TY  - JOUR
A1  - Galluzzi, L.
A1  - Bravo-San Pedro, J. M.
A1  - Vitale, I.
A1  - Aaronson, S. A.
A1  - Abrams, J. M.
A1  - Adam, D.
A1  - Alnemri, E. S.
A1  - Altucci, L.
A1  - Andrews, D.
A1  - Annicchiarico-Petruzelli, M.
A1  - Baehrecke, E. H.
A1  - Bazan, N. G.
A1  - Bertrand, M. J.
A1  - Bianchi, K.
A1  - Blagosklonny, M. V.
A1  - Blomgren, K.
A1  - Borner, C.
A1  - Bredesen, D. E.
A1  - Brenner, C.
A1  - Campanella, M.
A1  - Candi, E.
A1  - Cecconi, F.
A1  - Chan, F. K.
A1  - Chandel, N. S.
A1  - Cheng, E. H.
A1  - Chipuk, J. E.
A1  - Cidlowski, J. A.
A1  - Ciechanover, A.
A1  - Dawson, T. M.
A1  - Dawson, V. L.
A1  - De Laurenzi, V.
A1  - De Maria, R.
A1  - Debatin, K. M.
A1  - Di Daniele, N.
A1  - Dixit, V. M.
A1  - Dynlacht, B. D.
A1  - El-Deiry, W. S.
A1  - Fimia, G. M.
A1  - Flavell, R. A.
A1  - Fulda, S.
A1  - Garrido, C.
A1  - Gougeon, M. L.
A1  - Green, D. R.
A1  - Gronemeyer, H.
A1  - Hajnoczky, G.
A1  - Hardwick, J. M.
A1  - Hengartner, M. O.
A1  - Ichijo, H.
A1  - Joseph, B.
A1  - Jost, P. J.
A1  - Kaufmann, T.
A1  - Kepp, O.
A1  - Klionsky, D. J.
A1  - Knight, R. A.
A1  - Kumar, S.
A1  - Lemasters, J. J.
A1  - Levine, B.
A1  - Linkermann, A.
A1  - Lipton, S. A.
A1  - Lockshin, R. A.
A1  - López-Otín, C.
A1  - Lugli, E.
A1  - Madeo, F.
A1  - Malorni, W.
A1  - Marine, J. C.
A1  - Martin, S. J.
A1  - Martinou, J. C.
A1  - Medema, J. P.
A1  - Meier, P.
A1  - Melino, S.
A1  - Mizushima, N.
A1  - Moll, U.
A1  - Muñoz-Pinedo, C.
A1  - Nuñez, G.
A1  - Oberst, A.
A1  - Panaretakis, T.
A1  - Penninger, J. M.
A1  - Peter, M. E.
A1  - Piacentini, M.
A1  - Pinton, P.
A1  - Prehn, J. H.
A1  - Puthalakath, H.
A1  - Rabinovich, G. A.
A1  - Ravichandran, K. S.
A1  - Rizzuto, R.
A1  - Rodrigues, C. M.
A1  - Rubinsztein, D. C.
A1  - Rudel, T.
A1  - Shi, Y.
A1  - Simon, H. U.
A1  - Stockwell, B. R.
A1  - Szabadkai, G.
A1  - Tait, S. W.
A1  - Tang, H. L.
A1  - Tavernarakis, N.
A1  - Tsujimoto, Y.
A1  - Vanden Berghe, T.
A1  - Vandenabeele, P.
A1  - Villunger, A.
A1  - Wagner, E. F.
A1  - Walczak, H.
A1  - White, E.
A1  - Wood, W. G.
A1  - Yuan, J.
A1  - Zakeri, Z.
A1  - Zhivotovsky, B.
A1  - Melino, G.
A1  - Kroemer, G.
T1  - Essential versus accessory aspects of cell death: recommendations of the NCCD 2015
JF  - Cell Death and Differentiation
N2  - Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as 'accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. 'Regulated cell death' (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.
Y1  - 2015
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-121207
VL  - 22
ER  - 
TY  - JOUR
A1  - Chiorean, E. G.
A1  - Von Hoff, D. D.
A1  - Reni, M.
A1  - Arena, F. P.
A1  - Infante, J. R.
A1  - Bathini, V. G.
A1  - Wood, T. E.
A1  - Mainwaring, P. N.
A1  - Muldoon, R. T.
A1  - Clingan, P. R.
A1  - Kunzmann, V.
A1  - Ramanathan, R. K.
A1  - Tabernero, J.
A1  - Goldstein, D.
A1  - McGovern, D.
A1  - Lu, B.
A1  - Ko, A.
T1  - CA19-9 decrease at 8 weeks as a predictor of overall survival in a randomized phase III trial (MPACT) of weekly nab-paclitaxel plus gemcitabine versus gemcitabine alone in patients with metastatic pancreatic cancer
JF  - Annals of Oncology
N2  - Background
A phase I/II study and subsequent phase III study (MPACT) reported significant correlations between CA19-9 decreases and prolonged overall survival (OS) with nab-paclitaxel plus gemcitabine (nab-P + Gem) treatment for metastatic pancreatic cancer (MPC). CA19-9 changes at week 8 and potential associations with efficacy were investigated as part of an exploratory analysis in the MPACT trial.

