[Measures and Recommendations for Ensuring Adequate Inpatient Care Capacities for Pandemic Management within a Region: Results of a Hybrid Delphi Method].

Introduction: Since the beginning of the pandemic in spring 2020, inpatient healthcare has been under enormous burden, which is reflected especially in overworked staff, imprecise bed planning and/or data transfer. According to the recommendation of the Science Council, university clinics should play a controlling role in regional healthcare and act in conjunction with surrounding hospitals and practices.

Methods: In September 2021, 31 representatives from 18 university hospitals were invited to a hybrid Delphi study with a total of 4 survey rounds to discuss criteria for effective inpatient care in a pandemic situation, which were extracted from previous expert interviews.

Melatonin modifies cellular stress in the liver of septic mice by reducing reactive oxygen species and increasing the unfolded protein response.

Background & Aims: Melatonin's hepatoprotective actions have numerously been demonstrated in the past but the underlying molecular mechanisms are widely unknown. For a better understanding of melatonin's effects on hepatic stress response this study aimed to elucidate alterations in oxidative stress, unfolded protein response and acute phase response in septic mice.

Methods: Male C3H/HeN mice underwent sham operation or cecal ligation and incision and remained anesthetized for 5h.

Impact of melatonin receptor deletion on intracellular signaling in spleen cells of mice after polymicrobial sepsis.

Objective: Melatonin is known to influence immune functions and to ameliorate outcome after septic challenge but it is unknown whether this is mediated by melatonin receptor activation. This study aimed to elucidate molecular differences in spleen and ex vivo splenocytes of wild-type (WT) and melatonin receptor double knockout mice (KO) after polymicrobial sepsis.

Subjects And Methods: C3H/HeN wild-type and MT1-/-/MT2-/- mice underwent sham operation or cecum ligation and incision (CLI) and remained anesthetized for 1 h.

Inhibition of glycogen synthase kinase (GSK)-3-β improves liver microcirculation and hepatocellular function after hemorrhagic shock.

Ischemia and reperfusion may cause liver injury and are characterized by hepatic microperfusion failure and a decreased hepatocellular function. Inhibition of glycogen synthase kinase (GSK)-3β, a serine-threonine kinase that has recently emerged as a key regulator in the modulation of the inflammatory response after stress events, may be protective in conditions like sepsis, inflammation and shock. Therefore, aim of the study was to assess the role of GSK-3β in liver microcirculation and hepatocellular function after hemorrhagic shock and resuscitation (H/R).

Diagnosis and treatment of patients with stroke in a mobile stroke unit versus in hospital: a randomised controlled trial.

Background: Only 2-5% of patients who have a stroke receive thrombolytic treatment, mainly because of delay in reaching the hospital. We aimed to assess the efficacy of a new approach of diagnosis and treatment starting at the emergency site, rather than after hospital arrival, in reducing delay in stroke therapy.

Methods: We did a randomised single-centre controlled trial to compare the time from alarm (emergency call) to therapy decision between mobile stroke unit (MSU) and hospital intervention.

Delayed gastric emptying after pancreaticoduodenectomy: influence of the orthotopic technique of reconstruction and intestinal motilin receptor expression.

Background: Delayed gastric emptying (DGE) is still a common postoperative complication after pancreaticoduodenectomy (PD). Because different reconstruction techniques after PD and the influence of motilin receptor expression are controversially discussed, the present study analyzed the influence of a total orthotopic reconstruction technique on DGE after PD.

Methods: Data from patients undergoing PD and reconstruction using a total orthotopic technique were reviewed, and correlations between DGE and clinico-pathological variables were analyzed.

Bringing the hospital to the patient: first treatment of stroke patients at the emergency site.

Background: Early treatment with rt-PA is critical for favorable outcome of acute stroke. However, only a very small proportion of stroke patients receive this treatment, as most arrive at hospital too late to be eligible for rt-PA therapy.

Methods And Findings: We developed a "Mobile Stroke Unit", consisting of an ambulance equipped with computed tomography, a point-of-care laboratory system for complete stroke laboratory work-up, and telemedicine capabilities for contact with hospital experts, to achieve delivery of etiology-specific and guideline-adherent stroke treatment at the site of the emergency, well before arrival at the hospital.

Endothelin-1 contributes to hemoglobin glutamer-200-mediated hepatocellular dysfunction after hemorrhagic shock.

Hemoglobin glutamer-200 (HbG) might be an alternative to human blood. However, artificial oxygen carriers are initially successful to restore oxygen supply but may induce organ dysfunction and increase mortality several days after application in terms of delayed side effects. Impairment of microcirculation and an inflammatory cytokine response through induction of endothelin (ET) 1 may contribute.

Selective activation of melatonin receptors with ramelteon improves liver function and hepatic perfusion after hemorrhagic shock in rat.

Objective: Melatonin may attenuate organ damage via direct antioxidative properties, and was recently demonstrated to reduce cardiac and hepatic injury through receptor-dependent effects. However, the relevance of an isolated activation of melatonin receptors for organ protection, excluding direct antioxidant effects, has not been established yet. This study was designed to investigate whether therapy with melatonin receptor agonist and hypnotic substance ramelteon may improve liver function, hepatic perfusion, and hepatic integrity after hemorrhagic shock in rat.

