32459
2022
eng
1849-1853
12
24
article
1
--
--
--
Therapeutic effects of lipid lowering medications on myocardial blood flow, inflammation, and sympathetic nerve activity using nuclear techniques
Purpose of Review
Statins are routinely applied in patients with coronary artery disease, as they allow significantly to reduce blood cholesterol levels. Although those drugs are endorsed by current guidelines and prescribed routinely, a substantial portion of patients are still statin-intolerant and image-piloted strategies may then be helpful to identify patients that need further intensified treatment, e.g., to initiate treatment with proprotein convertase subtilisin / kexin type 9 inhibitors (PCSK9i). In addition, it has also been advocated that statins exhibit nonlipid, cardio-protective effects including improved cardiac nerve integrity, blood flow, and anti-inflammatory effects in congestive heart failure (HF) patients.
Recent Findings
In subjects after myocardial infarction treated with statins, \(^{123}\)I-metaiodobenzylguanidine (MIBG) scintigraphy has already revealed enhanced cardiac nerve function relative to patients without statins. In addition, all of those aforementioned statin-targeted pathways in HF can be visualized and monitored using dedicated cardiac radiotracers, e.g., \(^{123}\)I-MIBG or \(^{18}\)F-AF78 (for cardiac nerve function), \(^{18}\)F-flurpiridaz (to determine coronary flow) or \(^{68}\)Ga-PentixaFor (to detect inflammation).
Summary
Statins exhibit various cardio-beneficial effects, including improvement of cardiac nerve function, blood flow, and reduction of inflammation, which can all be imaged using dedicated nuclear cardiac radiotracers. This may allow for in vivo monitoring of statin-induced cardioprotection beyond lipid profiling in HF patients.
Current Cardiology Reports
10.1007/s11886-022-01792-4
urn:nbn:de:bvb:20-opus-324599
@articleHiguchi.2022, author = Higuchi, Takahiro and Serfling, Sebastian E. and Rowe, Steven P. and Werner, Rudolf A., year = 2022, title = Therapeutic Effects of Lipid Lowering Medications on Myocardial Blood Flow, Inflammation, and Sympathetic Nerve Activity Using Nuclear Techniques, pages = 1849–1853, volume = 24, number = 12, journal = Current cardiology reports, doi = 10.1007/s11886-022-01792-4
md5:ef79acbf8cc319618984a6199c746f03
2023-08-12T10:37:25+00:00
/tmp/phpKtPjJc
bibtex
64d760e520e2f0.54800151
Current Cardiology Reports (2022) 24:12, 1849-1853. DOI: 10.1007/s11886-022-01792-4
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Takahiro Higuchi
Sebastian E. Serfling
Steven P. Rowe
Rudolf A. Werner
eng
uncontrolled
sympathetic nervous system
eng
uncontrolled
cardiac nerve
eng
uncontrolled
MIBG
eng
uncontrolled
inflammation
eng
uncontrolled
blood flow
eng
uncontrolled
statin
Medizin und Gesundheit
open_access
Klinik und Poliklinik für Nuklearmedizin
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/32459/s11886-022-01792-4.pdf
30402
2023
eng
2
14
article
1
--
2023-02-14
--
Development of neovasculature in axially vascularized calcium phosphate cement scaffolds
Augmenting the vascular supply to generate new tissues, a crucial aspect in regenerative medicine, has been challenging. Recently, our group showed that calcium phosphate can induce the formation of a functional neo-angiosome without the need for microsurgical arterial anastomosis. This was a preclinical proof of concept for biomaterial-induced luminal sprouting of large-diameter vessels. In this study, we investigated if sprouting was a general response to surgical injury or placement of an inorganic construct around the vessel. Cylindrical biocement scaffolds of differing chemistries were placed around the femoral vein. A contrast agent was used to visualize vessel ingrowth into the scaffolds. Cell populations in the scaffold were mapped using immunohistochemistry. Calcium phosphate scaffolds induced 2.7–3 times greater volume of blood vessels than calcium sulphate or magnesium phosphate scaffolds. Macrophage and vSMC populations were identified that changed spatially and temporally within the scaffold during implantation. NLRP3 inflammasome activation peaked at weeks 2 and 4 and then declined; however, IL-1β expression was sustained over the course of the experiment. IL-8, a promoter of angiogenesis, was also detected, and together, these responses suggest a role of sterile inflammation. Unexpectedly, the effect was distinct from an injury response as a result of surgical placement and also was not simply a foreign body reaction as a result of placing a rigid bioceramic next to a vein, since, while the materials tested had similar microstructures, only the calcium phosphates tested elicited an angiogenic response. This finding then reveals a potential path towards a new strategy for creating better pro-regenerative biomaterials.
