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JLUdocs ist der Bereich für Open-Access-Publikationen von Mitgliedern und Angehörigen der JLU Gießen.

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Auflistung JLUdocs nach Auflistung nach Fachbereich/Einrichtung "FB 10 - Veterinärmedizin"

Gerade angezeigt 1 - 20 von 1809
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    24 hour hormone and serum electrolyte levels of dogs with pituitary-dependent hyperadrenocorticism treated with trilostane
    (2007) Lehnert, Claudia
    Ten dogs with PDH took part in this study. After confirming the diagnosis, treatment with once daily trilostane was started. On their 10th and 30th day of therapy, the dogs were controlled clinically and an ACTH stimulation test was performed 3 to 4 hours after trilostane dosing. On the 30th day of therapy, the dogs were hospitalized and over 24 hours, blood samples were taken for the measurement of trilostane, ketotrilostane, endogenous ACTH, cortisol, aldosterone, renin and serum electrolytes. On the 10th and 30th day of therapy, clinical improvement was good in all but one dog. Laboratory findings including the ACTH stimulation test results had generally improved on the 30th day of therapy, although some of the parameters still were not within the reference range. None of the patients showed any adverse effects. Nevertheless, on the 30th day of therapy, one of the dogs collapsed suddenly and, although regenerating quickly, was removed from further blood sampling. Trilostane absorption was quick and ketotrilostane was formed immediately. For both substances, peak concentrations were reached 1.5 to 3 (4) hours after trilostane administration. Accordingly, lowest serum cortisol and aldosterone levels were found at nearly the same time points. Although cortisol and aldosterone levels were very low in all dogs, none showed any adverse effects. Because the negative feedback mechanism caused by high cortisol levels was removed, all dogs showed highest endogenous ACTH levels 4 to 8 hours after trilostane dosing. At all time points, all dogs had endogenous ACTH levels well above the reference range. Because there was quite marked inter-individual variation over the 24 hours and in some dogs changes in endogenous ACTH levels were only minimal, its measurement is most likely not useful for the evaluation of therapeutical success of trilostane. Serum renin activity remained rather unchanged during the day. While changes in serum sodium and calcium were insignificant, serum potassium showed some astonishing development: At times when aldosterone was at its lowest concentration and high potassium levels would be expected, potassium levels were low, but nevertheless well inside the reference range. An aldosterone-like effect of trilostane or of accumulating steroid precursors seems possible, although further studies are necessary to verify these hypotheses. This may be one of the reasons why trilostane is more secure in the treatment of PDH than lysodren.
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    A contribution to age determination of cheetahs (Acinonyx jubatus) based on radiographic analysis of the skull and postcranial morphology.
    (2019) Schmidt, Martin J; Steenkamp, Gerhard; Failing, Klaus; Caldwell, Peter; Kirberger, Robert M
    The aim of this retrospective cross-sectional study was to present comprehensive information about the age-dependent change of skeletal characteristics in captive cheetahs with known age and to assess the benefit of these variables for age estimation in this species. Radiographs of 162 known-age captive and semi-captive cheetahs were retrospectively examined and age-related changes of skull, axial and appendicular skeletal systems were documented. Metric and non-metric variables were used. These parameters were checked for the best correlation with age using a multiple stepwise regression analysis. An overview about the time frames, in which ossification centers appeared and physeal closure occurred is presented. Multiple stepwise regression analysis revealed the status of closure of the coronal suture, the maximum length of the frontal sinus, the condylobasal-, hard palate, and facial length are most significantly correlated with age. Together with the pulp size of the upper canine, these values can be used for an age approximation in cheetahs.