Patients and methods
Untreated patients with MPC (N = 861) received nab-P + Gem or Gem alone. CA19-9 was evaluated at baseline and every 8 weeks.

Results
Patients with baseline and week-8 CA19-9 measurements were analyzed (nab-P + Gem: 252; Gem: 202). In an analysis pooling the treatments, patients with any CA19-9 decline (80%) versus those without (20%) had improved OS (median 11.1 versus 8.0 months; P = 0.005). In the nab-P + Gem arm, patients with (n = 206) versus without (n = 46) any CA19-9 decrease at week 8 had a confirmed overall response rate (ORR) of 40% versus 13%, and a median OS of 13.2 versus 8.3 months (P = 0.001), respectively. In the Gem-alone arm, patients with (n = 159) versus without (n = 43) CA19-9 decrease at week 8 had a confirmed ORR of 15% versus 5%, and a median OS of 9.4 versus 7.1 months (P = 0.404), respectively. In the nab-P + Gem and Gem-alone arms, by week 8, 16% (40/252) and 6% (13/202) of patients, respectively, had an unconfirmed radiologic response (median OS 13.7 and 14.7 months, respectively), and 79% and 84% of patients, respectively, had stable disease (SD) (median OS 11.1 and 9 months, respectively). Patients with SD and any CA19-9 decrease (158/199 and 133/170) had a median OS of 13.2 and 9.4 months, respectively.

Conclusion
This analysis demonstrated that, in patients with MPC, any CA19-9 decrease at week 8 can be an early marker for chemotherapy efficacy, including in those patients with SD. CA19-9 decrease identified more patients with survival benefit than radiologic response by week 8.
KW  - CA19-9
KW  - pancreatic cancer
KW  - chemotherapy
KW  - nab-paclitaxel
KW  - MPACT
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-189659
VL  - 27
IS  - 4
ER  - 
TY  - JOUR
A1  - Ungethüm, K.
A1  - Wiedmann, S.
A1  - Wagner, M.
A1  - Leyh, R.
A1  - Ertl, G.
A1  - Frantz, S.
A1  - Geisler, T.
A1  - Karmann, W.
A1  - Prondzinsky, R.
A1  - Herdeg, C.
A1  - Noutsias, M.
A1  - Ludwig, T.
A1  - Käs, J.
A1  - Klocke, B.
A1  - Krapp, J.
A1  - Wood, D.
A1  - Kotseva, K.
A1  - Störk, S.
A1  - Heuschmann, P. U.
T1  - Secondary prevention in diabetic and nondiabetic coronary heart disease patients: insights from the German subset of the hospital arm of the EUROASPIRE IV and V surveys
JF  - Clinical Research in Cardiology
N2  - Background
Patients with coronary heart disease (CHD) with and without diabetes mellitus have an increased risk of recurrent events requiring multifactorial secondary prevention of cardiovascular risk factors. We compared prevalences of cardiovascular risk factors and its determinants including lifestyle, pharmacotherapy and diabetes mellitus among patients with chronic CHD examined within the fourth and fifth EUROASPIRE surveys (EA-IV, 2012–13; and EA-V, 2016–17) in Germany.