Journal of Functional Biomaterials
2079-4983
10.3390/jfb14020105
urn:nbn:de:bvb:20-opus-304026
2023-03-14T05:53:15+00:00
sword
swordwue
attachment; filename=deposit.zip
f2adbbca8a571b62e8e40f3fa0c4e3c2
Journal of Functional Biomaterials (2023) 14:2, 105. https://doi.org/10.3390/jfb14020105
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Yassine Ouhaddi
Baptiste Charbonnier
Juliette Porge
Yu-Ling Zhang
Isadora Garcia
Uwe Gbureck
Liam Grover
Mirko Gilardino
Edward Harvey
Nicholas Makhoul
Jake Barralet
eng
uncontrolled
angiogenesis
eng
uncontrolled
axial vascularization
eng
uncontrolled
bioceramic
eng
uncontrolled
bioinorganic
eng
uncontrolled
calcium phosphate
eng
uncontrolled
NLRP3
eng
uncontrolled
inflammation
Medizin und Gesundheit
open_access
Abteilung für Funktionswerkstoffe der Medizin und der Zahnheilkunde
Import
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/30402/jfb-14-00105.pdf
34957
2024
eng
doctoralthesis
1
2024-02-19
--
2024-02-06
Dynamics of cardiac neutrophil diversity in murine myocardial infarction
Dynamik der Diversität kardialer neutrophiler Granulozyten im Mausmodell Herzinfarkt
After myocardial infarction, an inflammatory response is induced characterized by a sterile inflammation, followed by a reparative phase in order to induce cardiac healing. Neutrophils are the first immune cells that enter the ischemic tissue. Neutrophils have various functions in the ischemic heart, such as phagocytosis, production of reactive oxygen species or release of granule components. These functions can not only directly damage cardiac tissue, but are also necessary for initiating reparative effects in post-ischemic healing, indicating a dual role of neutrophils in cardiac healing after infarction.
In recent years, evidence has been growing that neutrophils show phenotypic and functional differences in distinct homeostatic and pathogenic settings.
Preliminary data of my working group using single-cell RNA-sequencing revealed the time- dependent heterogeneity of neutrophils, with different populations showing distinct gene expression profiles in ischemic hearts of mice, including the time-dependent appearance of a SiglecFhigh neutrophil population. To better understand the dynamics of neutrophil heterogeneity in the ischemic heart, my work aimed to validate previous findings at the protein level, as well as to investigate whether the distinct neutrophil populations show functional differences. Furthermore, in vivo depletion experiments were performed in order to modulate circulating neutrophil levels.
Hearts, blood, bone marrow and spleens were processed and analyzed from mice after 1 day and 3 days after the onset of cardiac ischemia and analyzed using flow cytometry.
Results showed that the majority of cardiac neutrophils isolated at day 3 after myocardial infarction were SiglecFhigh, whereas nearly no SiglecFhigh neutrophils could be isolated from ischemic hearts at day 1 after myocardial infarction.
No SiglecFhigh neutrophils could be found in the blood, spleen and bone marrow either after 1 day or 3 days after myocardial infarction, indicating that the SiglecFhigh state of neutrophils is unique to the ischemic cardiac tissue.
When I compared SiglecFhigh and SiglecFlow neutrophils regarding their phagocytosis activity and ROS production, SiglecFhigh neutrophils showed a higher phagocytosis ability than their SiglecFlow counterparts, as well as higher ROS production capacity.
