<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet href="/rss.css" type="text/css"?>
<rdf:RDF xmlns="http://purl.org/rss/1.0/"
    xmlns:cc="http://web.resource.org/cc/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:extra="http://www.w3.org/1999/xhtml"
    xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#">
    <channel rdf:about="http://www.medicalgasresearch.com/feeds/latestarticles/journal?quantity=&amp;format=rss&amp;version=">
        <title>Medical Gas Research - Latest Articles</title>
        <link>http://www.medicalgasresearch.com</link>
        <description>The latest research articles published by Medical Gas Research</description>
        <dc:date>2013-05-16T00:00:00Z</dc:date>
        <items>
            <rdf:Seq>
                                <rdf:li rdf:resource="http://www.medicalgasresearch.com/content/3/1/10" />
                                <rdf:li rdf:resource="http://www.medicalgasresearch.com/content/3/1/9" />
                                <rdf:li rdf:resource="http://www.medicalgasresearch.com/content/3/1/8" />
                                <rdf:li rdf:resource="http://www.medicalgasresearch.com/content/3/1/7" />
                                <rdf:li rdf:resource="http://www.medicalgasresearch.com/content/3/1/6" />
                                <rdf:li rdf:resource="http://www.medicalgasresearch.com/content/3/1/5" />
                                <rdf:li rdf:resource="http://www.medicalgasresearch.com/content/3/1/4" />
                                <rdf:li rdf:resource="http://www.medicalgasresearch.com/content/3/1/3" />
                                <rdf:li rdf:resource="http://www.medicalgasresearch.com/content/3/1/2" />
                                <rdf:li rdf:resource="http://www.medicalgasresearch.com/content/3/1/1" />
                            </rdf:Seq>
        </items>
                 <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </channel>
        <item rdf:about="http://www.medicalgasresearch.com/content/3/1/10">
        <title>The evolution of molecular hydrogen: a noteworthy potential therapy with clinical significance</title>
        <description>Studies on molecular hydrogen have evolved tremendously from its humble beginnings and have continued to change throughout the years. Hydrogen is extremely unique since it has the capability to act at the cellular level. Hydrogen is qualified to cross the blood brain barrier, to enter the mitochondria, and even has the ability to translocate to the nucleus under certain conditions. Once in these ideal locations of the cell, previous studies have shown that hydrogen exerts antioxidant, anti-apoptotic, anti-inflammatory, and cytoprotective properties that are beneficial to the cell. Hydrogen is most commonly applied as a gas, water, saline, and can be applied in a variety of other mediums. There are also few side effects involving hydrogen, thus making hydrogen a perfect medical gas candidate for the convention of novel therapeutic strategies against cardiovascular, cerebrovascular, cancer, metabolic, and respiratory diseases and disorders. Although hydrogen appears to be faultless at times, there still are several deficiencies or snares that need to be investigated by future studies. This review article seeks to delve and comprehensively analyze the research and experiments that alludes to molecular hydrogen being a novel therapeutic treatment that medicine desperately needs.</description>
        <link>http://www.medicalgasresearch.com/content/3/1/10</link>
                <dc:creator>Brandon Dixon</dc:creator>
                <dc:creator>Jiping Tang</dc:creator>
                <dc:creator>John Zhang</dc:creator>
                <dc:source>Medical Gas Research 2013, null:10</dc:source>
        <dc:date>2013-05-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/2045-9912-3-10</dc:identifier>
                                <prism:require>/content/figures/2045-9912-3-10-toc.gif</prism:require>
                <prism:publicationName>Medical Gas Research</prism:publicationName>
        <prism:issn>2045-9912</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>10</prism:startingPage>
        <prism:publicationDate>2013-05-16T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.medicalgasresearch.com/content/3/1/9">
        <title>Hydrogen sulfide as a vasculoprotective factor</title>
