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https://www.readbyqxmd.com/read/28437711/cardiomyocyte-ca-2-homeostasis-as-a-therapeutic-target-in-heart-failure-with-reduced-and-preserved-ejection-fraction
#1
REVIEW
Deborah Peana, Timothy L Domeier
Heart failure is a highly prevalent syndrome of multiple etiologies and associated comorbidities, and aberrant intracellular Ca(2+) homeostasis is a hallmark finding in heart failure patients. The cyclical changes in Ca(2+) concentration within cardiomyocytes control cycles of cardiac contraction and relaxation, and dysregulation of Ca(2+) handling processes leads to systolic dysfunction, diastolic dysfunction, and adverse remodeling. For this reason, greater understanding of Ca(2+) handling mechanisms in heart failure is critical for selection of appropriate treatment strategies...
April 21, 2017: Current Opinion in Pharmacology
https://www.readbyqxmd.com/read/28437123/distress-tolerance-and-physiological-reactivity-to-stress-predict-women-s-problematic-alcohol-use
#2
Cathryn Glanton Holzhauer, Stephanie Wemm, Edelgard Wulfert
Research has shown that measures of reactivity to distress-including distress tolerance and physiological reactivity to stress-are dysregulated in women who misuse alcohol. These variables may interact and create a risk profile for young adult women, reflecting patterns of stress reactivity that confer a risk for alcohol misuse. The current study tested this hypothesis by examining the independent and interactive associations of subjective distress tolerance, behavioral distress tolerance, and physiological stress reactivity with women's alcohol misuse...
April 24, 2017: Experimental and Clinical Psychopharmacology
https://www.readbyqxmd.com/read/28437065/a-macrocyclic-peptide-ligand-binds-the-oncogenic-microrna-21-precursor-and-suppresses-dicer-processing
#3
Matthew D Shortridge, Matthew J Walker, Tom Pavelitz, Yu Chen, Gabriele Varani
MicroRNAs (miRNAs) help orchestrate cellular growth and survival through post-transcriptional mechanisms. The dysregulation of miRNA biogenesis can lead to cellular growth defects, chemotherapeutic resistance and plays a direct role in the development of many chronic diseases. Among these RNAs, miR-21 is consistently overexpressed in most human cancers leading to the down regulation of key tumor suppressing and pro-apoptotic factors; suggesting that inhibition of miR-21 biogenesis could reverse these negative effects...
April 24, 2017: ACS Chemical Biology
https://www.readbyqxmd.com/read/28436955/vitamin-a-mediates-conversion-of-monocyte-derived-macrophages-into-tissue-resident-macrophages-during-alternative-activation
#4
Uma Mahesh Gundra, Natasha M Girgis, Michael A Gonzalez, Mei San Tang, Hendrik J P Van Der Zande, Jian-Da Lin, Mireille Ouimet, Lily J Ma, Jordan Poles, Nikollaq Vozhilla, Edward A Fisher, Kathryn J Moore, P'ng Loke
It remains unclear whether activated inflammatory macrophages can adopt features of tissue-resident macrophages, or what mechanisms might mediate such a phenotypic conversion. Here we show that vitamin A is required for the phenotypic conversion of interleukin 4 (IL-4)-activated monocyte-derived F4/80(int)CD206(+)PD-L2(+)MHCII(+) macrophages into macrophages with a tissue-resident F4/80(hi)CD206(-)PD-L2(-)MHCII(-)UCP1(+) phenotype in the peritoneal cavity of mice and during the formation of liver granulomas in mice infected with Schistosoma mansoni...
April 24, 2017: Nature Immunology
https://www.readbyqxmd.com/read/28436939/an-inflammatory-bowel-disease-risk-variant-in-inava-decreases-pattern-recognition-receptor-induced-outcomes
#5
Jie Yan, Matija Hedl, Clara Abraham
Inflammatory bowel disease (IBD) is characterized by dysregulation in both cytokines and responses to intestinal microbes, and proper regulation of pattern recognition receptor (PRR) signaling is critical for intestinal immune homeostasis. Altered functions for the IBD risk locus containing rs7554511, which encompasses the C1orf106 gene (recently named INAVA), and roles for the protein encoded by the INAVA gene are unknown. Here, we investigated the role of INAVA and INAVA genotype in regulating PRR-initiated outcomes in primary human cells...
