Equestrian-related injuries, predictors of fatalities, and the impact on the public health system in Sweden.

OBJECTIVES: Horse riding is a popular activity but has also been found to lead to many injuries and even fatalities. No reduction in the numbers of those being admitted to hospital for equestrian-related injuries have been seen in Sweden in recent years. The aim of this work was to examine injuries, fatalities, and predictors of fatalities in equestrian-related activities and to investigate the cost of these injuries to the public health system. STUDY DESIGN: The study is a retrospective analysis of hospital data. METHODS: National Swedish hospital and mortality registers were retrospectively examined, inclusive of the years 1997-2014. Logistic regression was used to examine the predictors of fatal injuries, and cost of hospital treatment was considered. RESULTS: Over the study period, there were an observed 29,850 injured cases and 51 fatalities. Women comprized almost 90% of those injured and 70% of fatalities. The average age was 26.8 years (range 0-91, standard deviation [SD] = 16.1) for injured and 43 years (range 7-78 years, SD = 20.5) for fatal cases. Men dominated both injured and fatal samples in the older age ranges (Fatal: >50 years; Injured: >70 years), although overall numbers were small. Injuries to the head contributed more than any other body region for both injured and fatal cases, and fractures were the most frequently seen injury type. A chi-squared analysis confirmed that injury type and injured body region were not independent of age. Logistic regression examining the association between fatality and age, gender, home region, and year of injury, indicating trends over time, found that there was an increase of 5.1% in the odds of fatality for every year increase in age of the patient and men had 2.2 times higher odds to be in the fatal sample than women. The conservative estimated cost of injury was 1800 Euro per injury event, equating to over 3 million Euro per year. CONCLUSION: Equestrian-related injury events present a major public health concern. Observed decreases in fatalities suggest improved health care, yet head injury and fatality rates are still high, indicating a need for further intervention. The type of injury changes with the age group, and a better understanding of injury patterns with age is needed to identify protective measures for the different user groups.

Electromagnetic hypersensitive Finns: Symptoms, perceived sources and treatments, a questionnaire study.

The aim was to analyze the subjective experiences of Finns who describe themselves as suffering from electromagnetic hypersensitivity (EHS), their symptoms, self-perceived sources of the health complaints and the effectiveness of medical and complementary alternative therapies. A total of 395 questionnaires were mailed to self-diagnosed EHS persons. Of the participants 345 belonged to a Finnish self-help group and 50 came from outside of the group. The return rate of the study was 52.1% (206) and 80.9% of the respondents were women. Before the onset of EHS the most common health complaints were different types of allergies (35.1%, 68). During the acute phase of EHS the most common symptoms were nervous system related: "stress" (60.3%, 117), "sleeping disorders" (59.3%, 115) and "fatigue" (57.2%, 111). The sources that were most often reported to have triggered EHS were: "personal computers" (50.8%, 94) and "mobile phones" (47.0%, 87). The same devices were also claimed to cause the most symptoms during the acute phase. After the acute phase of EHS had passed, the respondents still claimed to react to these same digital and wireless devices while their reactions to basic electrical appliances were reduced. According to 76% of 157 respondents the reduction or avoidance of electromagnetic fields (EMF) helped in their full or partial recovery. The best treatments for EHS were given as: "dietary change" (69.4%), "nutritional supplements" (67.8%) and "increased physical exercise" (61.6%). The official treatment recommendations of psychotherapy (2.6%) and medication (-4.2%) were not significantly helpful. According to the present results the official treatment protocols should take better account the EHS person's own experiences. The avoidance of electromagnetic radiation and fields effectively removed or lessened the symptoms in EHS persons.

Neuropeptide levels in Dercum's disease (adiposis dolorosa).

