Search

Vasoactive intestinal peptide (VIP) is an important modulatory peptide throughout the CNS acting as a neurotransmitter, neurotrophic or neuroprotective factor. In the hippocampus, a brain area implicated in learning and memory processes, VIP has a crucial role in the control of GABAergic transmission and pyramidal cell activity in response to specific network activity by either VIP-containing basket cells or interneuron-selective (IS) interneurons and this appears to have a differential impact in hippocampal-dependent cognition. At the cellular level, VIP regulates synaptic transmission by either promoting disinhibition, through activation of VPAC1 receptors, or enhancing pyramidal cell excitability, through activation of VPAC2 receptors. These actions also control several important synaptic plasticity phenomena such as long-term potentiation (LTP) and long-term depression (LTD). This paper reviews the current knowledge on the activation and multiple functions of VIP expressing cells in the hippocampus and their role in controlling synaptic transmission, synaptic plasticity and learning and memory processes, discussing also the role of VPAC1 and VPAC2 VIP receptors in the regulation of these different processes. Furthermore, we address the current knowledge regarding changes in VIP mediated neurotransmission in epileptogenesis and mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS), and discuss the therapeutic opportunities of using selective VIP receptor ligands to prevent epileptogenesis and cognitive decline in MTLE-HS. [ABSTRACT FROM AUTHOR]

• Review paper covering the engineering and material science involved in vacuum insulation panels (VIPs) relevant to refrigerators. • The factors affecting solid, gaseous and radiative conductivity are discussed in detail. • VIP thermal conductivity, ageing mechanisms and commercially available VIPs are described. Globally, the electrical energy consumption of domestic refrigerators is approximately 6% of the total consumed. Typically, refrigerators are insulated with materials, such as foams (thermal conductivity >20 mWm−1K−1). Alternatively, using Vacuum Insulation Panels (VIPs) (thermal conductivity < 7 mWm−1K−1) would significantly reduce their overall energy consumption and improve their energy efficiency index whilst maximising the usable inner volume. This paper reviews previous published research into VIPs covering core, envelope, heat transfer phenomena and ageing. The choice of core material significantly affects both the heat transfer coefficient and the overall cost of a VIP. To improve cost effectiveness and ageing properties, research has focused on the development of alternative core materials. This development requires a fundamental understanding of the effect of several interfering factors on the performance of VIPs. In this paper, these factors have been extensively reviewed and the results presented in a systematic manner. The factors are grouped into three sections viz. material properties (pore/particle size, particle's mechanical strength and conductivity), design properties (sealing pressure, compaction density) and operating conditions (mean operating temperature, relative humidity). The effect of each factor, on heat transfer modes, radiation and conduction, has been thoroughly discussed, along with the physics involved, by objectively reviewing studies reporting these. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Harbin Institute of Technology. Social Sciences Edition / Haerbin Gongye Daxue Xuebao. Shehui Kexue Ban is the property of Harbin Institute of Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Innervation of the intestinal mucosa has gained more attention with demonstrations of tuft and enteroendocrine cell innervation. However, the role(s) these fibers play in maintaining the epithelial and mucus barriers are still poorly understood. This study therefore examines the proximity of mouse ileal goblet cells to neuronal fibers, and the regulation of goblet cell production by vasoactive intestinal peptide (VIP). An organotypic intestinal slice model that maintains the cellular diversity of the intestinal wall ex vivo was used. An ex vivo copper‐free click‐reaction to label glycosaminoglycans was used to identify goblet cells. Pharmacological treatment of slices was used to assess the influence of VIP receptor antagonism on goblet cell production and neuronal fiber proximity. Goblet cells were counted and shown to have at least one peripherin immunoreactive fiber within 3 µm of the cell, 51% of the time. Treatment with a VIP receptor type I and II antagonist (VPACa) resulted in an increase in the percentage of goblet cells with peripherin fibers. Pharmacological treatments altered goblet cell counts in intestinal crypts and villi, with tetrodotoxin and VPACa substantially decreasing goblet cell counts. When cultured with 5‐Ethynyl‐2'‐deoxyuridine (EdU) as an indicator of cell proliferation, colocalization of labeled goblet cells and EdU in ileal crypts was decreased by 77% when treated with VPACa. This study demonstrates a close relationship of intestinal goblet cells to neuronal fibers. By using organotypic slices from mouse ileum, vasoactive intestinal peptide receptor regulation of gut wall goblet cell production was revealed. [ABSTRACT FROM AUTHOR]

Cortical circuit activity is shaped by the parvalbumin (PV) and somatostatin (SST) interneurons that inhibit principal excitatory (EXC) neurons and the vasoactive intestinal peptide (VIP) interneurons that suppress activation of other interneurons. To understand the molecular-genetic basis of functional specialization and identify potential drug targets specific to each neuron subtype, we performed a genome wide assessment of both gene expression and splicing across EXC, PV, SST and VIP neurons from male and female mouse brains. These results reveal numerous examples where neuron subtype-specific gene expression, as well as splice-isoform usage, can explain functional differences between neuron subtypes, including in presynaptic plasticity, postsynaptic receptor function, and synaptic connectivity specification. We provide a searchable web resource for exploring differential mRNA expression and splice form usage between excitatory, PV, SST, and VIP neurons (http://research-pub.gene.com/NeuronSubtypeTranscriptomes). This resource, combining a unique new dataset and novel application of analysis methods to multiple relevant datasets, identifies numerous potential drug targets for manipulating circuit function, reveals neuron subtype-specific roles for disease-linked genes, and is useful for understanding gene expression changes observed in human patient brains. [ABSTRACT FROM AUTHOR]