In vivo depletion experiments could not achieve successful and efficient depletion of cardiac neutrophils either 1 day or 3 days after myocardial infarction, but led to a shift of a higher percentage of SiglecFhigh expressing neutrophils in the depletion group. Bone marrow neutrophil levels only showed partial depletion at day 3 after MI. Regarding blood neutrophils, depletion efficiently reduced circulating neutrophils at both time points, 1 and 3 days after MI. To summarize, this work showed the time-dependent presence of different neutrophil states in the ischemic heart. The main population of neutrophils isolated 3 days after MI showed a high expression of SiglecF, a unique state that could not be detected at different time points or other organs. These SiglecFhigh neutrophils showed functional differences regarding their phagocytosis ability and ROS production. Further investigation is needed to reveal what role these SiglecFhigh neutrophils could play within the ischemic heart.
To better target neutrophil depletion in vivo, more efficient or different anti-neutrophil strategies are needed.
Nach Myokardinfarkt kommt es zu einer Entzündungsantwort, die durch eine sterile Entzündung und nachfolgende reparative Phase gekennzeichnet ist, um eine kardiale Heilung zu initiieren. Neutrophile Granulozyten sind die ersten Immunzellen, die das ischämische Gewebe infiltrieren. Neutrophile Granulozyten haben verschiedene Funktionen im ischämischen Herz, wie beispielsweise Phagozytose, Produktion reaktiver Oxigenspezies oder Entleerung von Granulae. Diese Funktionen können nicht nur das kardiale Gewebe direkt
schädigen, sondern sind auch notwendig, um die reparative Phase zu initiieren, was auf eine duale Rolle der neutrophilen Granulozyten hinsichtlich kardialer Heilung hinweist.
Evidenz der letzten Jahre zeigt, dass neutrophile Granulzyten phänotypische und funktionelle Unterschiede zeigen, sowohl in Homöostase als auch in verschiedenen pathologischen Umgebungen.
Vorangehende Ergebnisse meiner Arbeitsgruppe von Einzelzellsequenzierungen zeigten die
zeitabhängige Heterogenität neutrophiler Granulozyten, die in verschiedenen Populationen
und mit unterschiedlichen Expressions-Mustern in ischämischen Mäuseherzen auftauchten.
Unter anderem zeigte sich das zeitabhängige Auftauchen einer SiglecFhigh NeutrophilenPopulation. Um die Dynamik der Neutrophilen-Heterogenität im ischämischen Herz besser zu verstehen, war es das Ziel meiner Arbeit, vorangehende Ergebnisse auf Proteinbasis zu
bestätigen, und die verschiedenen Neutrophilen-Populationen hinsichtlich möglicher funktioneller Unterschiede zu untersuchen. Zusätzlich wurden in-vivo Depletionsversuche durchgeführt, um das Vorkommen zirkulierender neutrophiler Granulozyten zu modulieren
und mögliche Änderungen hinsichtlich des Vorkommens neutrophiler Granulozyten im Herzen zu untersuchen.
Herz, Blut, Knochenmark und Milz von Mäusen, die einen 1 oder 3 Tage alten Myokardinfarkt hatten, wurden prozessiert und mittels Durchflusszytometrie analysiert. Es zeigte sich, dass der
überwiegende Anteil kardialer neutrophiler Granulozyten die an Tag 3 nach Myokardinfarkt isoliert wurden SiglecFhigh waren, wohingegen quasi keine SiglecFhigh neutrophile Granulozyten an Tag 1 nach Myokardinfarkt gefunden werden konnten.
Es konnten keine SiglecFhigh neutrophile Granulozyten in Blut, Knochenmark oder Milz gefunden werden, weder 1 noch 3 Tage nach Myokardinfarkt, was darauf hinweist, dass der SiglecFhigh Status neutrophiler Granulozyten spezifisch für ischämisches Herzgewebe ist.
