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  • SAGE Publications  (30)
  • 1
    Online Resource
    Online Resource
    Sensitivity to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Males, Smokers, and Non-adenocarcinoma Lung Cancer in Patients with EGFR Mutations
    SAGE Publications ; 2013
    In:  The International Journal of Biological Markers Vol. 28, No. 3 ( 2013-07), p. 249-258
    Details
    In: The International Journal of Biological Markers, SAGE Publications, Vol. 28, No. 3 ( 2013-07), p. 249-258
    Abstract: The demographical/clinical characteristics of being Asian, having an adenocarcinoma, being female, and being a “never-smoker” are regarded as favorable predictors for epidermal growth factor receptor ( EGFR) tyrosine kinase inhibitor (TKI) efficacy in non-small cell lung cancer (NSCLC) with unknown EGFR gene status. In this study, we examined the effects of the supposedly unfavorable clinical variables in EGFR-mutant patients. Method In total, 159 EGFR-mutant NSCLC patients' clinical features were correlated with progression-free survival (PFS), response rate (RR), and overall survival (OS). Multivariate analysis of clinical characteristics was performed using the Cox and logistic regression methods. Result There were 90 females (56.6%), 112 never-smokers (70.4%), and 153 patients with adenocarcinomas (96.2%). All patients were treated with EGFR-TKI, and 52.8% received TKI in a first-line setting. The median PFS of patients receiving first-line TKI was similar, regardless of gender (males vs females: 9.1 vs 9.7 months, p=0.793), smoking status (never-smokers vs smokers: 9.9 vs 9.1 months, p=0.570), or histology (adenocarcinoma vs non-adenocarcinoma: 9.7 vs 9.2 months, p=0.644). OS curves of first-line TKI-treated patients were also not associated with gender (p=0.722), smoking status (p=0.579), or histology (p=0.480). Similar results of PFS and OS were obtained for patients who received TKI beyond first-line. Multivariate analysis indicated that none of these clinical factors was an independent predictor of survival. Conclusions The supposedly ‘favorable’ clinical factors of female gender, non-smoking status, and adenocarcinoma were not independent predictive factors for PFS or OS in this population of EGFR-mutant NSCLC patients.
    Type of Medium: Online Resource
    ISSN: 1724-6008 , 1724-6008
    URL: Article
    DOI: 10.5301/JBM.5000039
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2013
    detail.hit.zdb_id: 1475778-3
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  • 2
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    Rewarming from Therapeutic Hypothermia Induces Cortical Neuron Apoptosis in a Swine Model of Neonatal Hypoxic–Ischemic Encephalopathy
    SAGE Publications ; 2015
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 35, No. 5 ( 2015-05), p. 781-793
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 35, No. 5 ( 2015-05), p. 781-793
    Abstract: The consequences of therapeutic hypothermia for neonatal hypoxic–ischemic encephalopathy are poorly understood. Adverse effects from suboptimal rewarming could diminish neuroprotection from hypothermia. Therefore, we tested whether rewarming is associated with apoptosis. Piglets underwent hypoxia–asphyxia followed by normothermic or hypothermic recovery at 2 hours. Hypothermic groups were divided into those with no rewarming, rewarming at 0.5 °C/hour, or rewarming at 4 °C/hour. Neurodegeneration at 29 hours was assessed by hematoxylin and eosin staining, TUNEL assay, and immunoblotting for cleaved caspase-3. Rewarmed piglets had more apoptosis in motor cortex than did those that remained hypothermic after hypoxia–asphyxia. Apoptosis in piriform cortex was greater in hypoxic–asphyxic, rewarmed piglets than in naive/sham piglets. Caspase-3 inhibitor suppressed apoptosis with rewarming. Rapidly rewarmed piglets had more caspase-3 cleavage in cerebral cortex than did piglets that remained hypothermic or piglets that were rewarmed slowly. We conclude that rewarming from therapeutic hypothermia can adversely affect the newborn brain by inducing apoptosis through caspase mechanisms.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1038/jcbfm.2014.245
