Search PubMed⌕ Search

Biomedical subjects

M Berger

Publications and source records attributed to M Berger.

At least 1,207 records · Page 67Linked to original sources

Age-related changes in the concentration of cytosolic androgen receptors in the epididymis, vas deferens and seminal vesicle of maturing male mice.

In this study, changes in the number of androgen binding sites that occur in cytosols of epididymis, vas deferens and seminal vesicle of mice from 10 to 90 days of age are described. Specific saturable binding of [3H]R-1881 by cytosols of the three organs at all time points studied and age-related differences in the number of binding sites measured were observed. Cytosolic androgen receptor levels in all three organs studied were found to decrease with increasing age, regardless of whether the binding was expressed relative to weight of tissue, cytosolic protein or cellular DNA. The most pronounced change in androgen receptor levels (from 442 to 50 fmol/mg protein) was observed in the epididymis between 10 and 30 days of age. In these three organs there was no significant correlation between androgen (testosterone + dihydrotestosterone) levels and the concentration of androgen binding sites.

Aging↗

A calcium antagonist for the treatment of depressive episodes: single case reports.

Preclinical studies indicate that a disturbed intracellular calcium ion homeostasis is involved in the pathophysiology of affective disorders. Therefore some calcium antagonists were investigated, especially in the treatment of the manic syndrome. In the present study the calcium antagonist nimodipine was used in 10 out-patients with single or recurrent depressive episodes. As a result the mean HAMD scores changed from 26.5 to 9.9 after the individual nimodipine administration. These single case reports suggest an effective new therapy strategy for the treatment of affective dysregulations and give rise to controlled clinical studies with calcium antagonists.

Adult↗

Cholinergic REM induction test: muscarinic supersensitivity underlies polysomnographic findings in both depression and schizophrenia.

Disinhibition of rapid eye movement (REM) sleep (e.g. shortening of REM latency, heightened REM density) is frequently encountered in patients with a major depressive disorder (MDD). Administration of cholinomimetics prior to or during sleep leads to a more pronounced advance of REM sleep in depressed patients compared to healthy controls and patients with other psychiatric disorders. The present study tested whether the cholinergic REM induction test (CRIT) with 1.5 mg RS 86 (an orally acting muscarinic agonist) differentiates patients with MDD (n = 40) from those with schizophrenia (n = 43) and healthy controls (n = 36). The most pronounced shortening of REM latency after cholinergic stimulation occurred in patients with MDD. However, a significant number of patients with schizophrenia also displayed short REM latencies (REM latency < 25 minutes) under placebo conditions and after cholinergic stimulation. REM density measures more clearly differentiated patients with MDD from those with schizophrenia. It is concluded that a subgroup of patients suffering from schizophrenia displays signs of a muscarinic receptor supersensitivity.

Adolescent↗

Near-normotension and near-normoglycemia in blind type I diabetic patients with overt diabetic nephropathy.

In patients with diabetic nephropathy, near-normalization of blood pressure (BP) and blood sugar may have a beneficial impact on changes in kidney function, but visually impaired patients may face difficulties when striving for optimal control of hypertension and hyperglycemia. In a prospective feasibility study, we followed a group of nine blind Type I (insulin-dependent) diabetic patients (mean age 30 +/- 4 years) with overt diabetic nephropathy and uncontrolled hypertension. All patients received intensified insulin therapy after a structured diabetes treatment and teaching program, and adapted their antihypertensive drug treatment to self-monitored BP values. At recruitment, HbA1c values were 5.8 +/- 0.6%, and remained stable at 6.3 +/- 1.7% after a mean observation period of 27 months. BP pressure decreased from 150 +/- 14/99 +/- 14 mmHg to 130 +/- 17/86 +/- 10 mmHg after 1 year, and to 140 +/- 14/92 +/- 9 mmHg at the last examination, (p less than 0.05). Serum creatinine and creatinine clearance remained stable over the observation period at 165 +/- 56 mumol/L and 0.8 +/- 0.4 ml/s/1.72m2 at recruitment, and 152 +/- 47 mumol/L and 1.0 +/- 0.5 ml/s/1.72m2 at the final examination. Proteinuria decreased from 3.2 to 1.4 g/24 h (p less than 0.05). No patient needed renal replacement therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effects of intensification of antihypertensive care in diabetic nephropathy.

The overall quality of antihypertensive care in diabetic patients in Germany is poor. Only a minority of unselected hypertensive patients reach permanent normotensive blood pressure control. Previously, we have shown in a prospective randomized 3-year follow-up study in essential hypertension that implementation of a hypertension teaching and treatment program into routine care results in a significant improvement of blood pressure control. Subsequently, we have performed a prospective, controlled 5-year follow-up trial in hypertensive type I diabetic patients with nephropathy. One-half of a sequential sample of about 100 hypertensive patients with overt nephropathy participated in the program based on blood pressure self-monitoring with the goal of normalization of blood pressure values below 140/90 mm Hg (intensified care, IC). The remaining patients followed routine antihypertensive therapy and formed the control group (routine care, RC). During 5 years of follow-up in IC group patients, blood pressure control was significantly improved. The occurrence of primary study end points (need for dialysis and death) was significantly lower in the IC group patients. In conclusion, in patients with diabetic nephropathy, participation in a hypertension teaching treatment program results in a long-term improvement of blood pressure control and a decrease in mortality and morbidity.

