Inkrementelle Integritätsprüfung und Sichtenaktualisierung in SQL

Zentrales Problem der Implementierung von Integritätsbedingungen und materialisierten Sichten ist die effiziente Reaktion auf Basisfakten-änderungen. Ändert sich ein Basisfakt durch Einfügung, Löschung oder Modifikation, so müssen die Integritätsbedingungen geprüft und die abgeleiteten und gespeicherten Fakten materialisierter Sichten aktualisiert werden. Da die Dauer der Integritätsprüfung und Sichten-aktualisierung unmittelbar die Ausführungsdauer einer Transaktion beeinflußt, ist eine effiziente Durchführung von entscheidender Bedeutung. Effiziente Verfahren zur Integritätsprüfung und Aktualisierung materialisierter Sichten gehören seit mehr als 15 Jahren zu den wichtigsten Problemen der Forschungen zu deduktiven Datenbanken. Die im Kontext von Datalog und Relationaler Algebra entwickelten inkrementellen Verfahren haben jedoch bislang kaum Anwendung in SQL gefunden. Dies zeigt sich an den funktional sehr beschränkten Implementierungen beider Konzepte in SQL-basierten Datenbank-systemen kommerzieller Hersteller. Zentrale Idee inkrementeller Ansätze ist, dass Integritätsprüfung und Sichtenaktualisierung nur für die aktuell geänderten Fakten durchgeführt werden. Zu diesem Zweck werden im Rahmen eines Änderungspropagierungsprozesses die durch Basisfaktenänderungen induzierten Änderungen abgeleiteter Fakten ermittelt. Da bei den bisherigen inkrementellen Verfahren SQL-spezifische Konzepte wie das SQL-Transaktions- und Integritätskonzept nicht berücksichtigt wurden, ist eine Anwendung dieser Verfahren in SQL nicht direkt möglich. Aus diesem Grund werden im Rahmen der vorgelegten Dissertation inkrementelle Verfahren zur effizienten Integritätsprüfung und Sichtenaktualisierung im Kontext von SQL entwickelt. Bei den Verfahrensentwürfen werden SQL-spezifische Systemeigenschaften unverändert berücksichtigt. Die Implementierung dieser Verfahren in SQL-basierten, kommerziellen Datenbanksystemen würde diese Systeme funktional um leistungsfähige Komponenten zur Integritätsprüfung und zur Simulation und Aktualisierung materialisierter Sichten erweitern

SGLT2 is not expressed in pancreatic α- and β-cells, and its inhibition does not directly affect glucagon and insulin secretion in rodents and humans.

OBJECTIVE: Sodium-glucose cotransporter 2 (SGLT2) inhibitors (SGLT2i), or gliflozins, are anti-diabetic drugs that lower glycemia by promoting glucosuria, but they also stimulate endogenous glucose and ketone body production. The likely causes of these metabolic responses are increased blood glucagon levels, and decreased blood insulin levels, but the mechanisms involved are hotly debated. This study verified whether or not SGLT2i affect glucagon and insulin secretion by a direct action on islet cells in three species, using multiple approaches. METHODS: We tested the in vivo effects of two selective SGLT2i (dapagliflozin, empagliflozin) and a SGLT1/2i (sotagliflozin) on various biological parameters (glucosuria, glycemia, glucagonemia, insulinemia) in mice. mRNA expression of SGLT2 and other glucose transporters was assessed in rat, mouse, and human FACS-purified α- and β-cells, and by analysis of two human islet cell transcriptomic datasets. Immunodetection of SGLT2 in pancreatic tissues was performed with a validated antibody. The effects of dapagliflozin, empagliflozin, and sotagliflozin on glucagon and insulin secretion were assessed using isolated rat, mouse and human islets and the in situ perfused mouse pancreas. Finally, we tested the long-term effect of SGLT2i on glucagon gene expression. RESULTS: SGLT2 inhibition in mice increased the plasma glucagon/insulin ratio in the fasted state, an effect correlated with a decline in glycemia. Gene expression analyses and immunodetections showed no SGLT2 mRNA or protein expression in rodent and human islet cells, but moderate SGLT1 mRNA expression in human α-cells. However, functional experiments on rat, mouse, and human (29 donors) islets and the in situ perfused mouse pancreas did not identify any direct effect of dapagliflozin, empagliflozin or sotagliflozin on glucagon and insulin secretion. SGLT2i did not affect glucagon gene expression in rat and human islets. CONCLUSIONS: The data indicate that the SGLT2i-induced increase of the plasma glucagon/insulin ratio in vivo does not result from a direct action of the gliflozins on islet cells