Im Vergleich von SiglecFhigh und SiglecFlow neutrophilen Granulozyten hinsichtlich der Phagozytose und Produktion reaktiver Oxigenspezies, zeigten SiglecFhigh neutrophile Granulozyten sowohl eine höhere Phagozytose als auch eine höhere Produktion reaktiver Oxigenspezies.
In vivo Depletionsversuche konnten keine komplette und effiziente Depletion kardialer neutrophiler Granulozyten sowohl an Tag 1 als auch an Tag 3 nach Myokardinfarkt erzielen, führten jedoch zu einem höheren Prozentsatz an SiglecFhigh neutrophilen Granulozyten in der
Depletionsgruppe. Neutrophile Granulozyten im Knochenmark konnten nur an Tag 3 teilweise depletiert werden. Mit Blick auf neutrophile Granulozyten im Blut führte die Depletion zu einer effizienten Reduktion zirkulierender neutrophiler Granulozyten sowohl an Tag 1 als auch an Tag 3 nach Myokardinfarkt.
Zusammenfassend zeigt diese Arbeit die zeitabhängige Präsenz verschiedener neutrophiler Granulozyten im ischämischen Herzen. Der größte Anteil neutrophiler Granulozyten, die an Tag 3 isoliert wurden, zeigten eine hohe Expression von SiglecF, einem spezifischen und
einzigartigem Phänotypus, der weder zu anderen Zeitpunkten noch in anderen Organen gefunden wurde. Diese SiglecFhigh neutrophilen Granulozyten zeigten funktionelle Unterschiede hinsichtlich ihrer Phagozytose und Produktion reaktiver Oxigenspezies. Weitere Untersuchungen sind notwendig um aufzuzeigen, welche Rolle diese SiglecFhigh neutrophilen Granulozyten im ischämischen Herzen spielen könnten.Um eine effizientere Depletion neutrophiler Granulozyten in vivo zu erzielen, sind andere oder effizientere Anti-Neutrophilen Strategien notwendig.
urn:nbn:de:bvb:20-opus-349576
10.25972/OPUS-34957
publish
true
true
Deutsches Urheberrecht mit Print on Demand
Laura Krampert
deu
swd
Neutrophiler Granulozyt
eng
uncontrolled
neutrophils
deu
swd
Entzündung
deu
swd
Herzinfarkt
eng
uncontrolled
inflammation
eng
uncontrolled
myocardial infarction
Medizin und Gesundheit
open_access
Graduate School of Life Sciences
Universität Würzburg
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/34957/Krampert_Laura_Dissertation.pdf
31361
2023
eng
9
24
article
1
--
2023-04-25
--
Local inflammatory mediators involved in neuropathic pain
Polyneuropathy (PNP) is a term to describe diseases of the peripheral nervous system, 50% of which present with neuropathic pain. In some types of PNP, pain is restricted to the skin distally in the leg, suggesting a local regulatory process leading to pain. In this study, we proposed a pro-inflammatory pathway mediated by NF-κB that might be involved in the development of pain in patients with painful PNP. To test this hypothesis, we have collected nerve and skin samples from patients with different etiologies and levels of pain. We performed RT-qPCR to analyze the gene expression of the proposed inflammatory pathway components in sural nerve and in distal and proximal skin samples. In sural nerve, we showed a correlation of TLR4 and TNFα to neuropathic pain, and an upregulation of TNFα in patients with severe pain. Patients with an inflammatory PNP also presented a lower expression of TRPV1 and SIRT1. In distal skin, we found a reduced expression of TLR4 and miR-146-5p, in comparison to proximal skin. Our findings thus support our hypothesis of local inflammatory processes involved in pain in PNP, and further show disturbed anti-inflammatory pathways involving TRPV1 and SIRT1 in inflammatory PNP.
