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We apply Random Forests to detailed survey data of social relations in order to derive an inductive typology of egocentric networks. Beginning with over 40 descriptors of 1050 northern California respondents' networks, we combine 21 of these into seven dimensions, the extent to which those networks display: (1) interaction with nonkin, (2) proximity to kin, (3) overall involvement with kin (including support), (4) support from nonkin, and the extent to which (5) church, (6) work and (7) extra-curricular activities shape connections with others. We use these dimensions to reliably place 985 of the 1050 observations into types: career-and-friends (24%), family-and-community (20%), family-only (16%), untethered (8%), energetic (7%), withdrawn (6%), and home-and-church (5%). In the second part of the analysis, we describe the social and demographic attributes of respondents that predict membership in each cluster to present a richer picture of the network typology, as well as to confirm that the types have face validity.

Background: The growing diffusion of artificial intelligence, data science and digital health has highlighted the role of collection of data and biological samples, thus raising legal and ethical concerns regarding its use and dissemination. Further, the expansion of biobanking, from the basic collection of frozen specimens to the virtual biobanks of specimens and associated data that exist today, has given a revolutionary potential on healthcare systems, particularly in the field of neurological diseases, due to the inaccessibility of central nervous system and the need of non-invasive investigation approaches. Informed Consent (IC) is considered mandatory in all research studies and specimen collections, and must specifically take into account the ethical respect to the individuals to whom the used biological material and data belong., Methods: We evaluated the attitudes of patients with neurological diseases (NP) and healthy volunteers (HV) towards the donation of biological samples to a biobank for future research studies on neurological diseases, and limitations on the use of data, related to the requirements set by the General Data Protection Regulation (GDPR). The study involved a total of 1454 subjects, including 502 HVs and 952 NPs, recruited at Santa Lucia Foundation IRCCS, Rome, from 2020 to 2024., Results: We found that (i) almost all subjects agreed with the participation in biobanking (ii) and authorization to genetic studies (HV = 99.1%; NP = 98.3%); Regarding the return of results, (iii) we found a statistically significant difference between NP and HV, the latter preferring not to be informed of potential results (HV = 43%; NP = 11.3%; p < 0.0001); (iv) a small number limited the sharing inside European Union (EU) (HV = 4.6%; NP = 6.6%), whereas patients were more likely to refuse transfer outside EU (HV = 7.4%; NP = 10.7% p = 0.05); (v) nearly all patients agreed with the use of additional health data from EMR for research purposes (98.9%)., Conclusions: Consent for the donation of material for research purposes is crucial for biobanking and biomedical research studies that use biological material of human origin. Here, we have shown that choices regarding participation in a neurological biobank can be different between HVs and NPs, even if the benefit for research and scientific progress is recognized. NP have a strong interest in being informed of possible results but limit sharing of samples, highlighting a perception of greater individual or relative benefit, while HV prefer a wide dissemination and sharing of data but not to have the return of the results, favoring a possible benefit for society and knowledge. The results underline the need to carefully manage biological material and data collected in biobanks, in compliance with the GDPR and the specific requests of donors., (© 2024. The Author(s).)

Stroke is one of the leading causes of death and the primary source of disability in adults, resulting in neuronal necrosis of ischemic areas, and in possible secondary degeneration of regions surrounding or distant to the initial damaged area. Secondary neurodegeneration (SNDG) following stroke has been shown to have different pathogenetic origins including inflammation, neurovascular response and cytotoxicity, but can be associated also to regenerative processes. Aside from focal neuronal loss, ipsilateral and contralateral effects distal to the lesion site, disruptions of global functional connectivity and a transcallosal diaschisis have been reported in the chronic stages after stroke. Furthermore, SNDG can be observed in different areas not directly connected to the primary lesion, such as thalamus, hippocampus, amygdala, substantia nigra, corpus callosum, bilateral inferior fronto-occipital fasciculus and superior longitudinal fasciculus, which can be highlighted by neuroimaging techniques. Although the clinical relevance of SNDG following stroke has not been well understood, the identification of specific biomarkers that reflect the brain response to the damage, is of paramount importance to investigate in vivo the different phases of stroke. Actually, brain-derived markers, particularly neurofilament light chain, tau protein, S100b, in post-stroke patients have yielded promising results. This review focuses on cerebral morphological modifications occurring after a stroke, on associated cellular and molecular changes and on state-of-the-art of biomarkers in acute and chronic phase. Finally, we discuss new perspectives regarding the implementation of blood-based biomarkers in clinical practice to improve the rehabilitation approaches and post stroke recovery., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Brunelli, Giannella, Bizzaglia, De Angelis and Sancesario.)

