THE STRAIT OF MESSINA: A KEY AREA FOR PELAGIA NOCTILUCA (CNIDARIA, SCYPHOZOA)

The Strait of Messina is certainly a focal area for the biological cycle of the jellyfish Pelagia noctiluca in the Western Mediterranean Sea. By means of both original and literature data, a conceptual model outlining the biological cycle of this species is proposed. P. noctiluca reproduces from late winter to late spring in the Aeolian Island Archipelago. From late spring to early summer, currents transport newly produced young individuals (20-30 mm bell diameter) eastwards, towards the Strait. The Strait of Messina ecosystem is not a suitable reproduction area for its intense hydrodynamism that would surely lead to a very low reproductive success due to gamete dispersion. This area, however, represents an optimal site for growth, due to its intensive primary and secondary production, but also for an optimal temperature range, lower in summer and higher in winter in respect to the surrounding basins. Pelagia remains all the summer inside the Strait, increasing in bell diameter (50-70 mm) and biomass. Subsequently, in late summer-early autumn, the mature specimens, taking advantage of a typical autumnal downwelling transport, move to deep Tyrrhenian waters where overwinter, to upwell in the Aeolian Archipelago by late winter to start a new cycle

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Abstract Background: Elevated total homocysteine (tHcy) levels are associated with an increased risk of cerebrovascular disease. It is uncertain whether tHcy is also an independent risk factor for cognitive impairment. Methods: We examined 95 stroke subjects 3 months after their strokes, and 55 healthy comparison subjects, with a detailed neuropsychological assessment, and MRI brain scans in a proportion (n = 97). Baseline measurements of tHcy, serum folate and B 12 , creatinine and plasma fibrinogen levels were obtained. Results: tHcy levels were higher in the stroke subjects by a mean 34%. These levels were significantly correlated with the first factor of a principal component analysis of the neuropsychological data, after controlling for age, folate, B 12 and creatinine levels. The correlation of Hcy levels was particularly significant with frontal-executive functioning and attention. tHcy levels were significantly correlated with number of infarcts and total stroke volume in the stroke group, but not with T 2 -weighted deep white matter hyperintensity scores, after correction for age. In the control group, tHcy levels were significantly correlated with ventricle-tobrain ratios as measures of brain atrophy. Conclusion: This study provides evidence that high tHcy levels are associated with cognitive impairment, in particular that of frontal-executive function. The major component of this association is accounted for by small and large strokes, but non-vascular neurotoxic effects of tHcy also appear to play a role. tHcy must receive greater attention as a risk factor for cognitive impairment. Copyright © 2003 S. Karger AG, Basel Homocysteine (Hcy) is a sulfur-containing amino acid formed during the metabolism of the essential amino acid methionine. Elevated plasma homocysteine levels were first linked with vascular disease by McCully A high level of Hcy is both proatherogenic and prothrombotic If Hcy promotes cognitive impairment and is a risk factor for AD, it has important epidemiological implications. In this study, we examined plasma Hcy levels in a stroke sample to determine if there was an association between Hcy levels and cognition, and if this could be accounted for by infarct size or small vessel disease as detected by MRI. Methods Sample Subjects (n = 95) were consecutive patients admitted to two large teaching hospitals affiliated with the University of New South Wales who had recently suffered an ischemic stroke as diagnosed by two neurologists, and who met the diagnostic criteria for cerebral infarction Assessment Stroke subjects had a baseline assessment within 1 week of admission which included a detailed medical history and examination, history of risk factors for cerebrovascular disease and dementia, a functional assessment and the Mini-Mental State Examination Homocysteine Measurement Fasting blood was collected and centrifuged within 6 h, and the plasma stored at -20°C for later analysis. Total Hcy was measured using a fluorescence-based immunochemical technique with demonstrated high repeatability Neuropsychological Assessment Premorbid ability was estimated on the basis of performance on the National Adult Reading Test MRI Brain Scans MRI was performed on a proportion of subjects (n = 55 stroke; n = 42 controls) using a 1.5-T Signa GE magnet and the following protocol: a scout mid-sagittal cut (2D, TR 300 ms, TE 14 ms; 5 mm thick, number of excitations 1.5); 1.5-mm-thick T 1 -weighted contiguous coronal sections through whole brain using a FSPGR sequence and 3D acquisition (TR 14.3 ms, TE 5.4 ms); 4-mm-thick T 2 -weighted FLAIR coronal slices through whole brain (TR 8900, TE 145, TI 2200, FOV 25, 256 ! 192). Fifty-three subjects did not receive MRI scans because of claustrophobia or unwillingness to undergo the test. Analysis of Data Neuropsychological Tests. Raw scores were converted to agescaled scores using published norms [24-26, 28, 36, 38-41]. Composite z-scores were obtained for each domain. The raw scores from individual tests were also used in the exploratory analyses. MRI Scans. These were rated by a trained rater with good interrater (Î scores from 0.7 to 0.9 on various measures) and intra-rater (Î 0.8 to 0.9) reliability determined on five scans each. All ratings were carried out on a computer console using ANALYZE (Mayo Foundation) software. Brain infarctions were identified on T 1 -Homocysteine and Cognitive Impairment Dement Geriatr Cogn Disord 2003;15:155-162 15