International Journal of Molecular Sciences
1422-0067
10.3390/ijms24097814
urn:nbn:de:bvb:20-opus-313613
2023-05-05T11:06:41+00:00
sword
swordwue
attachment; filename=deposit.zip
5194e42384a5f042823ce8ee93d72dc4
International Journal of Molecular Sciences (2023) 24:9, 7814. https://doi.org/10.3390/ijms24097814
764860
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Patricia García-Fernández
Colette Reinhold
Nurcan Üçeyler
Claudia Sommer
eng
uncontrolled
polyneuropathy
eng
uncontrolled
pain
eng
uncontrolled
inflammation
eng
uncontrolled
NF-κB
eng
uncontrolled
TNFα
Medizin und Gesundheit
open_access
Neurologische Klinik und Poliklinik
OpenAIRE
Import
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/31361/ijms-24-07814.pdf
31105
2023
eng
5
24
article
1
--
2023-03-03
--
Imbalanced inflammatory responses in preterm and term cord blood monocytes and expansion of the CD14\(^+\)CD16\(^+\) subset upon toll-like receptor stimulation
Developmentally regulated features of innate immunity are thought to place preterm and term infants at risk of infection and inflammation-related morbidity. Underlying mechanisms are incompletely understood. Differences in monocyte function including toll-like receptor (TLR) expression and signaling have been discussed. Some studies point to generally impaired TLR signaling, others to differences in individual pathways. In the present study, we assessed mRNA and protein expression of pro- and anti-inflammatory cytokines in preterm and term cord blood (CB) monocytes compared with adult controls stimulated ex vivo with Pam3CSK4, zymosan, polyinosinic:polycytidylic acid, lipopolysaccharide, flagellin, and CpG oligonucleotide, which activate the TLR1/2, TLR2/6, TLR3, TLR4, TLR5, and TLR9 pathways, respectively. In parallel, frequencies of monocyte subsets, stimulus-driven TLR expression, and phosphorylation of TLR-associated signaling molecules were analyzed. Independent of stimulus, pro-inflammatory responses of term CB monocytes equaled adult controls. The same held true for preterm CB monocytes—except for lower IL-1β levels. In contrast, CB monocytes released lower amounts of anti-inflammatory IL-10 and IL-1ra, resulting in higher ratios of pro-inflammatory to anti-inflammatory cytokines. Phosphorylation of p65, p38, and ERK1/2 correlated with adult controls. However, stimulated CB samples stood out with higher frequencies of intermediate monocytes (CD14\(^+\)CD16\(^+\)). Both pro-inflammatory net effect and expansion of the intermediate subset were most pronounced upon stimulation with Pam3CSK4 (TLR1/2), zymosan (TR2/6), and lipopolysaccharide (TLR4). Our data demonstrate robust pro-inflammatory and yet attenuated anti-inflammatory responses in preterm and term CB monocytes, along with imbalanced cytokine ratios. Intermediate monocytes, a subset ascribed pro-inflammatory features, might participate in this inflammatory state.
International Journal of Molecular Sciences
1422-0067
10.3390/ijms24054919
urn:nbn:de:bvb:20-opus-311056
2023-04-05T12:30:48+00:00
sword
swordwue
attachment; filename=deposit.zip
fe4fd2356e5006a06ab3f6620a1cf25f
International Journal of Molecular Sciences (2023) 24:5, 4919. https://doi.org/10.3390/ijms24054919
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Kirsten Glaser
David Kern
Christian P. Speer
Nicolas Schlegel
Michael Schwab
Ulrich H. Thome
Christoph Härtel
Clyde J. Wright
eng
uncontrolled
neonatal immunology
eng
uncontrolled
inflammation
eng
uncontrolled
preterm infants
eng
uncontrolled
monocytes
eng
uncontrolled
cord blood
eng
uncontrolled
monocyte subsets
eng
uncontrolled
cytokines
eng
uncontrolled
Toll-like receptor signaling
Medizin und Gesundheit
open_access
Klinik und Poliklinik für Allgemein-, Viszeral-, Gefäß- und Kinderchirurgie (Chirurgische Klinik I)
Frauenklinik und Poliklinik
Kinderklinik und Poliklinik
Import
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/31105/ijms-24-04919.pdf
30413
