Publications
398 results found
Chen L, Zhao H, Yao S, et al., 2016, Epithelium-macrophage interaction promotes epithelial-to-mesenchymal transition after chemotherapy, BJA Research Forum, Publisher: OXFORD UNIV PRESS, Pages: E839-E840, ISSN: 0007-0912
Land WG, Agostinis P, Gasser S, et al., 2016, DAMP-Induced Allograft and Tumor Rejection: The Circle Is Closing, AMERICAN JOURNAL OF TRANSPLANTATION, Vol: 16, Pages: 3322-3337, ISSN: 1600-6135
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- Citations: 51
Ma D, Zhao H, 2016, The role of Nuclear factor-erythroid 2 related factor 2 (Nrf-2) in the protection against lung injury., American Journal of Physiology-Lung Cellular and Molecular Physiology
Zhao H, Eguchi S, Alam A, et al., 2016, The role of nuclear factor-erythroid 2 related factor 2 (Nrf-2) in the protection against lung injury., American Journal of Physiology-Lung Cellular and Molecular Physiology, ISSN: 1522-1504
Nuclear factor-erythroid 2 related factor 2 (Nrf2) is a ubiquitous master transcription factor that upregulates antioxidant response elements (AREs)-mediated expression of antioxidant enzyme and cytoprotective proteins. Activation of Nrf2 has been shown to be protective against lung injury. In the lung, diverse stimuli including environmental oxidants, medicinal agents and pathogens can activate Nrf2. Nrf2 translocates to the nucleus and binds to an antioxidant response element (ARE). Through transcriptional induction of ARE-bearing genes encoding antioxidant-detoxifying proteins, Nrf2 induces cellular rescue pathways against oxidative pulmonary injury, abnormal inflammatory and immune responses, and apoptosis. The Nrf2-antioxidant pathway has been shown to be important in the protection against various lung injury including acute lung injury/acute respiratory distress syndrome and bronchopulmonary dysplasia, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, asthma and allergy, and was widely examined for new therapeutic targets. The current review explores the protective role of Nrf-2 against lung injury and the therapeutic potential in targeting Nrf-2.
Wu X, Cui F, Zhang C, et al., 2016, Low-dose dexmedetomidine improves sleep quality pattern in elderly patients after noncardiac surgery in the intensive care unit: a pilot randomized controlled trial, Anesthesiology, ISSN: 1528-1175
Background: It has been shown that dexmedetomidine sedation can improve sleep architecture in mechanically ventilated patients. We hypothesized that low-dose dexmedetomidine infusion could also improve sleep architecture in non-mechanically ventilated elderly patients in the Intensive Care Unit (ICU) after surgery. Methods: This was a randomized, double-blind, placebo-controlled, parallel-arm pilot trial. Seventy-six patients of 65 years or older who were admitted to the ICU after non-cardiac surgery and did not require mechanical ventilation were randomized to receive dexmedetomidine (continuous infusion at a rate of 0.1 μg kg-1 h-1, n = 38) or placebo (n = 38) for 15 hours, i.e., from 5:00 PM on the day of surgery until 8:00 AM on the first day after surgery. Polysomnogram was monitored during the period of study drug infusion. The primary endpoint was the percentage of stage 2 non-rapid eye movement (stage N2) sleep. Results: Complete polysomnogram recordings were obtained in 61 patients (30 in the placebo group and 31 in the dexmedetomidine group). Compared with placebo, dexmedetomidine infusion significantly increased the percentage of stage N2 sleep (mean difference ***, 95% confidence interval **-**, P = ***); it also significantly prolonged the total sleep time, decreased the percentage of stage N1 sleep, and increased the sleep efficiency. However, the incidence of hypotension of all enrolled patients were significantly higher in the dexmedetomidine group than in the placebo group (39.5% [15/38] vs 13.2% [5/38], P = 0.009). Conclusions: In non-mechanically ventilated elderly patients who were admitted to ICU after non-cardiac surgery, the prophylactic low-dose dexmedetomidine infusion may improve sleep architecture but increases hypotension.