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    A genome-wide scan study identifies a single nucleotide substitution in MC1R gene associated with white coat colour in fallow deer (Dama dama)
    (2020) Reiner, Gerald; Weber, Tim; Nietfeld, Florian Georg; Fischer, Dominik; Wurmser, Christine; Fries, Ruedi; Willems, Hermann
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    A genome-wide scan study identifies a single nucleotide substitution in the tyrosinase gene associated with white coat colour in a red deer (Cervus elaphus) population
    (2020) Reiner, Gerald; Tramberend, Kirsten; Nietfeld, Florian; Volmer, Klaus; Wurmser, Christine; Fries, Ruedi; Willems, Hermann
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    A placebo-controlled, double-blind study evaluating the effect of orally administered polyunsaturated fatty acids on the oclacitinib dose for atopic dogs
    (2024) Schäfer, Laura; Thom, Nina
    Background: Supplementation of polyunsaturated fatty acids (PUFA) enables dose reduction of prednisolone and ciclosporin in canine atopic dermatitis (cAD). Objective: To determine if oral administration of PUFA reduces the dose of oclacitinib in cAD. Animals: Twenty-two client-owned dogs with cAD receiving oclacitinib. Materials and Methods: Dogs received a fish oil product (PUFA) or paraffin oil (placebo) for 16 weeks. Owners adjusted the oclacitinib dose according to daily pruritus assessments. On Day (D)0, D56 and D112, Canine Atopic Dermatitis Extent and Severity Index, fourth iteration (CADESI-04), pruritus Visual Analog Scale (PVAS), quality-of-life score (QoL), Global Assessment (GA), quality-of-coat (QoC) and adverse events were recorded. Results: Mean daily oclacitinib dose was significantly reduced in the PUFA group from 0.51 ± 0.20 mg/kg/24 h (D0) to 0.19 ± 0.14 mg/kg/24 h (D85–112; p < 0.00001) and not in the placebo group (D0: 0.70 ± 0.33 mg/kg/24 h; D85–112: 0.53 ± 0.35 mg/kg/24 h, p = 0.5422). CADESI-04 did not change over time or differ between groups. PVAS was significantly lower in the PUFA group (2.8 ± 1.5) compared to placebo (4.2 ± 1.6) at D112 (p = 0.0375). QoL and QoC improved only in the PUFA group (QoL: D0: 20 ± 7, D112: 12 ± 5, p = 0.0057; QoC: D0: 0 ± 0.5, D112: 1 ± 0.5, p = 0.0410). GA on D112 was higher in the PUFA group (p = 0.008). No adverse events were observed. Conclusion: Oral supplementation of PUFA allowed dose reduction of oclacitinib and improved PVAS, QoL, QoC and GA. The use of PUFA is recommended and was safe in the atopic study dogs receiving oclacitinib.
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    A rare case of multicentric eosinophilic granulocytic sarcoma as cause of hindlimb weakness and non-regenerative anaemia in a minipig
    (2021) Weyrich, Angelika; Becker, Sabrina; Vienenkötter, Julia; Reiner, Gerald; Herden, Christiane
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    A role for neutrophil granulocytes as afferent signals in immune-to-brain communication during systemic and localized organ-specific lung inflammation
    (2024) Hernandez, Jessica Kate
    The brain inflammatory response and brain-controlled sickness symptoms, such as fever, involve innate immune system activation through immune-to-brain signaling during systemic inflammatory insults. Neutrophil granulocytes (NG) are a crucial part of the carefully regulated immune system and contribute to the transmission of inflammatory information. Dysregulation of the immune response during an infection can have severe consequences, such as progression to septic inflammation. Indeed, sepsis is characterized by an overwhelming inflammatory response to infection and can be life-threatening or result in long-term impairments due, in part, to poor treatment options. Moreover, neutropenic