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Long-term management after stroke has not been standardized in contrast to acute and rehabilitative stroke care. The fragmented outpatient sector of healthcare allows a high degree of flexibility but also variability in the quality of care provided. The commission on long-term stroke care of the German Stroke Society developed a concept on how to provide standardized multiprofessional long-termstroke carewith a focus on patient-centered comprehensive care. We propose a diagnostic work-up in stages, with an initial patient-reported screening, followed by an adapted in-depth assessment of affected domains. This includes internistic domains (management of risk factors) and also genuine neurological domains (spasticity, cognitive deficits etc.) that must be considered. This information is then merged with patient expectations and prioritization to a standardized treatment plan. Special challenges for the implementation of such a comprehensive care system are the intersectoral and intrasectoral communication between healthcare providers, patients and relatives, the need to create a compensation system for providers and the establishment of appropriate quality management services. Digital health applications are helpful tools to provide aspects of diagnostics, treatment and communication in long-term stroke care., Die Schlaganfallnachsorge ist im Gegensatz zur akuten und rehabilitativen Versorgung des Schlaganfalls wenig standardisiert. Der fragmentierte ambulante Sektor erlaubt hierbei ein hohes Maß an Flexibilität, leidet aber folglich an variabler Qualität der Nachsorge. Die Kommission Nachsorge der Deutschen Schlaganfall-Gesellschaft formuliert in diesem Positionspapier ein inhaltliches Konzept, um eine strukturierte Nachsorge mit multiprofessionellem Ansatz zu entwickeln. Diese soll im Sinne einer „Comprehensive-care“-Versorgung und patientenzentriert erfolgen. Dazu schlagen wir ein diagnostisches Stufenkonzept mit Screening und ggf. weitergehender Untersuchung vor, das in Absprache mit den Betroffenen zu einem standardisierten Therapieplan führt, der im Langzeitverlauf entsprechend angepasst werden muss. Inhaltlich sind sowohl internistische Domänen (Management von Risikofaktoren) als auch genuin neurologische Domänen (Spastik, kognitive Defizite etc.) zu berücksichtigen. Besondere Herausforderungen an dieses Konzept sind die sektorenübergreifende (inter- und intrasektorale) Kommunikation zwischen den Akteuren im Gesundheitswesen untereinander sowie mit den Patienten und Angehörigen, die Notwendigkeit zur Schaffung eines Vergütungsmodells für eine solche Nachsorge und letztlich die Etablierung eines entsprechenden Qualitätsmanagements. Digitale Lösungen erachten wir als hilfreiche Werkzeuge für Aspekte der Diagnose, Therapie und Kommunikation in der Schlaganfallnachsorge.

To avoid innate sensing and immune control, human immunodeficiency virus type 1 (HIV-1) has to prevent the accumulation of viral complementary DNA species. Here, we show that the late HIV-1 accessory protein Vpu hijacks DNA repair mechanisms to promote degradation of nuclear viral cDNA in cells that are already productively infected. Vpu achieves this by interacting with RanBP2-RanGAP1*SUMO1-Ubc9 SUMO E3-ligase complexes at the nuclear pore to reprogramme promyelocytic leukaemia protein nuclear bodies and reduce SUMOylation of Bloom syndrome protein, unleashing end degradation of viral cDNA. Concomitantly, Vpu inhibits RAD52-mediated homologous repair of viral cDNA, preventing the generation of dead-end circular forms of single copies of the long terminal repeat and permitting sustained nucleolytic attack. Our results identify Vpu as a key modulator of the DNA repair machinery. We show that Bloom syndrome protein eliminates nuclear HIV-1 cDNA and thereby suppresses immune sensing and proviral hyper-integration. Therapeutic targeting of DNA repair may facilitate the induction of antiviral immunity and suppress proviral integration replenishing latent HIV reservoirs.