Background and Purpose: Parkinson disease (PD) presents relevant sex-related differences in epidemiology, pathophysiology, and clinical features, with males being more vulnerable to the disease. Sex hormones might have a role, as the experimental models suggest; however, human-based evidence is scarce. Here, we integrated multimodal biomarkers to investigate the relationships between circulating sex hormones and clinical-pathological features in male PD patients., Methods: A cohort of 63 male PD patients underwent comprehensive clinical evaluation of motor and nonmotor disturbances; measurement of estradiol, testosterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) blood levels; and cerebrospinal fluid (CSF) assay of total α-synuclein, amyloid-β-42, amyloid-β-40, total tau, and phosphorylated-181 tau levels. A subgroup of 47 PD patients underwent brain volumetry by 3-T magnetic resonance imaging for further correlations. A control group of 56 age-matched individuals was enrolled for comparative analyses., Results: Male PD patients had higher estradiol and testosterone levels than controls. Estradiol had independent inverse associations with Movement Disorder Society-Unified Parkinson's Disease Rating Scale Part 3 score and disease duration; it was also lower in nonfluctuating patients. Testosterone had inverse independent correlations with CSF α-synuclein and right globus pallidus volume. FSH and LH had age-dependent correlations with cognitive impairment and CSF amyloid-β-42/amyloid-β-40 ratio., Conclusions: The study suggested that sex hormones could differentially contribute to clinical-pathological features of PD in male patients. Whereas estradiol might have a protective role in motor impairment, testosterone might be involved in male vulnerability to PD neuropathology. Gonadotropins instead might mediate age-dependent phenomena of amyloidopathy and cognitive decline., (© 2023 European Academy of Neurology.)

Biobanking has emerged as a strategic challenge to promote knowledge on neurological diseases, by the application of translational research. Due to the inaccessibility of the central nervous system, the advent of biobanks, as structure collecting biospecimens and associated data, are essential to turn experimental results into clinical practice. Findings from basic research, omics sciences, and in silico studies, definitely require validation in clinically well-defined cohorts of patients, even more valuable when longitudinal, or including preclinical and asymptomatic individuals. Finally, collecting biological samples requires a great effort to guarantee respect for transparency and protection of sensitive data of patients and donors. Since the European General Data Protection Regulation 2016/679 has been approved, concerns about the use of data in biomedical research have emerged. In this narrative review, we focus on the essential role of biobanking for translational research on neurodegenerative diseases. Moreover, we address considerations for biological samples and data collection, the importance of standardization in the preanalytical phase, data protection (ethical and legal) and the role of donors in improving research in this field.

Millions of eligible families did not claim their 2021 expanded child tax credit (CTC), collectively forgoing billions of dollars. To address this problem, many policymakers focused on increasing awareness of the CTC by highlighting that families could receive up to $3,600 a year per child. However, people rarely budget on a yearly basis. We propose that communicating the CTC benefit amount in terms of commonly used budgeting periods (e.g., $300 a month) instead of uncommonly used budgeting periods (e.g., $3,600 a year) could increase interest in claiming the CTC. Two large-scale field experiments ([Formula: see text]) among low-income individuals support this account. Using common (vs. uncommon) budgeting periods to describe CTC benefit amounts increased CTC claiming intentions by 16 to 26%. A third large-scale field experiment ([Formula: see text]) demonstrated that encouraging people to consider different budgeting periods moderated these effects. These results suggest that communicating amounts in terms of common budgeting periods is a simple, cost-effective way to stimulate interest in claiming government benefits.