Activity-dependent neuroprotective protein (ADNP) was discovered and first characterized in the laboratory of Prof. Illana Gozes to be regulated by vasoactive intestinal peptide (VIP), and pituitary adenylate cyclase-activating peptide (PACAP) toward neuroprotection. Importantly, ADNP is a master regulator of >400 genes, essential for brain formation, while its haploinsufficiency causes cognitive impairments. Recently, de novo mutations in ADNP were identified as leading to the autism-like ADNP syndrome, mimicked by the Adnp -deficient mouse model. Furthermore, novel peptide derivatives of the neuroprotective ADNP-snippet NAP (NAPVSIPQ), developed in our laboratory, include SKIP and the mirroring all D-amino acid SKIP (D-SKIP). We now extended previous evidence suggesting potential antagonistic features for D-SKIP, compared with the neuroprotective peptide SKIP, as was observed by NMR analysis and social/olfactory functional testing. Here, an impact of the Adnp genotype was observed in the Morris Water Maze (MWM) test measuring cognition, coupled with improvement by SKIP, opposing the inert/exacerbating effect of D-SKIP. In the elevated plus-maze and open field tests measuring anxiety-related behaviors, contrasting effects of SKIP and D-SKIP were found, with SKIP improving/preserving the normal phenotype of the mouse, and D-SKIP causing alterations. Lastly, an in silico analysis suggested that SKIP and D-SKIP bind the microtubule end binding (EB) proteins EB1 and EB3 in different conformations, thereby indicating distinctive natures for the two peptides, potentially mediating differential in vivo effects. Altogether, our findings corroborate the notion of D-SKIP acting as an antagonist, thus distinguishing it from the neuroprotective SKIP. [ABSTRACT FROM AUTHOR]

Uterine receptivity and embryo implantation are two main processes that need a finely regulated balance between pro-inflammatory and tolerogenic mediators to allow a successful pregnancy. The neuroimmune peptide vasoactive intestinal peptide (VIP) is a key regulator, and it is involved in the induction of regulatory T cells (Tregs), which are crucial in both processes. Here, we analyzed the ability of endogenous and exogenous VIP to sustain a tolerogenic microenvironment during the peri-implantation period, particularly focusing on Treg recruitment. Wild-type (WT) and VIP-deficient mice [heterozygous (HT, +/−), knockout (KO, −/−)], and FOXP3-knock-in-GFP mice either pregnant or in estrus were used. During the day of estrus, we found significant histological differences between the uterus of WT mice vs. VIP-deficient mice, with the latter exhibiting undetectable levels of FOXP3 expression, decreased expression of interleukin (IL)-10, and vascular endothelial growth factor (VEGF)c, and increased gene expression of the Th17 proinflammatory transcription factor RORγt. To study the implantation window, we mated WT and VIP (+/−) females with WT males and observed altered FOXP3, VEGFc, IL-10, and transforming growth factor (TGF)β gene expression at the implantation sites at day 5.5 (d5.5), demonstrating a more inflammatory environment in VIP (+/−) vs. VIP (+/+) females. A similar molecular profile was observed at implantation sites of WT × WT mice treated with VIP antagonist at d3.5. We then examined the ability GFP-sorted CD4+ cells from FOXP3-GFP females to migrate toward conditioned media (CM) obtained from d5.5 implantation sites cultured in the absence/presence of VIP or VIP antagonist. VIP treatment increased CD4+FOXP3+ and decreased CD4+ total cell migration towards implantation sites, and VIP antagonist prevented these effects. Finally, we performed adoptive cell transfer of Tregs (sorted from FOXP3-GFP females) in VIP-deficient-mice, and we observed that FOXP3-GFP cells were mainly recruited into the uterus/implantation sites compared to all other tested tissues. In addition, after Treg transfer, we found an increase in IL-10 expression and VEGFc in HT females and allowed embryo implantation in KO females. In conclusion, VIP contributes to a local tolerogenic response necessary for successful pregnancy, preventing the development of a hostile uterine microenvironment for implantation by the selective recruitment of Tregs during the peri-implantation period. [ABSTRACT FROM AUTHOR]

The skin temperature (Tm) of the orofacial area influences orofacial functions and is related to the blood flow (BF). Marked increases in BF mediated by parasympathetic vasodilation may be important for orofacial Tm regulation. Therefore, we examined the relationship between parasympathetic reflex vasodilation and orofacial Tm in anesthetized rats. Electrical stimulation of the central cut end of the lingual nerve (LN) elicited significant increases in BF and Tm in the lower lip. These increases were significantly reduced by hexamethonium, but not atropine. VIP agonist increased both BF and Tm in the lower lip. The activation of the superior cervical sympathetic trunk (CST) decreased BF and Tm in the lower lip; however, these decreases were significantly inhibited by LN stimulation. Our results suggest that parasympathetic vasodilation plays an important role in the maintaining the hemodynamics and Tm in the orofacial area, and that VIP may be involved in this response. [ABSTRACT FROM AUTHOR]