Antihypertensive Agents↗

Delta sleep ratio as a predictor of sleep deprivation response in major depression.

The fast but short-lasting improvement of depressive symptoms by sleep deprivation (SD) in about 60% of patients with a major depressive disorder is well established, but the mechanisms of action are still not clear. Recent studies suggest that changes in non rapid eye movement (NREM) sleep, especially in slow wave activity (SWA), could be associated with the therapeutic outcome of SD. In the current study, spectral analysis of NREM sleep EEG directly prior to SD was performed to determine if automatically derived sleep parameters predict SD response. Sixteen pair matched and drug free patients with a major depressive disorder, 8 SD responders and 8 non-responders (response criterion: 50% reduction on the 6-item HAMD score), were included. Average EEG spectral power was calculated for the whole night before SD and for single NREM episodes. While whole-night averages of spectral power did not differ significantly between subgroups, SD responders showed a steady decrease of SWA across successive NREM episodes, whereas in non-responders an increase from the first to the second episode was observed. The different distribution of SWA was significantly expressed in the delta sleep ratio (quotient of SWA in the first to the second NREM episode). In conclusion, a high delta sleep ratio is a positive predictor for SD response. Referred to psycho- and pharmacotherapeutic results it is hypothesized that low and high values of the delta sleep ratio characterize subgroups of depressed patients with different neurobiological alterations, which could be relevant for further scientific and therapeutic approaches.

Adult↗

The value of REM sleep parameters in differentiating Alzheimer's disease from old-age depression and normal aging.

Pseudodementia as a common trait in elderly depressives presents a major problem in gerontopsychiatry, especially for the differential diagnosis between Old-Age Depression (OAD) and Dementia of the Alzheimer Type (DAT). The present polysomnographic study examined parameters of sleep continuity, sleep architecture, and REM sleep to differentiate DAT from OAD. The investigation was based on the theoretical framework of the cholinergic-aminergic imbalance model of depression, the cholinergic deficit hypothesis of Alzheimer's disease and the reciprocal interaction model of Non-REM/REM sleep regulation, according to which REM sleep parameters should have high discriminative value to differentiate OAD and DAT. We investigated 35 DAT patients, 39 OAD patients and 42 healthy controls for two consecutive nights in the sleep laboratory. The DAT patients were in relatively early/mild stages of the disease, the severity of depression in the OAD group was moderate to severe. Depressed patients showed characteristic 'depression-like' EEG sleep alterations, i.e. a lower sleep efficiency, a higher amount of nocturnal awakenings and decreased sleep stage 2. Sleep continuity and architecture in DAT was less disturbed. Nearly all REM sleep measures differentiated significantly between the diagnostic groups. OAD patients showed a shortened REM latency, increased REM density and a high rate of Sleep Onset REM periods (SOREM), whereas in DAT REM density was decreased in comparison to control subjects. REM latency in DAT was not prolonged as expected. To assess the discriminative power of REM sleep variables a series of discriminant analyses were conducted. Overall, 86% of patients were correctly classified, using REM density and REM latency measures. Our findings suggest that REM density as an indicator of phasic activity appears to be more sensitive as a biological marker for the differential diagnosis of OAD and DAT than REM latency. The results support the role of central cholinergic neurotransmission in REM sleep regulation and the pathogenesis of DAT and OAD.

Aged↗

Sleep and depression--results from psychobiological studies: an overview.

Disturbances of sleep are typical for most depressed patients and belong to the core symptoms of the disorder. Polysomnographic sleep research has demonstrated that besides disturbances of sleep continuity, in depression sleep is characterized by a reduction of slow wave sleep and a disinhibition of REM sleep, with a shortening of REM latency, a prolongation of the first REM period and increased REM density. These findings have stimulated many sleep studies in depressive patients and patients with other psychiatric disorders. In the meantime, several theoretical models, originating from basic research, have been developed to explain sleep abnormalities of depression, like the two-process-model of sleep and sleep regulation, the GRF/CRF imbalance model and the reciprocal interaction model of non-REM and REM sleep regulation. Interestingly, most of the effective antidepressant agents suppress REM sleep. Furthermore, manipulations of the sleep-wake cycle, like sleep deprivation or a phase advance of the sleep period, alleviate depressive symptoms. These data indicate a strong bi-directional relationship between sleep, sleep alterations and depression.

Brain↗

Atrial natriuretic factor in various stages of diabetic nephropathy.

Plasma concentrations of atrial natriuretic factor (ANF) were measured by radioreceptor assay in 148 insulin-dependent Type I diabetic patients with different stages of diabetic nephropathy. In patients with overt or incipient diabetic nephropathy as well as in patients with glomerular hyperfiltration only, ANF concentrations were elevated when compared with non-nephropathic diabetic and normal subjects. No correlations between ANF and blood pressure, age, diabetes duration, or parameters of metabolic control were found. These findings may indicate a pathophysiologic role of ANF in the development and progression of diabetic nephropathy.

Adult↗