Evans DRS, Fowler-Williams C, Ma D, 2016, Is Volatile Anesthesia During Cancer Surgery Likely to Increase the Metastatic Risk?, INTERNATIONAL ANESTHESIOLOGY CLINICS, Vol: 54, Pages: 92-107, ISSN: 0020-5907
Jaffer T, Ma D, 2016, The emerging role of chemokine receptor CXCR2 in cancer progression, TRANSLATIONAL CANCER RESEARCH, Vol: 5, Pages: S616-S628, ISSN: 2218-676X
Yang B, Fung A, Pac-Soo C, et al., 2016, Vascular surgery-related organ injury and protective strategies: update and future prospects, British Journal of Anaesthesia, Vol: 117, Pages: ii32-ii43, ISSN: 1471-6771
Whilst there has been a reduction in the prevalence of peripheral vascular disease worldwide, a significant proportion of the world's growing population is still affected by disease of the aorta, carotid, iliac and lower limb arteries. These if left untreated can result in severe morbidity and mortality. However vascular surgery, the main definitive treatment for such conditions, is associated with subsequent injury to vital organs including the kidneys, heart, brain, intestines and lungs, with a consequent increase in both morbidity and mortality. The current thinking is that the underlying mechanism of injury is direct organ ischaemia and ischaemia induced formation of free radicals, cytokine release and mitochondrial failure. Various methods to alleviate such injuries have been investigated including pre- and postconditioning strategies, pharmacological therapies including volatile anaesthetic and alpha2 adrenoceptor agonist drugs and more recently remote conditioning strategies. Although these interventions have demonstrated some reduction in the biomarkers for organ injury, attempts to translate these benefits into clinical practice have not been successful in terms of morbidity, mortality or length of hospital stay. For this reason, further research is needed in this area to facilitate the translation of the potential interventional benefits from bench to bedside.
Su X, Meng ZT, Wu XH, et al., 2016, Dexmedetomidine for prevention of delirium in elderly patients after non-cardiac surgery: a randomised, double-blind, placebo-controlled trial, Lancet, Vol: 388, Pages: 1893-1902, ISSN: 1474-547X
BACKGROUND: Delirium is a postoperative complication that occurs frequently in patients older than 65 years, and presages adverse outcomes. We investigated whether prophylactic low-dose dexmedetomidine, a highly selective α2 adrenoceptor agonist, could safely decrease the incidence of delirium in elderly patients after non-cardiac surgery. METHODS: We did this randomised, double-blind, placebo-controlled trial in two tertiary-care hospitals in Beijing, China. We enrolled patients aged 65 years or older, who were admitted to intensive care units after non-cardiac surgery, with informed consent. We used a computer-generated randomisation sequence (in a 1:1 ratio) to randomly assign patients to receive either intravenous dexmedetomidine (0·1 μg/kg per h, from intensive care unit admission on the day of surgery until 0800 h on postoperative day 1), or placebo (intravenous normal saline). Participants, care providers, and investigators were all masked to group assignment. The primary endpoint was the incidence of delirium, assessed twice daily with the Confusion Assessment Method for intensive care units during the first 7 postoperative days. Analyses were done by intention-to-treat and safety populations. This study is registered with Chinese Clinical Trial Registry, www.chictr.org.cn, number ChiCTR-TRC-10000802. FINDINGS: Between Aug 17, 2011, and Nov 20, 2013, of 2016 patients assessed, 700 were randomly assigned to receive either placebo (n=350) or dexmedetomidine (n=350). The incidence of postoperative delirium was significantly lower in the dexmedetomidine group (32 [9%] of 350 patients) than in the placebo group (79 [23%] of 350 patients; odds ratio [OR] 0·35, 95% CI 0·22-0·54; p<0·0001). Regarding safety, the incidence of hypertension was higher with placebo (62 [18%] of 350 patients) than with dexmedetomidine (34 [10%] of 350 patients; 0·50, 0·32-0·78; p=0·002). Tachycardia was also highe