fever is a severe life threatening condition in immunocompromised patients, such as those that have undergone chemotherapy. Therefore, an anti-inflammatory role for NGs during such inflammatory conditions was hypothesized. This hypothesis is supported by NG-dependent production of specialized pro-resolving mediators (SPM), like resolvin (Rv) E1. For my dissertation project, the role of NGs in two different mouse models of systemic and localized organ-specific lung inflammation was investigated. The first inflammatory model evaluated the effects of neutropenia during severe systemic inflammation. Mice received an intraperitoneal (IP) dose of anti-polymorphonuclear serum (PMN; 1 ml/kg), or normal rabbit serum (NRS) as a control, followed by an IP dose of lipopolysaccharide (LPS; 2.5 mg/kg) or phosphate buffered saline (PBS) 24 h later. The effects on sickness symptoms and peripheral and brain inflammation were investigated. Using a telemetric system, the following physiological parameters were continuously recorded: core body temperature, locomotor activity, and food and water intake. Mice were sacrificed at 4 h or 24 h post-inoculation (p.i.) with LPS and brain and plasma samples were collected. Alterations to peripheral and brain inflammation were assessed by hematological measurements, immunohistochemistry, immunoassays, and RT-qPCR. The second inflammatory model evaluated the effects of genetic omega (ω)-3 polyunsaturated fatty acid (PUFA) enrichment and two different RvE1 receptor (chemerin receptor 23 [CR] or leukotriene B4 receptor [LR]) deficiencies during acute respiratory distress syndrome (ARDS). To investigate the therapeutic potential of SPMs and the role of NGs during ARDS, C57BL/6N mice were bred with (Fat) or without (WT) fat-1 genetic ω-3 PUFA enrichment and crossbred with the RvE1 receptor knock-out (CR KO/LR KO) or unmodified (Norm) mice. Mice were treated with an intra-tracheal (i.t.) instillation of LPS (10 µg/mouse in 50 µl saline) and sacrificed at five different time points: 0 h, 4 h, 24 h, 72 h, or 120 h p.i. Lung, liver, and brain tissues were collected and analyzed by RT-qPCR, multiplex, Western blot, liquid chromatography-tandem mass spectrometry (LC-MS/MS), and immunohistochemistry to assess the peripheral and brain inflammatory response. Interestingly, during severe systemic inflammation, pretreatment with PMN not only reduced circulating levels of NGs but, at higher doses, increased lethality. Moreover, NG recruitment to the brain was attenuated by PMN. All physiological parameters were strongly affected by LPS, but only LPS-induced hypothermia was exacerbated and prolonged in PMN pretreated mice. Indeed, while LPS did increase circulating cytokines, neutropenic mice showed enhanced production of IL-10 as early as 4 h p.i. and by 24 h p.i. plasma levels of CXCL1, CXCL2, IL-10, IL-6, and tumor necrosis factor (TNF) α were all exacerbated in these mice compared to the immunocompetent controls. LPS-induced inflammation in the brain was detectable at 4 h p.i. for inflammatory mediators, enzymes for prostaglandin (PG) E2 synthesis, and markers for activation of inflammatory transcription factors, but these did not persist to 24 h p.i. and were unaffected by PMN pretreatment. However, at 24 h p.i., the mRNA expression of marker proteins for NFκB, STAT3, as well as the enzymes microsomal PGE synthase (mPGES), and cyclooxygenase (COX)2 were generally increased by pretreatment with PMN regardless of LPS treatment. Despite an overall weak PMN effect in the brain, LPS-induced circulating levels of corticosterone were dampened at 4 h but showed a prolonged increase in PMN pretreated compared to NRS pretreated mice. Taken together, these data suggest a peripheral action may be largely responsible for observed alterations