The principal circadian pacemaker in mammals, the suprachiasmatic nucleus (SCN), expresses a number of neuropeptides that facilitate intercellular synchrony, helping to generate coherent outputs to peripheral clocks throughout the body. In particular, arginine vasopressin (AVP)– and vasoactive intestinal peptide (VIP)–expressing neurons have been recognized as crucial subpopulations within the SCN and have thus been the focus of many chronobiological studies. Here, we analyze the neuropeptide expression of 2 popular transgenic mouse strains commonly used to direct or restrict Cre-mediated recombination to AVP- and VIP-ergic neurons. The Avp-IRES2-Cre (JAX #023530) and Vip-IRES-Cre (JAX #010908) "driver" mouse strains express the Cre recombinase under the control of the endogenous Avp or Vip gene, respectively, allowing scientists either to ablate their gene of interest or to overexpress a transgene in a cell type–specific manner. Although these are potentially very powerful tools for chronobiologists and other scientists studying AVP- and VIP-ergic neurons, we found that neuropeptide expression in these mice is significantly decreased when an IRES(2)-Cre cassette is inserted downstream of the neuropeptide-encoding gene locus. The impact of IRES(2)-Cre cassette insertion on neuropeptide expression may be a confounding factor in many experimental designs. Our findings suggest that extreme caution must be exercised when using these mouse models to avoid misinterpretation of empirical results. [ABSTRACT FROM AUTHOR]

Attentional modulation of sensory processing is a key feature of cognition; however, its neural circuit basis is poorly understood. A candidate mechanism is the disinhibition of pyramidal cells through vasoactive intestinal peptide (VIP) and somatostatin (SOM)-positive interneurons. However, the interaction of attentional modulation and VIP-SOM disinhibition has never been directly tested. We used all-optical methods to bi-directionally manipulate VIP interneuron activity as mice performed a cross-modal attention-switching task. We measured the activities of VIP, SOM, and parvalbumin (PV)-positive interneurons and pyramidal neurons identified in the same tissue and found that although activity in all cell classes was modulated by both attention and VIP manipulation, their effects were orthogonal. Attention and VIP-SOM disinhibition relied on distinct patterns of changes in activity and reorganization of interactions between inhibitory and excitatory cells. Circuit modeling revealed a precise network architecture consistent with multiplexing strong yet non-interacting modulations in the same neural population. • Attention and VIP interneurons both strongly modulate sensory responses in V1 • Attentional and VIP modulations do not interact and are orthogonal to each other • Imaging four cell classes shows the two modulations act through distinct mechanisms • Circuit modeling confirms that V1 can multiplex strong yet non-interacting modulations Attentional modulation of sensory processing is a critical aspect of cognition, but its neural circuit basis is poorly understood. Previous work implicates VIP interneurons as critical to this modulation. Myers-Joseph et al. demonstrate that modulations by VIP interneurons and attention are in fact orthogonal, allowing multiplexing diverse signals in V1. [ABSTRACT FROM AUTHOR]

This study evaluates three listed farmhouses in Ørland Municipality which are going to be relocated and rehabilitated according to current Norwegian standards and requirements. Accordingly, the study assesses possible challenges and solutions regarding energy upgrading and restoration while preserving their historic features and cultural heritage. The study suggests solutions for the energy rehabilitation of the three farmhouses based on a literature review, hygrothermal simulations and energy simulations. These solutions include thermal post-insulation of external walls and above the framework of joists against the cold attics with mineral wool, vacuum insulation panels (VIP), and aerogel blankets. Additionally, fenestration renovation options and the potential for implementation of building integrated photovoltaics (BIPV) are reviewed. Lastly, simulations of multiple energy-saving measures for each of the farmhouses have been conducted. A new foundation due to the relocation, together with post-insulation of the cold attic are found to be feasible measures considering the preservation of architectural appearance and authenticity. Regarding the external walls, post-insulating externally is preferable for the farmhouses considering moisture issues and interior space savings. However, it is important to consider any possible loss of cultural heritage value. Alternatively, internal thermal insulation with aerogel blankets may be a feasible solution due to its high thermal resistance applying small thicknesses. The results show that in some cases, enhancing old original windows with a secondary glazing is an equally good solution compared to a total replacement of the windows, and is recommended for cultural preservation. Implementation of BIPV contributed to meet the net energy demand requirement. Nevertheless, it is recommended that the chosen BIPV systems resemble an accepted roofing material from the regulatory requirements, e.g., slates, to accommodate the building's architectural aesthetics and authenticity. This study provides insight and recommendations for the rehabilitation of three listed traditional farmhouses in Trøndelag County, addressing energy efficiency while preserving their cultural significance. The findings show that it is possible to achieve today's energy requirements when rehabilitating listed heritage buildings. Results from energy simulations show that a reduction in net energy demand between 55 % and 75% is possible, while it is essential to note that each building is unique, and a case-by-case approach is needed. Nevertheless, the findings can be applicable for a general energy upgrading of heritage buildings. [ABSTRACT FROM AUTHOR]

