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Biomedical subjects

W Riedel

Publications and source records attributed to W Riedel.

At least 37 records · Page 2Linked to original sources

Tumor necrosis factor-alpha in macrophages of heart, liver, kidney, and in the pituitary gland.

Tumor necrosis factor-alpha (TNFalpha) is an important mediator in bacterial lipopolysaccharide (LPS)-induced fever and shock. New data on TNFalpha-producing macrophages in heart, pituitary gland, kidneys and liver in correlation with TNFalpha plasma levels are reported here. In adult rabbits, core temperature and TNFalpha plasma levels are significantly increased at 3 and 24 h after treatment with LPS. After a delay of 6-12 h, the number of TNFalpha-containing macrophages, determined by immunohistochemistry, increases more than fivefold in all organs investigated. With the exception of the pituitary gland, the increase in cell number is correlated with the degree of cellular injury, indicating the involvement of TNFalpha in LPS-induced organ damage that is accompanied by the synthesis of the cytokine. Cortisol levels also increase for at least 24 h after LPS treatment, show peak values 6 h after interleukin-1 treatment, and are unchanged after TNFalpha treatment, indicating the different effects of these factors on the hypothalamo-hypophyseal-adrenocortical axis. This study provides evidence that macrophageal TNFalpha of multi-organ origin is involved in LPS-induced tissue injury and supports the concept of a systemic inflammatory response syndrome. We also show for the first time that in the anterior lobe of the pituitary gland TNFalpha is a normal constituent in cells producing growth hormone but not ACTH. Moreover, most cells of the intermediate lobe are positive for TNFalpha.

Animals↗

Cognitive performance after strenuous physical exercise.

Stimulating as well as detrimental effects of exercise on cognitive functioning have been reported. In the present study, 15 endurance-trained athletes (aged 18 to 42 years) performed a bicycle ergometer endurance test at 75% of their maximal work capacity (Wmax). Psychomotor and cognitive tests were administered before and immediately after exercise. These consisted of simple reaction time (RT), 3-choice RT and Stimulus-Response (S-R) incompatible RT tasks, a finger-tapping task, and the Stroop test. Simple RT tasks, but also the more complex S-R in compatible RT, and Color Word Interference in the Stroop test showed an increase in speed of performance after exercise relative to baseline. An enhanced activation was probably responsible for this better performance on psychomotor and cognitive tests. Since performance on the most complex task, the Interference subtest of the Stroop, was especially improved after exercise, the expectancy of the subjects of a potential positive effect of exercise was thought to have been responsible.

Adolescent↗

Caffeine attenuates scopolamine-induced memory impairment in humans.

Caffeine consumption can be beneficial for cognitive functioning. Although caffeine is widely recognized as a mild CNS stimulant drug, the most important consequence of its adenosine antagonism is cholinergic stimulation, which might lead to improvement of higher cognitive functions, particularly memory. In this study, the scopolamine model of amnesia was used to test the cholinergic effects of caffeine, administered as three cups of coffee. Subjects were 16 healthy volunteers who received 250 mg caffeine and 2 mg nicotine separately, in a placebo-controlled double-blind cross-over design. Compared to placebo, nicotine attenuated the scopolamine-induced impairment of storage in short-term memory and attenuated the scopolamine-induced slowing of speed of short-term memory scanning. Nicotine also attenuated the scopolamine-induced slowing of reaction time in a response competition task. Caffeine attenuated the scopolamine-induced impairment of free recall from short- and long-term memory, quality and speed of retrieval from long-term memory in a word learning task, and other cognitive and non-cognitive measures, such as perceptual sensitivity in visual search, reading speed, and rate of finger-tapping. On the basis of these results it was concluded that caffeine possesses cholinergic cognition enhancing properties. Caffeine could be used as a control drug in studies using the scopolamine paradigm and possibly also in other experimental studies of cognitive enhancers, as the effects of a newly developed cognition enhancing drug should at least be superior to the effects of three cups of coffee.

Adult↗

Neuromediator and hormonal perturbations in fibromyalgia syndrome: results of chronic stress?