Dercum's disease (adiposis dolorosa) is characterised by adiposity and chronic pain in the adipose tissue. It has been proposed that conditions encompassing chronic pain have altered concentrations of neuropeptides involved in pain transmission. The aim of this investigation was to examine whether patients with Dercum's disease have abnormal concentrations of different neuropeptides. In cerebrospinal fluid (CSF) and in plasma (P) from 53 patients with Dercum's disease substance P-like immunoreactivity (SP-LI), neuropeptide Y-like immunoreactivity (NPY-LI), ß-endorphin-like immunoreactivity (ß-END-LI), calcitonin gene-related peptidelike immunoreactivity (CGRP-LI), met-enkephalin-like immunoreactivity (m-ENK-LI), vasoactive intestinal polypeptide-like immunoreactivity (VIP-LI), somatostatin (SOM-LI), γ2-melanocyte-stimulating hormone-like immunoreactivity (γ2-MSH-LI), and dynorphin-like immunoreactivity (DYN-LI) were measured. Three of the substances were also measured in a control group. The CSF concentration of SP was statistically significantly lower in the Dercum group than in the control group, whereas NPY-LI and b-END-LI were borderline statistically significantly lower and higher, respectively, in Dercum patients compared to controls. Compared with reference values, CSF-MSH-LI levels were slightly elevated and CSF-NPY-LI levels were slightly lowered in the Dercum group. The other substances in both CSF and plasma were within the reference values with a high degree of statistical significance. In conclusion, altered levels of neuropeptides that have previously been seen in different pain conditions cannot clearly be demonstrated in Dercum's disease.

Relativistic kinetic theory for spin-1/2 particles: Conservation laws, thermodynamics, and linear waves.

We study a recently derived fully relativistic kinetic model for spin-1/2 particles. First, the full set of conservation laws for energy, momentum, and angular momentum are given together with an expression for the (nonsymmetric) stress-energy tensor. Next, the thermodynamic equilibrium distribution is given in different limiting cases. Furthermore, we address the analytical complexity that arises when the spin and momentum eigenfunctions are coupled in linear theory by calculating the linear dispersion relation for such a case. Finally, we discuss the model and give some context by comparing with potentially relevant phenomena that are not included, such as radiation reaction and vacuum polarization.

The peptidergic innervation of the rat parotid gland: effects of section of the auriculo-temporal nerve and/or of otic ganglionectomy.

The origin/pathways of peptidergic nerves contributing to the parotid gland contents of vasoactive intestinal peptide (VIP), substance P and calcitonin gene-related peptide (CGRP) were investigated by performing surgery on one side of the rat. Comparisons (based on total amount of peptide) were made between the gland on the operated side and the contralateral gland 7 days postoperatively. Otic ganglionectomy showed that almost all of the parotid gland contents of VIP (98%) and substance P (98%) were due to the otic connection, while this was true for only a minor portion (32%) of the CGRP-gland content. Section of the auriculo-temporal nerve showed that almost all of the VIP- and substance P-containing nerve fibres reached the parotid gland via this nerve, as judged by a reduction in the VIP-content by 88% and in the substance P-content by 93%, while the CGRP-content was only reduced by 37%. Section of the auriculo-temporal nerve combined with otic ganglionectomy did not reduce the gland contents of CGRP and substance P further than just otic ganglionectomy. Thus, the auriculo-temporal nerve is not likely to innervate the parotid gland with CGRP- and/or substance P-containing nerve fibres from the trigeminal ganglion.

Renal handling of Zn-alpha2-glycoprotein as compared with that of albumin and the retinol-binding protein.

An unusual electrophoretic pattern of the urine from a patient with malignant lymphoma was observed. One of the major proteins, identified Zn-alpha2-glycoprotein (Zn-alpha2), was isolated from the urine and partly characterized. The Stokes radius was found to be 3.24 nm and the molecular weight, determined by sodium dodecyl sulfate polyacrylamide electrophoresis, 42,000. The plasma level in healthy individuals was 39 +/- 7 (SD) mg/liter. In 12 of 25 healthy individuals, Zn-alpha2 was measurable in the urine and was found to be 1.0 +/- 1.1 mg/liter. In 23 patients with chronic glomerulonephritis (CGN), in 9 with proximal tubular dysfunction (PTD), in 23 with various renal diseases (VRD), and in 10 with malignant lymphoma, the plasma level and the urinary excretion were compared with those of albumin (mol wt 67,000) and of the retinol-binding protein (RBP, mol wt 21,000). A close correlation was found between the urine-to-plasma (U/P) ratios of Zn-alpha2 and albumin in the patients with CGN, whereas in the PTD patients the U/P ratios of Zn-alpha2 and RBP were correlated. No significant renal arteriovenous difference in Zn-alpha2 could be demonstrated. The Zn-alpha2 excretion was increased also in two patients with malignant lymphoma and proteinuria of a tubular pattern. The plasma Zn-alpha2 varied inversely with the glomerular filtration rate in the patients with renal disease, but was normal in those with malignant lymphoma. The results are consistent with the assumption of a sieving coefficient of Zn-alpha2, substantially exceeding that of albumin, but notably lower than that of smaller low-molecular-weight proteins. An increased excretion of Zn-alpha2 may be due to increased glomerular permeability as well as to defective proximal tubular reabsorption.

