Data on unveiling the occurrence of transient, multi-contaminated mafic magmas inside a rhyolitic reservoir feeding an explosive eruption (Nisyros, Greece).

This data article includes the description and the geochemical and mineralogical dataset of 67 pyroclastic rock samples from the Upper Pumice (UP) explosive activity of Nisyros volcano (eastern South Aegean Active Volcanic Arc). A detailed field and petrographic description of the studied outcrops and samples are reported, including representative photomicrographs and SEM images, whole-rock major and trace elements compositions of 31 representative samples and Sr-Nd isotope ratios on 22 selected samples. Analytical methods and conditions used for data acquisition are also reported. The UP eruption produced a stratigraphic sequence constituted by a basal fallout deposit, gradually substituted by pyroclastic density current (PDC) deposits; these are overlaid by a lag-breccia unit, and the sequence is closed by a grey ash flow level. The juvenile is mainly constituted by white-yellow, moderately crystalline pumice with rhyolitic composition and homogenous Sr-Nd isotope values. Variable amounts of dense, grey, crystalline juvenile lapilli clasts (CRC, Crystal-Rich Clast), with rounded shape and less evolved composition (andesite to dacite) are also present in the deposit. These mafic CRCs are peculiar due to their large variability in textures (from distinctive diktytaxitic to strongly fragmented structure without a defined fabric) and in the geochemical and isotopic composition. The data acquired were fundamental to reconstruct the complex and peculiar history of ascent, storage and differentiation/assimilation processes of these mafic melts before their intrusion into the shallow, rhyolitic magma chamber, with important implication on the possible eruption trigger during the more recent explosive phase of activity at Nisyros volcano. Moreover, the geochemical and isotopic analyses provide new original data to the general knowledge of the Aegean volcanics. All the data reported in this paper are related to the research article Braschi et al. (2022).

Water flux management and phytoplankton communities in a Mediterranean coastal lagoon. Part I: How to promote dinoflagellate dominance?

The Biguglia lagoon is a shallow Mediterranean coastal ecosystem where eutrophication is increasing for years. A channel supplying freshwater was cleared in 2009 to enhance lagoon water circulation and alleviate dystrophic crises. Monthly monitoring was started in 2010 to document the impacts of this action on abiotic characteristics and phytoplankton communities. Three stations were surveyed (by microscopy and HPLC). Evidence suggests that this operation had an unexpected outcome. Salinity footprints indicated the succession of three main hydrological sequences that depended on rainfall and circulation pattern. Diatoms and dinoflagellates dominated the first sequence, characterized by heavy rainfall, while Prorocentrum minimum became progressively the dominant species in the second period (increasing salinities) with extensive bloom over the whole lagoon (5.93×10-(5) cells·L(-1)) during the third period. These phytoplankton successions and community structures underline the risk of pernicious effects arising from remediation efforts, in the present case based on increasing freshwater inputs.

The endogenous nociceptin/orphanin FQ-NOP receptor system as a potential therapeutic target for intestinal disorders.

In 1995, by reverse pharmacology approach, used here for the first time in the history of pharmacology, nociceptin/orphanin FQ (N/OFQ) has been discovered as the endogenous ligand of a preidentified receptor named opioid receptor like 1. Subsequent studies showed that N/OFQ and its receptor (N/OFQergic system) are widely distributed in central and peripheral nervous systems as well as in peripheral organs of human and animals, and represent a system that is involved in a very large range of biological functions such as pain perception, intestinal motility and secretion, immune modulation, stress. From the time of its discovery to now, a high number of NOP agonists and antagonists have been synthesized and tested in various pathologies. Nevertheless, none of the molecules targeting N/OFQergic system have currently succeeded in going through clinical trials concerning gut pathologies, indicating that further studies are required. The work from Dr. Fichna et al., published in the present issue of Neurogastroenterology and Motility, adds another brick in the wall of understanding the role of N/OFQergic system in IBS-D pathology by the pharmacological evaluation of a new NOP receptor agonist, SCH 221510, in animal models of intestinal alterations (diarrhea and visceral hyperalgesia). Interestingly, authors report clinical data confirming the involvement of N/OFQergic system in IBS-D patients and, consequently, suggest this system as a valuable therapeutic target for IBS-D pathology. This minireview aims to give a brief summary of experimental and clinical studies focusing on the N/OFQergic system as pharmacological target for the therapeutic treatment of intestinal pathologies such as IBS and IBD.