Since the first comprehensive description of the symptoms of FMS by Yunus et al (1981), numerous investigations have confirmed that FMS is a clinical entity. However, the aetiology of the syndrome is still not fully elucidated. It seems, however, logical to place the origin of the disorder in the muscle. Muscle pain, especially at the muscle-tendon junctions, fatigue and stiffness are the first symptoms. A malfunction of energy metabolism has been detected in part of the muscle fibres. However, it has to be considered that the muscle is not an isolated entity. Its activity is controlled by segmentally arranged motor units of the ventral horn of the spinal cord in response to proprioceptive afferent signals arising in the muscle spindles or in other sensory elements including nociceptors. Together with supraspinal descending inputs, the spinal motor neurone pool is the common final pathway for segmental and suprasegmental inputs, making the motor system extremely powerful for adaptive adjustments but also vulnerable if deficits occur in either of these input levels. A second, recently discovered abnormality seen in FMS is a lowered serotonin level in peripheral and most likely also central structures. The underlying mechanism seems to be defective absorption of the precursor amino acid tryptophan from the gut. Serotonin is involved centrally in the regulation of the sleep pattern, and at the spinal level it acts as a 'gain setter' of motoneurone excitability and suppresses signal transmission of noxious stimuli in dorsal horn neurones. Either of these two disturbances, muscle energy depletion or serotonin deficiency, could by itself evoke many of the symptoms of FMS, and their combined appearance will perpetuate the disease. Depressed levels of somatomedin C, caused by a deficit of stage 4 sleep-dependent release of GH, might represent an additional factor in preventing proper development or repair of myoskeletal structures. Malabsorption of certain amino acids, possibly due to a genetic disorder of gut transport mechanisms, may constitute an additional deleterious factor. The abnormalities found in the HPA and HPT axis may be seen as an attempt of the organism to restore homeostasis. The stimulus eliciting this counter-regulatory reaction may be pain or other afferent signals which normally do not reach the central nervous system. It is doubtful whether the unspecific activation of the HPA axis in a non-inflammatory disease is beneficial.(ABSTRACT TRUNCATED AT 400 WORDS)

Fibromyalgia↗

[The computed tomographic differentiation of endobronchial tumors and tumor-caused bronchial compression].

The efficiency of computed tomography in differentiating between a bronchial compression due to tumour formation and an endobronchial tumour was tested in comparison to bronchoscopy results. 624 bronchial segments were evaluated in 65 patients with masses in the pulmonary hilus area. Computed tomographical identification of pathological lesions (n = 71) was achieved with a sensitivity of 83% and a specificity of 96%. Out of 52 bronchial segments with endobronchial tumour, 90% showed pathological lesions and 85% were classified correctly. When the morphology of the bronchial lesions (endoluminal mass, smooth or irregularly demarcated bronchostenosis or bronchial displacement) was assessed with CT, only the CT identification of an endoluminal mass could distinguish endobronchial tumour growth with a probability of 91% from bronchial narrowing due to external causes and normal bronchi.

Adult↗

A sensitive sandwich ELISA for measuring erythropoietin in human serum.

A sandwich, non-competitive enzyme-linked immunosorbent assay (ELISA) for erythropoietin (EPO) is described. The ELISA utilizes a monospecific, polyclonal antibody raised in rabbits against human recombinant EPO (rhu EPO) and purified over a rhu EPO affinity chromatography column. The ELISA procedure can be summarized as follows: Anti-EPO is coated onto 96-well ELISA microtitre plates; standard EPO or sample is added and left to bind to this catching antibody; this is followed by the addition of the same antibody which has been biotinylated; finally, anti-biotin conjugated to alkaline phosphatase is added and the enzyme reaction developed and read at 405 nm. All parameters of the assay have been optimized. Recombinant human EPO was standardized against the World Health Organization 2nd International Reference Preparation for erythropoietin. The minimal detectable concentration of rhu EPO was 0.3-0.5 mU/ml, which corresponded to 1.2-2 mU/ml of EPO in serum (serum diluted 1:4). No reaction was obtained with a variety of blood components and cytokines, indicating that the anti-EPO antibody did not cross-react with those substances to produce false-positive results. The intra-assay variation ranged from 3% to 10%, while the inter-assay variation ranged from 8.5% to 24%. Serum dose-response curves were parallel to the standard dose-response curve. The assay is easy to use, rapid, reproducible, but above all quantitative, specific and sensitive to measure the EPO content in all serum samples.

Enzyme-Linked Immunosorbent Assay↗

Thyroid function in patients with fibromyalgia syndrome.

Thyroid function was tested in 13 female patients with primary fibromyalgia syndrome (FS) and 10 healthy age matched controls by intravenous injection of 400 micrograms thyrotropin-releasing hormone (TRH). Basal thyroid hormone levels of both groups were in the normal range. However, patients with primary FS responded with a significantly lower secretion of thyrotropin and thyroid hormones to TRH, within an observation period of 2 h, and reacted with a significantly higher increase of prolactin. Total and free serum calcium and calcitonin levels were significantly lower in patients with primary FS, while both groups exhibited parathyroid hormone levels in the normal range.

