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We propose Multi-Strategy Coevolving Aging Particles (MS-CAP), a novel population-based algorithm for black-box optimization. In a memetic fashion, MS-CAP combines two components with complementary algorithm logics. In the first stage, each particle is perturbed independently along each dimension with a progressively shrinking (decaying) radius, and attracted towards the current best solution with an increasing force. In the second phase, the particles are mutated and recombined according to a multi-strategy approach in the fashion of the ensemble of mutation strategies in Differential Evolution. The proposed algorithm is tested, at different dimensionalities, on two complete black-box optimization benchmarks proposed at the Congress on Evolutionary Computation 2010 and 2013. To demonstrate the applicability of the approach, we also test MS-CAP to train a Feedforward Neural Network modeling the kinematics of an 8-link robot manipulator. The numerical results show that MS-CAP, for the setting considered in this study, tends to outperform the state-of-the-art optimization algorithms on a large set of problems, thus resulting in a robust and versatile optimizer.

The influence of aging and of treatment with L-deprenyl on the structure of the kidney was investigated in 24-month-cld male Sprague Dawley rats by microanatomical techniques associated with image analysis. L-Deprenyl was administrated orally for 5 months at a dose not inhibiting monoamine oxidase (MAO) B activity (1.25/mg/kg/day) and at a dose inhibiting MAO B activity (5 mg/kg/day). In 24 month-old-rats the number and the volume of glomeruli was reduced in comparison with 12-month-old rats used as reference adult animals. Vascular changes characterised by increased thickness of the tunica media, decreased size of arterial lumen and increased wall-to-lumen ratio were also noticeable in 24-month-old rats. Moreover, an increased MAO B reactivity was noticeable within glomerular tufts and renal tubules. Treatment with the low dose of L deprenyl did not cause changes in MAO B reactivity, or in the number of glomeruli, but increased glomerular volume and reduced the wall-to-lumen ratio in medium-sized renal artery branches. The dose of 5 mg/kg/day of L-deprenyl significantly decreased MAO B reactivity within both glomerular tufts and tubules, increased the number and the volume of glomeruli and countered-age-related vascular changes. The above results suggest that treatment with L-deprenyl counters to some extent microanatomical changes occurring in the kidney of aged rats. The observation that the dose of the compound inactive on MAO B activity reduces in part age dependent renal microanatomical changes, indicates that the renal protective effect of L-deprenyl is only in part related to MAO B inhibition.

The effects of treatment with the dihydropyridine Ca+2 antagonist darodipine (PY 108-068) on age-related changes in the cerebral capillary network was studied using alkaline phosphatase histochemistry with quantitative image analysis. The investigation was performed on male Wistar rats of 12 months (adult reference group) and 27 months. The 27-month-old rats consisted of two groups, the first of control untreated animals and the second of rats receiving an oral dose of 5 mg/kg/day of darodipine from the 21st to the 27th month. The cerebral areas examined included the frontal cortex, the occipital cortex, Ammon's horn of the hippocampus, and the dentate gyrus. The number and the average length of alkaline phosphatase-positive capillaries were decreased in old rats, when compared with adult rats. The intercapillary distance, which is considered as a sensitive parameter for capillary density was increased in aged rats in comparison to adult rats. The capillary diameter was increased slightly or unchanged in old rats. The Ammon's horn and the frontal cortex were the cerebral areas most affected by age-dependent changes of the capillary network. Treatment with darodipine increased the number and the average length of alkaline phosphatase-reactive capillaries and reduced the intercapillary distance and the diameter of cerebral capillaries in old rats. The pericapillary microenvironment of the Ammon's horn was the most sensitive to treatment with darodipine. The above results showed that treatment with darodipine is capable of counteracting some microvascular changes occurring in the brain of aged rats. This suggests that the blockade of dihydropyridine-type Ca2+ channels has a positive effect on the brain microvascular system and may counteract the impairment of pericapillary microenvironment occurring with aging.

1. The density of nerve cells and of silver-gold impregnated fibres were evaluated in the hippocampus and in the cerebellar cortex in adult (12-month-old) and old (24-month-old) Sprague-Dawley rats. 2. The effects of long-term choline alfoscerate (GFC) treatment (100 mg/Kg/day for 6 months) on the above parameters were investigated in old rats. 3. The number of nerve cell profiles and the area occupied by silver-gold impregnated fibres were decreased both in the hippocampus and in the cerebellar cortex in old in comparison with adult rats. 4. GFC treatment countered the age-dependent reduction of nerve cells and silver-gold impregnated fibres. The hippocampus was more sensitive than the cerebellar cortex to the activity of GFC. 5. These results suggest that GFC treatment is effective in slowing down the expression of structural changes occurring in aging brain.

