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Journal articles on the topic 'Chronická nemoc'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

Kotolová, Hana, and Tomáš Hammer. "Chronic obstructive pulmonary disease." Praktické lékárenství 14, no. 4 (2018): 156–60. http://dx.doi.org/10.36290/lek.2018.030.

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2

Sova, Milan. "Chronic pulmonary disease and metabolic syndrome." Interní medicína pro praxi 20, no. 3 (2018): 118–20. http://dx.doi.org/10.36290/int.2018.022.

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3

Bártů, Václava. "Chronic obstructive pulmonary disease - benefit of dual bronchodilator therapy." Interní medicína pro praxi 18, no. 4 (2016): 198–202. http://dx.doi.org/10.36290/int.2016.045.

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4

Brat, Kristián, Jaromír Zatloukal, Kateřina Neumannová, et al. "Chronic obstructive pulmonary disease: diagnosis and treatment of stable phase of disease; personalized treatment approach using phenotype features of the disease." Vnitřní lékařství 67, no. 4 (2021): 230–39. http://dx.doi.org/10.36290/vnl.2021.058.

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5

Widimský, Jiří. "Pulmonary hypertension in chronic obstructive lung disease." Cor et Vasa 51, no. 7-8 (2009): 462–69. http://dx.doi.org/10.33678/cor.2009.119.

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6

Koblížek, Vladimír, and Karel Hejduk. "A targeted search for patients with chronic obstructive pulmonary disease: brief summary." Vnitřní lékařství 63, no. 11 (2017): 750–56. http://dx.doi.org/10.36290/vnl.2017.146.

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7

Adam, Zdeněk, Zdeněk Král, Jeroným Klimeš, Zdeněk Boleloucký, and Luděk Pour. "Chronic stress, mental discomfort, and depression increase the rates of infectious, autoimmune as well as malignant diseases." Vnitřní lékařství 66, no. 1 (2020): 34–38. http://dx.doi.org/10.36290/vnl.2020.006.

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8

Koblížek, Vladimír, Jaromír Zatloukal, Jan Chlumský, and Karel Hejduk. "An 2018 update of personalised Czech COPD guidelines; a country specificconsensus of The Czech Pneumological and Phthiseological Society." Medicína pro praxi 15, no. 3 (2018): 127–33. http://dx.doi.org/10.36290/med.2018.027.

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9

Nenci, Arianna, Christoph Becker, Andy Wullaert, et al. "Epithelial NEMO links innate immunity to chronic intestinal inflammation." Nature 446, no. 7135 (2007): 557–61. http://dx.doi.org/10.1038/nature05698.

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10

Beraza, Naiara, Yann Malato, Leif E. Sander, et al. "Hepatocyte-specific NEMO deletion promotes NK/NKT cell– and TRAIL-dependent liver damage." Journal of Experimental Medicine 206, no. 8 (2009): 1727–37. http://dx.doi.org/10.1084/jem.20082152.

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Nuclear factor κB (NF-κB) is one of the main transcription factors involved in regulating apoptosis, inflammation, chronic liver disease, and cancer progression. The IKK complex mediates NF-κB activation and deletion of its regulatory subunit NEMO in hepatocytes (NEMOΔhepa) triggers chronic inflammation and spontaneous hepatocellular carcinoma development. We show that NEMOΔhepa mice were resistant to Fas-mediated apoptosis but hypersensitive to tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) as the result of a strong up-regulation of its receptor DR5 on hepatocytes. Additional

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11

Lang, Otto, Helena R. Balon, Renata Píchová, Hana Křížová, and Ivana Kuníková. "Lung tissue density measured by low-dose CT during pulmonary perfusion SPECT/CT as a tool for differentiation pulmonary embolism from chronic obstructive pulmonary disease - A pilot study." Cor et Vasa 55, no. 6 (2013): e492-e496. http://dx.doi.org/10.1016/j.crvasa.2013.10.002.

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12

Cubero, F. J., A. Singh, E. Borkham-Kamphorst та ін. "TNFR1 determines progression of chronic liver injury in the IKKγ/Nemo genetic model". Cell Death & Differentiation 20, № 11 (2013): 1580–92. http://dx.doi.org/10.1038/cdd.2013.112.

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13

Hsu, Amy P., Christa S. Zerbe, Ladan Foruraghi, et al. "IKBKG (NEMO) 5′ Untranslated Splice Mutations Lead to Severe, Chronic Disseminated Mycobacterial Infections." Clinical Infectious Diseases 67, no. 3 (2018): 456–59. http://dx.doi.org/10.1093/cid/ciy186.