April 24, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28436449/metabolism-dysregulation-induces-a-specific-lipid-signature-of-nonalcoholic-steatohepatitis-in-patients
#6
Franck Chiappini, Audrey Coilly, Hanane Kadar, Philippe Gual, Albert Tran, Christophe Desterke, Didier Samuel, Jean-Charles Duclos-Vallée, David Touboul, Justine Bertrand-Michel, Alain Brunelle, Catherine Guettier, François Le Naour
Nonalcoholic steatohepatitis (NASH) is a condition which can progress to cirrhosis and hepatocellular carcinoma. Markers for NASH diagnosis are still lacking. We performed a comprehensive lipidomic analysis on human liver biopsies including normal liver, nonalcoholic fatty liver and NASH. Random forests-based machine learning approach allowed characterizing a signature of 32 lipids discriminating NASH with 100% sensitivity and specificity. Furthermore, we validated this signature in an independent group of NASH patients...
April 24, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28436424/the-immunopathology-of-sepsis-and-potential-therapeutic-targets
#7
REVIEW
Tom van der Poll, Frank L van de Veerdonk, Brendon P Scicluna, Mihai G Netea
Sepsis is defined as a life-threatening organ dysfunction that is caused by a dysregulated host response to infection. In sepsis, the immune response that is initiated by an invading pathogen fails to return to homeostasis, thus culminating in a pathological syndrome that is characterized by sustained excessive inflammation and immune suppression. Our understanding of the key mechanisms involved in the pathogenesis of sepsis has increased tremendously, yet this still needs to be translated into novel targeted therapeutic strategies...
April 24, 2017: Nature Reviews. Immunology
https://www.readbyqxmd.com/read/28436392/the-dna-damage-response-in-neurons-die-by-apoptosis-or-survive-in-a-senescence-like-state
#8
Edward Fielder, Thomas von Zglinicki, Diana Jurk
Neurons are exposed to high levels of DNA damage from both physiological and pathological sources. Neurons are post-mitotic and their loss cannot be easily recovered from; to cope with DNA damage a complex pathway called the DNA damage response (DDR) has evolved. This recognizes the damage, and through kinases such as ataxia-telangiectasia mutated (ATM) recruits and activates downstream factors that mediate either apoptosis or survival. This choice between these opposing outcomes integrates many inputs primarily through a number of key cross-road proteins, including ATM, p53, and p21...
April 18, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28436029/wnt4-acts-downstream-of-bmp2-to-mediate-the-regulation-of-atra-signaling-on-runx1-expression-implications-for-terminal-differentiation-of-antler-chondrocytes
#9
Hong-Liang Zhang, Zhan-Qing Yang, Cui-Cui Duan, Shuang Geng, Kai Wang, Hai-Fan Yu, Zhan-Peng Yue, Bin Guo
Although ATRA is involved in regulating the proliferation and differentiation of chondrocytes, its underlying mechanism remains unknown. Here we showed that ATRA could stimulate the proliferation of antler chondrocytes and expression of COL X and MMP13 which were two well-known markers for hypertrophic chondrocytes. Silencing of CRABP2 prevented the induction of ATRA on chondrocyte terminal differentiation, while overexpression of CRABP2 exhibited the opposite effects. CYP26A1 and CYP26B1 weakened the sensitivity of antler chondrocytes to ATRA...
April 24, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28435981/-iron-metabolism-and-neonatal-hypoxic-ischemic-brain-damage
#10
Kai-Yu Xu, Fan Li
Iron is an essential element for nervous system development, and maintaining a normal iron level in nervous system is controlled by multiple factors. Recent studies reported that iron dysregulation and the following iron metabolic pathways played an important role in hypoxic ischemic brain damage (HIBD) in neonates. Circulatory iron level is altered after hypoxia-ischemia exposure, which may cause abnormal iron deposition in the nervous system followed by neuronal injury. Finding the causing factors for abnormal iron metabolism after hypoxia-ischemia exposure, as well as understanding the mechanisms how iron metabolism contributes to HIBD, will shed lights on HIBD prevention and treatment...