Relativistic kinetic equation for spin-1/2 particles in the long-scale-length approximation.

In this paper, we derive a fully relativistic kinetic theory for spin-1/2 particles and its coupling to Maxwell's equations, valid in the long-scale-length limit, where the fields vary on a scale much longer than the localization of the particles; we work to first order in ℏ. Our starting point is a Foldy-Wouthuysen (FW) transformation, applicable to this regime, of the Dirac Hamiltonian. We derive the corresponding evolution equation for the Wigner quasidistribution in an external electromagnetic field. Using a Lagrangian method we find expressions for the charge and current densities, expressed as free and bound parts. It is furthermore found that the velocity is nontrivially related to the momentum variable, with the difference depending on the spin and the external electromagnetic fields. This fact that has previously been discussed as "hidden momentum" and is due to that the FW transformation maps pointlike particles to particle clouds for which the prescription of minimal coupling is incorrect, as they have multipole moments. We express energy and momentum conservation for the system of particles and the electromagnetic field, and discuss our results in the context of the Abraham-Minkowski dilemma.

Corticotropin-releasing factor and neuropeptide Y: role in emotional integration.

The amygdala complex integrates stressful stimuli and is critical in transducing their aversive value into autonomic, endocrine and behavioural responses. Stimulation within the amygdala complex produces signs of fear without a relevant external object, while lesions in this region abolish normal fear responses. In a manner characteristic of phylogenetically old limbic brain areas, the complex neurochemical anatomy of the amygdala involves a large number of phylogenetically old peptide mediators. The distribution and connectivity of these peptide systems have been extensively studied, but less is known about their functional role. Recent evidence suggests that two neuropeptides, corticotropin-releasing factor (CRF) and neuropeptide Y (NPY) exert a reciprocal regulation of responsiveness to stressful stimuli, possibly via an interaction of these two systems in the amygdala.

Prevention oriented epidemiologic study of accidental burns in rural areas of Ardabil, Iran.

PURPOSE OF STUDY: Burns are one of the leading causes of injury-related deaths in Iran. We conducted a study to investigate features of burns in rural areas of Ardabil Province from October 2004 through March 2005, with an aim to providing content for effective prevention programs. BASIC PROCEDURES: This study employed longitudinal prospective methodology. The study population included all patients presenting with burns to local health care facilities during the study period. MAIN FINDINGS: A total of 1179 cases were studied. Most of the cases (59.4%) were females. Mean of age of victims was 22.3+/-19 years in females and 13.6+/-17 years in males. The vast majority (91.2%) of burns occurred at home. More than two-thirds of burns were because of hot liquids or steam. The majority of scald burns resulted during use of heating devices such as samovars, gas stoves, valors and picnic gas stoves. Overturning and spilling of hot liquids were the most common injury mechanisms. PRINCIPLE CONCLUSIONS: Prevention programs should focus on children and adult women. Prevention efforts should target home environments and focus on prevention of scalding burns.

Sympathectomy-induced increases in calcitonin gene-related peptide (CGRP)-, substance P- and vasoactive intestinal peptide (VIP)-levels in parotid and submandibular glands of the rat.

The neuropeptide contents of rat salivary glands were increased four weeks after sympathetic postganglionic denervation (but not after preganglionic denervation): calcitonin gene-related peptide (CGRP) by 400 and 65% in the parotid and submandibular glands, respectively; substance P by 30% in the submandibular gland; and vasoactive intestinal peptide (VIP) by 30% in the parotid gland. The sensory neurotoxin capsaicin prevented the expected increases of CGRP and substance P in the submandibular glands and of VIP in the parotid glands. The CGRP-increase in the parotid gland was, however, only reduced (by 65%). Parasympathetic otic ganglionectomy reduced the peptide levels in the parotid glands (CGRP--50%, VIP--98% and substance P--99%). From these residual levels, CGRP increased almost 8-fold and substance P 3-fold in response to the sympathetic denervation, while VIP was unaffected. In the parasympathetically denervated glands, the capsaicin-sensitive contribution to the CGRP-response to sympathetic denervation was roughly estimated to be more than 25% but less than 40%, while the corresponding contribution to the substance P-response was roughly estimated to be more than 6% but less than 58%. Most likely not only CGRP/substance P-containing sensory C-fibres (submandibular and parotid glands) but also parasympathetic VIP-containing secretomotor and vasomotor fibres (parotid glands) contributed to the capsaicin-sensitive response to sympathetic denervation.