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2015
    detail.hit.zdb_id: 2039456-1
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  • 3
    Online Resource
    Online Resource
    Dopamine Receptor Modulation of Hypoxic—Ischemic Neuronal Injury in Striatum of Newborn Piglets
    SAGE Publications ; 2007
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 27, No. 7 ( 2007-07), p. 1339-1351
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 27, No. 7 ( 2007-07), p. 1339-1351
    Abstract: Dopamine receptors regulate glutamatergic neurotransmission and Na + ,K + -ATPase via protein kinase A (PKA) and dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32)-dependent signaling. Consequently, dopamine receptor activation may modulate neonatal hypoxic–ischemic (H–I) neuronal damage in the selectively vulnerable putamen enriched with dopaminergic receptors. Piglets subjected to two durations of hypoxia followed by asphyxic cardiac arrest were treated with a D1-like (SCH23390) or D2-like (sulpiride) receptor antagonist. At 4 days of recovery from less severe H–I, the remaining viable neurons in putamen were 60% of control, but nearly completely salvaged by pretreatment with SCH23390 or sulpiride. After more severe H–I in which only 18% of neurons were viable, partial neuroprotection was seen with SCH23390 pretreatment (50%) and posttreatment (39%) and with sulpiride pretreatment (35%), but not with sulpiride posttreatment (24%). Dopamine was significantly elevated in microdialysis samples from putamen during asphyxia and the first 15 mins of reoxygenation. Pretreatment with SCH23390 or sulpiride largely attenuated the increased nitrotyrosine and the decreased Na + ,K + -ATPase activity that occurred at 3 h after severe H–I. Pretreatment with SCH23390, but not sulpiride, also attenuated H–I-induced increases in PKA-dependent phosphorylation of Thr34 on DARPP-32, Ser943 on the α subunit of Na + ,K + -ATPase, and Ser897 of the N-methyl-d-aspartate (NMDA) receptor NR1 subunit. These findings indicate that D1 and D2 dopamine receptor activation contribute to neuronal death in newborn putamen after H–I in association with increased protein nitration and decreased Na + ,K + -ATPase activity. Furthermore, mechanisms of D1 receptor toxicity may involve DARPP-32-dependent phosphorylation of NMDA receptor NR1 and Na + ,K + -ATPase.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1038/sj.jcbfm.9600440
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2007
    detail.hit.zdb_id: 2039456-1
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  • 4
    Online Resource
    Online Resource
    Adenosine A 2A Receptor Contributes to Ischemic Brain Damage in Newborn Piglet
    SAGE Publications ; 2013
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 33, No. 10 ( 2013-10), p. 1612-1620
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 33, No. 10 ( 2013-10), p. 1612-1620
    Abstract: Pharmacologic inactivation or genetic deletion of adenosine A 2A receptors protects ischemic neurons in adult animals, but studies in neonatal hypoxia-ischemia (H-I) are inconclusive. The present study in neonatal piglets examined the hypothesis that A 2A receptor signaling after reoxygenation from global H-I contributes to injury in highly vulnerable striatal neurons where A 2A receptors are enriched. A 2A receptor immunoreactivity was detected in striatopallidal neurons. In nonischemic piglets, direct infusion of the selective A 2A receptor agonist CGS 21680 through microdialysis probes into putamen increased phosphorylation of N-methyl-D-aspartic acid (NMDA) receptor NR1 subunit and Na + , K + -ATPase selectively at protein kinase A (PKA)-sensitive sites. In ischemic piglets, posttreatment with SCH 58261, a selective A 2A receptor antagonist, improved early neurologic recovery and preferentially protected striatopallidal neurons. SCH 58261 selectively inhibited the ischemia-induced phosphorylation of NR1, Na + , K + -ATPase, and cAMP-regulated phosphoprotein 32 KDa (DARPP32) at PKA-sensitive sites at 3 hours of recovery and improved Na + , K + -ATPase activity. SCH 58261 also suppressed ischemia-induced protein nitration and oxidation. Thus, A 2A receptor activation during reoxygenation contributes to the loss of a subpopulation of neonatal putamen neurons after H-I. Its toxic signaling may be related to DARPP32-dependent phosphorylation of PKA-sensitive sites on NR1 and Na + , K + -ATPase, thereby augmenting excitotoxicity-induced oxidative stress after reoxygenation.