April 25, 2017: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/28435890/gene-expression-profile-of-human-cytokines-in-response-to-burkholderia-pseudomallei-infection
#11
Shivankari Krishnananthasivam, Harindra Darshana Sathkumara, Enoka Corea, Mohan Natesan, Aruna Dharshan De Silva
Melioidosis is an underreported infectious disease, caused by the Gram-negative bacterium Burkholderia pseudomallei. Understanding the disease susceptibility and pathogenesis is crucial for developing newer diagnostic and therapeutic strategies for this life-threatening infection. In this study, we aimed to analyze the gene expression levels of important cytokines in melioidosis patients and establish useful correlates with disease biomarkers compared to cases of sepsis infection caused by other pathogens and healthy individuals...
March 2017: MSphere
https://www.readbyqxmd.com/read/28435295/silencing-cdr1as-inhibits-colorectal-cancer-progression-through-regulating-microrna-7
#12
Wentao Tang, Meiling Ji, Guodong He, Liangliang Yang, Zhengchuan Niu, Mi Jian, Ye Wei, Li Ren, Jianmin Xu
An increasing number of studies have demonstrated that circular RNAs (circRNAs) can regulate gene expression through interacting with microRNAs. In this study, we analyzed the expression of antisense to CDR1as in colorectal cancer (CRC). CDR1as had a higher expression in CRC tissues compared to adjacent, normal mucosa and was positively associated with tumor size, T stage, lymph node metastasis, and poor overall survival (OS). Downregulation of CDR1as suppressed CRC cell proliferation and invasion and increased microRNA-7 (miR-7) expression...
2017: OncoTargets and Therapy
https://www.readbyqxmd.com/read/28435131/repression-of-acetaminophen-induced-hepatotoxicity-by-a-combination-of-celastrol-and-brilliant-blue-g
#13
Heba A Abdelaziz, Mohamed E Shaker, Mohamed F Hamed, Nariman M Gameil
The sterile inflammatory response is an eminent contributor to acetaminophen (APAP)-hepatotoxicity in humans. Recent advances unraveled an axial role of the NLRP3-inflammasome in APAP-post injury inflammation. Nevertheless, the role of signaling events preceded the NLRP3-inflammasome activation, like the transcription factor NF-κB and the purinergic receptor P2×7, is still unclear and needs further elucidation. Here, we investigated the pharmacological inhibition of these upstream signaling molecules by celastrol and brilliant blue G (BBG) (separately or simultaneously) in APAP-hepatotoxicity in mice...
April 20, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/28435083/subchronic-glucocorticoids-glutathione-depletion-and-a-postpartum-model-elevate-monoamine-oxidase-a-activity-in-the-prefrontal-cortex-of-rats
#14
Sofia Raitsin, Junchao Tong, Stephen Kish, Xin Xu, Lilia Magomedova, Carolyn Cummins, Ana C Andreazza, Gustavo Scola, Glen Baker, Jeffrey H Meyer
Recent human brain imaging studies implicate dysregulation of monoamine oxidase-A (MAO-A), in particular in the prefrontal cortex (PFC) and anterior cingulate cortex (ACC), in the development of major depressive disorder (MDD). This study investigates the influence of four alterations underlying important pathologies of MDD, namely, chronic elevation of glucocorticoid levels, glutathione depletion, changes in female gonadal sex hormones and serotonin concentration fluctuation, on MAO-A and MAO-B activity in rats...
April 20, 2017: Brain Research
https://www.readbyqxmd.com/read/28434941/dysregulation-of-the-sirt1-oct6-axis-contributes-to-environmental-stress-induced-neural-induction-defects
#15
Guoping Li, Zeyidan Jiapaer, Rong Weng, Yi Hui, Wenwen Jia, Jiajie Xi, Guiying Wang, Songcheng Zhu, Xin Zhang, Dandan Feng, Ling Liu, Xiaoqing Zhang, Jiuhong Kang
Environmental stresses are increasingly acknowledged as core causes of abnormal neural induction leading to neural tube defects (NTDs). However, the mechanism responsible for environmental stress-triggered neural induction defects remains unknown. Here, we report that a spectrum of environmental stresses, including oxidative stress, starvation, and DNA damage, profoundly activate SIRT1, an NAD(+)-dependent lysine deacetylase. Both mouse embryos and in vitro differentiated embryonic stem cells (ESCs) demonstrated a negative correlation between the expression of SIRT1 and that of OCT6, a key neural fate inducer...