This is a post-peer-review, pre-copyedit version of an article published in Polar Biology. The final authenticated version is available online at: http://dx.doi.org/https://doi.org/10.1007/s00300-019-02588-z. Although cryptogamic covers are important ecosystem engineers in high Arctic tundra, they were often neglected in vegetation surveys. Hence we conducted a systematic survey of cryptogamic cover and vascular plant coverage and composition at two representative, but differing Arctic sites (Ny-Ålesund, Svalbard) along catenas with a natural soil moisture gradient, and integrated these data with physical–chemical soil properties. Soil samples were taken for comprehensive pedological and mineralogical analyses. Vegetation surveys were conducted based on classification by functional groups. Vascular plants were identified to species level. Correlation and multivariate statistical analysis were applied to determine the key environmental factors explaining vegetation patterns along the soil moisture gradients. We observed significant differences in gravimetric water, soil organic matter and nutrient contents along the moisture gradients. These differences were coincident with a shift in vegetation cover and species composition. While chloro- and cyanolichens were abundant at the drier sites, mosses dominated the wetter and vascular plants the intermediate plots. Twenty four vascular plant species could be identified, of which only six were present at both sites. Cryptogamic covers generally dominated with maximum areal coverage up to 70% and hence should be considered as a new additional syntaxon in future ground-truth and remote sensing based vegetation surveys of Svalbard. Multivariate analysis revealed that soil moisture showed the strongest relation between vegetation patterns, together with NH4–N and pH. In conclusion, soil moisture is a key driver in controlling cryptogamic cover and vegetation coverage and vascular plant species composition in high Arctic tundra.

RNA-modulating factors not only regulate multiple steps of cellular RNA metabolism, but also emerge as key effectors of the immune response against invading viral pathogens including human immunodeficiency virus type-1 (HIV-1). However, the cellular RNA-binding proteins involved in the establishment and maintenance of latent HIV-1 reservoirs have not been extensively studied. Here, we screened a panel of 62 cellular RNA-binding proteins and identified NEDD4-binding protein 1 (N4BP1) as a potent interferon-inducible inhibitor of HIV-1 in primary T cells and macrophages. N4BP1 harbours a prototypical PilT N terminus-like RNase domain and inhibits HIV-1 replication by interacting with and degrading viral mRNA species. Following activation of CD4+ T cells, however, N4BP1 undergoes rapid cleavage at Arg 509 by the paracaspase named mucosa-associated lymphoid tissue lymphoma translocation 1 (MALT1). Mutational analyses and knockout studies revealed that MALT1-mediated inactivation of N4BP1 facilitates the reactivation of latent HIV-1 proviruses. Taken together, our findings demonstrate that the RNase N4BP1 is an efficient restriction factor of HIV-1 and suggest that inactivation of N4BP1 by induction of MALT1 activation might facilitate elimination of latent HIV-1 reservoirs. The interferon-inducible RNA-binding protein N4BP1 binds to and degrades HIV-1 mRNAs, thus inhibiting viral degradation and promoting viral latency. However, metacaspase-mediated degradation of N4BP1 following activation of CD4+ T cells facilitates HIV-1 latency reversal.

The members of the SepNet Critical Care Trials Group were provided in such a way that they could not be indexed as collaborators on PubMed. The publisher apologizes for this error and is pleased to list the members of the group here.