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1038/jcbfm.2013.117
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2013
    detail.hit.zdb_id: 2039456-1
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  • 5
    Online Resource
    Online Resource
    Augmentation of poly(ADP-ribose) polymerase-dependent neuronal cell death by acidosis
    SAGE Publications ; 2017
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 37, No. 6 ( 2017-06), p. 1982-1993
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 37, No. 6 ( 2017-06), p. 1982-1993
    Abstract: Tissue acidosis is a key component of cerebral ischemic injury, but its influence on cell death signaling pathways is not well defined. One such pathway is parthanatos, in which oxidative damage to DNA results in activation of poly(ADP-ribose) polymerase and generation of poly(ADP-ribose) polymers that trigger release of mitochondrial apoptosis-inducing factor. In primary neuronal cultures, we first investigated whether acidosis per sé is capable of augmenting parthanatos signaling initiated pharmacologically with the DNA alkylating agent, N-methyl- N′-nitro- N-nitrosoguanidine. Exposure of neurons to medium at pH 6.2 for 4 h after N-methyl- N′-nitro- N-nitrosoguanidine washout increased intracellular calcium and augmented the N-methyl- N′-nitro- N-nitrosoguanidine-evoked increase in poly(ADP-ribose) polymers, nuclear apoptosis-inducing factor , and cell death. The augmented nuclear apoptosis-inducing factor and cell death were blocked by the acid-sensitive ion channel-1a inhibitor, psalmotoxin. In vivo, acute hyperglycemia during transient focal cerebral ischemia augmented tissue acidosis, poly(ADP-ribose) polymers formation, and nuclear apoptosis-inducing factor , which was attenuated by a poly(ADP-ribose) polymerase inhibitor. Infarct volume from hyperglycemic ischemia was decreased in poly(ADP-ribose) polymerase 1-null mice. Collectively, these results demonstrate that acidosis can directly amplify neuronal parthanatos in the absence of ischemia through acid-sensitive ion channel-1a . The results further support parthanatos as one of the mechanisms by which ischemia-associated tissue acidosis augments cell death.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1177/0271678X16658491
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2017
    detail.hit.zdb_id: 2039456-1
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  • 6
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    Perinatal hypoxic-ischemic brain injury in large animal models: Relevance to human neonatal encephalopathy
    SAGE Publications ; 2018
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 38, No. 12 ( 2018-12), p. 2092-2111
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 38, No. 12 ( 2018-12), p. 2092-2111
    Abstract: Perinatal hypoxia-ischemia resulting in death or lifelong disabilities remains a major clinical disorder. Neonatal models of hypoxia-ischemia in rodents have enhanced our understanding of cellular mechanisms of neural injury in developing brain, but have limitations in simulating the range, accuracy, and physiology of clinical hypoxia-ischemia and the relevant systems neuropathology that contribute to the human brain injury pattern. Large animal models of perinatal hypoxia-ischemia, such as partial or complete asphyxia at the time of delivery of fetal monkeys, umbilical cord occlusion and cerebral hypoperfusion at different stages of gestation in fetal sheep, and severe hypoxia and hypoperfusion in newborn