Methods
The EA initiative iteratively conducts European-wide multicenter surveys investigating the quality of secondary prevention in chronic CHD patients aged 18 to 79 years. The data collection in Germany was performed during a comprehensive baseline visit at study centers in Würzburg (EA-IV, EA-V), Halle (EA-V), and Tübingen (EA-V).

Results
384 EA-V participants (median age 69.0 years, 81.3% male) and 536 EA-IV participants (median age 68.7 years, 82.3% male) were examined. Comparing EA-IV and EA-V, no relevant differences in risk factor prevalence and lifestyle changes were observed with the exception of lower LDL cholesterol levels in EA-V. Prevalence of unrecognized diabetes was significantly lower in EA-V as compared to EA-IV (11.8% vs. 19.6%) while the proportion of prediabetes was similarly high in the remaining population (62.1% vs. 61.0%).

Conclusion
Between 2012 and 2017, a modest decrease in LDL cholesterol levels was observed, while no differences in blood pressure control and body weight were apparent in chronic CHD patients in Germany. Although the prevalence of unrecognized diabetes decreased in the later study period, the proportion of normoglycemic patients was low. As pharmacotherapy appeared fairly well implemented, stronger efforts towards lifestyle interventions, mental health programs and cardiac rehabilitation might help to improve risk factor profiles in chronic CHD patients.
KW  - coronary heart disease
KW  - diabetes mellitus
KW  - secondary prevention
KW  - EUROASPIRE
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-324037
VL  - 112
IS  - 2
ER  - 
TY  - JOUR
A1  - Burns, Alan J.
A1  - Goldstein, Allan M.
A1  - Newgreen, Donald F.
A1  - Stamp, Lincon
A1  - Schäfer, Karl-Herbert
A1  - Metzger, Marco
A1  - Hotta, Ryo
A1  - Young, Heather M.
A1  - Andrews, Peter W.
A1  - Thapar, Nikhil
A1  - Belkind-Gerson, Jaime
A1  - Bondurand, Nadege
A1  - Bornstein, Joel C.
A1  - Chan, Wood Yee
A1  - Cheah, Kathryn
A1  - Gershon, Michael D.
A1  - Heuckeroth, Robert O.
A1  - Hofstra, Robert M.W.
A1  - Just, Lothar
A1  - Kapur, Raj P.
A1  - King, Sebastian K.
A1  - McCann, Conor J.
A1  - Nagy, Nandor
A1  - Ngan, Elly
A1  - Obermayr, Florian
A1  - Pachnis, Vassilis
A1  - Pasricha, Pankaj J.
A1  - Sham, Mai Har
A1  - Tam, Paul
A1  - Vanden Berghe, Pieter
T1  - White paper on guidelines concerning enteric nervous system stem cell therapy for enteric neuropathies
JF  - Developmental Biology
N2  - Over the last 20 years, there has been increasing focus on the development of novel stem cell based therapies for the treatment of disorders and diseases affecting the enteric nervous system (ENS) of the gastrointestinal tract (so-called enteric neuropathies). Here, the idea is that ENS progenitor/stem cells could be transplanted into the gut wall to replace the damaged or absent neurons and glia of the ENS. This White Paper sets out experts' views on the commonly used methods and approaches to identify, isolate, purify, expand and optimize ENS stem cells, transplant them into the bowel, and assess transplant success, including restoration of gut function. We also highlight obstacles that must be overcome in order to progress from successful preclinical studies in animal models to ENS stem cell therapies in the clinic.
KW  - Neural crest cells
KW  - Rat mynteric plexus
KW  - Intestinal pseudoobstruction
KW  - Hypertrophic pyloric-stenosis
KW  - Hirschsprung disease liability
KW  - Slow-transit constipation
KW  - Oxide synthase gene
KW  - Term follow-up
KW  - Nitric-oxide
KW  - In-vivo
KW  - Enteric nervous system
KW  - Enteric neuropathies
KW  - Stem cells
KW  - Cell replacement therapy
KW  - Hirschsprung disease
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-187415
VL  - 417
IS  - 2
ER  -