Background Stroke patients are often affected by long-term disabilities with needs concerning social issues. There is relatively little consideration of social recovery of patients and the support required to return to work, receive social benefits, participate in daily life activities, maintain contact with family and friends and to organize financial affairs. In our study we aimed to investigate if existing tools record social needs adequately. We analyzed the current provision of social support provided in long-term care after stroke and whether unmet social needs were associated with quality of life, caregiver burden, overall function and degree of disability. Methods Our analysis is part of the Managing Aftercare of Stroke study (MAS-I), a cross-sectional exploratory study of patient needs 2–3 years after initial stroke. Assessment tools included the Nikolaus-score (social situation), the EuroQoL (quality of life), the German Burden Scale for Family Caregivers (caregiver burden), the modified Rankin Scale (disability / dependence), Stroke Impact Scale (function and degree of disability) and the Stroke Survivor Needs Questionnaire (unmet needs). Results Overall 57 patients were included in MAS-I, with ten patients classified in urgent need of socio-economic support according to the Nikolaus-score. Patients with lower than normal Nikolaus-score had a higher degree of disability. Thirty percent of all patients had never received professional social support. Social worker contact happened mostly during the stay in acute hospital or rehabilitation institution. Only four patients (11%) reported long-term support after discharge. Apart from social worker contact during acute care, 43% of patients had unmet needs in the long-term aftercare. Forty percent of all patients included in MAS-I were recommended for social work intervention after an in-depth analysis of their situation. Finally, we saw that unmet social needs were associated with lower quality of life and higher caregiver burden. Conclusions Our data suggest significant unmet needs in social care in long-term stroke patients. Screening tools for unmet social needs such as the Nikolaus-score do not holistically report patients’ needs. Trial registration Clinicaltrials.Gov NCT02320994. Registered 19 December 2014 (retrospectively registered).

Lentiviral Nefs recruit assembly polypeptide complexes and target sorting motifs in cellular receptors to induce their internalization. While Nef-mediated CD4 downmodulation is conserved, the ability to internalize CD3 was lost in HIV-1 and its precursors. Although both functions play key roles in lentiviral replication and pathogenicity, the underlying structural requirements are poorly defined. Here, we determine the structure of SIVmac239 Nef bound to the ExxxLM motif of another Nef molecule at 2.5 Å resolution. This provides a basis for a structural model, where a hydrophobic crevice in simian immunodeficiency virus (SIV) Nef targets a dileucine motif in CD4 and a tyrosine-based motif in CD3. Introducing key residues into this crevice of HIV-1 Nef enables CD3 binding but an additional N-terminal tyrosine motif is required for internalization. Our resolution of the CD4/Nef/AP2 complex and generation of HIV-1 Nefs capable of CD3 downregulation provide insights into sorting motif interactions and target discrimination of Nef., HIV and simian immunodeficiency virus (SIV) Nef proteins both stimulate the clathrin-mediated endocytosis of CD4 but differ in downmodulation of the immune receptor CD3. Here, the authors present the structure of SIV Nef bound to the ExxxLM motif of another Nef molecule, which allows them to propose a model how Nef recognizes these motifs in CD3 and CD4.

This correction stands to the correct a spelling error to contributor name: Karin Glaser. The author group and the publisher wish all to recognize the name as Karin Glaser and not the former. The original article has been corrected.

Fuster, Josep et al., [Background]: Neutrophil gelatinase-associated lipocalin (NGAL) expression is increased in epithelial cancer patients, but studies showing its relation to prognosis are scarce. We aimed to test the ability of preoperative serum NGAL levels (pNGAL) to predict recurrence in metastatic and nonmetastatic colorectal cancer (CRC) patients. [Methods]: This retrospective study determined pNGAL levels in 60 healthy individuals, 47 patients with nonmetastatic CRC, and 70 patients with metastatic CRC undergoing curative neoplastic resection. Patients were divided into low- and high-pNGAL groups using a median series-based cutoff. [Results]: The mean ± SD pNGAL in CRC patients (nonmetastatic and metastatic) was 102.3 ± 66.6 (median 91.4). Nonmetastatic CRC and metastatic CRC patients had higher pNGAL than healthy controls (88 ± 64 and 112 ± 67 vs. 0.6 ± 0.3, respectively, both p < 0.0001). Nonmetastatic CRC patients with deeper tumor invasion and metastatic CRC patients with shorter disease-free interval after CRC resection had higher pNGAL. pNGAL levels correlated with neoplastic tissue volume. CRC patients with recurrence had higher pNGAL than those without recurrence (118 ± 64 vs. 88 ± 66, p = 0.013), and high-pNGAL patients had a higher recurrence rate (59.3 vs. 36.2 %, p = 0.016). Median pNGAL-based risk classification had a sensitivity of 62.5 % for predicting neoplastic progression in CRC patients and 74.3 % for predicting neoplastic progression during the first year after metastatic CRC resection. [Conclusions]: pNGAL is higher in CRC patients than in the healthy population, which indicates a potential screening role. High-pNGAL levels are associated with higher neoplastic tissue volume, characteristics of neoplastic invasion, and recurrence, showing a prognostic utility mainly in metastatic CRC patients, J.F. has been funded by an investigation grant from Abertis Infraestructuras S.A.