Adult↗

Neuropathy, myopathy and destructive arthropathy in primary hypothyroidism.

A 75-year-old woman with untreated primary hypothyroidism was found with peripheral neuropathy (including carpal tunnel syndrome), severe myopathy (high levels of creatine phosphokinase) and destructive arthropathy, affecting fingers, toes and the left knee. Radiographs of her knee showed destructive lesions of the tibial plateau similar to a pathologic compression fracture, while the joints of the fingers and toes showed all signs of severe erosive osteoarthritis (OA), radiographically documented over a period of 7 years. It is suggested that hypothyroidism is causally related to the development of erosive OA.

Aged↗

Nucleotide sequence of the full-length mouse lamin C cDNA and its deduced amino-acid sequence.

We have cloned and sequenced the cDNA comprizing the entire coding region and several hundred base-pairs of its flanks for the mouse nuclear envelope protein lamin C mRNA. The nucleotide sequence and the deduced amino-acid sequence of the mouse lamin C are compared with the previously published human lamin A/C sequences with respect to (a) the general organisation, (b) homologies, (c) predictions for the essential structural characteristics of lamins and (d) the localization of the most conserved region. Moreover, the mouse lamin C sequence presented allows the first intraspecies comparison between A/C-type and B-type lamins.

Amino Acid Sequence↗

Selective autonomic nervous control of thyroid hormone and calcitonin secretion during metabolic and cardiorespiratory activation by intracisternal thyrotropin-releasing hormone (TRH).

Injections of 10 micrograms/kg thyrotropin-releasing hormone (TRH) 150 microliter intracisternally (i.c.) in conscious rabbits evoked behavioral excitation and compulsive scratching, tachypnoea, an increase of heart rate and blood pressure, oxygen consumption and hyperthermia. TRH i.c. significantly increased free thyroid hormone and calcitonin secretion during depressed thyrotropin (TSH) secretion. The rise of calcitonin correlated with a fall of serum calcium. The ergotropic function of TRH i.c. was further demonstrated by rapid increases of glucagon, serum glucose, free fatty acid and free glycerol, with a delayed rise of insulin depending on glucose levels. The increases of free thyroid hormones, calcitonin, cortisol and lipolysis following TRH i.c. were augmented after spinal transection, while glucagon secretion increased at a slower rate, however, not accompanied by rises of glucose and insulin. Behavioral excitation and lipolysis were augmented by TRH i.c. after total thyroidal denervation, which completely prevented the rise in thyroid hormone and calcitonin secretion, although the thyroid follicles and C cells responded properly to TSH. Section of all thyroidal nerves except the recurrent laryngeal nerve reduced mainly calcitonin secretion following TRH i.c., while the behavioral, autonomic and other endocrine responses were augmented. Additional abdominal vagotomy in these rabbits diminished glucagon secretion by about 50% without significantly changing the other effector responses. Taking 125I-labelled TRH concentration in the cerebrospinal fluid at the site of i.c. injection as 100%, then 58% of TRH penetrated into outer parts of the dorsal and ventral medulla oblongata and pons, and 8% into the neuropil of the aqueductal region. Radioactivity in other brain areas including the hypothalamus was below 1%, while the hypophysis was practically devoid of radiolabelled TRH. It is suggested that the observed behavioral, autonomic and endocrine activity pattern elicited by injection of TRH into the cisterna magna was caused by excitation of neurons confined to that compartment and was mediated by pathways of the reticular formation of the lower brainstem, with the concept that TRH-containing neurons are intrinsic excitatory constituents of the 'activating reticular system'.

Animals↗

Caloric intake, stress, and menstrual function in athletes.

The cause of menstrual disturbance in athletes is still debated. Apart from the acute and chronic effects of exertion, other associated behavioral variables are suspected to play a key role. A longitudinal study with frequent blood sampling was undertaken to link information about nutrition and stress with a quantitative assessment of endocrine menstrual function in 18 endurance-trained athletes and 25 age-matched, nonathletic women. Four athletes did not show hormonal signs of follicular development. The 14 athletes with cyclic gonadal function did not differ from controls with regard to estradiol concentrations during the follicular phase and at midcycle. During the luteal phase, however, they showed significantly reduced areas under the estradiol and progesterone curves. Caloric intake, as assessed by nutritional diaries, correlated positively with the area under the progesterone curve during the luteal phase (rs = 0.70, P less than 0.01). Ratings of subjective stress in the area "partner, family, friends" correlated negatively with the luteal progesterone area (rs = 0.80; P less than 0.01). Data support the hypothesis that nutrition and stress may play a critical role in the genesis of menstrual disturbance in athletes.