Treatment with L-deprenyl increases mean and maximum life span in the rat and reverses memory and learning deficits associated with old age. Since only sparse information is available concerning the influence of L-deprenyl administration on the aging brain microanatomy, we have investigated the effect of long-term treatment with L-deprenyl on the structure of the cerebellar cortex in the aged rat. The cerebellar cortex was used since it represents a useful model for assessing age-related changes in nervous system anatomy and function. Male Sprague-Dawley rats were treated from the 19th to the 24th month of age with a daily oral dose of 1.25 mg/kg or 5 mg/kg L-deprenyl. Age-matched rats were left untreated and used as a control group. Eleven-month-old untreated rats were used as an adult reference group. The density of Purkinje and granule neuron profiles as well as the intensity of Nissl's staining within the cytoplasm of Purkinje neurons were reduced in 24-month in comparison with 11-month rats. Moreover, an increased accumulation of lipofuscin was noticeable in the cytoplasm of Purkinje neurons of old rats as well as an increase in MAO-B activity in the molecular layer of the cerebellar cortex. The two doses of L-deprenyl increased the density of both Purkinje and granule neuron profiles and the intensity of Nissl's staining in the cytoplasm of Purkinje neurons and reduced lipofuscin deposition within Purkinje neurons. The lower dose of L-deprenyl caused only a slight decrease in MAO-B activity, whereas the 5-mg/kg/day dose remarkably reduced it. These results suggest that long-term treatment with L-deprenyl counters the expression of some age-related microanatomical changes in the rat cerebellar cortex. The possible independence of the effects of the compound on age-related microanatomical changes of the cerebellar cortex and on MAO-B inhibitory activity is discussed.

The present study was designed to assess whether treatment with L-deprenyl has any effect on the age-related microanatomical changes in the rat frontal cortex. Male Sprague-Dawley rats of 19 months of age were treated until the 24th month with an oral daily dose of 1.25 mg/kg or of 5 mg/kg of L-deprenyl. Eleven-month-old untreated rats were used as an adult reference group. The density of nerve cell profiles and of glial fibrillary acidic protein-(GFAP) immunoreactive astroglial profiles, lipofuscin accumulation within the cytoplasm of pyramidal neurons, and MAO-B reactivity were assessed. A decreased density of nerve cell profiles and an increased density of astroglial profiles as well as augmented lipofuscin deposition and MAO-B reactivity were observed in the frontal cortex of rats of 24 months in comparison with 12-month-old animals. In the frontal cortex of rats treated with 5 mg/kg/day L-deprenyl, which is a dose inhibiting MAO-B activity, the density of nerve cell and GFAP-immunoreactive astrocyte profiles is increased and decreased respectively in comparison with age-matched untreated subjects. Lipofuscin deposition is reduced. The lower dose of L-deprenyl (1.25 mg/kg/day) which did not affect MAO-B activity, decreased lipofuscin deposition but was without effect on the density of nerve cell or GFAP-immunoreactive astrocyte profiles. The above findings suggest that treatment with L-deprenyl is able to counter some microanatomical changes occurring in the frontal cortex of aged rats. Some of these effects are probably not related to the inhibitory MAO-B activity of the compound.

The influence of ageing on the noradrenergic innervation of the ovary was studied in female Wistar rats using high pressure liquid chromatography (HPLC) with electrochemical detection and catecholamine histofluorescence techniques. Old age was accompanied by a significant decrease in ovarian noradrenaline levels. In young animals (3-month-old) noradrenergic nerve fibres were distributed primarily to blood vessels and in lesser amounts to the interstitial glands. In aged animals (24-month-old) perivascular noradrenergic fibres were reduced by more than 40%; interstitial gland nerve fibres were reduced by approximately 20%. The possibility that impaired noradrenergic ovarian innervation occurring in old age may be in some way related with age-dependent failure in reproductive activity is discussed.

The influence of ageing on the adrenaline content of the superior mesenteric artery and vein, renal artery and vein and portal vein was studied in 3-month- (young), 12-month- (adult) and 24-month-old (old) male Wistar rats using radioenzymatic assay for the measurement of catecholamine levels. Adrenaline concentrations were unchanged in the vascular wall of the blood vessels examined in adult rats, but were significantly decreased in the vascular wall of the superior mesenteric, renal and portal veins of old rats. In contrast, no age-dependent changes of adrenaline levels were found in the vascular wall of the superior mesenteric or renal arteries. The possibility that the loss of adrenaline concentrations in the venous vascular wall may be in some way related to the cardiovascular impairment occurring with age is discussed.