Ma D, 2016, Low-dose Dexmedetomidine Improves Sleep Quality Pattern in Elderly Patients after Noncardiac Surgery in the Intensive Care Unit: A Pilot Randomized Controlled Trial., Anesthesiology, ISSN: 1528-1175
Chen Q, Yi B, Ma J, et al., 2016, α2-adrenoreceptor modulated FAK pathway induced by dexmedetomidine attenuates pulmonary microvascular hyper-permeability following kidney injury, Oncotarget, Vol: 7, Pages: 55990-56001, ISSN: 1949-2553
Renal ischemia-reperfusion (rI/R) could cause remote acute lung injury (ALI) and combination of these two organ injuries can remarkably increase the mortality. This study aims to determine whether dexmedetomidine, an α2-adrenoreceptor agonist sedative, can ameliorate pulmonary microvascular hyper-permeability following rI/R injury and explore the underlying mechanisms. In vivo, C57BL/6J mice received dexmedetomidine (25µg/kg, i.p.) in the absence or presence of α2-adrenergic antagonist atipamezole (250µg/kg, i.p.) or focal adhesion kinase (FAK) inhibitor (30mg/kg, i.p.) before bilateral renal pedicle clamping for 45 minutes followed by 24 hours reperfusion. The lung histopathological changes and the permeability of pulmonary microvascular were assessed respectively. In vitro, the cultured C57BL/6J mice pulmonary microvascular endothelial cells (PMVECs) were treated with serum from mice with rI/R with or without dexmedetomidine and atipamezole. Trans-endothelial permeability and phospho-tyrosine397FAK, F-actin, VE-cadherin and ZO-1 in monolayer PMVECs were measured respectively in the presence or absence of rI/R serum, dexmedetomidine and FAK inhibitor. In vivo, dexmedetomidine remarkably attenuated lung injury and pulmonary microvascular hyper-permeability caused by rI/R injury, which was abolished by atipamezole or FAK inhibitor co-administration. In vitro, the permeability of PMVECs monolayer following exposure to serum from rI/R mice was increased significantly, and decreased by dexmedetomidine. Dexmedetomidine increased phospho-tyrosine397FAK in a time- and dose-dependent manner, which was correlated with the changes in trans-endothelial permeability. Our data indicated that dexmedetomidine is able to ameliorate remote pulmonary microvascular hyper-permeability induced by rI/R, at least in part, via FAK modulation.
Lian C, Xie Z, Wang Z, et al., 2016, Pediatric preoperative risk factors to predict postoperative ICU admission and death from a multicenter retrospective study, Pediatric Anesthesia, Vol: 26, Pages: 637-643, ISSN: 1155-5645
BackgroundAlthough some studies have investigated the potential predictors of perioperative mortality, there are few specifically for pediatrics.ObjectiveThe aim of the retrospective study was to analyze potential preoperative risk factors and to develop a pediatric preoperative risk prediction score (PRPS), and to predict postoperative ICU admission and the incidence of perioperative death in pediatric patients.MethodsPatients who postoperatively admitted to ICU or died (occurred within 30 days after the surgery) from 263 607 pediatric surgical patients with age from 1 day to 14 years old in eight centers in China from October 2010 to September 2013 were retrospectively analyzed. About 5500 non-ICU admission and death patients were randomly selected from those 263 607 patients as controls for analysis comparison. Independent risk factors and a risk model were derived from these analyses, and were further assessed with the likelihood ratio test and the area under the receiver operating characteristic (ROC) curve.ResultsThere were 1812 ICU admission or death patients but 187 patients’ records are incomplete. There were 487 patients with incomplete records among 5500 controls. Collectively, data from 6626 patients were enrolled in final analyses. With multiple logistic regression analysis, age, ASA physical status, SpO2, prematurity, and unfasted status were found to be independent predictors for critical patients. The AUC value of 0.905 indicated excellent predictive performance between critical and noncritical predictors.ConclusionsOur study revealed that age, ASA physical status, SpO2, prematurity, and unfasted status are risk factors to predict postoperative ICU admission and death in pediatric patients.
