Models for intra-hospital patient routing

Diese Magisterarbeit befasst sich mit dem in-house Transport von Patienten in pavillonartig strukturierten Krankenhäusern. Dieses Thema hat in den letzten Jahren an Bedeutung gewonnen, da Routing in Krankenhäusern große Kosten verursacht und ein effizienteres Routing sowohl die Kosten senken, als auch die Servicequalität, gemessen an der Patientenzufriedenheit, erhöhen kann. Ziel dieser Arbeit ist es, ein neues Modell für das in-house Routing von Patienten in Krankenhäusern zu entwickeln, das die Ansprüche von Patienten und Management gleichermaßen erfüllt. Patienten in Krankenhäusern haben fixe Termine, wie z.B. Röntgen- oder Ultraschalluntersuchungen, und müssen aus medizinischen Gründen oft von Trägern zu diesen Terminen begleitet werden. Im Modell werden die logistischen Kosten der Verwendung von Trägern und die Unannehmlichkeiten von Patienten minimiert. Außerdem gibt es zwei Erweiterungen, in der Ersten stehen primär patientenorientierte Sachverhalte im Vordergrund, in der Zweiten stehen krankenhaus- bzw. managementorientierte Sachverhalte im Vordergrund. Es wird gezeigt, dass die entwickelten Modelle in der Lage sind, reale Problemstellungen in mittelgroßen Krankenhäusern zu lösen. Das Modell gehört zur Gruppe der Pickup and Delivery-Probleme. Unter bestimmten Umständen kann das Model auch als Dial-a-Ride-Problem oder als spezielle Variante eines Stacker-Crane-Problems gesehen werden.This thesis deals with the in-house transportation of the patients in pavilion structured hospitals. This topic has gained increased attention over the last years, due to the fact that routing operations come at a high price and that efficient routing plan could not only help reduce the costs, but also to improve the service quality, which is reflected through patients’ satisfaction. The aim of this work is to introduce a new model for intra-hospital routing of patients, considering both client- and management related issues. Patients in a hospital have fixed appointments, such as x-rays or ultrasonic and due to medical reasons they may not be able to walk on their own, so they have to be escorted by porters. In the model logistical costs for the usage of porters and patient inconvenience are minimized. Furthermore, the model is expanded and changed accordingly in order to capture distinguish patient centred issues on one hand and hospital centred issues on the other hand. It has been shown that the different developed model variants are tractable for realistic problem instances in medium-sized hospitals. The model belongs to the group of pickup and delivery problems. Under some circumstances, the problem can be also seen as a dial-a-ride problem, or a special type of a stacker-crane problem

Enhancement of Cellular Antioxidant-Defence Preserves Diastolic Dysfunction via Regulation of Both Diastolic Zn 2+

We examined whether cellular antioxidant-defence enhancement preserves diastolic dysfunction via regulation of both diastolic intracellular free Zn2+ and Ca2+ levels (Zn2+i and Ca2+i) levels N-acetyl cysteine (NAC) treatment (4 weeks) of diabetic rats preserved altered cellular redox state and also prevented diabetes-induced tissue damage and diastolic dysfunction with marked normalizations in the resting Zn2+i and Ca2+i. The kinetic parameters of transient changes in Zn2+ and Ca2+ under electrical stimulation and the spatiotemporal properties of Zn2+ and Ca2+ sparks in resting cells are found to be normal in the treated diabetic group. Biochemical analysis demonstrated that the NAC treatment also antagonized hyperphosphorylation of cardiac ryanodine receptors (RyR2) and significantly restored depleted protein levels of both RyR2 and calstabin2. Incubation of cardiomyocytes with 10 µM ZnCl2 exerted hyperphosphorylation in RyR2 as well as higher phosphorphorylations in both PKA and CaMKII in a concentration-dependent manner, similar to hyperglycemia. Our present data also showed that a subcellular oxidative stress marker, NF-κB, can be activated if the cells are exposed directly to Zn2+. We thus for the first time report that an enhancement of antioxidant defence in diabetics via directly targeting heart seems to prevent diastolic dysfunction due to modulation of RyR2 macromolecular-complex thereby leading to normalized Ca2+i and Zn2+i in cardiomyocytes