Safety and efficacy of fluoxetine on functional outcome after acute stroke (AFFINITY): a randomised, double-blind, placebo-controlled trial

Background Trials of fluoxetine for recovery after stroke report conflicting results. The Assessment oF FluoxetINe In sTroke recoverY (AFFINITY) trial aimed to show if daily oral fluoxetine for 6 months after stroke improves functional outcome in an ethnically diverse population. Methods AFFINITY was a randomised, parallel-group, double-blind, placebo-controlled trial done in 43 hospital stroke units in Australia (n=29), New Zealand (four), and Vietnam (ten). Eligible patients were adults (aged ≥18 years) with a clinical diagnosis of acute stroke in the previous 2–15 days, brain imaging consistent with ischaemic or haemorrhagic stroke, and a persisting neurological deficit that produced a modified Rankin Scale (mRS) score of 1 or more. Patients were randomly assigned 1:1 via a web-based system using a minimisation algorithm to once daily, oral fluoxetine 20 mg capsules or matching placebo for 6 months. Patients, carers, investigators, and outcome assessors were masked to the treatment allocation. The primary outcome was functional status, measured by the mRS, at 6 months. The primary analysis was an ordinal logistic regression of the mRS at 6 months, adjusted for minimisation variables. Primary and safety analyses were done according to the patient's treatment allocation. The trial is registered with the Australian New Zealand Clinical Trials Registry, ACTRN12611000774921. Findings Between Jan 11, 2013, and June 30, 2019, 1280 patients were recruited in Australia (n=532), New Zealand (n=42), and Vietnam (n=706), of whom 642 were randomly assigned to fluoxetine and 638 were randomly assigned to placebo. Mean duration of trial treatment was 167 days (SD 48·1). At 6 months, mRS data were available in 624 (97%) patients in the fluoxetine group and 632 (99%) in the placebo group. The distribution of mRS categories was similar in the fluoxetine and placebo groups (adjusted common odds ratio 0·94, 95% CI 0·76–1·15; p=0·53). Compared with patients in the placebo group, patients in the fluoxetine group had more falls (20 [3%] vs seven [1%]; p=0·018), bone fractures (19 [3%] vs six [1%]; p=0·014), and epileptic seizures (ten [2%] vs two [<1%]; p=0·038) at 6 months. Interpretation Oral fluoxetine 20 mg daily for 6 months after acute stroke did not improve functional outcome and increased the risk of falls, bone fractures, and epileptic seizures. These results do not support the use of fluoxetine to improve functional outcome after stroke

The non\u2011indigenous Oithona davisae in a Mediterranean transitional environment: coexistence patterns with competing species