Effects of natalizumab on oligoclonal bands in the cerebrospinal fluid of multiple sclerosis patients: a longitudinal study.

Retrospective studies show that natalizumab modifies oligoclonal immunoglobulin (IgG) bands (OCBs) in the cerebrospinal fluid (CSF) of multiple sclerosis (MS) patients. In this study, we prospectively analyzed both serum and CSF samples from 24 MS patients, before and after 2 years of natalizumab-based therapy. Our results showed complete (55%) or partial (27%) disappearance of the OCBs in CSF samples that were taken after 2 years of therapy. Intrathecal IgG production, represented by the IgG index and IgGLoc, was also quantitatively reduced. Our data showed that natalizumab substantially modulates both intrathecal polyclonal and oligoclonal IgG production: This effect was much more potent than was previously reported.

Continuous exposure to Kaposi sarcoma-associated herpesvirus (KSHV) in healthcare workers does not result in KSHV infection.

Kaposi sarcoma (KS)-associated herpesvirus (KSHV or HHV-8) infection routes and risk of occupational exposure are still ill-defined. We analysed the risk for occupational acquisition of KSHV infection in healthcare workers (HCWs) with prolonged professional exposure to patients with classic KS, comparing the results to those obtained in healthy relatives of KS patients. Serum and/or saliva KSHV-specific antibodies and DNA were detected in five out of 35 healthy relatives of KS patients but in none of the eight HCWs, suggesting that, outside strict family contacts, horizontal transmission of KSHV is highly inefficient even for HCWs with prolonged contact with KS patients.

Contrast-enhanced ultrasound assessment of complex cystic lesions in renal transplant recipients with acquired cystic kidney disease: preliminary experience.

We prospectively studied the potential value of contrast-enhanced ultrasound (CEUS) to characterize complex acquired cystic kidney disease (ACKD) or suspected solid renal masses, avoiding the risk of inducing acute kidney injury in 138 renal transplant recipients by contrast-enhanced computed tomography (CT). Forty-three cases (31%) had ACKD; 15 ACKD patients (35%) showed suspicious or nondiagnostic ultrasound. The latter subgroup underwent CEUS and, if the suspicion was confirmed, a contrast-enhanced CT. Thirty five lesions were identified in the 15 patients studied by CEUS. According to the Bosniak classification, 27 cysts were type I (BI), four type II (BII), two type III (BIII) with enhancement at the level of thickened septa; we also identified two solid enhancing lesions (BIV). We followed the BI and BII lesions with serial CEUS, while the remaining four cases underwent contrast-enhanced CT showing two solid lesions and two complex cysts with contrast enhancement in the septea. The four patients underwent surgical resection yielding three renal cell carcinomas one papillary carcinoma as the pathological findings. This preliminary study characterized solid nodules and BIII lesions for further evaluation by CT. CEUS seems to correctly characterize BI and BII cysts that are not clearly defined by standard ultrasound.

A marketed fermented dairy product containing Bifidobacterium lactis CNCM I-2494 suppresses gut hypersensitivity and colonic barrier disruption induced by acute stress in rats.