        <description>Hydrogen sulfide is a novel mediator with the unique properties of a gasotransmitter and many and varied physiological effects. Included in these effects are a number of cardiovascular effects that are proving beneficial to vascular health. Specifically, H2S can elicit vasorelaxation, prevention of inflammation and leukocyte adhesion, anti-proliferative effects and anti-thrombotic effects. Additionally, H2S is a chemical reductant and nucleophile that is capable of inhibiting the production of reactive oxygen species, scavenging and neutralising reactive oxygen species and boosting the efficacy of endogenous anti-oxidant molecules. These result in resistance to oxidative stress, protection of vascular endothelial function and maintenance of blood flow and organ perfusion. H2S has been shown to be protective in hypertension, atherosclerosis and under conditions of vascular oxidative stress, and deficiency of endogenous H2S production is linked to cardiovascular disease states. Taken together, these effects suggest that H2S has a physiological role as a vasculoprotective factor and that exogenous H2S donors may be useful therapeutic agents. This review article will discuss the vascular effects and anti-oxidant properties of H2S as well as examine the protective role of H2S in some important vascular disease states.</description>
        <link>http://www.medicalgasresearch.com/content/3/1/9</link>
                <dc:creator>Eloise Streeter</dc:creator>
                <dc:creator>Hooi Ng</dc:creator>
                <dc:creator>Joanne Hart</dc:creator>
                <dc:source>Medical Gas Research 2013, null:9</dc:source>
        <dc:date>2013-04-29T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/2045-9912-3-9</dc:identifier>
                                <prism:require>/content/figures/2045-9912-3-9-toc.gif</prism:require>
                <prism:publicationName>Medical Gas Research</prism:publicationName>
        <prism:issn>2045-9912</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>9</prism:startingPage>
        <prism:publicationDate>2013-04-29T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.medicalgasresearch.com/content/3/1/8">
        <title>Serum leptin levels decrease after permanent MCAo in the rat and remain unaffected by delayed hyperbaric oxygen therapy</title>
        <description>Hyperbaric oxygen therapy (HBOT), referring to the medical use of oxygen at a level higher than atmospheric pressure, exerts neuroprotective effects after ischemic stroke via various mechanisms. It has been demonstrated that HBOT modulates the synthesis and degradation of hormones. Leptin, an adipose derived hormone, has been found to confer neuroprotection following experimental stroke. However, it is not known whether HBOT alters leptin concentrations after permanent middle cerebral artery occlusion (pMCAo) in the rat. In this present study, we aimed to investigate the effect of HBOT on the serum concentration of leptin in rats subjected to pMCAo. HBOT was initiated 48 hrs after experimental pMCAo, at 2.5 atmospheres absolutes with 100% oxygen, 1 hr a day for 10 consecutive days. Body weight, neurobehavioral deficits and infarct size were evaluated. Blood was collected on day 1 and day 16 following HBOT. Serum leptin concentrations were measured with ELISA. Delayed HBOT reduced infarct size and improved neurobehavioral scores. Decreased serum levels of leptin were found in treated and untreated pMCAo animals, compared to the sham group on day 1 (P&#8201;&gt;&#8201;0.05) and day 16 (P&#8201;&lt;&#8201;0.05). However, no statistical significance was found between HBOT and the air group. We concluded that the neuroprotective effects of delayed HBOT in pMCAo rats were unlikely to be exerted through changes in the serum concentration of leptin.</description>
        <link>http://www.medicalgasresearch.com/content/3/1/8</link>
                <dc:creator>Jun Mu</dc:creator>
                <dc:creator>Robert Ostrowski</dc:creator>
                <dc:creator>Paul Krafft</dc:creator>
                <dc:creator>Jiping Tang</dc:creator>
                <dc:creator>John Zhang</dc:creator>
                <dc:source>Medical Gas Research 2013, null:8</dc:source>
        <dc:date>2013-03-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/2045-9912-3-8</dc:identifier>
                                <prism:require>/content/figures/2045-9912-3-8-toc.gif</prism:require>
                <prism:publicationName>Medical Gas Research</prism:publicationName>
        <prism:issn>2045-9912</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2013-03-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.medicalgasresearch.com/content/3/1/7">
        <title>Quoth the Raven: carbon monoxide and nothing more</title>