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14

Neesse, Albrecht, and Volker Ellenrieder. "NEMO—CXCL12/CXCR4 axis: a novel vantage point for antifibrotic therapies in chronic pancreatitis?" Gut 66, no. 2 (2016): 211–12. http://dx.doi.org/10.1136/gutjnl-2016-312874.

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15

Dolgikh, M. A., M. A. Bolkov, I. A. Tuzankina, N. G. Sarkisyan, and N. A. Hovsepyan. "Oral manifestations of primary immunodeficiencies." Bulletin of Siberian Medicine 18, no. 3 (2019): 144–54. http://dx.doi.org/10.20538/1682-0363-2019-3-144-154.

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To understand the current state of the issue of dental manifestations of primary immunodeficiencies, foreign literature on the problem has been analyzed. The article describes the dental manifestations of many primary immunodeficiencies, which can be both secondary and major symptoms. The article presents the data on the following syndromes: severe combined immunodeficiency, hyper IgE, Wiskott – Aldrich, DiGeorge, deficiency of STIM1 and ORAI1, NEMO deficiency and IκBα deficiency, common variable immunodeficiency, X-linked agammaglobulinemia, hyper IgM, selective IgA deficiency, autoimmune lym

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16

Yanhua, Lan, Xie Zhijian, and Wang Yu. "NEMO‐binding domain peptide ameliorates inflammatory bone destruction in a Staphylococcus aureus induced chronic osteomyelitis model." Clinical Oral Implants Research 30, S19 (2019): 63. http://dx.doi.org/10.1111/clr.25_13509.

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17

ARORA, PRADEEP, ANNAMARIA T. KAUSZ, GREGORIO T. OBRADOR, et al. "Hospital Utilization among Chronic Dialysis Patients." Journal of the American Society of Nephrology 11, no. 4 (2000): 740–46. http://dx.doi.org/10.1681/asn.v114740.

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Abstract. Factors driving inpatient and outpatient utilization were studied among patients who began dialysis for chronic renal failure at the New England Medical Center (NEMC) between 1992 and 1997. Clinical, laboratory, and hospital resource utilization data were obtained from patient records and electronic databases. There were 2.2 hospitalizations and 14.8 hospital days per patient year at risk (PYAR). The number of hospitalizations and hospital days per PYAR were higher in the first 3 mo of initiating dialysis (4.3 and 28.3, respectively) compared to after 3 mo (1.9 and 12.9, respectively

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18

Mohs, Antje, Nadine Kuttkat, Tobias Otto, Sameh A. Youssef, Alain De Bruin, and Christian Trautwein. "MyD88-dependent signaling in non-parenchymal cells promotes liver carcinogenesis." Carcinogenesis 41, no. 2 (2019): 171–81. http://dx.doi.org/10.1093/carcin/bgy173.

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Abstract In Western countries, a rising incidence of obesity and type 2 diabetes correlates with an increase of non-alcoholic steatohepatitis (NASH)—a major risk factor for liver cirrhosis and hepatocellular carcinoma (HCC). NASH is associated with chronic liver injury, triggering hepatocyte death and enhanced translocation of intestinal bacteria, leading to persistent liver inflammation through activation of Toll-like receptors and their adapter protein myeloid differentiation factor 88 (MyD88). Therefore, we investigated the role of MyD88 during progression from NASH to HCC using a mouse mod

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19

Davé, Shaival H., Jeremy S. Tilstra, Katsuyoshi Matsuoka та ін. "Amelioration of Chronic Murine Colitis by Peptide-Mediated Transduction of the IκB Kinase Inhibitor NEMO Binding Domain Peptide". Journal of Immunology 179, № 11 (2007): 7852–59. http://dx.doi.org/10.4049/jimmunol.179.11.7852.

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20

Kondylis, V., H. Ehlken та M. Pasparakis. "O95 NF-κB-DEPENDENT AND INDEPENDENT ROLES OF NEMO (IKKg) IN THE DEVELOPMENT OF CHRONIC LIVER INFLAMMATION AND HCC". Journal of Hepatology 60, № 1 (2014): S39. http://dx.doi.org/10.1016/s0168-8278(14)60097-0.

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21

Vlantis, Katerina, Andy Wullaert, Apostolos Polykratis та ін. "NEMO Prevents RIP Kinase 1-Mediated Epithelial Cell Death and Chronic Intestinal Inflammation by NF-κB-Dependent and -Independent Functions". Immunity 44, № 3 (2016): 553–67. http://dx.doi.org/10.1016/j.immuni.2016.02.020.