BACKGROUND: Fermented milk (FM) containing Bifidobacterium lactis CNCM I-2494 and yogurt strains improves irritable bowel syndrome (IBS) symptoms in constipated IBS patients. In rats, stressful events exacerbate IBS symptoms and result in the alteration of gut sensitivity and permeability via epithelial cell cytoskeleton contraction. In a stress model, we aimed at evaluating the effect of B. lactis CNCM I-2494 as a pure strain or contained in an FM product on visceral sensitivity and the impact of this FM on intestinal barrier integrity. METHODS: Visceral sensitivity was analyzed in rats subjected to partial restraint stress (PRS). Rats received during 15 days the B. lactis as a pure strain (10(6) to 10(10) CFU mL(-1)), B. lactis in an FM product (10(8) CFU g(-1), diluted or not), or a control product. Gut paracellular permeability, colonic occluding and Jam-A proteins, and blood endotoxin levels were determined in rats receiving B. lactis in an FM product submitted or not to a PRS. KEY RESULTS: The FM product showed a dose-dependent inhibitory effect on stress-induced visceral hypersensitivity. A similar antihyperalgesic effect was observed at 10(10) CFU mL(-1) of pure B. lactis administration. The FM product prevented the increase in intestinal permeability induced by PRS and restored occludin and JAM-A expressions to control levels. The FM product abolished the increase concentration of blood endotoxin induced by PRS. CONCLUSIONS & INFERENCES: This study illustrates that a probiotic food containing B. lactis CNCM I-2494 strain reduces visceral hypersensitivity associated with acute stress by normalizing intestinal epithelial barrier via a synergistic interplay with the different probiotic strains and/or metabolites contained in this product.

Cannabinoid agonist WIN55,212 in vitro inhibits interleukin-6 (IL-6) and monocyte chemo-attractant protein-1 (MCP-1) release by rat pancreatic acini and in vivo induces dual effects on the course of acute pancreatitis.

BACKGROUND: Cannabinoids (CBs) evoke their effects by activating the cannabinoid receptor subtypes CB1-r and CB2-r and exert anti-inflammatory effects altering chemokine and cytokine expression. Various cytokines and chemokines are produced and released by rodent pancreatic acini in acute pancreatitis. Although CB1-r and CB2-r expressed in rat exocrine pancreatic acinar cells do not modulate digestive enzyme release, whether they modulate inflammatory mediators remains unclear. We investigated the CB-r system role on exocrine pancreas in unstimulated conditions and during acute pancreatitis. METHODS: We evaluated in vitro and in vivo changes induced by WIN55,212 on the inflammatory variables amylasemia, pancreatic edema and morphology, and on acinar release and content of the cytokine interleukin-6 (IL-6) and chemokine monocyte chemo-attractant protein-1 (MCP-1) in untreated rats and rats with caerulein (CK)-induced pancreatitis. KEY RESULTS: In the in vitro experiments, WIN55,212 (10(-6) mol L(-1)) inhibited IL-6 and MCP-1 release from acinar cells of unstimulated rats and after CK-induced pancreatitis. In vivo, when rats were pretreated with WIN55,212 (2 mg kg(-1), intraperitoneally) before experimentally-induced pancreatitis, serum amylase, pancreatic edema and IL-6 and MCP-1 acinar content diminished and pancreatic morphology improved. Conversely, when rats with experimentally-induced pancreatitis were post-treated with WIN55,212, pancreatitis worsened. CONCLUSIONS & INFERENCES: These findings provide new evidence showing that the pancreatic CB1-r/CB2-r system modulates pro-inflammatory factor levels in rat exocrine pancreatic acinar cells. The dual, time-dependent WIN55,212-induced changes in the development and course of acute pancreatitis support the idea that the role of the endogenous CB receptor system differs according to the local inflammatory status.

Markers of eosinophilic and neutrophilic inflammation in bronchoalveolar lavage of asthmatic and atopic children.

BACKGROUND: Recent studies performing fiberoptic bronchoscopy in children have improved our understanding of asthma pathophysiology. Eosinophilic, but also neutrophilic, inflammation has been described in asthma, but the relationship with atopy was incompletely investigated. The aim of this study is to examine inflammatory cells and mediators in children with asthma compared to the appropriate controls, i.e. atopic children without asthma and children with no atopy or asthma. Moreover, asthmatic children were analysed separately based on the presence of atopy and stratified by age. METHODS: We recruited 191 children undergoing fiberoptic bronchoscopy for appropriate indications: 91 asthmatics (aged 1.4-17 years), 44 atopics without asthma (1.6-17.8 years) and 56 nonasthmatic nonatopic controls (1.4-14 years). In bronchoalveolar lavage, total and differential cell counts and inflammatory mediators, including ECP, eotaxin, IL-8 and TNFalpha, were analysed. RESULTS: Eosinophils and ECP levels were increased in asthmatic children when compared to controls (P = 0.002 and P = 0.01, respectively), but also atopic children without asthma had increased ECP levels compared to controls (P = 0.0001). Among asthmatic children, eosinophils and ECP levels were not different between atopic and nonatopic individuals. Neither neutrophils nor the related mediators (IL-8 and TNFalpha) differed significantly in the three groups. This pattern of inflammation was observed in both preschool and school-aged asthmatic children. CONCLUSIONS: This study suggests that markers of eosinophilic, but not neutrophilic inflammation, are increased in asthmatic children and also in atopic children without asthma. Of interest, in asthmatic children, the activation of the eosinophilic response is not solely because of the presence of atopy.

