HOPE Fixation: A Novel Fixing Method and Paraffin-embedding Technique for Human Soft Tissues

Olert, J.; Wiedorn, Klaus-Hermann; Goldmann, Torsten; Kühl, Heike; Mehraein, Yasmin; Scherthan, Harry; Niketeghad, Fataneh; Vollmer, Ekkehard; Müller, Annette; Müller‐Navia, Jutta

doi:10.1078/0344-0338-00166

Cited by 124 publications

(111 citation statements)

References 7 publications

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“…Rats were ventilated with either 13/3 cmH 2 O or 45/10 cmH 2 O. These ventilation modes were chosen to minimise end-expiratory alveolar collapse and subsequent surfactant dysfunction [18]. Previous studies have shown that when animals are ventilated with a PIP of 45 cmH 2 O, lung injury can be reduced by applying a PEEP of 10 cmH 2 O [15,16], although at a PIP as high as 45 cmH 2 O, PEEP does not completely prevent lung injury, particularly at later time points.…”

Section: Discussionmentioning

confidence: 99%

“…The thorax was opened and lungs were collected sterile, snap frozen and stored. For immunohistochemistry, the thorax was opened, lungs were removed en bloc and filled with HOPE solution [18,19]. The lung was then inflated with a PEEP level of 10 cmH 2 O, the trachea was clamped and the lungs were stored in HOPE solution at 4uC until further analysis.…”

Section: Ventilation Of Rats In Vivomentioning

confidence: 99%

“…Sections of 4 mm thick were cut, mounted on Superfrostz slides (041300; Menzel-Glä ser Braunschweig, Germany) and deparaffinised as described elsewhere [18,19]. As well as positive reference sections, negative controls were included in every staining series to ensure even results.…”

Section: Ventilation Of Rats In Vivomentioning

confidence: 99%

“…Immunohistochemistry HOPE-fixed, paraffin-embedded specimens were prepared as previously described [18,19]. Sections of 4 mm thick were cut, mounted on Superfrostz slides (041300; Menzel-Glä ser Braunschweig, Germany) and deparaffinised as described elsewhere [18,19].…”

Section: Ventilation Of Rats In Vivomentioning

confidence: 99%

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Ventilation-induced activation of the mitogen-activated protein kinase pathway

Uhlig

Haitsma²,

Goldmann³

et al. 2002

Eur Respir J

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Mechanical ventilation of patients can be a life-saving treatment, but also imposes additional stress on the lung. Mitogen-activated protein kinases (MAPK) represent a family of protein kinases that become phosphorylated and activated by many different forms of stress.Using Western blot analysis, the present study analysed the effects of high distending pressure ventilation on the activation of the MAPK extracellular signal-related kinases (ERK)-1/2, c-Jun amino-terminal kinases (JNK) and p38 kinase, and on the MAPKactivated transcription factors c-Jun, ETS-like protein (Elk)-1 and activating transcription factor (ATF)-2.In adult rats, ventilation with high pressure (45/10 peak inspiratory pressure/positive end-expiratory pressure in cmH 2 O) for 30 or 60 min did not affect arterial oxygenation, but resulted in enhanced phosphorylation of ERK-1/2, JNK, c-Jun, Elk-1 and ATF-2 compared to normally ventilated (13/3) rats. The activation of ERK-1/2 and JNK was located to cells resembling alveolar type II cells. In addition, high pressure ventilation enhanced phosphorylation of the inhibitor of nuclear factor (NF)-kB and nuclear translocation of the transcription factor NF-kB. In isolated perfused mouse lungs, the MAPK/ERK kinase inhibitor U0126 prevented ventilation-induced activation of ERK-1/2 and Elk-1, but had no effect on ventilation-induced cytokine release.The present authors conclude that mechanical ventilation triggers specific signalling pathways, such as the mitogen-activated protein kinase and the nuclear factor-kB pathways, which may contribute to pulmonary inflammation and proliferation. Eur Respir J 2002; 20: 946-956.

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Section: Discussionmentioning

confidence: 99%

Section: Ventilation Of Rats In Vivomentioning

confidence: 99%

Section: Ventilation Of Rats In Vivomentioning

confidence: 99%

Section: Ventilation Of Rats In Vivomentioning

confidence: 99%

See 2 more Smart Citations

Ventilation-induced activation of the mitogen-activated protein kinase pathway

Uhlig

Haitsma²,

Goldmann³

et al. 2002

Eur Respir J

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“…CNS tissue was either fixed with 4% paraformaldehyde or in HOPE fixative (DCS Innovative; Olert et al, 2001) and was embedded in paraffin as described previously (Bergthaler et al, 2007). For light microscopy, endogenous peroxidases (PBS/3% H 2 O 2 ) were neutralized and unspecific binding blocked (PBS/10% FCS).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective intervention by interferon-γ blockade prevents CD8+ T cell-mediated dendrite and synapse loss

Kreutzfeldt¹,

Bergthaler²,

Fernandez³

et al. 2013

J Cell Biol

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Neurons are postmitotic and thus irreplaceable cells of the central nervous system (CNS). Accordingly, CNS inflammation with resulting neuronal damage can have devastating consequences. We investigated molecular mediators and structural consequences of CD8(+) T lymphocyte (CTL) attack on neurons in vivo. In a viral encephalitis model in mice, disease depended on CTL-derived interferon-(IFN-) and neuronal IFN-signaling. Downstream STAT1 phosphorylation and nuclear translocation in neurons were associated with dendrite and synapse loss (deafferentation). Analogous molecular and structural alterations were also found in human Rasmussen encephalitis, a CTL-mediated human autoimmune disorder of the CNS. Importantly, therapeutic intervention by IFN-blocking antibody prevented neuronal deafferentation and clinical disease without reducing CTL responses or CNS infiltration. These findings identify neuronal IFN-signaling as a novel target for neuroprotective interventions in CTLmediated CNS disease.

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