• PRL molecules of 4 stages (premature non-laying, laying, trans, and incubation) were identified. • Different isoform composition between pituitary PRL and secreted PRL was identified. • Increasing isoform numbers and ratios to non-posttranslational modified PRL were observed with reproductive stages. • Presence of isoforms which differ pI at least in part originate phosphorylation to the amino acid residue of PRL molecule. Endocrine changes during bird reproduction are well documented. Prolactin (PRL) exhibits a strong relationship between incubation and broody behavior. The molecular forms of PRL in the anterior pituitary gland during the reproductive cycle have already been previously identified but not those in the secreted form. To identify the molecular forms of secreted PRL during the reproductive cycle, we thus monitored the physiological status and incubation behavior of 10 Silkie hens by a video recording system over 1–2 years. Nine out of ten mature hens exhibited incubation behavior multiple times during the experiment. Ten hens demonstrated two interesting features. In a typical clutch, hens spent 10–15 min in the nest to lay an egg. Once they spent over 1 h in the nest, the nest occupancy increased incrementally. This shift in the nest occupancy occurred 7–10 days before the incubation onset and was highly repeatable. Based on the behavior of the hens, we cultured the anterior pituitary gland during four stages (premature non-laying, laying, trans, and incubation) with physiological PRL-releasing factor, vasoactive intestinal peptide (VIP). Based on our two-dimensional protein analysis, glycosylated PRL (G-PRL) displayed several isoforms with varying isoelectric points (pI), whereas we could detect one primary signal for non-glycosylated PRL (NG-PRL). However, 3–4 NG-PRL isoforms were detected in the anterior pituitary gland. These results suggested that secreted PRL, especially from the trans and incubation stages, contains various isoforms and it is post-translationally glycosylated and phosphorylated. [ABSTRACT FROM AUTHOR]

The subiculum, a key output region of the hippocampus, is increasingly recognized as playing a crucial role in seizure initiation and spread. The subiculum consists of glutamatergic pyramidal cells, which show alterations in intrinsic excitability in the course of epilepsy, and multiple types of GABAergic interneurons, which exhibit varying characteristics in epilepsy. In this study, we aimed to assess the role of the vasoactive intestinal peptide interneurons (VIP-INs) of the ventral subiculum in the pathophysiology of temporal lobe epilepsy. We observed that an anatomically restricted inhibition of VIP-INs of the ventral subiculum was sufficient to reduce seizures in the intrahippocampal kainic acid model of epilepsy, changing the circadian rhythm of seizures, emphasizing the critical role of this small cell population in modulating TLE. As we expected, permanent unilateral or bilateral silencing of VIP-INs of the ventral subiculum in non-epileptic animals did not induce seizures or epileptiform activity. Interestingly, transient activation of VIP-INs of the ventral subiculum was enough to increase the frequency of seizures in the acute seizure model. Our results offer new perspectives on the crucial involvement of VIP-INs of the ventral subiculum in the pathophysiology of TLE. Given the observed predominant disinhibitory role of the VIP-INs input in subicular microcircuits, modifications of this input could be considered in the development of therapeutic strategies to improve seizure control. [Display omitted] • First long-term study of VIP-expressing interneurons of ventral subiculum in epilepsy. • Permanent silencing of VIP-expressing interneurons dampened seizure activity. • Short-term activation of VIP-expressing interneurons increased seizure severity. • Disinhibitory role of VIP-expressing interneurons of ventral subiculum in epilepsy. [ABSTRACT FROM AUTHOR]

mammals, the circadian oscillators that drive daily behavioral and endocrine rhythms are located in the hypothalamic suprachiasmatic nucleus (SCN). While the SCN is anatomically well-situated to receive and transmit temporal cues to the rest of the brain and periphery, there are many holes in our understanding of how this temporal regulation occurs. Unanswered questions include how cell autonomous circadian oscillations within the SCN remain synchronized to each other as well as communicate temporal information to downstream targets. In recent years, it has become clear that neuropeptides are critically involved in circadian timekeeping. One such neuropeptide, vasoactive intestinal peptide (VIP), defines a cell population within the SCN and is likely used as a signaling molecule by these neurons. Converging lines of evidence suggest that the loss of VIP or its receptor has a major influence on the ability of the SCN neurons to generate circadian oscillations as well as synchronize these cellular oscillations. VIP, acting through the VPAC2 receptor, exerts these effects in the SCN by activating intracellular signaling pathways and, consequently, modulating synaptic transmission and intrinsic membrane currents. Anatomical evidence suggests that these VIP expressing neurons connect both directly and indirectly to endocrine and other output targets. Striking similarities exist between the role of VIP in mammals and the role of Pigment Dispersing Factor (PDF), a functionally related neuropeptide, in the Drosophila circadian system. Work in both mammals and insects suggests that further research into neuropeptide function is necessary to understand how circadian oscillators work as a coordinated system to impose a temporal structure on physiological processes within the organism./>

Keywords: PACAP; VIP; synaptic plasticity; learning; cognitive deficit EN PACAP VIP synaptic plasticity learning cognitive deficit 1 3 3 09/16/21 20210913 NES 210913 It is well-known that Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP), Vasoactive Intestinal Peptide (VIP) and related peptides act as neurotrophic and neuroprotective factors in the central nervous system (CNS). Solés-Tarrés et al. accurately describes the rescue processes of PACAP and VIP in AD, PD, and HD, and decipher the underlying molecular mechanisms, showing the role of each PACAP/VIP receptor subtype. In support of future clinical studies, this issue also reviews the most suitable administration routes for PACAP, VIP, and related peptides, as well as novel subtype-selective PACAP/VIP receptor agonists with improved systemic stability (Mosley et al.; Solés-Tarrés et al.; Sragovich et al.). [Extracted from the article]

Vasoactive intestinal peptide (VIP), a gut peptide hormone originally reported as a vasodilator in 1970, has multiple physiological and pathological effects on development, growth, and the control of neuronal, epithelial, and endocrine cell functions that in turn regulate ion secretion, nutrient absorption, gut motility, glycemic control, carcinogenesis, immune responses, and circadian rhythms. Genetic ablation of this peptide and its receptors in mice also provides new insights into the contribution of VIP towards physiological signaling and the pathogenesis of related diseases. Here, we discuss the impact of VIP on gastrointestinal function and diseases based on recent findings, also providing insight into its possible therapeutic application to diabetes, autoimmune diseases and cancer.