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22

Shiraki, Mayuka, Saori Kadowaki, Tomonori Kadowaki, Norio Kawamoto, and Hidenori Ohnishi. "Primary Immunodeficiency Disease Mimicking Pediatric Bechet’s Disease." Children 8, no. 2 (2021): 75. http://dx.doi.org/10.3390/children8020075.

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Behcet’s disease (BD) is a chronic inflammatory disease with multisystemic involvement. Its etiology is considered to involve complex environmental and genetic factors. Several susceptibility genes for BD, such as human leukocyte antigen (HLA)-A26, IL23R-IL12RB2, IL10 and ERAP1, in addition to the well-studied HLA-B51, were mainly identified by genome-wide association studies. A heterozygous mutation in TNFAIP3, which leads to A20 haploinsufficiency, was found to cause an early-onset autoinflammatory disease resembling BD in 2016. Several monogenic diseases associated with primary immunodefici

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23

Lutzny, Gloria, Thomas Kocher, Martina Rudelius та ін. "Protein Kinase C-β Dependent Activation of NF-κB in Stromal Cells Is Indispensable for the Survival of Chronic Lymphocytic Leukemia B-Cells in Vivo". Blood 120, № 21 (2012): 314. http://dx.doi.org/10.1182/blood.v120.21.314.314.

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Abstract Abstract 314 Defects in the apoptosis program are a hallmark of chronic lymphocytic leukemia (CLL), characterized by high expression levels of bcl2 and Mcl1. Notably, this de-regulation of anti-apoptotic proteins is not sufficient to maintain long-term survival of CLL cells, which remain highly dependent on pro-survival factors provided by the leukemia-microenvironment. Bone marrow stromal cells (BMSCs) play an important role for microenvironment mediated survival of CLL cells, based on the provision of soluble and membrane-bound factors. The stroma-CLL interactions not only protect C

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24

Cubero, F. J., G. Zhao, Y. A. Nevzorova, et al. "1037 DISRUPTION OF THE INTERPLAY BETWEEN IKKg/NEMO AND Jnk1 EXACERBATES CHRONIC LIVER DISEASE AND HCC THROUGH ALTERATION OF THE MAPK PATHWAY." Journal of Hepatology 58 (April 2013): S426. http://dx.doi.org/10.1016/s0168-8278(13)61038-7.

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25

Haeberle, Helene A., Antonella Casola, Zoran Gatalica та ін. "IκB Kinase Is a Critical Regulator of Chemokine Expression and Lung Inflammation in Respiratory Syncytial Virus Infection". Journal of Virology 78, № 5 (2004): 2232–41. http://dx.doi.org/10.1128/jvi.78.5.2232-2241.2004.

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ABSTRACT Respiratory syncytial virus (RSV) is the major etiologic agent of severe epidemic lower respiratory tract infections in infancy. Airway mucosal inflammation plays a critical role in the pathogenesis of RSV disease in both natural and experimental infections. RSV is among the most potent biological stimuli that induce the expression of inflammatory genes, including those encoding chemokines, but the mechanism(s) that controls virus-mediated airway inflammation in vivo has not been fully elucidated. Herein we show that the inoculation of BALB/c mice with RSV results in rapid activation

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26

Shamilov, Rambon, Olga Vinogradova, and Brian J. Aneskievich. "The Anti-Inflammatory Protein TNIP1 Is Intrinsically Disordered with Structural Flexibility Contributed by Its AHD1-UBAN Domain." Biomolecules 10, no. 11 (2020): 1531. http://dx.doi.org/10.3390/biom10111531.

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TNFAIP3 interacting protein 1 (TNIP1) interacts with numerous non-related cellular, viral, and bacterial proteins. TNIP1 is also linked with multiple chronic inflammatory disorders on the gene and protein levels, through numerous single-nucleotide polymorphisms and reduced protein amounts. Despite the importance of TNIP1 function, there is limited investigation as to how its conformation may impact its apparent multiple roles. Hub proteins like TNIP1 are often intrinsically disordered proteins. Our initial in silico assessments suggested TNIP1 is natively unstructured, featuring numerous poten

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27

Agarwal, Nitin, Chae Hwa Kim, Kranthi Kunkalla, et al. "Smoothened (SMO) Is an Adaptor Protein That Recruits TRAF6 and Phospholipase C Gamma 2 (PLCg2) to Enhance the Activation of NF-Kb Signaling Pathway." Blood 126, no. 23 (2015): 3907. http://dx.doi.org/10.1182/blood.v126.23.3907.3907.