        <description>The articles contained in this review series exemplify the diverse applications and succinct biological relevance of this simple gas. Articles summarizing the important effects of carbon monoxide in preventing the rejection of an organ, in its neuroprotective properties in piglets, regulation of mycobacterial growth, in its anti-inflammatory effects in the gut and in its use in new and innovative modalities and avenues by which to harness adjuvant therapies are eloquently and precisely described and reviewed. Each of these reports offers but a glimpse of continued prudent and sound evidence that this simple diatomic gas offers astonishingly potent and extremely diverse biological and medicinal qualities.</description>
        <link>http://www.medicalgasresearch.com/content/3/1/7</link>
                <dc:creator>Leo Otterbein</dc:creator>
                <dc:source>Medical Gas Research 2013, null:7</dc:source>
        <dc:date>2013-03-06T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/2045-9912-3-7</dc:identifier>
                                <prism:require>/content/figures/2045-9912-3-7-toc.gif</prism:require>
                <prism:publicationName>Medical Gas Research</prism:publicationName>
        <prism:issn>2045-9912</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>7</prism:startingPage>
        <prism:publicationDate>2013-03-06T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.medicalgasresearch.com/content/3/1/6">
        <title>Molecular hydrogen attenuates fatty acid uptake and lipid accumulation through downregulating CD36 expression in HepG2 cells</title>
        <description>Background:
There is accumulating evidence that obesity is closely associated with an impaired free fatty acid metabolism as well as with insulin resistance and inflammation. Excessive fatty acid uptake mediated by fatty acid translocase CD36 plays an important role in hepatic steatosis. Molecular hydrogen has been shown to attenuate oxidative stress and improve lipid, glucose and energy metabolism in patients and animal models of hepatic steatosis and atherosclerosis, but the underlying molecular mechanisms remain largely unknown.
Methods:
Human hepatoma HepG2 cells were exposed to palmitate-BSA complex after treatment with or without hydrogen for 24&#160;h. The fatty acid uptake was measured by using spectrofluorometry and the lipid content was detected by Oil Red O staining. JNK phosphorylation and CD36 expression were analyzed by Western blot and real-time PCR analyses.
Results:
Pretreatment with hydrogen reduced fatty acid uptake and lipid accumulation after palmitate overload in HepG2 cells, which was associated with inhibition of JNK activation. Hydrogen treatment did not alter CD36 mRNA expression but reduced CD36 protein expression.
Conclusion:
Hydrogen inhibits fatty acid uptake and lipid accumulation through the downregulation of CD36 at the protein level in hepatic cultured cells, providing insights into the molecular mechanism underlying the hydrogen effects in vivo on lipid metabolism disorders.</description>
        <link>http://www.medicalgasresearch.com/content/3/1/6</link>
                <dc:creator>Akio Iio</dc:creator>
                <dc:creator>Mikako Ito</dc:creator>
                <dc:creator>Tomohiro Itoh</dc:creator>
                <dc:creator>Riyako Terazawa</dc:creator>
                <dc:creator>Yasunori Fujita</dc:creator>
                <dc:creator>Yoshinori Nozawa</dc:creator>
                <dc:creator>Ikuroh Ohsawa</dc:creator>
                <dc:creator>Kinji Ohno</dc:creator>
                <dc:creator>Masafumi Ito</dc:creator>
                <dc:source>Medical Gas Research 2013, null:6</dc:source>
        <dc:date>2013-03-01T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/2045-9912-3-6</dc:identifier>
                                <prism:require>/content/figures/2045-9912-3-6-toc.gif</prism:require>
                <prism:publicationName>Medical Gas Research</prism:publicationName>
        <prism:issn>2045-9912</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>6</prism:startingPage>
        <prism:publicationDate>2013-03-01T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.medicalgasresearch.com/content/3/1/5">
        <title>The summer of hydrogen sulfide: highlights from two international conferences</title>
        <description>A great deal of interest has been paid recently to the hydrogen sulfide, the newest member of the gasotransmitter family. With the growing interest in the biology of H2S, the need for meetings and conferences dedicated solely to the field of H2S has also grown. In 2009, scientist from around the world met in Shanghai, China for the first time to discuss the physiological relevance of H2S. In 2012, two conferences were organized to bring scientists, clinicians, and industry representatives together to discuss the latest breakthroughs concerning the emergent field of H2S. The following is a summary report of The First European Conference on the Biology of Hydrogen Sulfide and the Second International Conference on Hydrogen Sulfide Biology and Medicine.</description>