Located in the midbrain, the inferior colliculus (IC) is the hub of the central auditory system. Although the IC plays important roles in speech processing, sound localization, and other auditory computations, the organization of the IC microcircuitry remains largely unknown. Using a multifaceted approach in mice, we have identified vasoactive intestinal peptide (VIP) neurons as a novel class of IC principal neurons. VIP neurons are glutamatergic stellate cells with sustained firing patterns. Their extensive axons project to long-range targets including the auditory thalamus, auditory brainstem, superior colliculus, and periaqueductal gray. Using optogenetic circuit mapping, we found that VIP neurons integrate input from the contralateral IC and the dorsal cochlear nucleus. The dorsal cochlear nucleus also drove feedforward inhibition to VIP neurons, indicating that inhibitory circuits within the IC shape the temporal integration of ascending inputs. Thus, VIP neurons are well-positioned to influence auditory computations in a number of brain regions.

The avian pineal gland is one of three central biological clocks that contain all the components of a circadian system: a photoreceptive input, oscillator, and rhythmically secreted melatonin (MEL) as an effector. The biosynthesis of MEL is regulated by the neurotransmitters noradrenaline (NA), vasoactive intestinal peptide (VIP), and pituitary adenylate cyclase-activating polypeptide (PACAP). The aim of the present study was to characterize the daily profile of neurotransmitters and their receptors in the pineal gland of male Hy-Line chickens housed under controlled light (12:12 light:dark) conditions. The pineal glands were isolated from 16-day-old birds every 2 h over a 24-h period, immediately after decapitation. The catecholamine content was measured using HPLC with electrochemical detection, whereas expression of VIP and PACAP was measured using quantitative real-time PCR (RT-qPCR) assays and Western blotting. Expression of the neurotransmitter receptors was also measured using RT-qPCR. We found daily changes in NA content, with elevated nocturnal levels, whereas the NA receptor was expressed in antiphase. Although we did not observe daily changes in VIP and PACAP protein levels, we found prominent diurnal changes in the expression of the Vip and Pacap genes. We also detected precursors of NA, 3,4-dihydroxy-L-phenylalanine (DOPA), and dopamine (DA) in the pineal glands, in addition to the DA metabolites. Our results provide the first evidence that the pineal gland itself may synthetize the neurotransmitters needed to regulate MEL biosynthesis.

Soil salinization is the primary obstacle to the sustainable development of agriculture and eco-environment in arid regions. The accurate inversion of the major water-soluble salt ions in the soil using visible-near infrared (VIS-NIR) spectroscopy technique can enhance the effectiveness of saline soil management. However, the accuracy of spectral models of soil salt ions turns out to be affected by high dimensionality and noise information of spectral data. This study aims to improve the model accuracy by optimizing the spectral models based on the exploration of the sensitive spectral intervals of different salt ions. To this end, 120 soil samples were collected from Shahaoqu Irrigation Area in Inner Mongolia, China. After determining the raw reflectance spectrum and content of salt ions in the lab, the spectral data were pre-treated by standard normal variable (SNV). Subsequently the sensitive spectral intervals of each ion were selected using methods of gray correlation (GC), stepwise regression (SR) and variable importance in projection (VIP). Finally, the performance of both models of partial least squares regression (PLSR) and support vector regression (SVR) was investigated on the basis of the sensitive spectral intervals. The results indicated that the model accuracy based on the sensitive spectral intervals selected using different analytical methods turned out to be different: VIP was the highest, SR came next and GC was the lowest. The optimal inversion models of different ions were different. In general, both PLSR and SVR had achieved satisfactory model accuracy, but PLSR outperformed SVR in the forecasting effects. Great difference existed among the optimal inversion accuracy of different ions: the predicative accuracy of Ca2+, Na+, Cl−, Mg2+ and SO42− was very high, that of CO32− was high and K+ was relatively lower, but HCO3− failed to have any predicative power. These findings provide a new approach for the optimization of the spectral model of water-soluble salt ions and improvement of its predicative precision.

This study assessed the impact of administering vasoactive intestinal polypeptide (VIP) on inflammation and intestinal VIP and tight junction mRNA expression in lambs fed grain-based finishing diets. Sixteen wether lambs (69.6 ± 1.9 kg) were individually housed, adapted to a corn-based diet containing no forage, and randomly assigned to 2 treatment groups. Lambs were intraperitoneally injected every other day for 28 d with either saline (0.9% NaCl) with no VIP (n = 8; control) or saline with VIP (n = 8; 1.3 nmol/kg BW). Blood samples were collected weekly for analysis of cytokine concentrations, and on days 0 and 28 for lipopolysaccharide (LPS), and LPS-binding protein (LBP) concentrations. Upon completion of the treatment period, lambs were euthanized and gastrointestinal tissues, including rumen, jejunum, cecum, and colon samples, were collected for analysis of the expression of tight junction mRNA (claudin-1, claudin-4, occludin, and ZO-1), endogenous VIP, and VIP receptor (VPAC-1). No treatment effects (P ≥ 0.38) were observed for VIP and VPAC-1 mRNA expression in the colon. Supplementation with VIP did not influence (P ≥ 0.28) the expression of claudin-1, claudin-4, occludin, and ZO-1 tight junction mRNA in the rumen, jejunum, cecum, and colon. Lambs treated with VIP had greater (P ≤ 0.01) plasma concentrations of the anti-inflammatory cytokines, IL-10 and IL-36RA. There were treatment-by-day interactions observed (P ≤ 0.02) for concentrations of the pro-inflammatory cytokines, MIP-1α and MIP-1β. Lambs that did not receive VIP had greater serum concentrations of LPS (P = 0.05) than the lambs receiving VIP. These data suggest that VIP administration may not influence tight junction mRNA expression but may decrease LPS concentrations and thus inflammation in lambs fed a grain-based diet., (© The Author(s) 2024. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