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Abstract Background: Constitutive activation of NF-κB signaling is a hallmark of DLBCL. Activation of NF-κB is a multifactorial process resulting from oncogenic mutations (CARD11, MYD88…), chromosomal abnormalities, chronic activation of B-cell receptor signaling (BCR) as well as stimuli from the microenvironment. Chronic activation of BCR is not only the result of gene mutations (e.g.CD79B) but also is the result of stimuli generated from the lymphoma microenvironment. We previously found that smoothened (SMO), transducer of hedgehog (Hh) signaling, enhanced NF-κB activation in lymphoma cells

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28

Danilov, Alexey V., Olga V. Danilova, Andreas K. Klein, and Brigitte T. Huber. "Apoptosis in Response to Inhibition of Dipeptidyl Peptidase 2 (DPP2) Defines Low Risk Chronic Lymphocytic Leukemia (CLL)." Blood 110, no. 11 (2007): 3094. http://dx.doi.org/10.1182/blood.v110.11.3094.3094.

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Abstract Maintenance of the G0 state is a key to survival of CLL B-cells. Heterogeneity of prognosis suggests that CLL is not a uniform disease. Molecules expressed in CLL with unfavorable prognosis, such as ZAP-70, Lyn, CD38 and others, provide stimuli which, coupled with B-cell receptor signaling, may alter cell cycle progression and delay apoptosis. We studied mechanisms of apoptosis in CLL B-cells via inhibition of Dipeptidyl Peptidase 2 (DPP2). DPP2 is a serine protease cloned in our lab, which is involved in the maintenance of the G0 (quiescent) state. Inhibition of DPP2 triggers apoptos

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29

Mulligan, Evan A., Jill E. Hunter, Arabella EG Baird та ін. "Relationships Between Aberrant Activity of the NF-κB Subunits and Outcome In Chronic Lymphocytic Leukemia: The Dual Role of DNA Damage Sensor Enzymes". Blood 116, № 21 (2010): 3588. http://dx.doi.org/10.1182/blood.v116.21.3588.3588.

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Abstract Abstract 3588 Poor prognosis patients with chronic lymphocytic leukaemia (CLL) can be identified by cytogenetic abnormalities such as del(17p), and del(11q) and corresponding mutations in TP53 and ATM (ataxia telangiectasia mutated kinase) respectively, which are associated with chemoresistance by virtue of defects in the DNA damage response pathway. We have demonstrated that overexpression of DNA-dependent protein kinase (DNA-PK), which mediates non-homologous end joining, is also associated with poor prognosis CLL1. Recent data show that constitutive activation of the p65 subunit of

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30

Haapaniemi, Emma M., Meri Kaustio, Helka Nurkkala, et al. "Dominant NFKB1 Mutations Cause Antibody Deficiency and Autoinflammatory Episodes." Blood 126, no. 23 (2015): 206. http://dx.doi.org/10.1182/blood.v126.23.206.206.

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Abstract The NFkB signaling pathway is a master regulator of the immune response. Recently, dominant mutations in NFKB2 have shown to cause antibody deficiency with adrenal insufficiency. We investigated two families with antibody deficiency and autoinflammatory features, with onset in teenage years and early adulthood (Fig. 1 and Table 1). In family 1, all patients available to study presented with respiratory tract infections and B cell dysfunction marked by hypogammaglobulinemia, poor antibody response to vaccines, or low switched memory B cell counts. Several experienced recurrent episodes

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31

Tse, William T., Jessica Ward, Jennifer Schneiderman, et al. "Robust Immune Reconstitution in Children with Severe Primary Immunodeficiency after Reduced-Intensity Conditioning Hematopoietic Stem Cell Transplantation." Blood 124, no. 21 (2014): 3923. http://dx.doi.org/10.1182/blood.v124.21.3923.3923.

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Abstract Hematopoietic stem cell transplantation (HSCT) is a potentially curative therapy for severe primary immunodeficiency diseases (PID), but it is still unclear what is the optimal transplant approach. To help answer this question, the stem cell transplant team at Ann & Robert H. Lurie Children's Hospital of Chicago (formerly Children's Memorial Hospital) evaluated the risks and benefits of a reduced-intensity conditioning (RIC) transplant approach for treatment of severe PID. Between 2000 and 2013, 42 children with severe PID were treated with allogeneic HSCT following a RIC regimen

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32

Wang, Yuan, Lei Cui, Guifang Yang та ін. "Hepatitis B e Antigen Inhibits NF-κB Activity by Interrupting K63-Linked Ubiquitination of NEMO". Journal of Virology 93, № 2 (2018). http://dx.doi.org/10.1128/jvi.00667-18.

