Biomedical subjects
Publications and source records attributed to M Kellner.
The PGE2 potentiated formalin arthritis can be only temporarily influenced by indomethacin. Azapropazone had a good therapeutic effect on chronic inflammation. According to the enzyme histochemical studies, azapropazone enhanced oxidative enzyme activity. This phenomenon may be interpreted as a sign of a favorable effect.
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A patient is described with a ruptured temporal cavernous hemangioma clinically presenting with recurrent panic attacks mimicking panic disorder. The role of temporal lobe structures in the pathogenesis of anxiety spells is highlighted, reviewing the published cases of temporal tumors leading to panic attacks.
Atrial natriuretic hormone (ANH) is found in heart myocytes, and also in the CNS. The inhibitory action of ANH on the hypothalamic-pituitary-adrenocortical (HPA) system has been established by in vivo and in vitro experiments, and could be of considerable importance: whereas several synergists to corticotropin-releasing hormone (CRH), the key hormone of the HPA system, are characterized in the past, until now ANH seems to be the only peptide which counterbalances the effects of CRH at the pituitary. As well as at the corticotroph, CRH has a stimulatory influence upon the lactotroph in vivo, and like ACTH and corticosteroids prolactin (PRL) is released in response to physical and cognitive challenges. To test the hypothesis of whether ANH also inhibits the CRH-mediated prolactin release a randomized, placebo-controlled, double-blind study in 12 males aged from 25 to 30 years was conducted. With regard to the diurnal variation of the HPA system activity we compared the prolactin release by 100 micrograms hCRH during a 30 min infusion of placebo, 150 micrograms ANH or 3 IU arginine vasopressin in the morning (08:00 h) and evening (19:00 h). Evaluation of morning and evening effects revealed that administration of hCRH led to a prompt rise of plasma PRL concentration. Infusion of ANH resulted in a significantly reduced maximum increment of PRL compared to placebo (0.83 +/- 0.87 vs 2.85 +/- 1.57 ng/ml, mean +/- SD, n = 12, p < .001). In addition, the AUC values were significantly lower under ANH than in the placebo condition. Infusion of AVP did not significantly change the PRL response to CRH vs placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
Given the anxiogenic effects of the type-B natriuretic peptide receptor agonist C-type natriuretic peptide (CNP) in rodents, we investigated the influence of CNP pretreatment upon the behavioral and endocrine action of the panicogen cholecystokinin tetrapeptide (CCK-4) in healthy men. In a randomized double-blind balanced design, 20 male volunteers were given an intravenous infusion of 300 microg of CNP vs. placebo followed by 25 microg of CCK-4. The behavior was assessed using panic, anxiety, and dissociation questionaires before the infusion and after the CCK-4 stimulus. Furthermore, the stress-sensitive hormones adrenocorticotropic hormone (ACTH), cortisol, and prolactin were measured. CNP pretreatment enhanced the anxiogenic and prodissociative effects of CCK-4 and significantly augmented the ACTH surge after CCK-4. However, no effect of CNP was seen upon panic symptoms. Our preliminary data support a role of type-B natriuretic peptide receptors in anxiety modulation in normal man.
Previous studies have shown unequivocally a lack of pituitary-adrenocortical stress hormone activation during lactate-induced panic attacks despite considerable psychopathological alterations, signs of arousal and several vegetative symptoms regularly occurring during stressful conditions. To study the possible inhibitory action of atrial natriuretic hormone (ANH) on adrenocorticotrophic hormone (ACTH) and cortisol release in humans, 10 patients with panic disorder (DSM-III-R) received sodium lactate and placebo (0.9% saline) infusions and ten healthy comparison subjects additionally received a 2.5% saline infusion and the response of ANH, vasopressin, ACTH, cortisol, and several biochemical and physiological cardiovascular parameters were measured. In comparison to placebo, lactate infusion led to enhanced ANH levels in both non-panicking comparison subjects and panickers. Importantly, panickers showed significantly lower baseline levels of ANH than comparison subjects followed by a faster release. No significant concomitant changes in vasopressin, ACTH, and cortisol were observed. During lactate infusion, heart rate was accelerated considerably in the two groups; in contrast, the reduction of pCO2 indicated an enhanced ventilation only in panickers. The pattern of ANH release cannot be attributed simply to either the volume load administered, the cardiac activation or an osmotic effect since neither 0.9 nor 2.5% saline resulted in comparable effects. Additional central nervous mechanisms must be considered for the increased ANH concentrations in lactate-induced panic attacks. We propose that the release of ANH is an intrinsic mechanism contributing to the apparent unresponsiveness of the pituitary-adrenocortical system in lactate-induced panic attacks. In addition, we surmise that ANH may also play a role in the yet unknown mechanisms for termination of panic attacks, e.g. either by inhibitory actions on the locus coeruleus or by bronchiorelaxation and consecutive decatastrophization.
A digoxin-like immunoreactivity (DLIS) was measured by two routinely used clinical digoxin-immunoassays (radio- and enzymeimmunoassay) in cord blood of 255 newborns, in sera of their mothers at birth and in sera of 211 newborns during the first two postpartal weeks. The highest DLIS levels were found in serum of neonates at the first day of life (median: 0.23 ng/ml, 25% and 75% percentile: 0.19 and 0.28 ng/ml) and in cord blood (median: 0.21 ng/ml, 25% and 75% percentile: 0.19 and 0.24 ng/ml); maternal serum was shown to have three times less DLIS (median: 0.08 ng/ml, 25% and 75% percentile: 0.05 and 0.10 ng/ml). There was no significant correlation between DLIS concentrations in serum of newborns, cord blood or pregnants. The DLIS serum levels of preterms with birthweight less than 2500 g and gestational age less than 37 weeks were significantly lower than those of normal neonates at term (p less than 0.01); concomitantly the lowest DLIS levels were found in maternal serum of preterms (p less than 0.01). These observations strongly suggest rather a DLIS origin in the newborn than in the mother. During the first two postpartal weeks the DLIS concentration of a vast majority of the 211 newborns (91%) decreased continuously to one half of the starting value. Within the second postpartal week preterms were found to have a significantly delayed decrease in the DLIS serum levels (p less than 0.01). Small for date newborns showed no difference in their postpartal DLIS time course compared to normal neonates.(ABSTRACT TRUNCATED AT 250 WORDS)
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This is the report of a case of a 41-year-old male patient with a rapidly progressing amyotrophic lateral sclerosis (ALS) combined with a severe presenile dementia. Screening for antibody binding on fresh-frozen human brain sections, we found that the patient's cerebrospinal fluid contained antibodies against microglia, the dominant and potentially cytotoxic immuneffector cell of the brain. This finding extends previous observations of CSF autoantibodies against microglia in neurodegenerative diseases. It demonstrates that in addition to antigens of neuronal origin (e.g. anti-Purkinje cell antibodies in paraneoplastic cerebellar dysfunction), glial antigens also appear to be under the surveillance of the CNS and/or the peripheral immune system. Our data provide evidence for a close link between neurodegeneration and the activation of microglia; a possible local antigen production against microglia/brain macrophages, which might regulate the concomitant glial activation in neurodegenerative diseases; and the presence of microglia-binding cerebrospinal antibodies as a marker for the acuity of the disease process underlying the acute deterioration of the neurological and cognitive performance in patients with, e.g., ALS. Future therapeutic strategies could therefore include the modulation of the possibly disease-promoting activation of microglia/brain macrophages.