2023
eng
2
11
article
1
--
2023-02-14
--
Complement 1q/tumor necrosis factor-related proteins (CTRPs): structure, receptors and signaling
Adiponectin and the other 15 members of the complement 1q (C1q)/tumor necrosis factor (TNF)-related protein (CTRP) family are secreted proteins composed of an N-terminal variable domain followed by a stalk region and a characteristic C-terminal trimerizing globular C1q (gC1q) domain originally identified in the subunits of the complement protein C1q. We performed a basic PubMed literature search for articles mentioning the various CTRPs or their receptors in the abstract or title. In this narrative review, we briefly summarize the biology of CTRPs and focus then on the structure, receptors and major signaling pathways of CTRPs. Analyses of CTRP knockout mice and CTRP transgenic mice gave overwhelming evidence for the relevance of the anti-inflammatory and insulin-sensitizing effects of CTRPs in autoimmune diseases, obesity, atherosclerosis and cardiac dysfunction. CTRPs form homo- and heterotypic trimers and oligomers which can have different activities. The receptors of some CTRPs are unknown and some receptors are redundantly targeted by several CTRPs. The way in which CTRPs activate their receptors to trigger downstream signaling pathways is largely unknown. CTRPs and their receptors are considered as promising therapeutic targets but their translational usage is still hampered by the limited knowledge of CTRP redundancy and CTRP signal transduction.
Biomedicines
2227-9059
10.3390/biomedicines11020559
urn:nbn:de:bvb:20-opus-304136
2023-03-14T05:54:24+00:00
sword
swordwue
attachment; filename=deposit.zip
d152bcf71c599da1e6b691beccdf2480
Biomedicines (2023) 11:2, 559. https://doi.org/10.3390/biomedicines11020559
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Constanze Schanbacher
Heike M. Hermanns
Kristina Lorenz
Harald Wajant
Isabell Lang
eng
uncontrolled
adiponectin
eng
uncontrolled
AMPK
eng
uncontrolled
C1q/TNF related protein (CTRP)
eng
uncontrolled
inflammation
eng
uncontrolled
metabolism
Medizin und Gesundheit
open_access
Institut für Pharmakologie und Toxikologie
Abteilung für Molekulare Innere Medizin (in der Medizinischen Klinik und Poliklinik II)
Medizinische Klinik und Poliklinik II
Import
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/30413/biomedicines-11-00559-v2.pdf
28830
2022
eng
19
23
article
1
--
2022-09-30
--
Hemorrhagic cerebral insults and secondary Takotsubo syndrome: findings in a novel in vitro model using human blood samples
Intracranial hemorrhage results in devastating forms of cerebral damage. Frequently, these results also present with cardiac dysfunction ranging from ECG changes to Takotsubo syndrome (TTS). This suggests that intracranial bleeding due to subarachnoid hemorrhage (SAH) disrupts the neuro–cardiac axis leading to neurogenic stress cardiomyopathy (NSC) of different degrees. Following this notion, SAH and secondary TTS could be directly linked, thus contributing to poor outcomes. We set out to test if blood circulation is the driver of the brain–heart axis by investigating serum samples of TTS patients. We present a novel in vitro model combining SAH and secondary TTS to mimic the effects of blood or serum, respectively, on blood–brain barrier (BBB) integrity using in vitro monolayers of an established murine model. We consistently demonstrated decreased monolayer integrity and confirmed reduced Claudin-5 and Occludin levels by RT-qPCR and Western blot and morphological reorganization of actin filaments in endothelial cells. Both tight junction proteins show a time-dependent reduction. Our findings highlight a faster and more prominent disintegration of BBB in the presence of TTS and support the importance of the bloodstream as a causal link between intracerebral bleeding and cardiac dysfunction. This may represent potential targets for future therapeutic inventions in SAH and TTS.
