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  1. Article ; Online: Genome-wide identification and functional characterization of CDPK gene family reveal their involvement in response to drought stress in Gossypium barbadense

    Guangzhen Shi / Xinxia Zhu

    PeerJ, Vol 10, p e

    2022  Volume 12883

    Abstract: Background Calcium dependent protein kinases (CDPKs) are a class of important calcium signal sensing response proteins, which play an important regulatory role in response to abiotic stress. However, researchers have not been excavated CDPKs’ role in ... ...

    Abstract Background Calcium dependent protein kinases (CDPKs) are a class of important calcium signal sensing response proteins, which play an important regulatory role in response to abiotic stress. However, researchers have not been excavated CDPKs’ role in drought in sea-island cotton(Gossypium barbadense L. ‘H7124’). Results Eighty-four CDPK genes have been identified in G. barbadense. These GbCDPK genes are unevenly distributed on 26 chromosomes, and segmental duplication is the significant way for the extension of CDPK family. Also, members within the same subfamily share a similar gene structure and motif composition. There are a large number of cis-elements involved in plant growth and response to stresses in the promoter regions of GbCDPKs. Additionally, these GbCDPKs show differential expression patterns in cotton tissues. The transcription levels of most genes were markedly altered in cotton under heat, cold, salt and PEG treatments, while the expressions of some GbCDPKs were induced in cotton under drought stress. Among these drought-induced genes, we selected GbCDPK32, GbCDPK68, GbCDPK74, GbCDPK80 and GbCDPK83 for further functional characterization by virus-induced gene silencing (VIGS) method. Conclusions In conclusion, the principal findings of this prospective study are that CDPKs were associated with drought. These findings provide a solid foundation for the development of future molecular mechanism in sea-island cotton.
    Keywords Identification ; CDPKs ; Drought ; Stress ; Gossypium barbadense ; Medicine ; R
    Subject code 572
    Language English
    Publishing date 2022-02-01T00:00:00Z
    Publisher PeerJ Inc.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Lipocalin 2 mediates appetite suppression during pancreatic cancer cachexia

    Brennan Olson / Xinxia Zhu / Mason A. Norgard / Peter R. Levasseur / John T. Butler / Abigail Buenafe / Kevin G. Burfeind / Katherine A. Michaelis / Katherine R. Pelz / Heike Mendez / Jared Edwards / Stephanie M. Krasnow / Aaron J. Grossberg / Daniel L. Marks

    Nature Communications, Vol 12, Iss 1, Pp 1-

    2021  Volume 15

    Abstract: Lipocalin 2 (LCN2) has been recently identified as an endogenous regulator of appetite. Here, using pancreatic cancer as a model of cachexia, the authors demonstrate that LCN2 is a critical mediator of cancer-associated anorexia and may be ... ...

    Abstract Lipocalin 2 (LCN2) has been recently identified as an endogenous regulator of appetite. Here, using pancreatic cancer as a model of cachexia, the authors demonstrate that LCN2 is a critical mediator of cancer-associated anorexia and may be therapeutically targeted to improve patient outcomes.
    Keywords Science ; Q
    Language English
    Publishing date 2021-04-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Circulating myeloid cells invade the central nervous system to mediate cachexia during pancreatic cancer

    Kevin G Burfeind / Xinxia Zhu / Mason A Norgard / Peter R Levasseur / Christian Huisman / Abigail C Buenafe / Brennan Olson / Katherine A Michaelis / Eileen RS Torres / Sophia Jeng / Shannon McWeeney / Jacob Raber / Daniel L Marks

    eLife, Vol

    2020  Volume 9

    Abstract: Weight loss and anorexia are common symptoms in cancer patients that occur prior to initiation of cancer therapy. Inflammation in the brain is a driver of these symptoms, yet cellular sources of neuroinflammation during malignancy are unknown. In a mouse ...

    Abstract Weight loss and anorexia are common symptoms in cancer patients that occur prior to initiation of cancer therapy. Inflammation in the brain is a driver of these symptoms, yet cellular sources of neuroinflammation during malignancy are unknown. In a mouse model of pancreatic ductal adenocarcinoma (PDAC), we observed early and robust myeloid cell infiltration into the brain. Infiltrating immune cells were predominately neutrophils, which accumulated at a unique central nervous system entry portal called the velum interpositum, where they expressed CCR2. Pharmacologic CCR2 blockade and genetic deletion of Ccr2 both resulted in significantly decreased brain-infiltrating myeloid cells as well as attenuated cachexia during PDAC. Lastly, intracerebroventricular blockade of the purinergic receptor P2RX7 during PDAC abolished immune cell recruitment to the brain and attenuated anorexia. Our data demonstrate a novel function for the CCR2/CCL2 axis in recruiting neutrophils to the brain, which drives anorexia and muscle catabolism.
    Keywords cachexia ; neuroimmunology ; neutrophils ; brain ; pancreatic cancer ; myeloid cells ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2020-05-01T00:00:00Z
    Publisher eLife Sciences Publications Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Dexamethasone Chemotherapy Does Not Disrupt Orexin Signaling.