This study evaluated if vasoactive intestinal polypeptide (VIP) influences growth performance, nutrient digestibility, nitrogen balance, and digestive enzyme activity. Sixteen wether lambs (69.6 ± 1.9 kg) were housed in individual pens, adapted to a corn grain-based diet, and randomly assigned to 2 treatment groups. Lambs were injected intraperitoneally every other day for 28 d with saline (0.9% NaCl) containing no VIP (n = 8; control) or containing VIP (n = 8; 1.3 nmol/kg body weight [BW]). All lambs were transferred to individual metabolic crates for the final 7 d of the experiment to measure nitrogen balance and nutrient digestibility. At the end of the treatment period, lambs were slaughtered, and pancreatic tissue, small intestinal tissue, and rumen fluid were collected for protein, digestive enzymes, ruminal pH, and volatile fatty acid (VFA) analyses. Lambs treated with VIP had greater final BW, average daily gain, and gain:feed (P = 0.01, 0.05, 0.03, respectively). No differences between treatment groups were observed (P ≥ 0.25) for nutrient intake, digestibility, nitrogen retention, ruminal pH, and VFA concentrations. Moreover, VIP treatment did not influence (P ≥ 0.19) plasma glucose, urea N, and insulin concentrations. Treatment with VIP increased (P = 0.03) relative cecum weight (g/kg BW) and decreased (P = 0.05) relative brain weight. Pancreatic and intestinal digestive enzyme activities, except for duodenal maltase (P = 0.02), were not influenced (P ≥ 0.09) by VIP treatment. These data suggest that the administration of VIP may have potential to improve average daily gain and gain:feed in lambs fed grain-based diets., (© The Author(s) 2024. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

In this study, differences in the chemical compositions of rebated excise duty diesel oil samples that were caused by fuel laundering were investigated. Two possible laundering pathways were simulated using either reduction or adsorption agents in model samples that were spiked with Solvent Yellow 124 and Solvent Red 19. The samples were characterized by their chromatographic fingerprints, which were recorded using gas chromatography coupled with a nitrogen chemiluminescence detector. The collections of fingerprints were further analyzed by discriminant partial least squares and the models with the optimal complexities presented the correct discrimination rates in the range of 69.1%–99.6%, respectively. The most informative fingerprint sections that were associated with the investigated differences were identified using the variable importance in projection, selectivity ratio and uninformative variable elimination methods. The reduced multivariate discriminant models presented a relatively high performance with the correct classification rates in the range of 74.9%–99.8%, respectively. O -toluidine and 2,5-diaminotoluene were identified as potential markers of diesel oil counterfeiting by laundering through a reduction agent. Image 1 • Chemical analysis of counterfeited rebated excise duty diesel oil was conducted. • Discoloration treatments based on the absorption and reduction were simulated. • Nitrogen chemiluminescence detector was used for chemical fingerprints registration. • PLS-DA models were constructed based on chromatographic signals. • Potential marker of rebated excise diesel oil 'laundering' was determined. [ABSTRACT FROM AUTHOR]

Purpose: The aim of this study is to evaluate the effects of adrenalectomy (ADX) and glucocorticoid in the changes induced by intracerebroventricular (ICV) administration of vasoactive intestinal peptide (VIP) on food intake and plasma parameters, as well as VIP receptor subtype 2 (VPAC2) mRNA expression in different hypothalamic nuclei of male rats. Methods: Male Wistar rats (260–280 g) were subjected to ADX or sham surgery, 7 days before the experiments. Half of ADX animals received corticosterone (ADX + CORT) in the drinking water. Animals with 16 h of fasting received ICV microinjection of VIP or saline (0.9% NaCl). After 15 min: (1) animals were fed, and the amount of food ingested was quantified for 120 min; or (2) animals were euthanized and blood was collected for biochemical measurements. Determination of VPAC2 mRNA levels in LHA, ARC, and PVN was performed from animals with microinjection of saline. Results: VIP treatment promoted the anorexigenic effect, which was not observed in ADX animals. Microinjection of VIP also induced an increase in blood plasma glucose and corticosterone levels, and a reduction in free fatty acid plasma levels, but adrenalectomy abolished these effects. In addition, adrenalectomy reduced mRNA expression of VPAC2 in the lateral hypothalamic area and arcuate nucleus, but not in the paraventricular nucleus. Conclusions: These results suggest that adrenal glands are required for VIP-induced changes in food intake and plasma parameters, and these responses are associated with reduction in the expression of VPAC2 in the hypothalamus after adrenalectomy. [ABSTRACT FROM AUTHOR]