Wu L, Zhao H, Ma D, 2016, Small intestinal injury after injurious renal allograft transplantation in rats, Meeting of the Difficult-Airway-Society, Publisher: OXFORD UNIV PRESS, Pages: E934-E935, ISSN: 0007-0912
Zhao H, Kilgas S, Alam A, et al., 2016, The Role of Extracellular Adenosine Triphosphate in Ischemic Organ Injury., Critical Care Medicine, Vol: 44, Pages: 1000-1012, ISSN: 1530-0293
OBJECTIVES: Ischemic tissue injury contributes to significant morbidity and mortality and is implicated in a range of pathologic conditions, including but not limited to myocardial infarction, ischemic stroke, and acute kidney injury. The associated reperfusion phase is responsible for the activation of the innate and adaptive immune system, further accentuating inflammation. Adenosine triphosphate molecule has been implicated in various ischemic conditions, including stroke and myocardial infarction. STUDY SELECTION: Adenosine triphosphate is a well-defined intracellular energy transfer and is commonly referred to as the body's "energy currency." However, Laboratory studies have demonstrated that extracellular adenosine triphosphate has the ability to initiate inflammation and is therefore referred to as a damage-associated molecular pattern. Purinergic receptors-dependent signaling, proinflammatory cytokine release, increased Ca influx into cells, and subsequent apoptosis have been shown to form a common underlying extracellular adenosine triphosphate molecular mechanism in ischemic organ injury. CONCLUSIONS: In this review, we aim to discuss the molecular mechanisms behind adenosine triphosphate-mediated ischemic tissue injury and evaluate the role of extracellular adenosine triphosphate in ischemic injury in specific organs, in order to provide a greater understanding of the pathophysiology of this complex process. We also appraise potential future therapeutic strategies to limit damage in various organs, including the heart, brain, kidneys, and lungs.
Zhao T, Li C, Wei W, et al., 2016, Prenatal ketamine exposure causes abnormal development of prefrontal cortex in rat., Scientific Reports, Vol: 6, ISSN: 2045-2322
Ketamine is commonly used for anesthesia and as a recreational drug. In pregnant users, a potential neurotoxicity in offspring has been noted. Our previous work demonstrated that ketamine exposure of pregnant rats induces affective disorders and cognitive impairments in offspring. As the prefrontal cortex (PFC) is critically involved in emotional and cognitive processes, here we studied whether maternal ketamine exposure influences the development of the PFC in offspring. Pregnant rats on gestational day 14 were treated with ketamine at a sedative dose for 2 hrs, and pups were studied at postnatal day 0 (P0) or P30. We found that maternal ketamine exposure resulted in cell apoptosis and neuronal loss in fetal brain. Upon ketamine exposure in utero, PFC neurons at P30 showed more dendritic branching, while cultured neurons from P0 PFC extended shorter neurites than controls. In addition, maternal ketamine exposure postponed the switch of NR2B/2A expression, and perturbed pre- and postsynaptic protein expression in the PFC. These data suggest that prenatal ketamine exposure impairs neuronal development of the PFC, which may be associated with abnormal behavior in offsprings.
Singh M, Nabavi E, Zhou Y, et al., 2016, Application of Gold Nanorods in Cancer Theranostics (plenary presentation winner), Society for Surgery of the Alimentary Tract Annual Meeting, 31st Annual SSAT Residents and Fellows Research Conference
Xuan W, Zhao H, Hankin J, et al., 2016, Local anaesthetic bupivacaine induced ovarian and prostate cancer apoptotic cell death and underlying mechanisms in vitro, Scientific Reports, Vol: 6, ISSN: 2045-2322
Retrospective studies indicate that the use of regional anesthesia can reduce cancer recurrence after surgery which could be due to ranging from immune function preservation to direct molecular mechanisms. This study was to investigate the effects of bupivacaine on ovarian and prostate cancer cell biology and the underlying molecular mechanisms. Cell viability, proliferation and migration of ovarian carcinoma (SKOV-3) and prostate carcinoma (PC-3) were examined following treatment with bupivacaine. Cleaved caspase 3, 8 and 9, and GSK-3β, pGSK-3βtyr216 and pGSK-3βser9 expression were assessed by immunofluorescence. FAS ligand neutralization, caspase and GSK-3 inhibitors and GSK-3β siRNA were applied to further explore underlying mechanisms. Clinically relevant concentrations of bupivacaine reduced cell viability and inhibited cellular proliferation and migration in both cell lines. Caspase 8 and 9 inhibition generated partial cell death reversal in SKOV-3, whilst only caspase 9 was effective in PC-3. Bupivacaine increased the phosphorylation of GSK-3βTyr216 in SKOV-3 but without measurable effect in PC3. GSK-3β inhibition and siRNA gene knockdown decreased bupivacaine induced cell death in SKOV-3 but not in PC3. Our data suggests that bupivacaine has direct ‘anti-cancer’ properties through the activation of intrinsic and extrinsic apoptotic pathways in ovarian cancer but only the intrinsic pathway in prostate cancer.