April 19, 2017: Stem Cell Reports
https://www.readbyqxmd.com/read/28434922/association-of-autoimmune-thyroiditis-and-celiac-disease-with-juvenile-polyposis-due-to-10q23-1q23-31-deletion-potential-role-of-pi3k-akt-pathway-dysregulation
#16
Federica Guaraldi, Giovanni Di Nardo, Luigi Tarani, Luca Bertelli, Francesco Claudio Susca, Rosanna Bagnulo, Nicoletta Resta
Juvenile Polyposis (JP) is a rare hereditary condition characterized by diffuse hamartomatous gastrointestinal polyposis, associated with a significantly increased risk of neoplastic transformation. Most of the cases are caused by SMAD and BMPR1A mutations, while 10q23 microdeletions, encompassing both PTEN and BMPR1A oncogenes, are extremely rare, typically associated with more aggressive JP, and extraintestinal features overlapping with PTEN Hamartoma Tumor Syndrome. We present the first case of a young female with multiple autoimmune disorders (i...
April 18, 2017: European Journal of Medical Genetics
https://www.readbyqxmd.com/read/28434671/resveratrol-improves-mitochondrial-function-in-the-remnant-kidney-from-5-6-nephrectomized-rats
#17
Yan Hui, Miaomiao Lu, Yarong Han, Hongli Zhou, Wei Liu, Lijing Li, Ruixia Jin
Mitochondrial dysfunction is involved in the pathogenesis of chronic kidney disease (CKD). Resveratrol has been demonstrated to be beneficial for the recovery of kidney diseases. In this study, the 5/6 nephrectomized rat was used as a CKD model and the TGF-β1-exposed mouse mesangial cells were used as an in vitro model. Pathological examination showed that resveratrol treatment attenuated glomerular injury in the remnant kidney of 5/6 nephrectomized rat. Additionally, resveratrol improved mitochondrial function in vivo and in vitro, as evidenced by increasing mitochondrial membrane potential, increasing ATP, decreasing reactive oxygen species production and enhancing activities of complex I and III...
April 20, 2017: Acta Histochemica
https://www.readbyqxmd.com/read/28434262/the-emergence-of-acid-ceramidase-as-a-therapeutic-target-for-acute-myeloid-leukemia
#18
Su-Fern Tan, Jennifer M Pearson, David J Feith, Thomas P Loughran
Acute myeloid leukemia (AML) is the most common adult leukemia. Only a fraction of AML patients will survive with existing chemotherapy regimens. Hence, there is an urgent and unmet need to identify novel targets and develop better therapeutics in AML. In the past decade, the field of sphingolipid metabolism has emerged into the forefront of cancer biology due to its importance in cancer cell proliferation and survival. In particular, acid ceramidase (AC) has emerged as a promising therapeutic target due to its role in neutralizing the pro-death effects of ceramide...
April 24, 2017: Expert Opinion on Therapeutic Targets
https://www.readbyqxmd.com/read/28434145/mtorc1-signaling-in-hepatic-lipid-metabolism
#19
REVIEW
Jinbo Han, Yiguo Wang
The mechanistic target of rapamycin (mTOR) signaling pathway regulates many metabolic and physiological processes in different organs or tissues. Dysregulation of mTOR signaling has been implicated in many human diseases including obesity, diabetes, cancer, fatty liver diseases, and neuronal disorders. Here we review recent progress in understanding how mTORC1 (mTOR complex 1) signaling regulates lipid metabolism in the liver.
April 22, 2017: Protein & Cell
https://www.readbyqxmd.com/read/28434044/faulty-rna-splicing-consequences-and-therapeutic-opportunities-in-brain-and-muscle-disorders
#20
REVIEW
Vittoria Pagliarini, Piergiorgio La Rosa, Claudio Sette
Alternative splicing is a powerful mechanism that largely expands the coding potential of eukaryotic genomes. Indeed, its complex and flexible regulation is exploited by cells to adapt to various environmental conditions, through production of protein variants displaying different functions. Such flexibility, however, is accompanied by high risk of errors, and dysregulation of splicing is now recognized as an important factor in human diseases. Notably, the RNA-based nature of splicing, which involves high specificity through base pair recognition, offers a remarkable therapeutic opportunity by allowing design of tools with elevated target selectivity...
April 22, 2017: Human Genetics
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