Adult↗

Effect of bombesin on thermoregulation of the rabbit.

Injections of bombesin (BOM, 125, 250 and 500 ng) into the preoptic/anterior hypothalamus caused dose-related decreases of threshold temperatures for metabolic cold defence, cutaneous vasomotor tone and respiratory rate, combined with a reduced sensitivity of these thermoregulatory effectors in response to core temperature changes induced at thermoneutral or warm ambient conditions. Intracisternal (i.c.) injections of BOM (250 ng) produced qualitatively identical thermoregulatory effector changes in response to core temperature changes. Injections of BOM into the posterior hypothalamus did not affect body temperature control. Increased locomotor behavior, licking and grooming was elicited, however, from all injection sites. The results explain the prevailing hypothermic effect of BOM as the consequence of the concerted decrease in threshold temperatures and "gains" of all autonomic thermoregulatory effectors and suggest the activation of warm inputs, relative to cold inputs, at the hypothalamic level as the underlying mechanism. Direct or indirect inhibition of the intrinsic hypothalamic system involving thyrotropin-releasing hormone (TRH) and consequent deactivation of central noradrenergic pathways known to generate the entire autonomic pattern of cold defence might be involved in the neuro-humoral changes resulting in hypothermic effects of centrally applicated BOM.

Animals↗

Long-term recording of core temperatures with chronically implanted silicon diodes.

An electronic circuit for measurement of temperatures is described utilizing silicon diodes as temperature sensors and the feature that the reverse current flow of a diode is linearly related to temperature. Once calibrated and implanted into various sites of the body core of rabbits, the diodes preserved their precise temperature sensing qualities for periods longer than a year. Temperature changes of the atlanto-occipital membrane were found to be close to simultaneously measured intracisternal temperature, both temperatures being some 0.3 degree C higher than rectal temperature. This temperature-relationship persisted under conditions with different states of cutaneous vasoconstriction and thermal panting as observed in fever and during defervescence. These results indicate that extrahypothalamic brain regions as the cerebellum and the medulla oblongata do not benefit from the proposed protective function of brain cooling during stimulation of heat dissipating effector mechanisms.

Animals↗

The renal sympathetic baroreflex in the rabbit. Arterial and cardiac baroreceptor influences, resetting, and effect of anesthesia.

Curves relating renal sympathetic nerve activity and mean arterial pressure were derived in conscious rabbits during ramp changes in mean arterial pressure, elicited by perivascular balloon inflation. The renal sympathetic nerve activity-mean arterial pressure relationship consisted of a high-gain sigmoidal region about resting, where renal sympathetic nerve activity rose or fell in response to moderate falls and rises of mean arterial pressure. With larger pressure rises, renal sympathetic nerve activity first fell to a lower plateau and then reversed at even higher mean arterial pressure. When mean arterial pressure was lowered below resting, renal sympathetic nerve activity rose to an upper plateau and then reversed abruptly toward resting at low mean arterial pressure. Both arterial and cardiac baroreceptors exerted substantial inhibitory influences on renal sympathetic nerve activity at all pressure levels. These effects appeared additive over the central high gain region of the curve, but beyond this region there were non-additive interactions. The latter were affected considerably by alfathesin anesthesia. In other experiments, we studied the effects of sustained alterations in resting mean arterial pressure induced by infusing nitroprusside and phenylephrine, which produced rapid resetting of the renal baroreflex. The latter could be accounted for, in part, by resetting of the threshold of the arterial baroreceptors and in part by contributions from other afferents, probably the cardiac receptors. During resetting associated with nitroprusside-induced falls in resting blood pressure, high-gain reflex adjustments in renal sympathetic nerve activity to moderate changes in mean arterial pressure were preserved, but during resetting associated with phenylephrine-induced rises in resting mean mean arterial pressure, the resting renal sympathetic nerve activity lay on the lower curve plateau, resulting in reduction in the apparent gain of the reflex renal sympathetic nerve activity response to moderate changes in mean arterial pressure.

Alfaxalone Alfadolone Mixture↗