Zhao H, Mitchell S, Koumpa S, et al., 2016, Heme Oxygenase-1 mediates neuro-protection conferred by argon in combination with hypothermia in neonatal hypoxia-ischemia brain injury, Anesthesiology, Vol: 125, Pages: 180-192, ISSN: 1528-1175
Argon–hypothermia treatment reduced both neuronal death in an in vitro neuronal culture model and brain infarct size in an in vivo rat model of neonatal asphyxia. The protective effects of argon–hypothermia involve both inhibition of apoptosis and neuroinflammation mechanisms and activation of cell survival pathways.
Ning J, Mo L, Yi B, et al., 2016, Therapeutic Whole-body Hypothermia Protects Remote Lung, Liver, and Kidney Injuries after Blast Limb Trauma in Rats., Anesthesiology, Vol: 124, Pages: 1360-1371, ISSN: 0003-3022
Background: Severe blast limb trauma (BLT) induces distant multiple-organ injuries. In the current study, the authors determined whether whole-body hypothermia (WH) and its optimal duration (if any) afford protection to the local limb damage and distant lung, liver, and kidney injuries after BLT in rats.Methods: Rats with BLT, created by using chartaceous electricity detonators, were randomly treated with WH for 30 min, 60 min, 3 h, and 6 h (n = 12/group). Rectal temperature and arterial blood pressure were monitored throughout. Blood and lung, liver, and kidney tissue samples were harvested for measuring tumor necrosis factor-α, interleukin-6 and interleukin-10, myeloperoxidase activity, hydrogen sulfide, and biomarkers of oxidative stress at 6 h after BLT. The pathologic lung injury and the water content of the lungs, liver, and kidneys and blast limb tissue were assessed.Results: Unlike WH for 30 min, WH for 60 min reduced lung water content, lung myeloperoxidase activity, and kidney myeloperoxidase activity by 10, 39, and 28% (all P < 0.05), respectively. WH for 3 h attenuated distant vital organs and local traumatic limb damage and reduced myeloperoxidase activity, hydrogen peroxide and malondialdehyde concentration, and tumor necrosis factor-α and interleukin-6 levels by up to 49% (all P < 0.01). Likewise, WH for 6 h also provided protection to such injured organs but increased blood loss from traumatic limb.Conclusions: Results of this study indicated that WH may provide protection for distant organs and local traumatic limb after blast trauma, which warrants further study.
Ma D, 2016, Volatile anaesthetics enhance the metastasis related cellular signalling including CXCR2 of ovarian cancer cells, Oncotarget, Vol: 7, ISSN: 1949-2553
The majority of ovarian cancer patients relapse after surgical resection. Evidence is accumulating regarding the role of surgery in disseminating cancer cells; in particular anaesthesia may have an impact on cancer re-occurrence. Here, we have investigated the metastatic potential of volatile anaesthetics isoflurane, sevoflurane and desflurane on ovarian cancer cells.Human ovarian carcinoma cells (SKOV3) were exposed to isoflurane (2%), sevoflurane (3.6%) or desflurane (10.3%) for 2 hours. Metastatic related gene expression profiles were measured using the Tumour Metastasis PCR Array and qRT-PCR. Subsequently vascular endothelial growth factor A (VEGF-A), matrix metalloproteinase 11 (MMP11), transforming growth factor beta-1 (TGF-β1) and chemokine (C-X-C motif) receptor 2 (CXCR2) proteins expression were determined using immunofluorescent staining. The migratory capacities ofSK-OV3 cells were assessed with a scratch assay and the potential role of CXCR2 in mediating the effects of volatile anaesthetics on cancer cell biology were further investigated with CXCR2 knockdown by siRNA.All three volatile anaesthetics altered expression of 70 out of 81 metastasic related genes with significant increases in VEGF-A, MMP-11, CXCR2 and TGF-β genes and protein expression with a magnitude order of desflurane (greatest), sevoflurane and isoflurane.Scratch analysis revealed that exposure to these anesthetics increased migration, which was abolished by CXCR2 knockdown.Volatile anaesthetics at clinically relevant concentrations have strong cancer cell biology which in turn could enhance ovarian cancer metastatic potential. This work raises the urgency for further in vivo studies and clinical trials before any conclusions can be made in term of the alteration of clinical practice.