Radioimmunoassay of pro-gamma-melanotropin, the amino-terminal fragment of proopiolipomelanocortin.

A RIA has been developed for natural porcine pro-gamma MSH, the 103-amino acid peptide that represents the amino-terminal part of proopiolipomelanocortin. Rabbits were immunized with the purified peptide polymerized with glutaraldehyde. The antiserum is directed against the amino-terminal end of the antigen and does not cross-react with corticotropin, beta-lipotropin, beta-endorphin, gamma 3MSH, or gamma 2MSH. The minimum detectable concentration is 0.15 ng/ml standard pro-gamma MSH (15 pg/tube). Pro-gamma MSH-like immunoreactivity was detected in plasma and extracts of the hypothalamus and pituitary of pigs. Gel chromatography of these extracts revealed at least three immunoreactive peaks in the anterior and neurointermediate lobes of the pituitary, whereas two immunoreactive peaks were found in extracts of the hypothalamus.

Calcitonin gene-related peptide in thyroid nerve fibers and C cells: effects on thyroid hormone secretion and response to hypercalcemia.

Calcitonin gene-related peptide (CGRP) in the thyroid has a dual localization to nerve fibers around blood vessels and follicles and to parafollicular (C) cells. CGRP was found to coexist with substance P (SP) in most of the nerve fibers; a few CGRP fibers seemed to lack SP, and a few SP fibers seemed to be devoid of CGRP. In the C cells, CGRP coexisted with calcitonin (CT). Cervical vagotomy (extirpation of the nodose ganglion) eliminated approximately 50% of the CGRP/SP fibers in the thyroid without any overt influence on CGRP/CT in the C cells. Removal of the superior cervical ganglion or chemical sympathectomy (6-hydroxydopamine treatment) affected neither thyroid CGRP/SP nerve fibers nor CGRP/CT-storing C cells. CGRP nerve cell bodies were numerous in the jugular-nodose ganglionic complex (notably in the jugular portion); in many of them, CGRP coexisted with SP. A few scattered CGRP nerve cell bodies also occurred in the laryngeal ganglion, whereas none was found in the thyroid ganglion. Hypercalcemia evoked by vitamin D2 treatment, which is known to degranulate thyroid C cells, reduced the thyroid content of both CGRP and CT. As tested in mice in vivo, CGRP and SP alone or together had no effect on basal or TSH- or isoprenaline-induced thyroid hormone secretion. Vasoactive intestinal peptide-stimulated iodothyronine release, on the other hand, was enhanced by CGRP, but not by SP. SP had no effect on combined vasoactive intestinal peptide-CGRP-stimulated iodothyronine release. These findings suggest that CGRP participates in the control of thyroid hormone secretion and that, like CT, CGRP in the C cells is under control of the serum calcium level.

Neuropeptides in the thyroid gland: distribution of substance P and gastrin/cholecystokinin and their effects on the secretion of iodothyronine and calcitonin.

Previously, vasoactive intestinal polypeptide was localized to intrathyroidal nerve fibers. It stimulates iodothyronine secretion in mice. In the present study two populations of nerve fibers containing substance P and gastrin/cholecystokinin (CCK)-like immunoreactivity, respectively, were demonstrated in the thyroid gland of several mammals. The substance P fibers occurred around blood vessels and follicles, whereas the gastrin/CCK fibers occurred mainly around follicles. In the chicken thyroid and ultimobranchial glands only substance P-containing fibers could be demonstrated. Such fibers were particularly numerous in the ultimobranchial gland. CCK-4, CCK-8, and substance P did not increase thyronine secretion measured as release of radioiodine into the circulation of mice pretreated with Na125I and T4. The TSH-induced release of radioiodine was also unaffected. Calcitonin secretion in rats was stimulated by CCK-4, CCK-8, substance P, and vasoactive intestinal polypeptide.