Wallnofer S. and Hotter M. 2008. Syntaxonomy and site ecology of mixed oak forest communities in the Inner and Intermedial Alps of Tyrol (Austria). Bot. Helv. 118: 21 – 43.

Ischemic preconditioning has shown to reduce apoptosis in the intestinal mucosa during ischemia/reperfusion. This study evaluated if the decrease of apoptotic events found during preconditioning could be related with a reduction of the substrate (i.e., xanthine/hypoxanthine) available for xanthine oxidase (XO). Animals were randomly assigned to the following study groups: C, control; I/R, ischemia/reperfusion; P+I/R, ischemic preconditioning; P+I/R+H/X, ischemic preconditioning plus hypoxanthine/xanthine, and P+I/R+H/X+Allo, ischemic preconditioning plus hypoxanthine/xanthine plus allopurinol. Caspase-3 activity, DNA fragmentation and TUNEL staining increased in the I/R group compared to control. Ischemic preconditioning (P+I/R group) was able to reverse these apoptotic variables to a level similar to that of control rats. The addition of hypoxanthine/xanthine to rats subjected to ischemic preconditioning (P+I/R+H/X group) showed the highest apoptotic activity; however, further addition of allopurinol (P+I/R+H/X+Allo group) decreased significantly apoptotic activity and events. In conclusion, intestinal ischemic preconditioning is able to reduce apoptosis during the following sustained ischemia/reperfusion event because of a reduced accumulation of xanthine/hypoxanthine nucleotide., This study was supported by EU grant QLK6-CT-2000-00064, SAF 2000/ 3090-CE0057 and FISS 01/1691. A. Sola is supported by CSIC into I3P Programme

Renal injury due to ischaemia/reperfusion (I/R) leads to impaired renal function. One of the essential pathological changes thereby is cell death due to apoptosis. This study investigated the effect of adenosine administration on caspase-3 (C3) activity and expression during warm renal ischaemia in rat kidney and the role of nitric oxide (NO) as a mediator of the adenosine-induced effect. The following experimental groups were studied: control, ischaemia, ischaemia with adenosine administration, ischaemia with adenosine and N-nitro-L-arginine methyl ester (L-NAME) treatment and ischaemia with NO donor administration. C3 activity was measured and its protein expression determined by Western blot analysis. Supplementation of adenosine or NO during ischaemia increased C3 activity and protein expression but the effect of adenosine was reversed in rats treated with L-NAME. We conclude that adenosine increases C3 activity through an NO-dependent mechanism., This work was supported by the European Community (QLK6-2000-00064), Ministerio de Ciencia y Tecnología (Spain) (FISS 01/1691) and Ministerio de Ciencia y Tecnología (SAF 2000-3090-CE)

We examined 77 obese patients treated with bariatric surgery in order to analyse treatment success, and compare those with a good or a poor outcome. The subjects, who were recruited one year after undergoing adjustable gastric banding, were asked questions concerning their sociodemographic status, postoperative course, past and present weight status, eating behaviours and difficulties in changing eating habits. Furthermore, we also used two body image questionnaires, and considered the patients' evaluations of positive and negative changes, as well as their wishes for the future. There were no preoperative differences between the 71% of patients in the good outcome group and the 29% in the poor outcome group. With regard to the postoperative course, the poor outcome group had more problems in adapting to new eating behaviours, experienced significantly more post-surgical complications, and had a persistently negative body evaluation. Both groups were satisfied with their achieved weight loss achieved, and their improved self-esteem and mobility. Adjustable gastric banding seems to be successful in inducing weight loss and allowing a better quality of life. However, factors such as postoperative complications, the ability and willingness to adopt new eating attitudes, and an improved body image seem to be crucial for therapeutic outcome.