Molecular and Electrophysiological Role of Diabetes-Associated Circulating Inflammatory Factors in Cardiac Arrhythmia Remodeling in a Metabolic-Induced Model of Type 2 Diabetic Rat

Background: Diabetic patients have prolonged cardiac repolarization and higher risk of arrhythmia. Besides, diabetes activates the innate immune system, resulting in higher levels of plasmatic cytokines, which are described to prolong ventricular repolarization. Methods: We characterize a metabolic model of type 2 diabetes (T2D) with prolonged cardiac repolarization. Sprague-Dawley rats were fed on a high-fat diet (45% Kcal from fat) for 6 weeks, and a low dose of streptozotozin intraperitoneally injected at week 2. Body weight and fasting blood glucose were measured and electrocardiograms of conscious animals were recorded weekly. Plasmatic lipid profile, insulin, cytokines, and arrhythmia susceptibility were determined at the end of the experimental period. Outward K+ currents and action potentials were recorded in isolated ventricular myocytes by patch-clamp. Results: T2D animals showed insulin resistance, hyperglycemia, and elevated levels of plasma cholesterol, triglycerides, TNFα, and IL-1b. They also developed bradycardia and prolonged QTc-interval duration that resulted in increased susceptibility to severe ventricular tachycardia under cardiac challenge. Action potential duration (APD) was prolonged in control cardiomyocytes incubated 24 h with plasma isolated from diabetic rats. However, adding TNFα and IL-1b receptor blockers to the serum of diabetic animals prevented the increased APD. Conclusions: The elevation of the circulating levels of TNFα and IL-1b are responsible for impaired ventricular repolarization and higher susceptibility to cardiac arrhythmia in our metabolic model of T2D.This work was supported by grants from the Gobierno Vasco PIBA2018-58 and GIC18/150 and MICINN PID2020-118814RB-I00. JZ-A is a predoctoral Fellow of the UPV/EHU and had a STSM from the EU COST Action CA16225

A Benign Rare Lesion of the Breast: Giant Epidermal Inclusion Cyst

An epidermal inclusion cyst can be seen at any location. Epidermal cysts are commonly found on the scalp, face, trunk, neck, and extremities. They are rarely seen in the breast parenchyma. These benign lesions are important in that they may undergo neoplastic differentiation, although very rarely. Epidermoid cysts usually develop as a result of the implantation of superficial epidermal tissue into the dermis or subcutaneous tissue after trauma or surgical procedures. In this study, a 37-year-old female patient who underwent a histopathological examination that showed a 10-cm epidermal cyst without a history of trauma or a surgical procedure was discussed

Altered mitochondrial metabolism in the insulin-resistant heart.

Obesity-induced insulin resistance and type 2 diabetes mellitus can ultimately result in various complications, including diabetic cardiomyopathy. In this case, cardiac dysfunction is characterized by metabolic disturbances such as impaired glucose oxidation and an increased reliance on fatty acid (FA) oxidation. Mitochondrial dysfunction has often been associated with the altered metabolic function in the diabetic heart, and may result from FA-induced lipotoxicity and uncoupling of oxidative phosphorylation. In this review, we address the metabolic changes in the diabetic heart, focusing on the loss of metabolic flexibility and cardiac mitochondrial function. We consider the alterations observed in mitochondrial substrate utilization, bioenergetics and dynamics, and highlight new areas of research which may improve our understanding of the cause and effect of cardiac mitochondrial dysfunction in diabetes. Finally, we explore how lifestyle (nutrition and exercise) and pharmacological interventions can prevent and treat metabolic and mitochondrial dysfunction in diabetes.COST Action MitoEAGL

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery