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Purpose: Human infection with Dobrava-Belgrade virus (DOBV) in Northern Germany causes a mild form of hantavirus disease predominantly characterized by acute kidney injury due to interstitial nephritis. We evaluated the largest number of DOBV-infected patients so far regarding clinical course, proteinuria, and prognostic markers., Patients and Methods: Patients with DOBV-associated hantavirus disease admitted to the Renal Division of the University of Lübeck (Germany) between 1997 and 2012 were included in this study. Symptoms, clinical course, laboratory parameters, and urinary protein analysis were investigated at admission (baseline, t 0 ), 3-5 days (t 3-5 ), 10-17 days (t 10-17 ), and after 1 year of follow-up (t 365 )., Results: Of the 34 patients (male/female ratio: 23/11; age: 41 ± 14 years) included in the study, 4 underwent hemodialysis (HD). Glomerular filtration rate was 17 ± 14 mL/min at t 0 and increased to 27 ± 26 mL/min (t 3-5 ), 57 ± 20 mL/min (t 10-17 ), and 84 ± 16 mL/min (t 365 ). Albuminuria and tubular proteinuria (α 1 - and β 2 -microglobulin) decreased during follow-up; the urinary α 1 -microglobulin concentration in patients who required HD was significantly higher than that in patients not requiring HD (t 0 : 186 ± 51 vs. 45 ± 26 mg/g creatinine; t 3-5 : 87 ± 14 vs. 32 ± 16 mg/g creatinine; t 10-17 : 63 ± 18 vs. 28 ± 12 mg/g creatinine; p < 0.001)., Conclusions: DOBV infection of inpatients in Northern Germany is associated with severe kidney injury that recovers within a few weeks and normalizes within 1 year. Tubular proteinuria is associated with the severity of kidney injury and the necessity of renal replacement therapy in these DOBV-infected patients.

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 < 0.001) at t(0) also predicted increased problems with diabetes-related health behavior at t(1). Adjusted ORs for poor glycemic control (HbA(1c) >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., ((c) 2010 S. Karger AG, Basel.)

Insulin and leptin are well known to be involved in the regulation of food intake and body weight. Recent studies have suggested that both hormones may also affect memory and learning processes. We explored whether the intrahippocampal administration of insulin or leptin improved spatial memory formation in rats following a radial maze task and whether the insulin and leptin receptor expression in different areas of the hippocampus was affected. Animals without a learning task were also investigated in order to differentiate between the influence of spatial learning and hormone application on receptor expression. Spatial memory formation was found unaltered following the different applications. The application of insulin increased the expression of the long form of the leptin receptor in the Ammon's horn and dentate gyrus region of the hippocampus in the learning group only. These data clearly show that learning is a prerequisite for the effect of insulin on leptin receptor expression., (Copyright 2005 S. Karger AG, Basel.)

In recent years, clear evidence has accumulated that insulin affects central nervous functions. Besides controlling metabolic processes such as energy homeostasis by the regulation of food intake through hypothalamic receptors, the peptide hormone also appears to be capable of modulating cognitive functions. Experimental and clinical evidence for insulin supports effects on learning and memory. This study explores the impact of insulin on neuronal activity using a picture encoding task in a functional magnetic resonance imaging approach. Ten subjects performed two independent scanning sessions, each session divided into one part of four baseline runs and a second part of four runs during either insulin or saline was infused. A hyperinsulinemic- euglycemic clamp technique was applied to keep the blood glucose concentrations normal during insulin infusion. Contrast images between the two parts revealed identical activation patterns during baseline and saline conditions while during the insulin condition a higher level of activation was detected within the fusiform gyrus in both hemispheres. Shorter reaction times during the insulin condition underlined the cognitive benefit. For the first time, we were able to demonstrate that insulin enhances neuronal activity within the medio-temporal lobe and increased performance in humans under in-vivo conditions., (Copyright (c) 2005 S. Karger AG, Basel.)

Growth hormone (GH) possesses multiple metabolic effects, in particular with regard to glucose and lipid homeostasis. Studies on the effects of GH on body weight and food and water intake are scarce and have yielded controversial results. We investigated the effects of different modes of GH administration on the parameters of body weight and food intake as well as on insulin and leptin concentrations in fa/fa Zucker rats. In control experiments, aqua pro injection was given. GH was administered over a time period of 11 days at a daily dose of 250 microg intraperitoneally (i.p.) and 25 microg intracerebroventricularly (i.c.v.). While both food intake and body weight were found to be unaltered in the four groups after this observation period, there was an enhanced food intake and consecutively an increase in body weight over the day period when compared to the night period in the groups of rats that received GH i.c.v. or i.p. This tendency was also shown for water intake. Insulin and leptin concentrations were similar in all groups. Thus, injection of GH appears to modify food intake-related behavior, since the periods of enhanced food and water intake were shifted from night- to daytime. Thus, while in general the metabolic parameters remained unchanged, the activity pattern was clearly modified., (Copyright 2002 S. Karger AG, Basel)

In the present study the effects of different doses of corticotropin-releasing factor (CRF) and the CRF antagonist alpha-helical CRF on locus coeruleus (LC) neurons were studied in anesthetized male Wistar rats. To monitor the release of noradrenaline (NA) and its metabolite 3-methoxy-4-hydroxyphenylethylene glycol (MHPG), a microdialysis probe was implanted into the parietal cortex, a major projection area of the LC. Saline, 0.17, 0.51 nmol CRF and a combination of 5.1 nmol alpha-helical CRF and 0.51 nmol CRF were applied to the LC via a fused silica capillary. While both doses of CRF augmented NA in parietal cortex dialysates (0.51 nmol CRF: from 0.0206 to 0.0266 pmol/sample; 0.17 nmol CRF: from 0.0147 to 0.0170 pmol/sample), saline did not affect NA concentration. The metabolite MHPG also increased, but in a more prolonged time course. The antagonist alpha-helical CRF attenuated the CRF effects. The increase of extraneuronal NA concentration monitored in the cortical samples indicates an augmented depolarization rate of noradrenergic LC neurons. This clearly demonstrates the activation of these neurons by CRF, suggesting physiological interactions of CRF and noradrenergic neurons.

The neuropeptides thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH) have been found to be potent stimulators of the autonomic nervous system in both experimental animals and humans. We studied the effects of different doses of CRH and TRH given intracerebroventricularly in the urethane-anesthetized rat and a single dose of CRH in the chloral hydrate-anesthetized rat to elucidate the effects of these peptides in the unconscious state. All TRH doses studied enhanced blood pressure and noradrenaline and adrenaline secretion. Surprisingly, there were no blood pressure increases following administration of 0.4, 1.3 and 1.7 nmol CRH. In general, there was a tendency for blood pressure to decrease with the largest drop observed after 1.7 nmol CRH. Our data suggest that only TRH clearly augments blood pressure and catecholamine secretion in the anesthetized animal, while CRH does not exert major effects under the two anesthetic conditions employed.

Besides their regulation of the pituitary-adrenal and pituitary-thyroidal axis, respectively, the neurohormones CRH and TRH act within the central nervous system to evoke and modulate a number of behavioral and physiological processes. In particular, an increase in the sympathetic nervous system and respiratory activity has been observed. The data communicated in this review article emphasize the role of these neurohormones with regard to the neuroendocrine regulation of the autonomic nervous system, sleep and cognitive performance. Moreover, a possible therapeutic role is suggested by the beneficial effects in patients at risk of hypoventilation-associated disorders.

Brain catecholamine and serotonin neurons are intimately involved in a number of physiological functions such as cardiovascular regulation, neuroendocrine secretion, regulation of behavior, mood and appetite control. The synthesis and release of these neurotransmitters appear to be remarkably correlated with the subsequent physiological changes observed. While there are numerous pharmacological approaches that affect the neurotransmitters involved (i.e., the catecholamines dopamine, noradrenaline and adrenaline as well as the indoleamine serotonin), one particularly attractive (while specific) approach involves the administration of a precursor amino acid. It is thus a prerequisite for the physiological and possibly therapeutic properties of the precursor amino acids l-tyrosine and l-tryptophan that they affect synthesis and release of their transmitter product. We will describe in detail the nature of the different neurochemical mechanisms guiding transmitter synthesis and their dependent physiological responses, in particular appetite control and neuroendocrine regulation.

Tumor anorexia can be defined as a continuous reduction in dietary intake with a steadily increased cost of energy of the organism. A possible basis for this nutritional imbalance during the course of the illness is provided by metabolic dysfunction, changes in taste, neuroendocrine alterations and behavioral factors. At the present time no uniform explanation exists, thus only adjuvant therapeutic strategies can be deducted.

Plasma concentrations of the major brain metabolite of norepinephrine, 3-methoxy-4-hydroxyphenethyleneglycol (MHPG), were assayed in patients with essential, renovascular hypertension, pheochromocytoma and in controls. The concentration of MHPG was significantly elevated in patients suffering from pheochromocytoma and was found to be related to tumor size.

The effects of tryptophan in combination with two different diets (high-carbohydrate and high-protein diet) on behavioral parameters such as mood, sleep and performance were chronically studied in a group of 34 hypertensive patients undergoing a trial of testing the antihypertensive properties of l-tryptophan. While no major changes in mood were observed, there was a tendency for sleep latency to decrease and sleep duration to increase following tryptophan intake in the intragroup analysis. The administration of tryptophan caused a significant improvement on performance in a concentration task. No significant dietary effects were observed either in combination with tryptophan or in the placebo group. These data again demonstrate behavioral relevance of the precursor amino acid l-tryptophan and suggest a long-term improvement in partial aspects of performance behavior.

Clinical and experimental data demonstrate that hormonal factors are involved in magnesium regulation. It is possible that the parathyroid hormone could play an important role in the maintenance of normal calcium and magnesium concentrations. The action of other hormones in magnesium metabolism appears to be an indirect response to factors such as calcium concentration or changes in volume. Alterations of the magnesium concentrations are important for the intracellular potassium, sodium and calcium content. Magnesium deficiency appears to lower intracellular potassium and to increase intracellular sodium and calcium concentrations. Therefore, magnesium is essential to avoid cardiovascular diseases (acute myocardial infarction, arrhythmias, hypertension) and to restore cellular potassium concentrations.