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ABSTRACTViruses have adopted diverse strategies to suppress antiviral responses. Hepatitis B virus (HBV), a virus that is prevalent worldwide, manipulates the host’s innate immune system to evade scavenging. It is reported that the hepatitis B e antigen (HBeAg) can interfere with NF-κB activity, which then leads to high viral loads, while HBV with the G1896A mutation remains infectious without the production of HBeAg but can induce more severe proinflammatory response and liver damage. The aim of current work was to study the molecular mechanism by which HBeAg suppresses interleukin-1β (IL-1β)

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33

Wang, Hai-Yan, Hai-Mei Zhao, Yao Wang, et al. "Sishen Wan® Ameliorated Trinitrobenzene-Sulfonic-Acid-Induced Chronic Colitis via NEMO/NLK Signaling Pathway." Frontiers in Pharmacology 10 (March 6, 2019). http://dx.doi.org/10.3389/fphar.2019.00170.

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34

"Best Paper Selection." Yearbook of Medical Informatics 29, no. 01 (2020): 158. http://dx.doi.org/10.1055/s-0040-1702017.

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Hendriks MP, Verbeek XAAM, van Vegchel T, van der Sangen MJC, Strobbe LJA, Merkus JWS, Zonderland HM, Smorenburg CH, Jager A, Siesling S. Transformation of the National Breast Cancer Guideline into data-driven clinical decision trees. JCO Clin Cancer Inform 2019 May;3:1-14 https://ascopubs.org/doi/full/10.1200/CCI.18.00150 Kamišalić A, Riaño D, Kert S, Welzer T, Nemec Zlatolas L. Multi-level medical knowledge formalization to support medical practice for chronic diseases. Data & Knowledge Engineering 2019; 119:36–57 https://www.sciencedirect.com/science/article/abs/pii/S0169023X16303937 Kh

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35

Lan, Yanhua, Huizhi Xie, Yang Shi, et al. "NEMO‑binding domain peptide ameliorates inflammatory bone destruction in a Staphylococcus�aureus‑induced chronic osteomyelitis model." Molecular Medicine Reports, February 20, 2019. http://dx.doi.org/10.3892/mmr.2019.9975.

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36

Xu, Chang-Peng, Ya Chen, Hong-Tao Sun, et al. "Efficacy of NEMO-binding domain peptide used to treat experimental osteomyelitis caused by methicillin-resistant Staphylococcus aureus: an in-vivo study." Antimicrobial Resistance & Infection Control 8, no. 1 (2019). http://dx.doi.org/10.1186/s13756-019-0627-y.

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Abstract Purpose Treatment of chronic osteomyelitis (bone infection) remains a clinical challenge. Our previous study had demonstrated that NEMO-binding domain (NBD) peptide effectively ameliorates the inhibition of osteoblast differentiation by TNF-α in vitro. In this work, NBD peptide was evaluated in vivo for treating chronic osteomyelitis induced by methicillin-resistant Staphylococcus aureus (MRSA) in a rabbit model. Methods Tibial osteomyelitis was induced in 50 New Zealand white rabbits by tibial canal inoculation of MRSA strain. After 3 weeks, 45 rabbits with osteomyelitis were randoml

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37

Paccione, Charles Ethan, Lien My Diep, Audun Stubhaug, and Henrik Børsting Jacobsen. "Motivational nondirective resonance breathing versus transcutaneous vagus nerve stimulation in the treatment of fibromyalgia: study protocol for a randomized controlled trial." Trials 21, no. 1 (2020). http://dx.doi.org/10.1186/s13063-020-04703-6.

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Abstract Background Chronic widespread pain (CWP), including fibromyalgia (FM), affects one in every ten adults and is one of the leading causes of sick leave and emotional distress. Due to an unclear etiology and a complex pathophysiology, FM is a condition with few, if any, effective and safe treatments. However, current research within the field of vagal nerve innervation suggests psychophysiological and electrical means by which FM may be treated. This study will investigate the efficacy of two different noninvasive vagal nerve stimulation techniques for the treatment of FM. Methods The st

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