Introduction: Prodromal constipation (PC) at Parkinson's disease (PD) onset may mark a distinct neurodegenerative trajectory; accordingly, presenting phenotype, biochemical signature, and progression of PD patients with PC (PD + PC) might differ from those without (PDwoPC). We compared the clinical-biochemical profile of de novo PD patients with and without PC, and the respective mid-term progression, to establish the grouping effect of PC., Methods: Motor and non-motor scores were collected at diagnosis in n = 57 PD + PC patients and n = 73 PDwoPC. Paired CSF biomarkers (α-synuclein, amyloid and tau peptides, lactate, CSF/serum albumin ratio or AR) were assessed into a smaller sample and n = 46 controls. Clinical progression was estimated as Hoehn and Yahr stage (HY) and levodopa equivalent daily dose (LEDD) change 2.06 ± 1.35 years after diagnosis., Results: At onset, PD + PC patients had higher HY and MDS-UPDRS-part III scores, and higher CSF AR. PDwoPC had higher Non-Motor Symptoms Scale domain-2 score, and lower CSF α-synuclein level. At follow-up, PD + PC had greater LEDD., Conclusions: PC identifies a group of de novo patients with more severe motor impairment, possible blood brain barrier disruption, and greater dopaminergic requirement at mid-term; conversely, de novo PDwoPC patients had prominent fatigue, and pronounced central synucleinopathy., Competing Interests: Declaration of competing interest None. TS, PG: conceptualized the study; PG, DM, LG, HZ: collected and processed data; PG, TS: wrote the initial draft; DM, LG, HZ, GMS, EG, NBM, DDM: supported data interpretation and reviewed the manuscript. All authors have approved the final article., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Each year, eligible individuals forgo billions of dollars in financial assistance in the form of government benefits. To address this participation gap, we identify psychological ownership of government benefits as a factor that significantly influences individuals' interest in applying for government benefits. Psychological ownership refers to how much an individual feels that a target is their own. We propose that the more individuals feel that government benefits are their own, the less likely they are to perceive applying for them as an aversive ask for help, and thus, the more likely they are to pursue them. Three large-scale field experiments among low-income individuals demonstrate that higher psychological ownership framing of government benefits significantly increases participants' pursuit of benefits and outperforms other common psychological interventions. An additional experiment shows that this effect occurs because greater psychological ownership reduces people's general aversion to asking for assistance. Relative to control messages, these psychological ownership interventions increased interest in claiming government benefits by 20% to 128%. These results suggest that psychological ownership framing is an effective tool in the portfolio of potential behavioral science interventions and a simple way to stimulate interest in claiming benefits., Competing Interests: Competing interest statement: W.D.L.R., S.M.T., and M.L. are affiliated with Stanford University. W.D.L.R and S.M.T have not collaborated with M.L., (Copyright © 2021 the Author(s). Published by PNAS.)

In this study, we use population-based linked administrative data to document the full child protective service (CPS) histories of arrested youth and young adults. We extracted records for all individuals aged 24 and under who were arrested in California in 2014 and 2015. These records were probabilistically linked to statewide CPS records dating back to 1998. Overall, 43.4% of those arrested had a history of CPS involvement. Among individuals with uncensored CPS records (born in 1998 or later), 60.2% had past CPS involvement. Findings indicate that youth and young adults booked for a felony offense were more likely to have a history of CPS involvement than those booked for misdemeanors. A multinomial model served to confirm bivariate findings. This study provides further evidence that community concerns of childhood maltreatment were common among criminal justice-involved young adults.

Background: The jurisdiction where an offense is prosecuted significantly affects the severity of punishment for drug possession, creating geographic disparities in exposure to a social determinant of health. In California, felony conviction rates after drug possession arrests have historically varied enormously between counties. California Proposition 47 (Prop-47), passed in 2014, reduced drug possession offenses previously classified as felonies or wobblers (offenses for which prosecutors have discretion to file felony or misdemeanor charges) to misdemeanors. This study examines whether geographic variation in felony convictions after drug possession arrests was reduced, and whether effects were offset by changes in felony convictions for other offenses not addressed by Prop-47., Methods: Arrests made after the implementation of Prop-47 were propensity score matched to similar arrests prior to Prop-47 to account for compositional changes in arrests. This approach compares the outcomes of individuals likely to be arrested with or without the reclassification of drug offenses. We used mixed models to estimate the change in county variance in the probability of felony conviction., Results: The probability of a felony conviction among those arrested for Prop-47 drug offenses declined by 14 percentage points (95% CI: -0.16, -0.12), from 0.20 (95% CI: 0.18, 0.23) to 0.06 (95% CI: 0.06, 0.07). Counties with higher felony conviction probabilities pre-Prop-47 declined most, reducing cross-county variance. For those arrested for drug offenses unaffected by Prop-47, the probability of felony conviction declined by 7 percentage points (95% CI: -0.08, -0.05), from 0.34 (95% CI: 0.31, 0.37) to 0.27 (0.25, 0.29). Declines in both groups were driven by fewer felony convictions for Prop-47 drug offenses, with no increases in felony convictions for concurrent offenses., Conclusion: Reducing offense classifications for drug possession reduced previously large differences in the probability of felony convictions for people arrested for drug offenses in different counties., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Objectives: To evaluate the effects of California Proposition 47, which reclassified felony drug offenses to misdemeanors in 2014, on racial/ethnic disparities in drug arrests., Methods: Using data on all drug arrests made in California from 2011 to 2016, we compared racial/ethnic disparities in drug arrests between Whites, Blacks, and Latinos, immediately and 1 year after policy changes, controlling for secular and seasonal trends., Results: In the month following passage, absolute Black-White disparities in monthly felony drug arrests decreased from 81 to 44 per 100 000 and continued to decrease over time. There was an immediate increase of 27% in the relative disparity, however, because a higher proportion of felony offense types among Whites was reclassified. Total drug arrest rates also declined, suggesting drug law enforcement was deprioritized. During the first year after enactment, felony drug arrests fell by an estimated 51 985 among Whites, 15 028 among Blacks, and 50 113 among Latinos., Conclusions: Reducing criminal penalties for drug possession can reduce racial/ethnic disparities in criminal justice exposure and has implications for improving health inequalities linked to social determinants of health.