International Journal of Molecular Sciences
1422-0067
10.3390/ijms231911557
urn:nbn:de:bvb:20-opus-288305
2022-10-06T14:54:05+00:00
sword
swordwue
attachment; filename=deposit.zip
f59af8ade65d0d3ecf79aae32c5d996e
International Journal of Molecular Sciences (2022) 23:19, 11557. https://doi.org/10.3390/ijms231911557
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Serge C. Thal
Manuel Smetak
Kentaro Hayashi
Carola Y. Förster
eng
uncontrolled
Takotsubo syndrome
eng
uncontrolled
subarachnoid hemorrhage
eng
uncontrolled
inflammation
eng
uncontrolled
in vitro
eng
uncontrolled
blood
eng
uncontrolled
blood–brain barrier
eng
uncontrolled
human
eng
uncontrolled
patient
eng
uncontrolled
endothelial cells
Medizin und Gesundheit
open_access
Klinik und Poliklinik für Anästhesiologie (ab 2004)
Import
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/28830/ijms-23-11557.pdf
28458
2022
eng
10
23
article
1
--
2022-05-11
--
Short-chain fatty acids in Chronic Kidney Disease: focus on inflammation and oxidative stress regulation
Chronic Kidney Disease (CKD) is a debilitating disease associated with several secondary complications that increase comorbidity and mortality. In patients with CKD, there is a significant qualitative and quantitative alteration in the gut microbiota, which, consequently, also leads to reduced production of beneficial bacterial metabolites, such as short-chain fatty acids. Evidence supports the beneficial effects of short-chain fatty acids in modulating inflammation and oxidative stress, which are implicated in CKD pathogenesis and progression. Therefore, this review will provide an overview of the current knowledge, based on pre-clinical and clinical evidence, on the effect of SCFAs on CKD-associated inflammation and oxidative stress.
International Journal of Molecular Sciences
1422-0067
10.3390/ijms23105354
urn:nbn:de:bvb:20-opus-284587
2022-09-04T02:31:44+00:00
sword
swordwue
attachment; filename=deposit.zip
f44c6848e3c94496fe93c7e03357eb51
International Journal of Molecular Sciences (2022) 23:10, 5354. https://doi.org/10.3390/ijms23105354
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Giorgia Magliocca
Pasquale Mone
Biagio Raffaele Di Iorio
August Heidland
Stefania Marzocco
eng
uncontrolled
chronic kidney disease
eng
uncontrolled
short-chain fatty acids
eng
uncontrolled
oxidative stress
eng
uncontrolled
inflammation
eng
uncontrolled
uremic toxins
Medizin und Gesundheit
open_access
Medizinische Klinik und Poliklinik I
Import
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/28458/ijms-23-05354.pdf
31818
2023
eng
S38
S49
47
article
1
--
--
--
Overview of oxidative stress and the role of micronutrients in critical illness
Inflammation and oxidative stress represent physiological response mechanisms to different types of stimuli and injury during critical illness. Its proper regulation is fundamental to cellular and organismal survival and are paramount to outcomes and recovery from critical illness. A proper maintenance of the delicate balance between inflammation, oxidative stress, and immune response is crucial for resolution from critical illness with important implications for patient outcome. The extent of inflammation and oxidative stress under normal conditions is limited by the antioxidant defense system of the human body, whereas the antioxidant capacity is commonly significantly compromised, and serum levels of micronutrients and vitamins significantly depleted in patients who are critically ill. Hence, the provision of antioxidants and anti-inflammatory nutrients may help to reduce the extent of oxidative stress and therefore improve clinical outcomes in patients who are critically ill. As existing evidence of the beneficial effects of antioxidant supplementation in patients who are critically ill is still unclear, actual findings about the most promising anti-inflammatory and antioxidative candidates selenium, vitamin C, zinc, and vitamin D will be discussed in this narrative review. The existing evidence provided so far demonstrates that several factors need to be considered to determine the efficacy of an antioxidant supplementation strategy in patients who are critically ill and indicates the need for adequately designed multicenter prospective randomized control trials to evaluate the clinical significance of different types and doses of micronutrients and vitamins in selected groups of patients with different types of critical illness.