Glucose stimulation of pancreatic beta-cell lines induces expression and secretion of dynorphin.

To investigate adaptive responses of pancreatic beta-cells to hyperglycemia, genes induced by glucose stimulation were identified by subtraction cloning. Among 53 clones representing differentially expressed genes, 20 encoded the endogenous opioid precursor, prodynorphin. The amino acid sequence of murine prodynorphin is identical to the rat protein in sequences comprising the opioid peptides and 86% identical in the remainder of the molecule. Stimulation of MIN6 cells increased prodynorphin RNA levels to more than 20-fold in proportion to physiological glucose concentrations. Similar induction levels were observed in murine betaTC3 and rat Rinm5F beta-cell lines. Prodynorphin RNA expression increased within 1 h of glucose stimulation, achieved maximal levels by 4 h, and remained elevated for at least 24 h. By using RIA, MIN6 cells were shown to contain and secrete increased amounts of dynorphin-A following glucose stimulation. Treatment of MIN6 cells with KCl, forskolin, or isobutyl-methyl-xanthine strongly induced prodynorphin RNA expression, suggesting that induction may be related to secretion-coupled signaling pathways. The induction of prodynorphin in several beta-cell lines is consistent with previous demonstrations of beta-cell synthesis of other endogenous opioids, including beta-endorphin, and suggests that opioids may have a potentially significant role in regulating beta-cell secretion.

Antihistone and anti-dsDNA autoantibodies in Alzheimer's disease and vascular dementia.

In order to evaluate their prevalence in senile dementias, serum titer of antibodies against histones and double stranded deoxyribonucleic acid (dsDNA) were measured by means of the ELISA test in patients suffering from vascular dementia (VD), presenile Alzheimer's disease (AD), and senile dementia of the Alzheimer's type (SDAT). Only three subjects out of 87 had dsDNA autoantibodies. On the contrary, VD and SDAT showed high titers of antibodies against histones when compared to healthy controls. A significant relationship was also found between antihistone serum titer and degree of dementia in AD. Results were not influenced by gender, age, or duration of illness. Presence of antihistone antibodies in dementias might reflect an alteration of membrane fluidity and integrity with leakage of nuclear immunogens or disturbances of immune functions, as frequently observed in dementia disorders.

High delta sleep-inducing peptide-like immunoreactivity in plasma in suicidal patients with major depressive disorder.

BACKGROUND: Delta sleep-inducing peptide (DSIP) supposedly involves the hypothalamus-pituitary-adrenal (HPA) axis. Previous studies have shown deviated plasma DSIP-like immunoreactivity (DSIP-LI) levels, as well as abnormal DSIP-LI responses to corticotropin-releasing hormone in patients with major depressive disorder (MDD). This study was performed to investigate plasma-DSIP-LI and its association with the dexamethasone suppression test (DST) in suicide attempters. METHODS: Plasma-DSIP and serum cortisol were measured before and after dexamethasone intake in 34 suicide attempters and in healthy age- and sex-matched controls. RESULTS: We found significantly elevated DSIP-LI levels in MDD patients (p < .005), and a significant correlation between predexamethasone cortisol and predexamethasone DSIP-LI levels in healthy controls. Postdexamethasone DSIP-LI levels increased in subjects with low predexamethasone DSIP-LI levels, whereas they decreased in subjects with high predexamethasone DSIP-LI levels. CONCLUSIONS: Results give some support to the theory of glucocorticoid involvement in the regulation of DSIP, and suggest altered DSIP-LI levels in suicidal MDD patients.

Cerebrospinal fluid neuropeptides in Alzheimer's disease and vascular dementia.

Cerebrospinal fluid (CSF) levels of several neuropeptides have been suggested as candidate markers in neurodegenerative disorders. We have examined the levels of corticotropin-releasing hormone (CRH), beta-endorphine (BEND), delta sleep-inducing peptide (DSIP), somatostatin (SRIF), and neuropeptide Y (NPY) in CSF samples obtained under highly standardized conditions from healthy aged controls and from patients suffering from Alzheimer's disease (AD) or vascular dementia (VAD). The influence of some potentially confounding factors was evaluated. CRH and BEND were markedly decreased in both AD and VAD patients, and BEND levels correlated negatively with degree of dementia within the patient population. SRIF was decreased in both AD and VAD patients. DSIP was slightly increased in AD, but not in VAD. NPY did not differ between groups. For none of the peptides did CSF concentrations correlate significantly with duration of illness, nor, with the exception of BEND, with its degree. Present data do not support the hypothesis that specific neuropeptide changes occur in different neurodegenerative disorders, but are in agreement with previous reports suggesting that neuropeptide systems are differentially affected by neurodegeneration.