Zhao H, Mitchell S, Ciechanowicz S, et al., 2016, Argon protects against hypoxic-ischemic brain injury in neonatal rats through activation of Nuclear factor (erythroid-derived 2)-like 2, Oncotarget, Vol: 7, ISSN: 1949-2553
Perinatal hypoxic ischaemic encephalopathy (HIE) has a high mortality rate with neuropsychological impairment. This study investigated the neuroprotective effects of argon against neonatal hypoxic-ischaemic brain injury.In vitro cortical neuronal cell cultures derived from rat foetuses were subjected to an oxygen and glucose deprivation (OGD) challenge for 90 minutes and then exposed to 70% argon or nitrogen with 5% carbon dioxide and balanced with oxygen for 2 hours.In vivo, seven-day-old rats were subjected to unilateral common carotid artery ligation followed by hypoxic (8% oxygen balanced with nitrogen) insult for 90 minutes. They were exposed to 70% argon or nitrogen balanced with oxygen for 2 hours. In vitro, argon treatment of cortical neuronal cultures resulted in a significant increase of p-mTOR and Nuclear factor (erythroid-derived 2)-like 2(Nrf2) and protection against OGD challenge. Inhibition of m-TOR through Rapamycin or Nrf2 through siRNA abolished argon-mediated cyto-protection. In vivo, argon exposure significantly enhanced Nrf2 and its down-stream effector NAD(P)H Dehydrogenase, Quinone 1(NQO1) and superoxide dismutase 1(SOD1). Oxidative stress, neuroinflammation and neuronal cell death were significantly decreased and brain infarction was markedly reduced. Blocking PI-3K through wortmannin or ERK1/2 through U0126 attenuated argon-mediated neuroprotection.These data provide a new molecular mechanism for the potential application of Argon as a neuroprotectant in HIE.
Elson DS, Singh M, Nabavi E, et al., 2016, Application of Gold Nanorods in Cancer Theranostics, Association of Surgeons in Training
Saczewski J, Hudson A, Scheinin M, et al., 2016, Transfer of SAR information from hypotensive indazole to indole derivatives acting at alpha-adrenergic receptors: In vitro and in vivo studies, European Journal of Medicinal Chemistry, Vol: 115, Pages: 406-415, ISSN: 0223-5234
In a search for novel antihypertensive drugs we applied scaffold hopping from the previously described α1-adrenergic receptor antagonists, 1-[(imidazolin-2-yl)methyl]indazoles. The aim was to investigate whether the α-adrenergic properties of the indazole core were transferable to the indole core. The newly obtained 1-[(imidazolin-2-yl)methyl]indole analogues were screened in vitro for their binding affinities for α1-and α2-adrenoceptors, which allowed the identification of the target-based SAR transfer (T_SAR transfer) as well as structure-based SAR transfer (S_SAR transfer) events. However, when screened in vivo with use of anaesthetized male Wistar rats, the new indole ligands showed a different hemodynamic profile than expected. Instead of the immediate hypotensive effect characteristic of peripheral vasodilatator α1 blockers, a biphasic effect was observed, reminiscent of clonidine-like centrally acting antihypertensive agents. This was supported by subsequent in vitro functional studies in [35S]GTPγS binding assay, where the indole analogues displayed partial agonist properties at α2-adrenergic receptors. Since no correlation was found between the in vitro binding to α-adrenoceptors and the in vivo hemodynamic effects of the two series of indazole and indole bioisosteric compounds, in a search for new imidazoline-containing adrenergic drugs, the structure-based SAR transfer information obtained from in vitro binding studies should be treated with caution.