The density and pattern of the sympathetic noradrenergic innervation of the extramedullary and intramedullary blood vessels of the spinal cord was studied in 3-, 12- and 25-month-old male Wistar rats using combined catecholamine histofluorescence and quantitative image analysis techniques. The study of innervation of intramedullary vessels was accomplished in spinal cord-transected rats to avoid the interference of descending spinal monoamine fibres in the observations. No age-related changes in the density of noradrenergic innervation of the anterior spinal artery or of sympathetic fibres associated with spinal cord blood vessels occurred. These results suggest that unlike perivascular noradrenergic nerves supplying the cerebrovascular tree, the sympathetic innervation of spinal cord blood vessels does not undergo age-dependent changes. It cannot be excluded that the lesser vulnerability of the spinal compared to the cerebral vascular tree to certain kinds of age-related diseases, may depend on the unchanged sympathetic trophic regulation of spinal vessels with age.

By using fluorescence microscopy and microfluorimetric techniques, the effects of ageing and of 11 months acetyl-L-carnitine (ALCAR) treatment on lipofuscin deposition within the cytoplasm of pyramidal neurons of rat prefrontal cortex and hippocampus (CA3 field) were assessed. No lipofuscin autofluorescence was observed in the nerve cell bodies of neurons under study in young rats (3 months of age), but lipopigment had accumulated in the same nerve cells of senescent rats (22 months of age). ALCAR administration significantly reduced the accumulation of lipofuscin within pyramidal neurons of the brain areas examined.

Vasoactive intestinal polypeptide (VIP) levels and distribution were studied in the penis of young-adult (3-month-old) and old (30-month-old) Wistar rats by radioimmunoassay and immunofluorescence. No significant changes in tissue VIP concentrations or distribution occurred in the penis of old rats compared to young-adult rats. The present data indicate that the age-related impairment of male sexual function is not dependent on modifications of the VIP-ergic innervation of penile tissue.

The influence of ageing on the metabolic profile of lateral ventricle choroid plexus epithelial cells from young (3-month-old) and aged (26-month-old) male Wistar rats was studied using enzyme histochemical techniques. The following enzymatic activities related to energy transduction were examined: lactate-(LDH) and succinate- (SDH) dehydrogenases; NADH2-tetrazolium reductase (NADHD) and alpha-glycerophosphate-dehydrogenase (GPDH). The intensity of enzymatic staining within single choroid plexus epithelial cells from young and old animals was assessed microphotometrically. In the choroid plexus epithelial cells of young rats NADHD was the enzymatic activity more heavily stained; cell levels of LHD and GPDH were approximately the same and SDH reactivity was less intense. In old age LDH was reduced by 9.3%, SDH was reduced by 26.1%, NADHD was reduced by 8.6% and GPDH was reduced by 3.6%. The possibility that impaired energy transduction mechanisms at the level of choroid plexus epithelium in old age may influence functional activity of the choroid plexus is discussed.

The influence of aging on the metabolic profile of cerebellar cortex was studied in young (3-month-old), adult (12-month-old) and aged (26-month-old) male Sprague-Dawley rats using enzyme histochemical techniques. The following enzymatic activities related to energy transduction were examined: lactate-(LDH) and succinate-(SDH) dehydrogenases; NADH2-tetrazolium reductase (NADHD) and alpha-glycerophosphate-dehydrogenase (GPDH). The intensity of enzymatic staining within the neuropil of molecular and granular layers as well as within the cytoplasm of Purkinje neurons of young, adult and aged animals was assessed microphotometrically. In the molecular layer LSH, SDH and NADHD levels were reduced in old rats; GPDH was decreased both in adult and old animals. In Purkinje neurons no age-related changes of the enzymatic activities under study were observed. In the granular layer LDH and GPDH showed an age-dependent loss; SDH and NADHD were unchanged. The possibility that age-related changes of the enzymatic activities under study may be due to impaired energy production mechanisms and/or represent the consequence of reduced energetic needs resulting from the documented age-dependent loss of synapses in the molecular or in the granular layers of cerebellar cortex is discussed.

The effects of ageing and of 6 months of Hydergine treatment on lipofuscin deposition within the cytoplasma of pyramidal neurons of rat prefrontal cortex, hippocampus (fields CA1 and CA3) and of Purkinje neurons were assessed microfluorimetrically. No lipofuscin autofluorescence was detected in the nerve cell populations of 3-month-old rats, but lipopigment had accumulated in nerve cell bodies of 16-month-old animals and increased significantly thereafter in rats of 22 months of age. In 22-month-old rats, Hydergine administration (0.6 and 1 mg/kg p.o.) started at 16 months caused a significant dose-related decrease in lipofuscin accumulation within the cytoplasm of the various kinds of nerve cells examined.