in sickness symptoms in neutropenic animals. LPS-induced ARDS resulted in milder inflammation compared to the severe LPS-induced systemic model. The inflammatory response was largely localized to the lung where mediators of inflammation appeared enhanced at 24 h p.i., and alterations by genetic ω-3 PUFA enrichment and RvE1 receptor deficiencies changed over time. These data indicate that both ω-3 PUFA enrichment and RvE1 receptor deficiencies were enough to cause minor alterations in LPS-induced lung inflammation. In contrast, LPS-induced production of inflammatory mediators in the liver was less pronounced. Despite low inflammatory signaling in the periphery (liver), signs of inflammation in the brain were detected in the hypothalamus, similar to the lung with a peak at 24 h p.i. Overall, deficiency in CR had a stronger effect than LR deficiency in the hypothalamus as evidenced by reduced expression of CXCL1 and IL-1β in Fat-CR KO mice compared to Fat-Norm controls. In addition, GFAP expression was increased by CR deficiency regardless of ω-3 PUFA enrichment. Immunohistochemical staining also revealed that NG recruitment to different brain structures were present during inflammation. In combination with the liver’s modest inflammatory response, these effects suggest a minor role of circulating cytokines in lung-to-brain communication. However, NGs trafficking to the brain may contribute to inflammatory signaling from the lung to the brain. Enrichment with ω-3 PUFA and RvE1 receptor deficiencies modulated lipid mediator profiles in the lung and hypothalamus. Such changes in lipids may significantly contribute to lung-brain communication and inflammatory resolution during LPS-induced ARDS. In summary, by analyzing NGs during two different models of inflammation, I found that NGs can be recruited to different brain structures during LPS-induced severe systemic inflammation and ARDS, and potentially participate in immune-to-brain communication. In the case of severe systemic inflammation, neutropenia increases mortality, exacerbates peripheral inflammation, prolongs HPA activation, and worsens inflammatory hypothermia. In this model of inflammation, a peripheral anti-inflammatory action of NGs is most likely contributing to alterations in disease severity. Exaggerated peripheral inflammation during neutropenia could be instrumental in exacerbating sickness symptoms, possibly through interactions with the blood-brain barrier (BBB) or at brain structures with a leaky BBB such as the so-called circumventricular organs. In the milder inflammatory ARDS model, lung-to-brain communication includes low humoral signaling and recruitment of NGs. Both genetic ω-3 PUFA enrichment and RvE1 receptor deficiencies had an effect on the inflammatory response in the lung and hypothalamus. Within the hypothalamus, CR deficiency enhanced GFAP immunoreactivity. The actions of RvE1, as well as ω-3 PUFA enrichment, modulate NG recruitment to the brain most likely through CR. Further investigations into the anti-inflammatory roles of NGs and their ability to participate in immune-to-brain communication are warranted. This will help to gain further insights into underlying mechanisms of the pathophysiology in individuals suffering from neutropenia or when being at risk for brain inflammatory insults as a complication of ARDS.
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    A special issue on “New technologies in parasitology”
    (2022) Brehm, Klaus; Taubert, Anja; Grevelding, Christoph G.
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    ACE (CD143) in granulomatösen Entzündungen von Mensch und Tier : Speziesspezifische Expression in Endothel und Makrophagen
    (2001) Georg, Melanie