        <link>http://www.medicalgasresearch.com/content/3/1/5</link>
                <dc:creator>John Calvert</dc:creator>
                <dc:source>Medical Gas Research 2013, null:5</dc:source>
        <dc:date>2013-02-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/2045-9912-3-5</dc:identifier>
                                <prism:require>/content/figures/2045-9912-3-5-toc.gif</prism:require>
                <prism:publicationName>Medical Gas Research</prism:publicationName>
        <prism:issn>2045-9912</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2013-02-25T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.medicalgasresearch.com/content/3/1/4">
        <title>XENON in medical area: emphasis on neuroprotection in hypoxia and anesthesia</title>
        <description>Xenon is a medical gas capable of establishing neuroprotection, inducing anesthesia as well as serving in modern laser technology and nuclear medicine as a contrast agent. In spite of its high cost, its lack of side effects, safe cardiovascular and organoprotective profile and effective neuroprotective role after hypoxic-ischemic injury (HI) favor its applications in clinics. Xenon performs its anesthetic and neuroprotective functions through binding to glycine site of glutamatergic N-methyl-D-aspartate (NMDA) receptor competitively and blocking it. This blockage inhibits the overstimulation of NMDA receptors, thus preventing their following downstream calcium accumulating cascades. Xenon is also used in combination therapies together with hypothermia or sevoflurane. The neuroprotective effects of xenon and hypothermia cooperate synergistically whether they are applied synchronously or asynchronously. Distinguishing properties of Xenon promise for innovations in medical gas field once further studies are fulfilled and Xenon&#8217;s high cost is overcome.</description>
        <link>http://www.medicalgasresearch.com/content/3/1/4</link>
                <dc:creator>Ecem Esencan</dc:creator>
                <dc:creator>Simge Yuksel</dc:creator>
                <dc:creator>Yusuf Tosun</dc:creator>
                <dc:creator>Alexander Robinot</dc:creator>
                <dc:creator>Ihsan Solaroglu</dc:creator>
                <dc:creator>John Zhang</dc:creator>
                <dc:source>Medical Gas Research 2013, null:4</dc:source>
        <dc:date>2013-02-01T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/2045-9912-3-4</dc:identifier>
                                <prism:require>/content/figures/2045-9912-3-4-toc.gif</prism:require>
                <prism:publicationName>Medical Gas Research</prism:publicationName>
        <prism:issn>2045-9912</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>4</prism:startingPage>
        <prism:publicationDate>2013-02-01T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.medicalgasresearch.com/content/3/1/3">
        <title>Xenon preconditioning: molecular mechanisms and biological effects</title>
        <description>Xenon is one of noble gases and has been recognized as an anesthetic for more than 50&#8201;years. Xenon possesses many of the characteristics of an ideal anesthetic, but it is not widely applied in clinical practice mainly because of its high cost. In recent years, numerous studies have demonstrated that xenon as an anesthetic can exert neuroprotective and cardioprotective effects in different models. Moreover, xenon has been applied in the preconditioning, and the neuroprotective and cardioprotective effects of xenon preconditioning have been investigated in a lot of studies in which some mechanisms related to these protections are proposed. In this review, we summarized these mechanisms and the biological effects of xenon preconditioning.</description>
        <link>http://www.medicalgasresearch.com/content/3/1/3</link>
                <dc:creator>Wenwu Liu</dc:creator>
                <dc:creator>Ying Liu</dc:creator>
                <dc:creator>Han Chen</dc:creator>
                <dc:creator>Kan Liu</dc:creator>
                <dc:creator>Hengyi Tao</dc:creator>
                <dc:creator>Xuejun Sun</dc:creator>
                <dc:source>Medical Gas Research 2013, null:3</dc:source>
        <dc:date>2013-01-10T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/2045-9912-3-3</dc:identifier>
                                <prism:require>/content/figures/2045-9912-3-3-toc.gif</prism:require>
                <prism:publicationName>Medical Gas Research</prism:publicationName>