In this study, the fabrication of laminated composite grids, as a new class of grid structures, is presented. These structures can be constituted from a various number of grid layers, with different patterns, fibers and orientations. This concept yields to a large variety of laminated grid configurations with different coupling effects compare to conventional grids. In the current study, the fabrication of a laminated grid plate, which composed of four orthogrid layers, is presented. The vacuum infusion process (VIP) is employed to manufacture the specimen. Moreover, a simulation is conducted using COMSOL Multiphysics software to determine the appropriate locations of resin inlet and air vent tubes. The degrees of cure and temperature profiles of the specimen are obtained in simulation and experimental studies. The results show, the simulation fits the experimental observations reasonably well and the VIP method is confirmed to be appropriate for manufacturing the high-quality laminated grid. [ABSTRACT FROM AUTHOR]

Highlights • The dead zone phase of SCN showed a slow phase shift after abrupt shift of LD cycle. • The dead zone phase corresponded with a slow phase shift of the rest-activity cycles. • The dead zone phase of SCN is adjusted by the shell region of the SCN. Abstract The suprachiasmatic nucleus (SCN) is the center of the mammalian circadian system. Environmental photic signals shifts the phase of the circadian rhythm in the SCN except during the dead zone, when the photic signal is gated somewhere on the way from the retina to the neurons in the SCN. Here we examined the phase of the dead zone after an abrupt delay of the LD cycles for several days by observing the mc -Fos induction in the SCN by light pulses. After an abrupt shift of the LD cycles, the dead zone showed a slow phase shift, about two hours per day, which was well corresponded with the slow phase shift of the rest-activity cycles. In our previous study we demonstrated that, after an abrupt shift of the LD cycles, the SCN showed transient endogenous desynchronization between shell and core regions that showed a slow and a rapid shift of the circadian rhythms, respectively. Therefore, the present findings on the phase shift of the dead zone after the LD cycles shift suggest that the phase of the dead zone is under the control of the timing signals from the shell region of the SCN. [ABSTRACT FROM AUTHOR]

Obesity arises from disrupted energy balance and is caused by chronically higher energy intake compared to expenditure via basal metabolic rate, exercise, and thermogenesis. The brown adipose tissue (BAT), the primary thermogenic organ, has received considerable attention as a potential therapeutic target due to its ability to burn lipids in the production of heat. Pituitary adenylate cyclase-activating polypeptide (PACAP) has been identified as a key regulator of the physiological stress response both centrally and peripherally. While PACAP has been shown to increase thermogenesis by acting at the hypothalamus to increase sympathetic output to BAT, a peripheral role for PACAP-activated thermogenesis has not been studied. We identified PACAP receptor (PAC1, VPAC1/2) expression for the first time in murine BAT and confirmed their expression in white adipose tissues. PAC1 receptor expression was significantly altered in all three adipose tissues studied in response to 3.5-week cold acclimation, with expression patterns differing by depot type. In primary cell culture, VPAC1 was increased in differentiated compared to non-differentiated brown adipocytes, and the same trend was observed for the PACAP-specific receptor PAC1 in gonadal white fat primary cultures. The primary PAC1R mRNA splice variant in interscapular BAT was determined as isoform 2 by RNA-Seq. These results show that PACAP receptors are present in adipose tissues and may have important functional roles in adipocyte differentiation, lipid metabolism, or adipose sensitization to sympathetic signaling in response to thermogenic stimuli. [ABSTRACT FROM AUTHOR]

In order to achieve a high-quality composite, a proper manufacturing technique should be used. Glass Fiber Reinforced Plastic (GFRP) structures are commonly manufactured using hand layup, vacuum bag and vacuum infusion process (VIP) which are cost effective techniques. This paper compares the tensile strength, modulus, inter-laminar bonding and surface macroscopy of GFRP composites made by hand layup, vacuum bag and VIP process. For this reason, at first GFRP sample were manufactured using these three methods and then tested for tensile properties. In the next step, these samples were modeled numerically and compared. The results show that the strength of the sample made by VIP process is 20 % higher than the hand layup and 11 % higher than vacuum bag sample. Also, the modulus of the sample achieved using VIP is 21 % higher that hand layup and 15% higher than vacuum bag technique. By comparing the failure mechanism of the samples, it was observed that the inter-laminar bonding is highest in VIP and then vacuum bag and lastly hand layup due to a smaller number of voids. Lastly the numerical results showed to have a good agreement with the experimental results. [ABSTRACT FROM AUTHOR]

Objective: To investigate the role of calcitonin gene-related peptide, pituitary adenylate cyclase-activating polypeptide-38 (PACAP38) and vasoactive intestinal polypeptide in cluster headache, we measured these vasoactive peptides interictally and during experimentally induced cluster headache attacks.Methods: We included patients with episodic cluster headache in an active phase (n = 9), episodic cluster headache patients in remission (n = 9) and patients with chronic cluster headache (n = 13). Cluster headache attacks were induced by infusion of calcitonin gene-related peptide (1.5 µg/min) in a randomized, double-blind, placebo controlled, two-way cross-over study. At baseline, we collected interictal blood samples from all patients and during 11 calcitonin gene-related peptide-induced cluster headache attacks.Results: At baseline, episodic cluster headache patients in remission had higher plasma levels of calcitonin gene-related peptide, 100.6 ± 36.3 pmol/l, compared to chronic cluster headache patients, 65.9 ± 30.5 pmol/l, ( p = 0.011). Episodic cluster headache patients in active phase had higher PACAP38 levels, 4.0 ± 0.8 pmol/l, compared to chronic cluster headache patients, 3.3 ± 0.7 pmol/l, ( p = 0.033). Baseline levels of vasoactive intestinal polypeptide did not differ between cluster headache groups. We found no attack-related increase in calcitonin gene-related peptide, PACAP38 or vasoactive intestinal polypeptide levels during calcitonin gene-related peptide-induced cluster headache attacks.Conclusions: This study suggests that cluster headache disease activity is associated with alterations of calcitonin gene-related peptide expression. Future studies should investigate the potential of using calcitonin gene-related peptide measurements in monitoring of disease state and predicting response to preventive treatments, including response to anti-calcitonin gene-related peptide monoclonal antibodies. [ABSTRACT FROM AUTHOR]