    Vorkommen und Verteilungsmuster von Angiotensin I-converting enzyme (ACE, Kininase II, CD143), das die Auswirkungen des RAS unddes KKS über die Gewebespiegel bioaktiver Angiotensine und Kinine reguliert, ist in Geweben von Mensch und Tier unzureichendcharakterisiert. Erst kürzlich fiel seine endotheliale Heterogenität mit bemerkenswerter Gefäß-, Organ- und Speziesspezifität auf. Fernersind die bei Sarkoidose und einigen histiozytären Entzündungen abnorm erhöht gefundenen ACE-Serumspiegel morphogenetisch nichterklärt. Ziele dieser Arbeit waren daher, mit sechs gegen denaturiertes menschliches ACE hergestellten neu zur Verfügung stehendenmonoklonalen Antikörpern (mAk) (CG1, CG2, CG3, CG4, CG5 und 5F1) das Expressionsmuster von ACE (1.) in Makrophagen undätiologisch verschiedenen granulomatösen Entzündungen des Menschen zu vergleichen, (2.) diese mAk hinsichtlich einer möglichenKreuzreaktivität mit dem ACE verschiedener Tierarten zu prüfen, um dadurch (3.) mögliche speziesspezifische Unterschiede in derendothelialen, makrophagozytären und granulomatösen ACE-Expression zu analysieren. Außerdem wurden die mAk JC/70A gegenCD31, mAk KP1 gegen CD68 und mAk MR12/53 (unspezifisch) zu Kontrollzwecken eingesetzt. Grundlage bildeten formalinfixierte und in Paraffin eingebettete Gewebeproben von Patienten mit klinisch abgesicherter Tuberkulose (n=41), Sarkoidose (n= 29), Toxoplasmose (n= 30), Fremdkörpergranulomen unterschiedlicher Ätiologie (n= 14) und 20 Patientenfälle mitbesonderen granulomatösen und histiozytären Entzündungen wie Schistosomiasis, Blastomykose, mykobakterieller Histiozytose undMorbus Hansen (Lepra). Ferner wurden in Paraffin eingebettete Gewebeproben von 21 verschiedenen Tierarten untersucht. Histiozytäreund granulomatöse Gewebereaktionen konnten hier jeweils an der Tuberkulose von Menschenaffe, Hund, Katze und Großkatzen, an derLungenmykose des Kaninchens und an Fremdkörperreaktionen des Hundes erfasst werden. Das Gewebematerial entstammte denInstituten für Pathologie und Veterinär-Pathologie der JLU Giessen, die Sonderfälle der Abteilung für Pathologie der Universität Campinas,Brasilien. Als Detektionsmethode der Immunreaktivität diente die APAAP-Technik. Die geweblichen Expressionsmuster von ACE wurdeneinheitlich analysiert, wobei eine semiquantitative Erfassung morphologisch und immunhistologisch relevanter Gewebeveränderungen beiSarkoidose, Tuberkulose und Toxoplasmose eine vergleichende statistische Analyse zuließ. Von den analysierten mAk gegen humanes ACE reagierte der mAk CG2 kreuz mit dem ACE des Menschenaffen, der Carnivoren Hund,Katze und aller Großkatzen, des Kaninchens und des Gürteltieres, nicht jedoch mit dem ACE der Kleinnager Hamster, Maus, Ratte undMeerschweinchen oder der Omni- und Herbivoren wie Schwein, Schaf, Ziege, Rind und Pferd. Dies spricht für konservierteACE-Proteindomänen mit immunogener Ähnlichkeit untereinander verwandter Tierarten. Der mAk CG2 lokalisierte ACE in den Gewebender kreuzreaktiv gefundenen Tierarten jeweils eindeutig. Auffallende gefäß-, organ- und speziesspezifische Unterschiede betrafen jedochdie endotheliale Expression, besonders deutlich im direkten Vergleich der Lungen-, Nieren- und Lebervaskularisation. WährendAlveolarendothel allgemein stark und einheitlich exprimierte, fehlte ACE in den Endothelien aller Nierengefäße von Kaninchen und Affe, undnur die Carnivoren Hund und Katze zeigten eine Expression in venösen Endothelien des splanchnalen (und portalen) Gefäßsystems. DieErgebnisse bestätigen - über Mensch und Ratte hinaus - die Heterogenität der endothelialen ACE-Verteilung für zahlreiche weitereTierarten. Eine unterschiedliche Regulation von zirkulierendem RAS, KKS und Blutdruck ist daher zu vermuten, jeweils angepasst an dieBedürfnisse der betreffenden Spezies und des betreffenden Organsystems. In einer überraschenden Heterogenität