Nabavi E, Singh M, Zhou Y, et al., 2016, Preliminary studies of fluorescence image-guided photothermal therapy of human oesophageal adenocarcinoma in vivo using multifunctional gold nanorods, Conference on Optical Methods for Tumor Treatment and Detection - Mechanisms and Techniques in Photodynamic Therapy XXV, Publisher: SPIE-INT SOC OPTICAL ENGINEERING, ISSN: 0277-786X
We present a preliminary in vivo study of fluorescence imaging and photothermal therapy (PTT) of human oesophageal adenocarcinoma using multi-functionalised gold nanorods (GNRs). After establishing tumour xenograft in mouse functionalised GNRs were administrated intravenously (IV). Fluorescence imaging was performed to detect the tumour area. The intensity of the fluorescence signal varied significantly across the tumour site and surrounding tissues. PTT was then performed using a 808 nm continuous wave diode laser to irradiate the tumour for 3 minutes, inducing a temperature rise of ~44°C, which photothermally ablated the tumour.
Gallina ME, Zhou Y, Johnson CJ, et al., 2016, Aptamer-conjugated, fluorescent gold nanorods as potential cancer theradiagnostic agents, Materials Science and Engineering C-Biomimetic and Supramolecular Systems, Vol: 59, Pages: 324-332, ISSN: 0928-4931
GNRs are emerging as a new class of probes for theradiagnostic applications thanks to their unique optical properties. However, the achievement of proper nanoconstructs requires the synthesis of highly pure GNRs with well-defined aspect ratio (AR), in addition to extensive surface chemistry modification to provide them with active targeting and, possibly, multifunctionality.In this work, we refined the method of the seed mediated growth and developed a robust procedure for the fabrication of GNRs with specific AR. We also revealed and characterized unexplored aging phenomena that follow the synthesis and consistently alter GNRs' final AR. Such advances appreciably improved the feasibility of GNRs fabrication and offered useful insights on the growth mechanism.We next produced fluorescent, biocompatible, aptamer-conjugated GNRs by performing ligand exchange followed by bioconjugation to anti-cancer oligonucleotide AS1411. In vitro studies showed that our nanoconstructs selectively target cancer cells while showing negligible cytotoxicity. As a result, our aptamer-conjugated GNRs constitute ideal cancer-selective multifunctional probes and promising candidates as photothermal therapy agents.
Ciechanowicz SJ, Ma D, 2016, Anaesthesia for oncological surgery - can it really influence cancer recurrence?, ANAESTHESIA, Vol: 71, Pages: 127-131, ISSN: 0003-2409
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Li X-Y, Wan Y, Tang S-J, et al., 2016, Maladaptive plasticity and neuropathic pain, Neural Plasticity, Vol: 2016, ISSN: 1687-5443
Fung A, Zhao H, Yang B, et al., 2016, Ischaemic and inflammatory injury in renal graft from brain death donation: an update review., Journal of Anesthesia, Vol: 30, Pages: 307-316, ISSN: 1438-8359
Renal transplantation remains an important therapy in treating renal failure and can be considered to be a curative treatment. The demand for renal grafts outstrips supply available each year, making it increasingly important to look at improving the treatment of both renal grafts and recipients, and thereby improving patient outcomes and increasing the pool of potential donor grafts. Important to this, however, is knowledge of the underlying mechanisms leading to damage to the graft and rejection from the recipient. This includes ischaemia and consequently the priming of the organ during storage for ischaemia reperfusion injury (IRI) on implantation and the importance of the innate immune system which can be activated via multiple pathways, often via TLR-4, and the consequent production of danger-associated molecular patterns. This makes the time period involving both explantation and storage an important therapeutic window for improving outcomes. Other windows explored include treatment of IRI and improvement in immunosuppressive therapy. The multiple windows of potential therapeutic input have spawned a large body of work exploring both the underlying mechanisms and also how to exploit these mechanisms to improve overall outcomes and to allow for more marginal organs to be used.
Ma D, 2016, Is volatile anesthesia during cancer surgery likely to increase the metastatic risk?, Anaesthesia, ISSN: 1365-2044
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