    David E Kram / Stephanie M Krasnow / Peter R Levasseur / Xinxia Zhu / Linda C Stork / Daniel L Marks

    PLoS ONE, Vol 11, Iss 12, p e

    2016  Volume 0168731

    Abstract: Steroid-induced sleep disturbance is a common and highly distressing morbidity for children receiving steroid chemotherapy for the treatment of pediatric acute lymphoblastic leukemia (ALL). Sleep disturbance can negatively impact overall quality of life, ...

    Abstract Steroid-induced sleep disturbance is a common and highly distressing morbidity for children receiving steroid chemotherapy for the treatment of pediatric acute lymphoblastic leukemia (ALL). Sleep disturbance can negatively impact overall quality of life, neurodevelopment, memory consolidation, and wound healing. Hypothalamic orexin neurons are influential wake-promoting neurons, and disturbances in orexin signaling leads to abnormal sleep behavior. A new class of drug, the orexin receptor antagonists, could be an intriguing option for sleep disorders caused by increased orexinergic output. Our aim was to examine the impact of ALL treatment doses of corticosteroids on the orexin system in rodents and in children undergoing treatment for childhood ALL.We administered repeated injections of dexamethasone to rodents and measured responsive orexin neural activity compared to controls. In children with newly diagnosed standard risk B-cell ALL receiving dexamethasone therapy per Children's Oncology Group (COG) induction therapy from 2014-2016, we collected pre- and during-steroids matched CSF samples and measured the impact of steroids on CSF orexin concentration.In both rodents, all markers orexin signaling, including orexin neural output and orexin receptor expression, were preserved in the setting of dexamethasone. Additionally, we did not detect a difference in pre- and during-dexamethasone CSF orexin concentrations in children receiving dexamethasone.Our results demonstrate that rodent and human orexin physiology is largely preserved in the setting of high dose dexamethasone. The data obtained in our experimental model fail to demonstrate a causative role for disruption of the orexin pathway in steroid-induced sleep disturbance.
    Keywords Medicine ; R ; Science ; Q
    Subject code 610
    Language English
    Publishing date 2016-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: The TLR7/8 agonist R848 remodels tumor and host responses to promote survival in pancreatic cancer

    Katherine A. Michaelis / Mason A. Norgard / Xinxia Zhu / Peter R. Levasseur / Shamilene Sivagnanam / Shannon M. Liudahl / Kevin G. Burfeind / Brennan Olson / Katherine R. Pelz / Diana M. Angeles Ramos / H. Carlo Maurer / Kenneth P. Olive / Lisa M. Coussens / Terry K. Morgan / Daniel L. Marks

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 15

    Abstract: In the treatment of pancreatic ductal adenocarcinoma (PDAC), comorbidities such as cachexia limit quality of life and survival. Here, the authors show TLR7/8 agonist R848 remodels host and tumour immune responses, promoting survival and attenuating ... ...

    Abstract In the treatment of pancreatic ductal adenocarcinoma (PDAC), comorbidities such as cachexia limit quality of life and survival. Here, the authors show TLR7/8 agonist R848 remodels host and tumour immune responses, promoting survival and attenuating cachexia in murine models of PDAC.
    Keywords Science ; Q
    Language English
    Publishing date 2019-10-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Publisher Correction

    Katherine A. Michaelis / Mason A. Norgard / Xinxia Zhu / Peter R. Levasseur / Shamilene Sivagnanam / Shannon M. Liudahl / Kevin G. Burfeind / Brennan Olson / Katherine R. Pelz / Diana M. Angeles Ramos / H. Carlo Maurer / Kenneth P. Olive / Lisa M. Coussens / Terry K. Morgan / Daniel L. Marks

    Nature Communications, Vol 10, Iss 1, Pp 1-

    The TLR7/8 agonist R848 remodels tumor and host responses to promote survival in pancreatic cancer

    2019  Volume 1

    Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

    Abstract An amendment to this paper has been published and can be accessed via a link at the top of the paper.
    Keywords Science ; Q
    Language English
    Publishing date 2019-11-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: The TLR7/8 agonist R848 remodels tumor and host responses to promote survival in pancreatic cancer

    Katherine A. Michaelis / Mason A. Norgard / Xinxia Zhu / Peter R. Levasseur / Shamilene Sivagnanam / Shannon M. Liudahl / Kevin G. Burfeind / Brennan Olson / Katherine R. Pelz / Diana M. Angeles Ramos / H. Carlo Maurer / Kenneth P. Olive / Lisa M. Coussens / Terry K. Morgan / Daniel L. Marks

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 15

    Abstract: In the treatment of pancreatic ductal adenocarcinoma (PDAC), comorbidities such as cachexia limit quality of life and survival. Here, the authors show TLR7/8 agonist R848 remodels host and tumour immune responses, promoting survival and attenuating ... ...