Introduction: Recent evidence suggests that sexually antagonistic genetic factors in the maternal line promote homosexuality in men and fecundity in female relatives. However, it is not clear if and how these genetic factors are phenotypically expressed to simultaneously induce homosexuality in men and increased fecundity in their mothers and maternal aunts., Aims: The aim of the present study was to investigate the phenotypic expression of genetic factors that could explain increased fecundity in the putative female carriers., Methods: Using a questionnaire-based approach, which included also the Big Five Questionnaire personality inventory based on the Big Five theory, we investigated fecundity in 161 female European subjects and scrutinized possible influences, including physiological, behavioral, and personality factors. We compared 61 female probands who were either mothers or maternal aunts of homosexual men. One hundred females who were mothers or aunts of heterosexual men were used as controls., Main Outcome Measures: Personality traits, retrospective physiological and clinical data, behavior and opinions on fecundity-related issues were assessed and analyzed to illustrate possible effects on fecundity between probands and control females., Results: Our analysis showed that both mothers and maternal aunts of homosexual men show increased fecundity compared with corresponding maternal female relatives of heterosexual men. A two-step statistical analysis, which was based on t-tests and multiple logistic regression analysis, showed that mothers and maternal aunts of homosexual men (i) had fewer gynecological disorders; (ii) had fewer complicated pregnancies; (iii) had less interest in having children; (iv) placed less emphasis on romantic love within couples; (v) placed less importance on their social life; (vi) showed reduced family stability; (vii) were more extraverted; and (viii) had divorced or separated from their spouses more frequently., Conclusions: Our findings are based on a small sample and would benefit from a larger replication, however they suggest that if sexually antagonistic genetic factors that induce homosexuality in males exist, the factors might be maintained in the population by contributing to increased fecundity greater reproductive health, extraversion, and a generally relaxed attitude toward family and social values in females of the maternal line of homosexual men., (© 2012 International Society for Sexual Medicine.)

Unlabelled: The network model of innovation widely adopted among researchers in the economics of science and technology posits relatively porous boundaries between firms and academic research programs and a bi-directional flow of inventions, personnel, and tacit knowledge between sites of university and industry innovation. Moreover, the model suggests that these bi-directional flows should be considered as mutual stimulation of research and invention in both industry and academe, operating as a positive feedback loop. One side of this bi-directional flow--namely; the flow of inventions into industry through the licensing of university-based technologies--has been well studied; but the reverse phenomenon of the stimulation of university research through the absorption of new directions emanating from industry has yet to be investigated in much detail. We discuss the role of federal funding of academic research in the microarray field, and the multiple pathways through which federally supported development of commercial microarray technologies have transformed core academic research fields., Results and Conclusion: Our study confirms the picture put forward by several scholars that the open character of networked economies is what makes them truly innovative. In an open system innovations emerge from the network. The emergence and diffusion of microarray technologies we have traced here provides an excellent example of an open system of innovation in action. Whether they originated in a startup company environment that operated like a think-tank, such as Affymax, the research labs of a large firm, such as Agilent, or within a research university, the inventors we have followed drew heavily on knowledge resources from all parts of the network in bringing microarray platforms to light. Federal funding for high-tech startups and new industrial development was important at several phases in the early history of microarrays, and federal funding of academic researchers using microarrays was fundamental to transforming the research agendas of several fields within academe. The typical story told about the role of federal funding emphasizes the spillovers from federally funded academic research to industry. Our study shows that the knowledge spillovers worked both ways, with federal funding of non-university research providing the impetus for reshaping the research agendas of several academic fields.