In vitro and in vivo pharmacological role of TLQP-21, a VGF-derived peptide, in the regulation of rat gastric motor functions.

BACKGROUND AND PURPOSE: Vgf gene expression has been detected in various endocrine and neuronal cells in the gastrointestinal tract. In this study we investigated the pharmacological activity of different VGF-derived peptides. Among these, TLQP-21, corresponding to the 556-576 fragment of the protein was the unique active peptide, and its pharmacological profile was further studied. EXPERIMENTAL APPROACH: The effects of TLQP-21 were examined in vitro by smooth muscle contraction in isolated preparations from the rat gastrointestinal tract and, in vivo, by assessing gastric emptying in rats. Rat stomach tissues were also processed for immunohistochemical and biochemical characterization. KEY RESULTS: In rat longitudinal forestomach strips, TLQP-21 (100 nmol x L(-1)-10 micromol x L(-1)) concentration-dependently induced muscle contraction (in female rats, EC(50) = 0.47 micromol.L(-1), E(max): 85.7 +/- 7.9 and in male rats, 0.87 micromol x L(-1), E(max): 33.4 +/- 5.3; n = 8), by release of prostaglandin (PG)E(2) and PGF(2a) from the mucosal layer. This effect was significantly antagonized by indomethacin and selective inhibitors of either cyclooxygenase-1 (S560) or cyclooxygenase-2 (NS398). Immunostaining and biochemical studies confirmed the presence of VGF in the gastric neuronal cells. TLQP-21, injected i.c.v. (2-32 nmol per rat), significantly decreased gastric emptying by about 40%. This effect was significantly (P < 0.05) blocked by i.c.v. injection of indomethacin, suggesting that, also in vivo, this peptide acts in the brain stimulating PG release. CONCLUSIONS AND IMPLICATIONS: The present results demonstrate that this VGF-derived peptide plays a central and local role in the regulation of rat gastric motor functions.

Involvement of cannabinoid CB1- and CB2-receptors in the modulation of exocrine pancreatic secretion.

The role of the cannabinoid system in the regulation of exocrine pancreatic secretion was investigated by studying the effects of the synthetic CB1- and CB2-receptors agonist, WIN55,212, on amylase secretion in isolated lobules and acini of guinea pig and rat, and the expression of CB-receptors in rat pancreatic tissue by immuno-chemistry and Western-blot analysis in both basal and cerulein (CK)-induced pancreatitis condition. In pancreatic lobules of guinea pig and rat, WIN55,212 significantly inhibited amylase release stimulated by KCl depolarization through inhibition of presynaptic acetylcholine release, but did not modify basal, carbachol- or CK-stimulated amylase secretion. The effect of WIN55,212 was significantly reduced by pre-treatment with selective CB1- and CB2-receptor antagonists. The antagonists, when given alone, did not affect the KCl-evoked response. Conversely, WIN55,212 was unable to affect basal and CK- or carbachol-stimulated amylase release from pancreatic acini of guinea pig and rat. Immunofluorescent staining of rat pancreatic tissues showed that CB1- and CB2-receptors are expressed in lobules and in acinar cells and their presence in acinar cells was also shown by Western-blot analysis. After CK-induced pancreatitis, the expression of CB1-receptors in acinar cells was not changed, whilst a down-regulation of CB2-receptors was observed. In conclusion, the present study shows that WIN55,212 inhibits amylase release from guinea pig and rat pancreatic lobules and, for the first time, that cannabinoid receptors are expressed in lobules of the rat pancreas, suggesting an inhibitory presynaptic role of this receptor system. Finally, in rat pancreatic acinar cells, CB1- and CB2-receptors, expressed both in basal conditions and after CK-induced pancreatitis but inactive on amylase secretion, have an unknown role both in physiological and pathological conditions.