The Venice lagoon (VL) has been recognized as a hot spot of introduction of non-indigenous species (NIS), due to several anthropogenic factors and environmental stressors that combined may facilitate NIS invasions. In the last decades an increasing number of zooplankton NIS have been observed in the VL. This work aims to provide a picture of the annual cycle and distribution of the recently recorded non-indigenous copepod Oithona davisae, considering the coexistence patterns with the congeneric resident Oithona nana. Therefore, zooplankton samplings were carried out monthly from August 2016 to July 2017 at five Long-Term Ecological Research LTER stations in the VL. Oithona davisae showed a persistent occurrence throughout the year with the highest abundances in the warm season and in the inner areas, while the congeneric O. nana, showing a different distribution pattern, resulted more abundant near the inlets of the Lagoon, where O. davisae reached the minimum density. Oithona davisae seems to find local conditions that promote its settlement and distribution, especially in the inner and more trophic lagoon sites. In other European coastal embayments or transitional waters, O. davisae occupied the niche left by the indigenous O. nana or can replace this congeneric species through competitive exclusion mechanisms. Our data indicate that, for now, such species replacement has not occurred in the VL. One of the causes is the extreme variety of habitats and niches offered by this environment allowing a balanced coexistence with O. nana and in general with the resident copepod community

Does somatostatin have a role to play in migraine headache?

Migraine is a condition without apparent pathology. Its cardinal symptom is the prolonged excruciating headache. Theories about this pain have posited pathologies which run the gamut from neural to vascular to neurovascular, but no observations have detected a plausible pathology. We believe that no pathology can be found for migraine headache because none exists. Migraine is not driven by pathology – it is driven by neural events produced by triggers – or simply by neural noise- noise that has crossed a critical threshold. If these ideas are true, how does the pain arise? We hypothesise that migraine headache is a consequence of withdrawal of descending pain control, produced by “noise” in the cerebral cortex. Nevertheless, there has to be a neural circuit to transform cortical noise to withdrawal of pain control. In our hypothesis, this neural circuit extends from the cortex, synapses in two brainstem nuclei (the periaqueductal gray matter and the raphe magnus nucleus) and ultimately reaches the first synapse of the trigeminal sensory system. The second stage of this circuit uses serotonin (5HT) as a neurotransmitter, but the neuronal projection from the cortex to the brainstem seems to involve relatively uncommon neurotransmitters. We believe that one of these is somatostatin (SST). Temporal changes in levels of circulating SST mirror the temporal changes in the incidence of migraine, particularly in women. The SST2 receptor agonist octreotide has been used with some success in migraine and cluster headache. A cortical to PAG/NRM neural projection certainly exists and we briefly review the anatomical and neurophysiological evidence for it and provide preliminary evidence that SST may the critical neurotransmitter in this pathway. We therefore suggest that the withdrawal of descending tone in SST-containing neurons, might create a false pain signal and hence the headache of migraine

Pituitary adenylate cyclase activating polypeptide and migraine

Pituitary adenylate cyclase activating peptide (PACAP) is found in human trigeminocervical complex and can trigger migraine. PACAP levels were measured using a sensitive radioimmunoassay. Stimulation of the superior sagittal sinus (SSS) in cat elevated PACAP levels in cranial blood. Patients with moderate or severe migraine headache had elevated PACAP in the external jugular vein during headache (n = 15), that was reduced 1 h after treatment with sumatriptan 6 mg (n = 11), and further reduced interictally (n = 9). The data suggest PACAP, or its receptors, are a promising target for migraine therapeutics

Pituitary adenylate cyclase activating polypeptide and migraine.

Pituitary adenylate cyclase activating peptide (PACAP) is found in human trigeminocervical complex and can trigger migraine. PACAP levels were measured using a sensitive radioimmunoassay. Stimulation of the superior sagittal sinus (SSS) in cat elevated PACAP levels in cranial blood. Patients with moderate or severe migraine headache had elevated PACAP in the external jugular vein during headache (n = 15), that was reduced 1 h after treatment with sumatriptan 6 mg (n = 11), and further reduced interictally (n = 9). The data suggest PACAP, or its receptors, are a promising target for migraine therapeutics