präsentierte sich ebenfalls das von Makrophagen exprimierte ACE, das spezies- und zudemaktivierungsabhängigen Mustern folgte. Alveolarmakrophagen und andere aktivierte Makrophagen zeigten sich beim Menschen geringimmunreaktiv für ACE, jedoch in keiner der untersuchten Tierarten. Eine dem Menschen vergleichbare Morphologie und stets ausgeprägteACE-Immunreaktivität waren kennzeichnend für die epitheloidzellig granulomatöse Entzündungsreaktion des Menschenaffen beiTuberkulose, wurden aber nur unregelmäßig und sporadisch bei Hund und Katze und nicht bei Großkatzen gefunden. Trotz massiverTuberkulose gehörte eine ACE-Expression bei Großkatzen offenbar nicht zu dem Reaktionsspektrum aktivierter Makrophagen,ebensowenig wie bei aktivierten Makrophagen des Kaninchens. Beim Menschen dagegen unterschieden sich Sarkoidose, Tuberkuloseund Toxoplasmose nicht substanziell in der histiozytären Fähigkeit zur ACE-Expression. Die hinsichtlich zellulärer Art und Intensität faktischgleichartigen Expressionsmuster von Sarkoidose und Tuberkulose erklären ihre unterschiedlich beschriebenen ACE-Serumspiegel nicht.Daher müssen hier andere Einflußfaktoren diskutiert werden, wie eine unterschiedliche Aktivität von Sekretasen, die das plasmatischerfassbare ACE generieren. Die multifaktorielle Analyse ergab, dass nicht Lymphozyten, sondern die Makrophagen selbst signifikantenEinfluss auf ihre Akkumulation und ACE-Expression in der granulomatösen Entzündungsreaktion haben. Diese Befunde decken sich gutmit der kürzlich bekanntgewordenen Beziehung zwischen ACE und dem von Makrophagen gebildeten Zytokin MCP-1, das - zumindestexperimentell von Angiotensin II induziert - für die Makrophagen-akkumulation verantwortlich ist und beim Menschen mit ACE-Gehalt undAusprägungsgrad granulomatöser Gewebereaktionen korreliert. Die eigenen Befunde sprechen dafür, dass Tierarten, denen dasReaktionsspektrum mit lokal ausgeprägter ACE-Expression fehlt, tatsächlich keine vergleichbare epitheloidzellig granulomatöseEntzündungsreaktion aufbauen können.
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    Activated platelets and platelet-leukocyte aggregates in the equine systemic inflammatory response syndrome
    (2022) Theuerkauf, Kim; Obach-Schröck, Carmen; Staszyk, Carsten; Moritz, Andreas; Roscher, Katja A.
    In humans, activated platelets contribute to sepsis complications and to multiple organ failure. In our prospective analytical study of cases of the equine systemic inflammatory response syndrome (SIRS), we adapted a standard human protocol for the measurement of activated platelets and platelet-leukocyte aggregates (PLAs) in equine platelet-leukocyte-rich plasma (PLRP) by flow cytometry, and we investigated the hypothesis that activated platelets and PLAs are increased in clinical cases of SIRS. We included 17 adult horses and ponies fulfilling at least 2 SIRS criteria, and 10 healthy equids as controls. Activation of platelets was determined by increased expression of CD62P on platelets. Activated platelets and PLAs were measured before and after in vitro activation of platelets with collagen. Median expression of CD62P on platelets was significantly increased after activation in the control group: 1.45% (interquartile range [IQR]: 1.08–1.99%) initially versus 8.78% (IQR: 6.79–14.78%, p = 0.002) after activation. The equids with SIRS had significantly more activated platelets and PLAs in native PLRP than controls: CD62P 4.92% (median, IQR: 2.21–12.41%) versus 1.45% in controls (median, IQR: 1.08–1.99%, p = 0.0007), and PLAs 4.16% (median, IQR: 2.50–8.58%) versus 2.95% in controls (median, IQR: 1.57–3.22%, p = 0.048). To our knowledge, increased platelet activation and PLAs have not been demonstrated previously with flow cytometry in clinical cases of equine SIRS.
