared with adult hearts. (jci.org)
  • Hypoxia/reoxygenation (H/R) as well as hypoxic preconditioning (HPC) is widely used for simulating in vivo myocardial I/R and ischemic preconditioning (IPC) in a cell culture model. (spandidos-publications.com)
  • Global hypoxia-ischemia interrupts oxygen delivery and blood flow to the entire brain. (cdc.gov)
  • Global brain hypoxia-ischemia during cardiac arrest has a long-term impact on processing and transfer of sensory information by thalamic circuitry. (cdc.gov)
  • We have recently shown that postischemic administration of intralipid protects the heart against ischemia-reperfusion injury. (silverchair.com)
  • Thus, liver surgeons have the option to apply vascular inflow control procedures and sometimes total vascular exclusion to reduce intraoperative bleeding. (123dok.net)
  • Abstract Hepatic ischemia/reperfusion (I/R) injury is a common clinical challenge. (123dok.net)
  • We previously demonstrated that chronic pretreatment with a thiazolidinedione peroxisome proliferator-activated receptor (PPAR)-γ activator, troglitazone, improves recovery of left ventricular (LV) function and substrate metabolism after ischemia and reperfusion, without causing arrhythmias. (diabetesjournals.org)
  • in vivo cardiac function and metabolism were assessed with CINE MRI and hyperpolarized magnetic resonance respectively. (ox.ac.uk)
  • Ischemia-reperfusion (I/R) injury is a process whereby parenchymal damage caused by blood flow deprivation is accentuated upon organ reperfusion. (123dok.net)
  • Here we investigate the effect of EUK-134, a synthetic superoxide dismutase and catalase mimetic, (i) on renal dysfunction and injury caused by I/R in vivo and (ii) on proximal tubular cell (PTC) injury and death caused by oxidative and nitrosative stress. (scienceopen.com)
  • Urinary N -acetyl-β- D -glucosaminidase activity, an indicator of tubular damage, was reduced from 42 ± 5 (n = 12, I/R only) to 22 ± 3 IU/l (n = 12, I/R +3 mg/kg EUK-134). (scienceopen.com)
  • These sequelae of renal ischemia are a result of endothelial dysfunction, which is most probably responsible for the 'no-reflow' phenomenon and further aggravation of tubular ischemia during the early reperfusion period. (scienceopen.com)
  • A characteristic reaction of ONOO − is the nitration of protein-bound tyrosine residues to produce nitrotyrosine, and the production of nitrotyrosine has been used extensively as a footprint for ONOO − in vivo. (hindawi.com)
  • The anti-ischemic drug meldonium may provide a route to counteract this by reducing l-carnitine levels, resulting in improved cardiac glucose utilization. (ox.ac.uk)
  • Herein, we utilize in vivo imaging of luminol chemiluminescence to noninvasively monitor neutrophil activation after PDT administration. (bioxcell.com)
  • Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings. (frontiersin.org)
  • In this study, clinical data from 84 patients showed that loss or reduced expression of IL-37 in lung adenocarcinoma tissues was significantly associated with tumor metastasis. (nature.com)
  • Ischemia/reperfusion (I/R) injury of the spinal cord is a dynamic process that frequently occurs during a variety of clinical situations such as thoracoabdominal aortic surgery or spinal cord injury [ 1 ]. (biomedcentral.com)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • We will also investigate the role of NADA, and the other components of the endocannabinoid system, in vivo using mouse models of infectious and non-infectious inflammation. (ucsf.edu)
  • EUK-134 produced a significant reduction in renal dysfunction and injury caused by I/R. Specifically, serum creatinine levels, an indicator of renal dysfunction, were reduced from 227 ± 11 (n = 12, I/R only) to 146 ± 9 µ M (n = 12, I/R +3 mg/kg EUK-134). (scienceopen.com)
  • In conclusion, the intricate relations between endothelial and epithelial cells, based in part on the relations between endothelial and inducible nitric oxide synthases, are perturbed in renal ischemia primarily as a result of endothelial dysfunction precipitating epithelial injury. (scienceopen.com)
  • and the underlying mechanism of CLU4A in myocardial ischemia/reperfusion injury needs to be investigated. (engreen.com.cn)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • Cardiac ischemia-reperfusion injury (IRI) occurs intra-operatively during heart transplantation (HTx), underpinning graft survival. (uwo.ca)
  • The conducted study focuses on how we can reduce injury to the heart during heart transplantation. (uwo.ca)
  • Cardiac ischemia-reperfusion injury (IRI) occurs when transplanting a heart from donor to recipient. (uwo.ca)
  • The "ischemia" phase of cardiac IRI occurs when the donor heart is being collected and blood/oxygen is not going to the heart. (uwo.ca)
  • By analyzing these questions, this research might be useful in humans to potentially reduce the rate of injury during heart transplantation. (uwo.ca)
  • The cAMP analogue 8-Br-cAMP-AM (8-Br) confers marked protection against global ischaemia/reperfusion of isolated perfused heart. (mdpi.com)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • Heart disease is caused by blood vessels hardening and plaque buildup over time, which reduces cardiovascular function. (myoptivida.com)
  • Using Hemp Extract has been proven effective as a way of reducing metabolic issues of increased glucose responses, a major factor in heart disease. (myoptivida.com)
  • In conclusion, meldonium improves in vivo pyruvate dehydrogenase flux in the diabetic heart, contributing to improved cardiac recovery after ischemia. (ox.ac.uk)
  • Taking N-acetyl cysteine by mouth seems to reduce homocysteine levels, a possible risk factor for heart disease. (medlineplus.gov)
  • We first demonstrated the presence of IL-36(α/β) and its receptor (IL-36R) in ischemia/reperfusion-injured (IR-injured) mouse hearts and, interestingly, noted that expression of both increased with aging. (jci.org)
  • In conclusion, CLU4A expression was up-regulated in myocardial ischemia/reperfusion. (engreen.com.cn)
  • Results: All groups fed a HFD presented with significantly enhanced body weight, visceral fat content and reduced glucose clearance compared to corresponding ND groups. (uib.no)
  • The objective of the present study was to determine whether an alternate MMP activatable probe with a shorter optical imaging time, MMPSense ™ 750 FAST (MMPSense750), could be used for visualization of MMP activity in the early stages of ischemia reperfusion in a mouse model of stroke. (biomedcentral.com)
  • It has been shown that the Fas pathway is functional in cardiac myocytes and plays a critical role in myocardial death due to ischemia-reperfusion in vivo [ 4 ]. (ac.ir)
  • Therefore, we hypothesized that hydrogen/oxygen therapy for ordinary coronavirus disease 2019 (COVID-19) patients might reduce the length of hospitalization and increase hospital discharge rates. (researchgate.net)
  • The system was validated in vivo against complementary techniques, including white light and diffuse reflectance spectroscopy. (lu.se)