    Abstract In the treatment of pancreatic ductal adenocarcinoma (PDAC), comorbidities such as cachexia limit quality of life and survival. Here, the authors show TLR7/8 agonist R848 remodels host and tumour immune responses, promoting survival and attenuating cachexia in murine models of PDAC.
    Keywords Science ; Q
    Language English
    Publishing date 2019-10-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  8. Article ; Online: Publisher Correction

    Katherine A. Michaelis / Mason A. Norgard / Xinxia Zhu / Peter R. Levasseur / Shamilene Sivagnanam / Shannon M. Liudahl / Kevin G. Burfeind / Brennan Olson / Katherine R. Pelz / Diana M. Angeles Ramos / H. Carlo Maurer / Kenneth P. Olive / Lisa M. Coussens / Terry K. Morgan / Daniel L. Marks

    Nature Communications, Vol 10, Iss 1, Pp 1-

    The TLR7/8 agonist R848 remodels tumor and host responses to promote survival in pancreatic cancer

    2019  Volume 1

    Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

    Abstract An amendment to this paper has been published and can be accessed via a link at the top of the paper.
    Keywords Science ; Q
    Language English
    Publishing date 2019-11-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Mechanism of protection by soluble epoxide hydrolase inhibition in type 2 diabetic stroke.

    Kristen L Zuloaga / Stephanie M Krasnow / Xinxia Zhu / Wenri Zhang / Sari A Jouihan / Robert E Shangraw / Nabil J Alkayed / Daniel L Marks

    PLoS ONE, Vol 9, Iss 5, p e

    2014  Volume 97529

    Abstract: Inhibition of soluble epoxide hydrolase (sEH) is a potential target of therapy for ischemic injury. sEH metabolizes neuroprotective epoxyeicosatrienoic acids (EETs). We recently demonstrated that sEH inhibition reduces infarct size after middle cerebral ... ...

    Abstract Inhibition of soluble epoxide hydrolase (sEH) is a potential target of therapy for ischemic injury. sEH metabolizes neuroprotective epoxyeicosatrienoic acids (EETs). We recently demonstrated that sEH inhibition reduces infarct size after middle cerebral artery occlusion (MCAO) in type 1 diabetic mice. We hypothesized that inhibition of sEH would protect against ischemic injury in type 2 diabetic mice. Type 2 diabetes was produced by combined high-fat diet, nicotinamide and streptozotocin in male mice. Diabetic and control mice were treated with vehicle or the sEH inhibitor t-AUCB then subjected to 60-min MCAO. Compared to chow-fed mice, high fat diet-fed mice exhibited an upregulation of sEH mRNA and protein in brain, but no differences in brain EETs levels were observed between groups. Type 2 diabetic mice had increased blood glucose levels at baseline and throughout ischemia, decreased laser-Doppler perfusion of the MCA territory after reperfusion, and sustained larger cortical infarcts compared to control mice. t-AUCB decreased fasting glucose levels at baseline and throughout ischemia, improved cortical perfusion after MCAO and significantly reduced infarct size in diabetic mice. We conclude that sEH inhibition, as a preventative treatment, improves glycemic status, post-ischemic reperfusion in the ischemic territory, and stroke outcome in type 2 diabetic mice.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Regulation of lean mass, bone mass, and exercise tolerance by the central melanocortin system.

    Theodore P Braun / Benjamin Orwoll / Xinxia Zhu / Peter R Levasseur / Marek Szumowski / My Linh T Nguyen / Mary L Bouxsein / Robert F Klein / Daniel L Marks

    PLoS ONE, Vol 7, Iss 7, p e

    2012  Volume 42183

    Abstract: Signaling via the type 4-melanocortin receptor (MC4R) is an important determinant of body weight in mice and humans, where loss of function mutations lead to significant obesity. Humans with mutations in the MC4R experience an increase in lean mass. ... ...

    Abstract Signaling via the type 4-melanocortin receptor (MC4R) is an important determinant of body weight in mice and humans, where loss of function mutations lead to significant obesity. Humans with mutations in the MC4R experience an increase in lean mass. However, the simultaneous accrual of fat mass in such individuals may contribute to this effect via mechanical loading. We therefore examined the relationship of fat mass and lean mass in mice lacking the type-4 melanocortin receptor (MC4RKO). We demonstrate that MC4RKO mice display increased lean body mass. Further, this is not dependent on changes in adipose mass, as MC4RKO mice possess more lean body mass than diet-induced obese (DIO) wild type mice with equivalent fat mass. To examine potential sources of the increased lean mass in MC4RKO mice, bone mass and strength were examined in MC4RKO mice. Both parameters increase with age in MC4RKO mice, which likely contributes to increases in lean body mass. We functionally characterized the increased lean mass in MC4RKO mice by examining their capacity for treadmill running. MC4R deficiency results in a decrease in exercise performance. No changes in the ratio of oxidative to glycolytic fibers were seen, however MC4RKO mice demonstrate a significantly reduced heart rate, which may underlie their impaired exercise performance. The reduced exercise capacity we report in the MC4RKO mouse has potential clinical ramifications, as efforts to control body weight in humans with melanocortin deficiency may be ineffective due to poor tolerance for physical activity.
    Keywords Medicine ; R ; Science ; Q
    Subject code 796
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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