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    Activation of the inflammatory transcription factor nuclear factor interleukin-6 during inflammatory and psychological stress in the brain
    (2013) Fuchs, Franziska; Damm, Jelena; Gerstberger, Rudiger; Roth, Joachim; Rummel, Christoph
    BACKGROUND:The transcription factor nuclear factor interleukin 6 (NF-IL6) is known to be activated by various inflammatory stimuli in the brain. Interestingly, we recently detected NF-IL6-activation within the hypothalamus-pituitary-adrenal (HPA)-axis of rats after systemic lipopolysaccharide (LPS)-injection. Thus, the aim of the present study was to investigate whether NF-IL6 is activated during either, inflammatory, or psychological stress in the rat brain. METHODS:Rats were challenged with either the inflammatory stimulus LPS (100mug/kg, i.p.) or exposed to a novel environment. Core body temperature (Tb) and motor activity were monitored using telemetry, animals were killed at different time points, brains and blood removed, and primary cell cultures of the anterior pituitary lobe (AL) were investigated. Analyses were performed using immunohistochemistry, RT-PCR, and cytokine-specific bioassays. RESULTS:Stress stimulation by a novel environment increased NF-IL6-immunoreactivity (IR) in the pituitary´s perivascular macrophages and hypothalamic paraventricular cells and a rise in Tb lasting approximately 2h. LPS stimulation lead to NF-IL6-IR in several additional cell types including ACTH-IR-positive corticotrope cells in vivo and in vitro. Two other proinflammatory transcription factors, namely signal transducer and activator of transcription (STAT)3 and NFkappaB, were significantly activated and partially colocalized with NF-IL6-IR in cells of the AL only after LPS-stimulation, but not following psychological stress. In vitro NF-IL6-activation was associated with induction and secretion of TNFalpha in folliculostellate cells, which could be antagonized by the JAK-STAT-inhibitor AG490. CONCLUSIONS:We revealed, for the first time, that NF-IL6 activation occurs not only during inflammatory LPS stimulation, but also during psychological stress, that is, a novel environment. Both stressors were associated with time-dependent activation of NF-IL6 in different cell types of the brain and the pituitary. Moreover, while NF-IL6-IR was partially linked to STAT3 and NFkappaB activation, TNFalpha production, and ACTH-IR after LPS stimulation; this was not the case after exposure to a novel environment, suggesting distinct underlying signaling pathways. Overall, NF-IL6 can be used as a broad activation marker in the brain and might be of interest for therapeutic approaches not only during inflammatory but also psychological stress.
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    Adaptation of Campylobacter field isolates to propionic acid and sorbic acid is associated with fitness costs
    (2021) Peh, E.; Kittler, S.; Seinige, D.; Valero, A.; Kehrenberg, C.
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    Adipose tissue derived mesenchymal stem cells for musculoskeletal repair in veterinary medicine
    (2015) Arnhold, Stefan; Wenisch, Sabine
    Adipose tissue derived stem cells (ASCs) are mesenchymal stem cells which can be obtained from different adipose tissue sources within the body. It is an abundant cell pool, which is easy accessible and the cells can be obtained in large numbers, cultivated and expanded in vitro and prepared for tissue engineering approaches, especially for skeletal tissue repair. In the recent years this cell population has attracted a great amount of attention among researchers in human as well as in veterinary medicine. In the meantime ASCs have been well characterized and their use in regenerative medicine is very well established. This review focuses on the characterization of ASCs for their use for tissue engineering approaches especially in veterinary medicine and also highlights a selection of clinical trials on the basis of ASCs as the relevant cell source.
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    Aetiology and 30-Year Long-Term Outcome of Children with Cardiomyopathy Necessitating Heart Transplantation
    (2020) Zschirnt, Martin; Thul, Josef; Akintürk, Hakan; Valeske, Klaus; Schranz, Dietmar; Skrzypek, Susanne; Müller, Matthias; Jux, Christian; Hahn, Andreas; Rupp, Stefan