Hemin arginate-induced heme oxygenase 1 expression improves liver microcirculation and mediates an anti-inflammatory cytokine response after hemorrhagic shock.

Microvascular failure is a major determinant for the development of hepatocellular dysfunction after hemorrhagic shock. Induction of heme oxygenase (HO) 1 may confer hepatocellular protection. Hemin arginate (HAR) induces HO-1 and protects against shock-induced organ failure.

Failure of two commercial indexes and spectral parameters to reflect the pharmacodynamic effect of desflurane on EEG.

Objective: We compared two PK/PD models, one with and one without a plateau effect. Bispectral (BIS, Aspect Medical Systems, Natick, MA, version XP) and Narcotrend (NCT, MonitorTechnik, Bad Bramstedt, Germany, Version 4.0) indices were used as an electroencephalographic measure of desflurane drug effect.

Melatonin receptors mediate improvements of liver function but not of hepatic perfusion and integrity after hemorrhagic shock in rats.

Objective: Melatonin has been demonstrated to attenuate organ damage in models of ischemia and reperfusion. Melatonin treatment before hemorrhagic shock has been shown to improve liver function and hepatic perfusion. Proposed mechanisms of the pineal hormone involve direct inactivation of reactive oxygen species and induction of antioxidative enzymes.

Melatonin pretreatment improves liver function and hepatic perfusion after hemorrhagic shock.

Exogenous administration of pineal hormone melatonin (MEL) has been demonstrated to attenuate organ damage in models of I/R and inflammation by antioxidative effects. However, specific organ-protective effects of MEL with respect to hemorrhagic shock have not been investigated yet. In the present study, we evaluated the role of MEL pretreatment for hepatic perfusion, redox state, and function after hemorrhage and resuscitation, with emphasis on MEL receptor activation.

Dobutamine improves liver function after hemorrhagic shock through induction of heme oxygenase-1.

Rationale: Induction of heme oxygenase-1 (HO-1) protects the liver against reperfusion injury after hemorrhagic shock. Previous data suggest that the beta(1)-adrenoceptor agonist dobutamine induces HO-1 in hepatocytes.

Objectives: To investigate the functional significance of dobutamine pretreatment for liver function after hemorrhagic shock in vivo.

Influence of heme-based solutions on stress protein expression and organ failure after hemorrhagic shock.

Objective: Hemoglobin-based oxygen carriers (e.g., diaspirin-cross-linked hemoglobin [DCLHb] and hemoglobin glutamer-200 [HbG]) may have potential in the treatment of hemorrhagic shock.

Mechanism of the delay phenomenon: tissue protection is mediated by heme oxygenase-1.

Induction of the "delay phenomenon" by chronic ischemia is an established clinical procedure, but the mechanisms conferring tissue protection are still incompletely understood. To elucidate the role of heme oxygenase-1 [HO-1 or heat shock protein-32 (HSP-32)] in delay, we examined in the skin-flap model of the ear of the hairless mouse, 1) whether chronic ischemia (delay) is capable to induce expression of HO-1, and 2) whether delay-induced HO-1 affects skin-flap microcirculation and survival by either its carbon monoxide-associated vasodilatory action or its biliverdin-associated anti-oxidative mechanism. Chronic ischemia was induced by transsection of the central feeding vessel of the ear 7 days before flap creation.

Heme oxygenase-1 gene expression in pericentral hepatocytes through beta1-adrenoceptor stimulation.

Induction of heme oxygenase (HO)-1 may confer hepatocellular protection, e.g., in reperfusion injury.

Perflubron emulsion in prolonged hemorrhagic shock: influence on hepatocellular energy metabolism and oxygen-dependent gene expression.

Background: Liver dysfunction as a result of impaired oxygen availability frequently occurs following hemorrhage and contributes to delayed mortality. Artificial oxygen carriers may improve oxygen supply to vital organs while avoiding the need for allogeneic transfusion.

Methods: Rats were subjected to hemorrhagic hypotension (mean arterial pressure = 35-40 mmHg for 120 min) and were subsequently resuscitated with (1) stored whole rat blood, (2) pentastarch, or (3) pentastarch combined with perflubron emulsion (PFE; 2.

Hyperthermia preconditioning induces renal heat shock protein expression, improves cold ischemia tolerance, kidney graft function and survival in rats.

Background: Evidence indicates that hyperthermia preconditioning (HP) can be protective in kidney transplantation, possibly through increased heat shock protein (HSP) expression. A detailed study about individual HSPs and functional preservation is lacking, however. Therefore, we studied the effects of HP on kidney graft survival, function and HSP expression.

Connective tissue growth factor gene expression alters tumor progression in esophageal cancer.

The ability of cancer cells to initiate specific fibroblast reactions may subsequently determine tumor evolution. In the present study we examined the coordinated expression of transforming growth factor-beta-1 (TGF-beta1), its signaling receptors, and its downstream mediator-connective tissue growth factor (CTGF)--and their impact on tumor progression and fibrogenesis in esophageal carcinomas. Messenger ribonucleic acid (mRNA) expression of TGF-beta1, CTGF, TGF-beta receptor subtype I ALK5 (TbetaR-IALK5), and TGF-beta receptor type II (TbetaR-II) was studied by Northern blot analysis in esophageal cancer and the normal esophagus.