piglets, have largely overcome these limitations. In monkey, complete asphyxia produces preferential injury to cerebellum and primary sensory nuclei in brainstem and thalamus, whereas partial asphyxia produces preferential injury to somatosensory and motor cortex, basal ganglia, and thalamus. Mid-gestational fetal sheep provide a valuable model for studying vulnerability of progenitor oligodendrocytes. Hypoxia followed by asphyxia in newborn piglets replicates the systems injury seen in term newborns. Efficacy of post-insult hypothermia in animal models led to the success of clinical trials in term human neonates. Large animal models are now being used to explore adjunct therapy to augment hypothermic neuroprotection.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1177/0271678X18797328
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2018
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  • 7
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    A comparison and review of three sets of classification criteria for systemic lupus erythematosus for distinguishing systemic lupus erythematosus from pure mucocutaneous manifestations in the lupus disease spectrum
    SAGE Publications ; 2020
    In:  Lupus Vol. 29, No. 14 ( 2020-12), p. 1854-1865
    Details
    In: Lupus, SAGE Publications, Vol. 29, No. 14 ( 2020-12), p. 1854-1865
    Abstract: Although the original purpose of the systemic lupus erythematosus (SLE) classification criteria was to distinguish SLE from other mimic diseases, and to facilitate sample selection in scientific research, they have become widely used as diagnostic criteria in clinical situations. It is not known yet if regarding classification criteria as diagnostic criteria, what problems might be encountered? This is the first study comparing the three sets of classification criteria for SLE, the 1997 American College of Rheumatology (ACR’97), 2012 Systemic Lupus International Collaborating Clinics (SLICC’12) and 2019 European League Against Rheumatism/American College of Rheumatology (EULAR/ACR’19), for their ability to distinguish patients with SLE from patients with pure mucocutaneous manifestations (isolated cutaneous lupus erythematosus without internal disease, i-CLE) in the lupus disease spectrum. 1,865 patients with SLE and 232 patients with i-CLE were recruited from a multicenter study. We found that, due to low specificity, none of the three criteria are adept at distinguishing patients with SLE from patients with i-CLE. SLICC’12 performed best among the original three criteria, but if a positive ANA was removed as an entry criterion, EULAR/ACR’19 would performed better. A review of previous studies that compared the three sets of criteria was presented in this work.
    Type of Medium: Online Resource
    ISSN: 0961-2033 , 1477-0962
    URL: Article
    DOI: 10.1177/0961203320959716
    RVK:
    XA 10000
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2020
    detail.hit.zdb_id: 2008035-9
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  • 8
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    Synthesis of Transition Metal Complexes with Aza-Crown Substituted Unsymmetrical Salicylaldimine Bis-Schiff Base Ligands and Metal Schiff Base Complex Catalysed Oxidation of P-Xylene to P-Toluic Acid
    SAGE Publications ; 2012
    In:  Journal of Chemical Research Vol. 36, No. 7 ( 2012-07), p. 425-428
    Details
    In: Journal of Chemical Research, SAGE Publications, Vol. 36, No. 7 ( 2012-07), p. 425-428
    Abstract: Four unsymmetrical, salicylaldimine bis-Schiff bases with pendant benzo-10-aza-15-crown-5- or morpholino-groups and their 1:1 (ligand /metal) complexes with cobalt, copper and manganese have been synthesised and studied as catalysts in the aerobic oxidation of p-xylene to p-toluic acid. Significant selectivity (up to −90%) and conversion levels (up to −70%) were obtained. The effects of the pendant aza-crown ether group in Mn(III) Schiff base complexes on the oxidation of p-xylene were also investigated by comparison with analogues having pendant morpholino-groups.