This work studied the activation of hepatic macrophages during acute pancreatitis and the involvement of these cells in the lung inflammatory response. Pancreatitis was induced in Wistar rats by intraductal administration of 5% sodium taurocholate. Three hours after pancreatitis induction, the degree of pulmonary inflammation, TNF-α levels, and P-selectin expression were evaluated. The generation of TNF-α by Kupffer cells was also measured. Pancreatitis increases the serum concentration of TNF-α, neutrophil infiltration, and P-selectin expression in pancreas and lung. In addition, Kupffer cells generate increased levels of TNF-α. When Kupffer cells were inhibited, the increase in serum TNF-α levels and the infiltration of neutrophils in the lung were prevented, but P-selectin expression remained unmodified. We conclude that pulmonary inflammation induced by acute pancreatitis is mediated by Kupffer cell activation and that pancreatitis induces the expression of P-selectin on pulmonary endothelial cells but this effect is not mediated by Kupffer cells.

Formation of nitric oxide (NO) inischemia-reperfusion (I-R) associated with pancreastransplantation could modulate the inflammatoryresponse. In this sense, previous studies havedemonstrated the action of NO on vasoactive substances likeprostacyclin or endothelin. The present study wasdesigned to evaluate the contribution of endothelin tothe inflammatory events induced by NO in the I-R processassociated with pancreas transplantation. For thispurpose, pancreatic levels of endothelin, neutrophilinfiltration, and prostacyclin were evaluated in anexperimental model of pancreas transplantation afterinhibition of NO synthesis or after NO inhibition plusaddition of endothelin. Results show significantposttransplantation increases in endothelin, neutrophilinfiltration, and prostacyclin production. Theseincreases were prevented by NO inhibition. Endothelinadministration plus nitric oxide inhibition reversedthis effect, resulting in an increase in myeloperoxidaseand 6-ketoprostaglandin F1α. Theseresults suggest that the proinflammatory effects of NO in I-Rassociated with pancreas transplantation are mediated bythe induction of endothelin generation.

Rhizobium loti strain PN4115 (NZP2213 str-1) ineffectively nodulates Leucaena leucocephala, i.e., strain PN4115 induces nodulation (Nod+) and is able to invade these nodules (Inv+), but fails to fix nitrogen (Fix–). Strain PN4115 does not synthesize a flavolan-binding polysaccharide (FBP), which is synthesized by the fully effective (Nod+Inv+Fix+) R. loti strain PN184 (NZP2037 str-1). The FBP may offer protection from prodelphinidin-rich flavolans synthesized by Lc. leucocephala. In this work, we show that exopolysaccharide (EPS)-negative mutants derived from strain PN4115 have a more severe ineffective phenotype (Nod+Inv–Fix–) on Lc. leucocephala than strain PN4115. This suggests that EPS from strain PN4115 is functional during invasion of Lc. leucocephala and that the requirement for EPS precedes the requirement for FBP.