Central and peripheral role of the nociceptin/orphaninFQ system on normal and disturbed colonic motor function and faecal pellet output in the rat.

In this study, seeking further information on the role of the nociceptin/orphanin FQ (N/OFQ)-ergic system in normal and disturbed colonic motor function in rats, we compared the colonic effects of UFP-112, a novel highly potent agonist, with those of N/OFQ. When injected intracerebroventricularly (i.c.v.) and intraperitoneally (i.p.), UFP-112 and N/OFQ increased bead expulsion time in a statistically significant and dose-related manner and reduced the percentage of rats with castor oil-induced diarrhoea. UFP-112 showed greater efficacy, higher potency and longer-lasting inhibitory effects than N/OFQ, and pretreatment with UFP-101, a selective antagonist, blocked the N/OFQ analogue-induced responses in both tests. When injected i.c.v., UFP-112 and N/OFQ inhibited corticotrophin releasing factor- and restrain stress-stimulated faecal pellet excretion significantly and in a dose-related manner. Conversely, when injected peripherally both peptides significantly inhibited colonic propulsive motility but did so in a non-dose-related manner. In conclusion, these findings indicate that, in the rat, the central and peripheral N/OFQ systems have an inhibitory role in modulating distal colonic propulsive motility under physiological and pathological conditions. UFP-112 therefore promises to be a useful pharmacological tool for investigating the role of the N/OFQ system in motor functions in the distal colonic tract under physiological and pathological conditions.

General and specific factors associated with severity of cognitive impairment in systemic lupus erythematosus.

OBJECTIVE: To determine factors affecting the severity of cognitive impairment in systemic lupus erythematosus (SLE) and to analyze its anatomic location. METHODS: Fifteen cognitive functions grouped into 8 domains were evaluated in 52 patients with SLE and 20 with rheumatoid arthritis. Patients were classified according to severity of impairment as normal, mild, or moderate/severe. Multivariate analysis was performed to identify the main factors affecting severity of cognitive deficits. The most likely anatomic site of damage according to neuropsychological performance was compared with the lesion's location on magnetic resonance imaging (MRI). RESULTS: In SLE patients, a stepwise regression analysis showed that the number of impaired functions (dependent variable) was associated with antiphospholipid antibody positivity (aPL+; P = 0.04), the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI; P = 0.001), hypertension (P = 0.032), and was inversely related to educational level (P = 0.021). Including MRI, the number of impaired functions was associated with severity of MRI (P < 0.001), the SDI (P = 0.013), and the presence of Raynaud's phenomenon (P = 0.04). The contemporary presence of aPL+ and Raynaud's phenomenon resulted in a higher probability to develop moderate/severe cognitive deficits (P = 0.015). Two logistic multiple regression analyses identified hypertension (P < 0.05), the SDI (P < 0.01), and moderate/severe MRI findings as main predictors of moderate/severe impairment (dependent variable). The damage site hypothesized through neuropsychological testing corresponded with MRI findings in 71.7% of SLE patients K = 0.42, P = 0.005). CONCLUSION: Hypertension, aPL+, accumulated damage, and MRI lesions are the main factors affecting severity of cognitive impairment in SLE. The hypothesized sites of central nervous system involvement according to neuropsychological testing correlated with MRI findings in most patients.

The gastric effects of UFP-112, a new nociceptin/orphanin receptor agonist, in physiological and pathological conditions.