We previously reported that hypoxic coronary vasodilatation (HCVD) is initiated by endothelial NO and sustained by adenosine. Prolonged ischemia/reperfusion impairs endothelium-dependent coronary vasodilatation, whereas transient ischemia (ie, preconditioning) protects the myocardium from subsequent ischemic events. Accordingly, we assessed whether prolonged ischemia/reperfusion impairs HCVD and whether preconditioning prevents this dysfunction. HCVD, elicited in isolated guinea pig hearts by a 1-minute exposure to 100% N2, consisted of an approximately 70% increase in coronary flow associated with enhanced nitrite/nitrate and adenosine overflow (+40% and 5-fold, respectively). After 30-minute global ischemia and 20-minute reperfusion, HCVD was decreased by approximately 60%, and the increases in nitrite/nitrate and adenosine overflow were abolished. Preconditioning (ie, three cycles of 5-minute global ischemia+5-minute reperfusion) prevented the impairment of HCVD and fully restored the increase in nitrite/nitrate overflow, but not that of adenosine. The protective effect of preconditioning was mimicked by perfusion with the adenosine A1 receptor agonist N6-cyclopentyladenosine and prevented by the A1 receptor antagonist N-0861. In addition, the A3 receptor agonist N6-(3-iodobenzyl)adenosine-5'-N-methyl-carboxamide had a similar protective effect. The bradykinin B2 receptor antagonist HOE 140 abolished the protective effect of preconditioning, whereas the NO synthase inhibitor N(omega)-methyl-L-arginine and the cycloxygenase inhibitor indomethacin did not. Our data indicate that preconditioning restores HCVD by a process that is triggered by activation of adenosine A1/A3 and bradykinin B2 receptors. The action of bradykinin is independent of NO and prostacyclin production. Once restored by preconditioning, HCVD is mediated by NO but no longer sustained by adenosine.

Polyunsaturated fatty acids (PUFA: arachidonic and linoleic acid) release histamine from isolated purified rat serosal mast cells only in the presence of oxidizing systems such as phenobarbital-induced rat liver microsomes, prostaglandin-H-synthetase (PHS) or soybean lipoxygenase. The release of mast cell histamine by activated PUFA has a long time-course and the electron microscopical features are consistent with an exocytotic secretion in the case of arachidonic acid and cell lysis in the case of linoleic acid. The phenomenon is associated with a significant increase in malonyldialdehyde (MDA) and conjugated diene generation, suggesting a relationship between histamine release and membrane lipid peroxidation. The secretion of histamine was inhibited by anti-free radical interventions such as D-mannitol, reduced glutathione and alpha-tocopherol. Some cyclooxygenase and lipoxygenase inhibitors, cimetidine and carnitine derivatives, are differentially active in the inhibition of mast cell histamine release by activated arachidonic acid. These results suggest that free radical derivatives of PUFA, generated by metabolic activation, trigger mast cell histamine release.

Flavonols are a group of naturally occurring compounds which are widely distributed in nature where they are found glycosylated primarily in vegetables and fruits. A number of studies have found both anti- and prooxidant effects for many of these compounds. The most widely studied because of their ubiquitous nature have been quercetin, a B-dihydroxylated and myricetin, a B-trihydroxylated flavonol. Some of their prooxidant properties have been attributed to the fact that they can undergo autooxidation when dissolved in aqueous buffer. Studying a number of factors affecting autooxidation, we found the rate of autooxidation for both quercetin and myricetin to be highly pH dependent with no autooxidation detected for quercetin at physiologic pH. Both the addition of iron for the two flavonols and the addition of iron followed by SOD for quercetin at physiologic pH. Both the addistantially. Neither kaempferol, a monohydroxylated flavonol nor rutin, a glycosylated quercetin showed any ability to autooxidize. The results with rutin differ from what we expected based on the B-ring structural similarity to quercetin. The autooxidation of quercetin and myricetin was further studied by electron spin resonance spectroscopy (ESR). Whereas quercetin produced a characteristic DMPO-OH radical, it was not detected below a pH of 9. However, the addition of iron allowed the signal to be detected at a pH as low as 8.0. On the other hand, myricetin autooxidation yielded a semiquinone signal which upon the addition of iron, converted to a DMPO-OH signal detected at a pH of 7.5. In a microsome-NADPH system, quercetin produced an increase in oxygen utilization and with ESR, an ethanol-derived radical signal which could be completely suppressed by catalase indicating the dependence of the signal on hydrogen peroxide. These studies demonstrate that the extracellular production of active oxygen species by dietary flavonols is not likely to occur in vivo but the potential for intracellular redox cycling may have toxicologic significance.