Cerebrospinal fluid monoamines in Prader-Willi syndrome.

BACKGROUND: The behavioral phenotype of Prader-Willi syndrome (PWS) suggests hypothalamic dysfunction and altered neurotransmitter regulation. The purpose of this study was to examine whether there was any difference in the concentrations of monoamine metabolites in the cerebrospinal fluid (CSF) in PWS and non-PWS comparison cases. METHODS: The concentration of monoamine metabolites in CSF was determined in 13 children and adolescents with PWS diagnosed on clinical and genetic criteria. The concentrations were compared with those from 56 comparison cases in healthy and other contrast groups. RESULTS: The concentrations of dopamine and particularly serotonin metabolites were increased in the PWS group. The differences were most prominent for 5-hydroxyindoleacetic acid. The increased concentrations were found in all PWS cases independently of age, body mass index, and level of mental retardation. CONCLUSIONS: The findings implicate dysfunction of the serotonergic system and possibly also of the dopamine system in PWS individuals, and might help inform future psychopharmacologic studies.

Delta sleep-inducing peptide response to human corticotropin-releasing hormone (CRH) in major depressive disorder. Comparison with CRH-induced corticotropin and cortisol secretion.

Twenty-four subjects (12 patients with major depressive disorder and 12 controls matched for sex and age) received 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) as an iv bolus dose. Healthy subjects exhibited a slight, but sustained, increase of plasma delta sleep-inducing peptide (DSIP) concentrations, whereas a marked reduction of DSIP levels was found in depressives. Compared to controls, depressed patients showed a significant attenuation of corticotropin (ACTH) responses, whereas cortisol secretion in response to hCRH was normal. Basal DSIP and cortisol concentrations were highly correlated and were higher in depressives than in controls. Both were negatively correlated with the DSIP responses to hCRH. These findings are compatible with the hypothesis that hypothalamic-pituitary-adrenal (HPA) overactivity in the depressive state is primarily due to central hypersecretion of CRH and support the view of a modulatory function of DSIP in the complex regulatory mechanism of the HPA system and of its pathophysiological significance for aberrant HPA axis function in major depressive disorder.

Calcitonin gene-related peptide and cerebral blood vessels: distribution and vasomotor effects.

The innervation of cerebral blood vessels by nerve fibers containing calcitonin gene-related peptide (CGRP) and the vasomotor effects of this peptide are described for a number of different mammalian species. CGRP-immunoreactive nerve fibers were present in the adventitia of cerebral arteries in all species examined (guinea pig, cat, rabbit, rat, and mouse). Numerous perikarya containing CGRP immunoreactivity are demonstrable in the trigeminal ganglion of all species. In the cerebral perivascular nerve fibers and in trigeminal perikarya, CGRP is often colocalized with substance P and neurokinin A. Marked interspecies differences exist both in the density of CGRP-immunoreactive nerve fibers and in the cerebrovascular levels measured with radioimmunoassay. The highest concentrations were observed in cerebral vessels from guinea pigs, the lowest concentration in rabbit vessels, and intermediate levels in the feline and human cerebral vasculature. CGRP is a potent dilator of cerebral arteries in all species examined (human pial, feline middle cerebral, rabbit, guinea pig and rat basilar arteries). The concentration of CGRP eliciting half-maximal responses ranged from 0.4 nM (human pial artery) to 3 nM (rat and rabbit basilar arteries). Pretreatment of cerebral arteries with low concentrations of either substance P (0.1 nM) or neurokinin A (3 nM) attenuated slightly the CGRP-induced relaxations of guinea pig basilar arteries. Calcitonin was found to be a very weak dilator of cerebral arteries from human and guinea pig. Thus, cardiovascular nerve fibers containing CGRP appear to be present in all mammalian species (although to varying degrees) and CGRP is invariably a potent dilator of the cerebral arteries for all species.