Nociceptin/orphanin FQ (N/OFQ), the endogenous NOP receptor ligand, centrally modulates gastric motor and secretory functions and prevents ethanol-induced gastric lesions in rats. A recently synthesized N/OFQ analog, [(pF)Phe(4)Aib(7)Arg(14)Lys(15)]N/OFQ-NH(2) (UFP-112), acts as a highly potent and selective peptide agonist for NOP receptors and produces longer-lasting in vitro and in vivo effects in mice than the natural ligand N/OFQ. In this study, we evaluated the effects of centrally (intracerebroventricularly/icv) and peripherally (intraperitoneally/ip) injected UFP-112 on gastric emptying and gastric acid secretion, and on the development of gastric mucosal lesions induced by 50% ethanol in the rat. When injected icv, it dose-dependently delayed gastric emptying of a phenol red meal (by up to 70%), decreased gastric secretion in water-loaded rats after 90 pylorus ligature, and reduced ethanol-induced gastric lesions (by up to 87%). In all three assays, UFP-112 was more effective than N/OFQ. The highly selective NOP receptor antagonist, UFP-101, decreased the efficacy of UFP-112, thus confirming that central NOP receptors mediate inhibitory control on these functional and pathological conditions in rats. Ip injected N/OFQ and UFP-112 induced non-dose-related gastric hypersecretory and antiulcer effects, which UFP-101 partially abolished. Ip N/OFQ appeared equiactive but about 30-100 times less potent than ip UFP-112 in stimulating gastric acid secretion and preventing lesion formation. When ip injected, both UFP-112 and N/OFQ left gastric emptying in rats unchanged, suggesting that peripheral NOP receptors have a role in mediating gastric hypersecretory and antiulcer effects but are not involved in regulating gastric motility. In addition, the inhibitory effects induced by this novel NOP receptor agonist lasted longer than those induced by N/OFQ. In conclusion, UFP-112 is a promising new pharmacological tool for studying the functional roles of the central and peripheral N/OFQ receptor system.

Assessment of the main pancreatic duct using computed tomography with multiplanar reconstructions.

UNLABELLED: The aim of this study was to assess the morphology of the main pancreatic duct (MPD) using multiplanar reconstructions and to compare this with the morphology of the MPD of anatomic subjects. MATERIALS AND METHODS: The morphology of the MPD was studied by means of multiplanar reconstructions obtained on the one hand from thin tomodensitometric slices and on the other hand from the dissection of anatomic subjects. This study involved 15 subjects in each group. RESULTS: Full multiplanar reconstruction was obtained in 13 cases. In 2 cases, the isthmus did not appear in the reconstructions. The morphology of the MPD was similar in both groups. The length of the MPD was identical at the head and isthmus of the pancreas in both groups but was greater in the dissection group than in the reconstruction group in the body and tail areas of the pancreas. The diameter of the MPD was greater at the head of the pancreas in the dissection group and was identical in both groups for the other segments of the MPD. CONCLUSIONS: Multiplanar tomodensitometric reconstruction of the main pancreatic duct is feasible. This new technique, currently under evaluation, could allow the study of canalar pathologies of the pancreas through tomodensitometry.

Nociceptin/orphanin FQ-induced delay in gastric emptying: role of central corticotropin-releasing factor and glucocorticoid receptors.

When injected intracerebroventricularly (i.c.v.) in rats, nociceptin/orphanin FQ (N/OFQ) delays gastric emptying and increases plasma corticosterone levels. Our aim in this study was to investigate changes in gastric emptying of a phenol red meal, and the plasma corticosterone response to N/OFQ in adrenalectomized (ADX) rats, in ADX rats injected with corticosterone at 1, 24 and 72 h before the gastric emptying assay, and in intact rats i.c.v. pretreated with a glucocorticoid antagonist (RU486) and with a corticotropin-releasing factor receptor antagonist (alpha-helical CRF9-41). In adrenal intact rats, i.c.v. injection of N/OFQ (2.5 nmol rat-1) significantly delayed gastric emptying (by 70%) and increased plasma corticosterone concentrations. Conversely, in ADX rats, N/OFQ left gastric emptying unchanged. In ADX rats, corticosterone injected at 1, 24 and 72 h before the gastric emptying assay almost restored the N/OFQ-induced delay in gastric emptying. Finally, pretreatment with RU486- and alpha-helical CRF9-41 abolished the N/OFQ-induced inhibition of gastric emptying. These findings suggest that central N/OFQ inhibits gastric emptying through an integrated orphaninergic system-CRF interaction in which corticosterone plays a permissive role.