Free radicals are produced by perfusion of isolated guinea pig heart with FeCl3/ADP (10 microM/100 microM) and/or occlusion and opening of the left anterior descending coronary artery. Cardiac histopathology was correlated with histamine and lactate dehydrogenase release and with malondialdehyde production. A differential release of histamine and lactate dehydrogenase in the perfusate was detected, showing a preferential liberation of histamine in the reperfusion phase. The increase in lipid peroxidation product in left ventricular tissues after left coronary artery occlusion was maximal at the end of ischemia.

The effects of histamine and of H1- and H2-receptor agonists on the response to specific antigen were studied in isolated hearts taken from actively sensitized guinea-pigs. Histamine and H2-receptor agonists (dimaprit, impromidine) dose-dependently decrease the positive chronotropic and inotropic effects, and the severity of arrhythmias evoked by the challenge of sensitized hearts with specific antigen. Nordimaprit and the selective H1-receptor agonist 2-pyridyl-ethyl-amine (2-PEA) did not modify the patterns of cardiac anaphylaxis. The positive inotropic and chronotropic responses of the isolated heart to exogenous histamine appear to be partly reduced in the presence of dimaprit. The H2-receptor agonists decrease the amount of histamine released during cardiac anaphylaxis which is increased by cimetidine, while nordimaprit and PEA were ineffective, indicating an inhibitory function afforded by H2-receptors in cardiac anaphylaxis.

In isolated rat serosal mast cells, studies with the fluorescent Ca2+ indicator, quin 2, and with [3H]-myoinositol to label endogenous polyphosphoinositides have established that an increase in cytosol Ca2+ levels was obligatory for histamine release by free radicals. No substantial breakdown of phosphatidylinositol and related polyphosphoinositides was associated with generation of the Ca2+ signal and histamine release, suggesting that the release of histamine by free radicals entails different pathways than the calcium-mobilizing receptors linked to polyphosphoinositides as second messengers.

This study was performed to evaluate the role of intermediate products of arachidonic acid metabolism on histamine release from rat serosal mast cells. Arachidonic acid in concentrations ranging from 10(-9) to 10(-4) M caused no histamine release from purified rat peritoneal mast cells. High concentrations (10(-6)-10(-6) M) of the terminal products of the arachidonic acid metabolism were also devoid of any significant histamine-releasing properties. The metabolic activation of arachidonic acid with prostaglandin-H-(PGH)-synthase isolated from calf seminal vesicles, evoked a significant release of histamine from rat serosal mast cells. The liberation of histamine was not accompanied by a significant leakage of lactic dehydrogenase (LDH) and the electron microscopical features were consistent with an exocytotic release. The phenomenon was blocked by reduced glutathione (GSSH) and by D-mannitol, a hydroxyl free-radical scavenger. These results suggest that free radical derivatives of arachidonic acid are generated during the catalysis which triggers mast cell histamine release.

Parasympathetic innervation of nasal mucosa plays an important role in the pathogenesis of chronic hypertrophic non-allergic rhinitis (C.H.N.A.R.). The present study investigated the effect of Vidian nerve stimulation and resection on the histamine contents and on the morphological pattern in mucosal samples of patients with C.H.N.A.R. Vidian nerve stimulation determines a significant decrease in histamine content in the samples examined; microscopical observations showed significant variations in the glandular, stromal and vascular components. The changes indicate an enhanced secretory activity, intensive vasodilatation and active degranulation of mast cells, which were significantly decreased in number in the samples obtained after 90 sec of stimulation. The neurectomy of the Vidian nerve resolves quite completely the clinical symptomatology and in parallel decreases the mucosal histamine contents, which are increased in patients with C.H.N.A.R. before the operation in comparison with the normal controls.