    Type of Medium: Online Resource
    ISSN: 1747-5198 , 2047-6507
    URL: Article
    DOI: 10.3184/174751912X13377751456987
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2012
    detail.hit.zdb_id: 3010810-X
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  • 9
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    Stroke prevention and control system in China: CSPPC-Stroke Program
    SAGE Publications ; 2021
    In:  International Journal of Stroke Vol. 16, No. 3 ( 2021-04), p. 265-272
    Details
    In: International Journal of Stroke, SAGE Publications, Vol. 16, No. 3 ( 2021-04), p. 265-272
    Abstract: In China, stroke is a major cause of mortality, and long-term physical and cognitive impairment. To meet this challenge, the Ministry of Health China Stroke Prevention Project Committee (CSPPC) was established in April 2011. This committee actively promotes stroke prevention and control in China. With government financial support of 838.4 million CNY, 8.352 million people from 536 screening points in 31 provinces have received stroke screening and follow-up over the last seven years (2012–2018). In 2016, the CSPPC issued a plan to establish stroke centers. To shorten the pre-hospital period, the CSPPC established a stroke center network, stroke map, and stroke “Green Channel” to create three 1-h gold rescue circles, abbreviated as “1-1-1” (onset to call time 〈 1 h; pre-hospital transfer time  〈  1 h, and door-to-needle time  〈  1 h). From 2017 to 2018, the median door-to-needle time dropped by 4.0% (95% confidence interval (CI), 1.4–9.4) from 50 min to 48 min, and the median onset-to-needle time dropped by 2.8% (95% CI, 0.4–5.2) from 180 min to 175 min. As of 31 December 2018, the CSPPC has established 380 stroke centers in mainland China. From 1 November 2018, the CSPPC has monitored the quality of stroke care in stroke center hospitals through the China Stroke Data Center Data Reporting Platform. The CSPPC Stroke program has led to a significant improvement in stroke care. This program needs to be further promoted nationwide.
    Type of Medium: Online Resource
    ISSN: 1747-4930 , 1747-4949
    URL: Article
    DOI: 10.1177/1747493020913557
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2021
    detail.hit.zdb_id: 2211666-7
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  • 10
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    Establishing an hTERT-driven immortalized umbilical cord-derived mesenchymal stem cell line and its therapeutic application in mice with liver failure
    SAGE Publications ; 2023
    In:  Journal of Tissue Engineering Vol. 14 ( 2023-01)
    Details
    In: Journal of Tissue Engineering, SAGE Publications, Vol. 14 ( 2023-01)
    Abstract: Acute liver failure (ALF) is characterized by rapid liver cell destruction. It is a multi-etiological and fulminant complication with a clinical mortality of over 80%. Therapy using mesenchymal stem cells (MSCs) or MSCs-derived exosomes can alleviate acute liver injury, which has been demonstrated in animal experiments and clinical application. However, similar to other stem cells, different cell sources, poor stability, cell senescence and other factors limit the clinical application of MSCs. To achieve mass production and quality control on stem cells and their exosomes, transfecting umbilical cord mesenchymal stem cell (UCMSC) with lentivirus overexpressing human telomerase reverse transcriptase (hTERT) gene, the hTERT-UCMSC was constructed as an immortalized MSC cell line. Compared with the primary UCMSC (P3) and immortalized cell line hTERT-UCMSC at early passage (P10), the hTERT-UCMSC retained the key morphological and physiological characteristics of UCMSC at the 35th passage (P35), and showed no signs of carcinogenicity and toxic effect in mice. There was no difference in either exosome production or characteristics of exosomes among cultures from P3 primary cells, P10 and P35 immortalized hTERT-UCMSCs. Inoculation of either hTERT-UCMSC (P35) or its exosomes improved the survival rate and liver function of ALF mice induced by thioacetamide (TAA). Our findings suggest that this immortalized cell line can maintain its characteristics in long-term culture. Inoculation of hTERT-UCMSC and its exosomes could potentially be used in clinics for the treatment of liver failure in the future.
    Type of Medium: Online Resource
    ISSN: 2041-7314 , 2041-7314
    URL: Article
    DOI: 10.1177/20417314231200328
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2023
    detail.hit.zdb_id: 2573915-3
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