        <prism:issn>2045-9912</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2013-01-10T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.medicalgasresearch.com/content/3/1/2">
        <title>Normobaric hyperoxia-based neuroprotective therapies in ischemic stroke</title>
        <description>Stroke is a leading cause of death and disability due to disturbance of blood supply to the brain. As brain is highly sensitive to hypoxia, insufficient oxygen supply is a critical event contributing to ischemic brain injury. Normobaric hyperoxia (NBO) that aims to enhance oxygen delivery to hypoxic tissues has long been considered as a logical neuroprotective therapy for ischemic stroke. To date, many possible mechanisms have been reported to elucidate NBO&#8217;s neuroprotection, such as improving tissue oxygenation, increasing cerebral blood flow, reducing oxidative stress and protecting the blood brain barrier. As ischemic stroke triggers a battery of damaging events, combining NBO with other agents or treatments that target multiple mechanisms of injury may achieve better outcome than individual treatment alone. More importantly, time loss is brain loss in acute cerebral ischemia. NBO can be a rapid therapy to attenuate or slow down the evolution of ischemic tissues towards necrosis and therefore &#8220;buy time&#8221; for reperfusion therapies. This article summarizes the current literatures on NBO as a simple, widely accessible, and potentially cost-effective therapeutic strategy for treatment of acute ischemic stroke.</description>
        <link>http://www.medicalgasresearch.com/content/3/1/2</link>
                <dc:creator>Zhifeng Qi</dc:creator>
                <dc:creator>Wenlan Liu</dc:creator>
                <dc:creator>Yumin Luo</dc:creator>
                <dc:creator>Xunming Ji</dc:creator>
                <dc:creator>Ke Jian Liu</dc:creator>
                <dc:source>Medical Gas Research 2013, null:2</dc:source>
        <dc:date>2013-01-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/2045-9912-3-2</dc:identifier>
                                <prism:require>/content/figures/2045-9912-3-2-toc.gif</prism:require>
                <prism:publicationName>Medical Gas Research</prism:publicationName>
        <prism:issn>2045-9912</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2013-01-09T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.medicalgasresearch.com/content/3/1/1">
        <title>The immunomodulatory role of carbon monoxide during transplantation</title>
        <description>The number of organ and tissue transplants has increased worldwide in recent decades. However, graft rejection, infections due to the use of immunosuppressive drugs and a shortage of graft donors remain major concerns. Carbon monoxide (CO) had long been regarded solely as a poisonous gas. Ultimately, physiological studies unveiled the endogenous production of CO, particularly by the heme oxygenase (HO)-1 enzyme, recognizing CO as a beneficial gas when used at therapeutic doses. The protective properties of CO led researchers to develop uses for it, resulting in devices and molecules that can deliver CO in vitro and in vivo. The resulting interest in clinical investigations was immediate. Studies regarding the CO/HO-1 modulation of immune responses and their effects on various immune disorders gave rise to transplantation research, where CO was shown to be essential in the protection against organ rejection in animal models. This review provides a perspective of how CO modulates the immune system to improve transplantation and suggests its use as a therapy in the field.</description>
        <link>http://www.medicalgasresearch.com/content/3/1/1</link>
                <dc:creator>Mariane Amano</dc:creator>
                <dc:creator>Niels Camara</dc:creator>
                <dc:source>Medical Gas Research 2013, null:1</dc:source>
        <dc:date>2013-01-07T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/2045-9912-3-1</dc:identifier>
                                <prism:require>/content/figures/2045-9912-3-1-toc.gif</prism:require>
                <prism:publicationName>Medical Gas Research</prism:publicationName>
        <prism:issn>2045-9912</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>1</prism:startingPage>
        <prism:publicationDate>2013-01-07T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <cc:License rdf:about="http://creativecommons.org/licenses/by/2.0/">
        <cc:permits rdf:resource="http://creativecommons.org/ns#Reproduction" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#Distribution" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#DerivativeWorks" />
    </cc:License>
</rdf:RDF>