Acute kidney injury and tools for risk-stratification in 456 patients with hantavirus-induced nephropathia epidemica

BACKGROUND Puumala virus (PUUV) is the most common species of hantavirus in Central Europe. Nephropathia epidemica (NE), caused by PUUV, is characterized by acute kidney injury (AKI) and thrombocytopenia. The major goals of this study were to provide a clear clinical phenotyping of AKI in patients with NE and to develop an easy prediction rule to identify patients, who are at lower risk to develop severe AKI. METHODS A cross-sectional prospective survey of 456 adult patients with serologically confirmed NE was performed. Data were collected from medical records and prospectively at follow-up visit. Severe AKI was defined by standard criteria according to the RIFLE (Risk, Injury, Failure, Loss, End-stage kidney disease) classification. Fuller statistical models were developed and validated to estimate the probability for severe AKI. RESULTS During acute NE, 88% of the patients had AKI according to the RILFE criteria during acute NE. A risk index score for severe AKI was derived by using three independent risk factors in patients with normal kidney function at time of diagnosis: thrombocytopenia [two points; odds ratios (OR): 3.77; 95% confidence intervals (CI): 1.82, 8.03], elevated C-reactive protein levels (one point; OR: 3.02; 95% CI: 1.42, 6.58) and proteinuria (one point; OR: 3.92; 95% CI: 1.33, 13.35). On the basis of a point score of one or two, the probability of severe AKI was 0.18 and 0.28 with an area under the curve of 0.71. CONCLUSION This clinical prediction rule provides a novel and diagnostically accurate strategy for the potential prevention and improved management of kidney complications in patients with NE and, ultimately, for a possible decrease in unnecessary hospitalization in a high number of patient

Diabetes in primary care: prospective associations between depression, nonadherence and glycemic control

BACKGROUND Findings are inconsistent regarding the degree to which depression may exert a negative impact on glycemic control in patients with type 2 diabetes. We therefore aimed to examine the longitudinal relationship between depression, behavioral factors, and glycemic control. METHODS In a prospective component of a nationally representative sample, 866 patients with type 2 diabetes aged >or=18 years completed a standardized assessment including a laboratory screening, questionnaires, and diagnostic measures. Subsequent to baseline (t(0)), patients were tracked over a period of 12 months (t(1)). Depression was assessed according to DSM-IV and ICD-10 criteria. Glycemic control was determined by levels of glycosylated hemoglobin (HbA(1c)); a level of >or=7% was judged as unsatisfactory. Regression analyses were performed to analyze the prospective relationship between depression, medication adherence, diabetes-related health behavior, and HbA(1c). RESULTS Patients with depression at t(0) revealed increased rates of medication nonadherence (adjusted OR: 2.67; CI: 1.38-5.15) at t(1). Depression (adjusted regression coefficient: beta = 0.96; p = 0.001) and subthreshold depression (beta = 1.01; p or=7%) at t(1) were also increased for patients with baseline depression (2.01; CI: 1.10-3.69). However, problems with medication adherence as well as problems with diabetes-related health behavior at t(0) did not predict poor glycemic control at t(1). CONCLUSIONS In a prospective representative study of patients with type 2 diabetes, baseline depression predicted problems with medication adherence, problems with health-related behaviors, and unsatisfactory glycemic control at follow-up

Clinical course and long-term outcome of hantavirus-associated nephropathia epidemica, Germany

Human infection with Puumala virus (PUUV), the most common hantavirus in Central Europe, causes nephropathia epidemica (NE), a disease characterized by acute kidney injury and thrombocytopenia. To determine the clinical phenotype of hantavirus-infected patients and their long-term outcome and humoral immunity to PUUV, we conducted a cross-sectional prospective survey of 456 patients in Germany with clinically and serologically confirmed hantavirus-associated NE during 2001-2012. Prominent clinical findings during acute NE were fever and back/limb pain, and 88% of the patients had acute kidney injury. At follow-up (7-35 mo), all patients had detectable hantavirus-specific IgG; 8.5% had persistent IgM; 25% had hematuria; 23% had hypertension (new diagnosis for 67%); and 7% had proteinuria. NE-associated hypertension and proteinuria do not appear to have long-term consequences, but NE-associated hematuria may. All patients in this study had hantavirus-specific IgG up to years after the infection