Journal of Parenteral and Enteral Nutrition
10.1002/jpen.2421
urn:nbn:de:bvb:20-opus-318186
@articleDresen.2023b, author = Dresen, Ellen and Pimiento, Jose M. and Patel, Jayshil J. and Heyland, Daren K. and Rice, Todd W. and Stoppe, Christian, year = 2023, title = Overview of oxidative stress and the role of micronutrients in critical illness, pages = S38-S49, volume = 47 Suppl 1, journal = JPEN. Journal of parenteral and enteral nutrition, doi = 10.1002/jpen.2421,
md5:99e2ab7a1040796f2e40832f58827d83
2023-06-06T12:36:48+00:00
/tmp/phpqnoJwR
bibtex
647f286071dce5.55788422
Journal of Parenteral and Enteral Nutrition 2023, 47:S38-S49. DOI: 10.1002/jpen.2421
false
true
CC BY-NC-ND: Creative-Commons-Lizenz: Namensnennung, Nicht kommerziell, Keine Bearbeitungen 4.0 International
Ellen Dresen
Jose M. Pimiento
Jayshil J. Patel
Daren K. Heyland
Todd W. Rice
Christian Stoppe
eng
uncontrolled
critical illness
eng
uncontrolled
vitamins
eng
uncontrolled
vitamin C
eng
uncontrolled
inflammation
eng
uncontrolled
medical nutrition therapy
eng
uncontrolled
oxidative stress
eng
uncontrolled
selenium
eng
uncontrolled
trace elements
eng
uncontrolled
micronutrients
eng
uncontrolled
vitamin D
eng
uncontrolled
zinc
Medizin und Gesundheit
open_access
Klinik und Poliklinik für Anästhesiologie (ab 2004)
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/31818/Dresen_JPEN.pdf
29377
2022
eng
1253
1261
12
49
article
1
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Oral health status of adult hypophosphatasia patients: A cross‐sectional study
Aim
This study evaluated the oral health status of adult patients with hypophosphatasia (HPP).
Materials and Methods
Parameters of oral health assessment comprised decayed/missing/filled teeth (DMFT) index, probing pocket depth and clinical attachment level (CAL) as well as documentation of tooth loss and periodontal health status according to CCD/AAP criteria. Findings were compared with national reference data (DMS V survey) reporting oral health status in age‐related controls. Within‐group comparisons were made between the HPP patients harbouring one versus two alkaline phosphatase liver/bone/kidney type (ALPL) gene variants.
Results
Of 80 HPP patients (64 female) with a mean age of 46.4 years (range 24–78) and one (n = 55) or two (n = 18) variants (n = 7 lacking testing) within the ALPL gene, those with two variants displayed substantially higher tooth loss rate (14.0 ± 9.3) than those affected by only one ALPL variant (4.1 ± 5.4), who did not differ substantially from healthy DMS V controls. While DMFT score and severe periodontal diseases (PDs) of HPP patients with one variant only increased with progressing age, the two‐variant sub‐cohort age independently exhibited increased DMFT scores and a higher rate of severe PDs.
Conclusions
HPP patients affected by two variants of the ALPL gene exhibited a higher risk of periodontitis and tooth loss than the general population, while patients with one variant developed clinically relevant oral disease symptoms with progressing ageing.
Journal of Clinical Periodontology
10.1111/jcpe.13718
urn:nbn:de:bvb:20-opus-293777
2022-12-05T10:00:56+00:00
sword
swordwue
attachment; filename=deposit.zip
a1a73b9747f163782e38acd01704feb5
Journal of Clinical Periodontology 2022, 49(12):1253-1261. DOI: 10.1111/jcpe.13718
false
true
CC BY-NC: Creative-Commons-Lizenz: Namensnennung, Nicht kommerziell 4.0 International
Margareta Weider
Ulrich Schlagenhauf
Lothar Seefried
eng
uncontrolled
dental status
eng
uncontrolled
hypophosphatasia
eng
uncontrolled
inflammation
eng
uncontrolled
periodontal disease
eng
uncontrolled
tooth loss
Medizin und Gesundheit
open_access
Lehrstuhl für Orthopädie
Abteilung für Parodontologie (in der Poliklinik für Zahnerhaltung und Parodontologie)
Import
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/29377/Weider_Clinical.pdf