Blur adaptation: clinical and refractive considerations

The human visual system is amenable to a number of adaptive processes; one such process, or collection of processes, is the adaptation to blur. Blur adaptation can be observed as an improvement in vision under degraded conditions, and these changes occur relatively rapidly following exposure to blur. The potential important future directions of this research area and the clinical implications of blur adaptation are discussed.     

Alpha 2-adrenoceptor-mediated inhibition of nerve stimulation-evoked release of neuropeptide Y (NPY)-like immunoreactivity in the pithed guinea-pig

Clonidine (10 micrograms X kg-1) reduced by almost 50% the increase in plasma neuropeptide (NPY)-like immunoreactivity (-LI) induced by preganglionic nerve stimulation at 8 Hz. This effect was reversed by yohimbine (1 mg X kg-1) which caused a three-fold increase of the plasma NPY-LI. Prazosin (1 mg X kg-1) had no such effect. Guanethidine (5 mg X kg-1) reduced the stimulation-evoked increase in plasma NPY-LI. It is concluded that the release of NPY-LI evoked by nerve stimulation from sympathetic nerve terminals is controlled by a presynaptic alpha 2-adrenoceptor-mediated mechanism.     

Occurrence of anti-C1q antibodies in IgA nephropathy

Background: The pathogenic mechanisms and the antigens involved in the establishment and progress of IgA nephropathy are unknown. As antibodies against C1q have been reported to correlate with SLE nephritis, we analysed the occurrence of these antibodies in IgA nephropathy in order to investigate the possibility of pathogenetic similarities in these renal disorders. Methods: The occurrence of IgA- and IgG anti-C1q antibodies (anti-C1q) were determined by ELISA in patients with IgA nephropathy (n=36) and SLE nephritis (n=37), diseases both known to be associated with circulating immune complexes. Levels of these antibodies were also determined in two other glomerular diseases, i.e. idiopathic membranous glomerulo-nephritis (n=7) and minimal change disease (n=2), in which circulating immune complexes are usually not present, and in 40 healthy controls. Results: IgA anti-C1q was observed in increased titres in 11/36 of the patients with IgA nephropathy, in 2/37 of the patients with SLE nephritis (both with proliferative disease) and in 1/9 of the patients with membranous and minimal change disease (P<0.001). Increased titres of IgG anti-C1q were observed in 1/36 of the patients with IgA nephropathy, in 17/37 of the patients with SLE nephritis and in 0/9 of the patients with membranous and minimal change disease (P<0.001). There were no correlations between the levels of anti-C1q antibodies and clinical parameters such as degree of proteinuria, haematuria, or renal function. Nor was there any correlation to the concentration of C3a and the terminal complement complex (TCC) in patients with IgA nephropathy. Conclusions: The occurrence of anti-C1q antibodies in both IgA nephropathy and SLE nephritis, albeit of different predominating isotypes, indicates the possibility of a similar pathogenic mechanism involved in these renal disorders. The occurrence of IgA anti-C1q antibodies in patients with IgA nephropathy has to our knowledge not previously been reported.     

Screening of an elderly population in primary care for primary hyperparathyroidism.

In order to assess the diagnostic outcome of a screening for primary hyperparathyroidism (PHPT) in an elderly population, we determined ionized calcium in serum from 368 individuals participating in a health control at M?lnlycke Primary Care Centre (200 women, 168 men; age range 75-95 years); four-fifths of the individuals living in their homes, the remainder in homes for aged or nursing homes. Intact parathyroid hormone was determined in the samples with oinized calcium concentration greater than mean + 3SD of the truncated population sample, and these individuals were also recalled for another blood sample. Moderate hypercalcaemia, probably due to PHPT, was found in eight individuals (2% of the complete sample, 3% of the women), five having neuropsychiatric or neuromuscular symptoms consistent with PHPT. Surgical intervention is probably indicated in only a small proportion of elderly patients. We conclude that optimal benefits in relation to costs of screening for PHPT in old people will depend on the availability of a safe and simple pharmacological treatment that could determine any causal relationship between hypercalcaemia and symptoms.     

Urinary monoamine metabolites as indices of mental stress in healthy males and females

Concentrations of the serotonin metabolite 5-hydroxyindole acetic acid (5-HIAA), the dopamine metabolite homovanillic acid (HVA) and the noradrenaline metabolite 4-hydroxy-3-methoxyphenyl glycol (HMPG) were determined in urine samples from healthy male and female students by mass fragmentography. Urine samples were obtained after a demanding examination (mental stress) and a day of ordinary school work (control condition). Self-ratings were obtained of feelings induced by the examination, and of habitual psychosomatic symptoms. The results for both sexes showed that the examination stress induced a significant increase of HVA and HMPG excretion, but not of 5-HIAA. The males excreted significantly more of each of the metabolites than the females. The pattern of correlations between metabolite levels and psychological and psychosomatic variables were strikingly different for the two sexes.     

Elevations of neuropeptide Y-like immunoreactivity and catecholamines in plasma on increased intracranial pressure in the pig

Graded increases of intracranial pressure (ICP) in anaesthetized pigs induced elevations of plasma levels of neuropeptide Y (NPY)-like immunoreactivity (LI) and catecholamines, simultaneously with hypertension and tachycardia. Plasma adrenaline (ADR) increased at a lower ICP-level than did the plasma levels of noradrenaline (NA) and NPY-LI. At the maximal ICP elevation, 22.9 kPa (172 mmHg), plasma NPY-LI was increased about 10-fold, from 48 +/- 8 pmol/l in the basal state, while NA and ADR concentrations increased more than 100-fold. At this maximal ICP-level the plasma levels of NPY-LI were correlated to the concentrations of both NA (r = 0.87, P less than 0.01) and ADR (r = 0.92, P less than 0.001). Plasma NPY-LI continued to increase to about 1000 pmol/l, 10 min after the maximal elevation of ICP was discontinued, while the catecholamines then had declined considerably. A slight cardiac release of NPY-LI was observed at the maximal elevation of ICP. The half-life of NPY-LI in plasma was about 6 min upon systemic infusion. At plasma levels similar to those obtained upon maximal ICP elevation, exogenous NPY caused slight vasoconstriction in the spleen and skeletal muscle, but had no effects on coronary blood flow or systemic blood pressure. This suggests that NPY mainly exerts local actions after release from nerve endings, while levels of circulating NPY in plasma must be very high to influence blood flow in some organs. It is concluded that elevation of ICP results in hypertension and tachycardia related to elevated plasma levels of NPY-LI and catecholamines.(ABSTRACT TRUNCATED AT 250 WORDS)