The role of nitric oxide, produced during reperfusion as a function of preservation time, in the development of the inflammatory process in pancreas transplantation has been explored. For this purpose, the effect of nitric oxide synthase inhibition, as well as 6-keto-prostaglandin F1alpha, leukotriene B4, and lipoperoxidation levels were evaluated in an experimental model of rat pancreas transplantation after different periods of cold preservation. The results show posttransplantation increases in 6-keto-prostaglandin F1alpha, leukotriene B4, and lipoperoxidation levels in pancreatic tissue and in plasma lipase. When ischemia was induced for 30 min, nitric oxide synthase inhibition prevented these increases, and L-arginine was able to reverse this effect. By contrast, nitric oxide synthase inhibition has no effect when ischemia was prolonged for 12 hr. In summary, this study suggests that, during reperfusion, nitric oxide modulates 6-keto-prostaglandin F1alpha synthesis, lipoperoxidation levels, and the development of pancreatic injury but only when the ischemic period is quite short.

The role of nitric oxide in lipoxygenase metabolism after a process of ischemia-reperfusion in pancreas transplantation has been evaluated in this study. Sprague-Dawley rats were randomized into three groups, as follows: Group I--Control animals not surgically manipulated; Group II.--Pancreas transplantation, after 12 h of organ preservation; Group III.--Same as II but with administration of NG-nitro-L-arginine methyl esther (a nitric oxide synthase inhibitor) (10 mg/Kg) prior to organ revascularization. The results show post-transplantation increases in leukotriene B4 and 12-hydroxyeicosatraenoic acid levels in pancreatic tissue. Nitric oxide synthase inhibition reversed the increases in 12-hydroxyeicosatetraenoic acid, but was unable to modify leukotriene B4 increases suggesting the existence of a direct effect of nitric oxide on the 12-lipoxygenase metabolism in pancreas transplantation.

A nuclear factor (SBF-1) has previously been identified in Phaseolus vulgaris L. (bean) suspension cell nuclear extracts that binds in vitro to three DNase I-footprinted elements (SBF-1 boxes I, II, and III, 5' to 3') in the 5' region of the bean CHS15 (chalcone synthase) gene promoter. To define the functional role of the three SBF-1 boxes in development, we examined transgenic tobacco plants carrying a series of nested CHS15 promoter-beta-glucuronidase (GUS) fusions for GUS activity by histochemical staining. We show that the CHS15 promoter deleted to position -173 and lacking all three SBF-1 boxes directs the same qualitative pattern of expression in initiating lateral roots and in developing seeds as the full length promoter (-326). Thus, activation of expression in these organs is mediated by sequence elements located downstream of the three SBF-1 boxes. However, specific deletions within the -326 to -173 region modulate expression. Thus, deletion of box II abolishes GUS activity in initiating lateral roots. Further deletion of box III fails to restore expression but subsequent deletion of an additional 43 bp to position -173 re-establishes expression. We show that sequence-specific DNA-binding activities consistent with these results are present in nuclear extracts of bean roots and seeds. These studies reveal cis elements within the CHS15 promoter, and potential trans factors, that permit organ- and tissue-specific developmental patterns of regulation to be combined with a flexible response to environmental cues.

The role of nitric oxide in eicosanoid and oxygen-free radical production in the early stages of sodium taurocholate-induced acute necrotizing pancreatitis has been studied. Male Wistar rats were divided into three groups: group I: control group, a volume of 0.1 ml/100 g body wt saline solution was injected at low pressure in the pancreatic duct; group II: acute pancreatitis was induced by administration of 3.5% sodium taurocholate; and group III: intravenous administration of NG-nitro-L-arginine methyl esther (a nitric oxide synthase inhibitor) 5 min before induction of acute pancreatitis as stated for group II. At 5 and 60 min after induction of pancreatitis, blood and pancreas tissue samples were taken for assays. Increases in 6-keto PGF1 alpha, TXB2, PGE2, PGF2 alpha, and 12-HETE were observed in the pancreatic tissue. Lipoperoxidation was also enhanced and remained unaltered after nitric oxide inhibition. The fact that nitric oxide synthase inhibition could only reverse the increases in 6-keto PGF1 alpha and TXB2 levels indicates that in acute pancreatitis endothelial and platelet eicosanoid generation is mediated through an nitric oxide-dependent mechanism. In contrast, nitric oxide appears to be not related with oxygen free radical damage associated with acute pancreatitis.

The aim of this study has been the evaluation of an automated system for on-line sample preparation using solid phase extraction and HPLC purification for the measurement of prostanoids in urine. We have established the optimum precolumn and column conditions for this analysis. The manual extraction —HPLC procedure furnishes lower recoveries and higher coefficients of variation than those obtained by the automated on-line procedure. The automated system has been applied to prostanoid analysis of human urine samples from subjects exposed to lead.

The differentiation of HL-60 human promyelocytic leukaemia cells into specific monocytic or granulocytic lineage cells depending of the inductor agent is accompanied by selective regulation of several key enzymes involved in the synthesis of eicosanoids. In this communication we have investigated the changes in arachidonic acid metabolic profiles during phorbol 12-myristate 13-acetate (PMA)-induced monocytic differentiation of HL-60 cells. Our results show that HL-60 cells have spontaneous capacity to synthesize large amounts of LTB4, but PMA-differentiated cells lose the ability to release LTB4. Significant differences are found between HL-60 cells and PMA-treated cells in basal conditions and under ionophore stimulation. The addition of LTB4 at the time of PMA differentiation did not have effects on cell proliferation, but nordihydroguaiaretic acid (NDGA), a potent 5-lipoxygenase inhibitor, also inhibited HL-60 cell proliferation and did not have any effect on PMA-differentiated cell proliferation.

Systemic prostacyclin and thromboxane A2 production in rat experimental acute pancreatitis has been evaluated by measuring the urinary excretion of the 2,3-dinor 6-keto prostaglandin F1 alpha and 2,3-dinor thromboxane B2, respectively. Acute pancreatitis was induced by intraductal administration of 4.5% sodium taurocholate (0.1 ml/100 mg body weight) and intravenous cerulein perfusion (5 micrograms/kg/hr) for 6 hr, respectively. Urinary excretion of 2,3-dinor 6-keto prostaglandin F1 alpha and 2,3-dinor thromboxane B2 were much more important in sodium taurocholate- than in cerulein-induced acute pancreatitis. These data confirm an altered prostacyclin and thromboxane metabolism occurring in experimental acute pancreatitis. Phospholipase A2 activity and the effect of gabexate mesilate on the arachidonate metabolism were also evaluated.

This work is licensed under the Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 Unported License.-- et al., Injury due to cold ischemia reperfusion (I/R) is a major cause of primary graft non-function following liver transplantation. We postulated that I/R-induced cellular damage during liver transplantation might affect the secretory pathway, particularly at the endoplasmic reticulum (ER). We examined the involvement of ER stress in organ preservation, and compared cold storage in University of Wisconsin (UW) solution and in Institute Georges Lopez-1 (IGL-1) solution. In one group of rats, livers were preserved in UW solution for 8 h at 4 °C, and then orthotopic liver transplantation was performed according to Kamada's cuff technique. In another group, livers were preserved in IGL-1 solution. The effect of each preservation solution on the induction of ER stress, hepatic injury, mitochondrial damage and cell death was evaluated. As expected, we found increased ER stress after liver transplantation. IGL-1 solution significantly attenuated ER damage by reducing the activation of three pathways of unfolded protein response and their effector molecules caspase-12, C/EBP homologous protein-10, X-box-binding protein 1, tumor necrosis factor-associated factor 2 and eukaryotic translation initiation factor 2. This attenuation of ER stress was associated with a reduction in hepatic injury and cell death. Our results show that IGL-1 solution may be a useful means to circumvent excessive ER stress reactions associated with liver transplantation, and may optimize graft quality. © 2012 Macmillan Publishers Limited All rights reserved., This work was supported by The Ministry of Health and Consumption (PI 081988), CIBER-ehd, Carlos III Institute, Madrid, Spain; Ministry of Foreign Affairs and International Cooperation (A/020255/08 and A/02987/09).