Abstract Nerve injuries often result in neuropathic pain with co-morbid changes in social behaviours, motivation, sleep-wake cycles and neuroendocrine function. In an animal model of neuropathic injury (CCI) similar co-morbid changes are evoked in a subpopulation (~30%) of injured rats. In addition to anatomical evidence of altered neuronal and glial function, the periaqueductal grey (PAG) of these rats shows evidence of cell death. These changes in the PAG may play a role in the disruption of the normal emotional coping responses triggered by nerve injury. Cell death can occur via a number of mechanisms, including the disruption of neuroprotective mechanisms. Pituitary adenylate cyclase activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are two endogenous neuropeptides whose activities are tightly regulated by two receptors subtypes, namely the PAC1 and VPAC receptors. These peptides and their receptors exert robust neuroprotective roles. In these studies, we hypothesized that rats expressing disabilities following CCI showed altered expression of PACAP and VIP in the PAG. Rats were categorized as having either Pain alone, Transient or Persistent disability, based on changes in social behaviours pre- and post-CCI. Social interaction behavioural tested (BT), sham-injured and naïve untested rats were also included. For measurements of mRNA and protein expression we utilised micro-dissected PAGs blocks taken from each group. At the mRNA level, VIP was downregulated and PAC1 was upregulated in BT animals, whilst VPAC1 mRNA was specifically increased in the Pain alone group. Interestingly, protein levels of both PACAP and VIP were remarkably increased in the Persistent Disability group. Taken together, sciatic nerve CCI that triggers neuropathic pain and persistent disability results in abnormally increased VIP and PACAP expression in the PAG. Our data also suggest that these effects are likely to be governed by post-transcriptional mechanisms. Highlights • VPAC1 mRNA is selectively increased in the Pain alone group. • VPAC1 protein expression is sensitive to various components of the experimental model. • PACAP and VIP expression is increased in CCI rats with persistent disability. • PACAP and VIP protein levels correlate with the degree of behavioural disability. [ABSTRACT FROM AUTHOR]

Intrinsically photosensitive retinal ganglion cells (ipRGCs), which express the photopigment melanopsin, are photosensitive neurons in the retina and are essential for non-image-forming functions, circadian photoentrainment, and pupillary light reflexes. Five subtypes of ipRGCs (M1-M5) have been identified in mice. Although ipRGCs are spared in several forms of inherited blindness, they are affected in Alzheimer's disease and aging, which are associated with impaired circadian rhythms. Huntington's disease (HD) is an autosomal neurodegenerative disease caused by the expansion of a CAG repeat in th e huntingtin gene. In addition to motor function impairment, HD mice also show impaired circadian rhythms and loss of ipRGC. Here, we found that, in HD mouse models (R6/2 and N171-82Q male mice), the expression of melanopsin was reduced before the onset of motor deficits. The expression of retinal T-box brain 2, a transcription factor essential for ipRGCs, was associated with the survival of ipRGCs. The number of M1 ipRGCs in R6/2 male mice was reduced due to apoptosis, whereas non-Ml ipRGCs were relatively resilient to HD progression. Most importantly, the reduced innervations of Ml ipRGCs, which was assessed by X-gal staining in R6/2-OPN4Lacz/+ male mice, contributed to the diminished light-induced c-fos and vasoactive intestinal peptide in the suprachiasmatic nuclei (SCN), which may explain the impaired circadian photoentrainment in HD mice. Collectively, our results show that Ml ipRGCs were susceptible to the toxicity caused by mutant Huntingtin. The resultant impairment of Ml ipRGCs contributed to the early degeneration of the ipRGC-SCN pathway and disrupted circadian regulation during HD progression. [ABSTRACT FROM AUTHOR]

Rat pancreatic acinar cells possess only the p21-activated kinase (PAKs), PAK4 of the group II PAK, and it is activated by gastrointestinal hormones/neurotransmitters stimulating PLC and by a number of growth factors. However, little is known generally of cAMP agents causing PAK4 activation, and there are no studies with gastrointestinal hormones/neurotransmitters activating cAMP cascades. In the present study, we examined the ability of VIP and secretin, which stimulate cAMP generation in pancreatic acini, to stimulate PAK4 activation, the signaling cascades involved, and their possible role in activating sodium-potassium adenosine triphosphatase (Na+,K+- ATPase). PAK4 activation was compared with activation of the well-established cAMP target, cyclic AMP response element binding protein (CREB). Secretin-stimulated PAK4 activation was inhibited by KT-5720 and PKA Type II inhibitor (PKI), protein kinase A (PKA) inhibitors, whereas VIP activation was inhibited by ESI-09 and HJC0197, exchange protein directly activated by cAMP (EPAC) inhibitors. In contrast, both VIP/secretin-stimulated phosphorylation of CREB (pCREB) via EPAC activation; however, it was inhibited by the p44/42 inhibitor PD98059 and the p38 inhibitor SB202190. The specific EPAC agonist 8-CPT-2-O-Me-cAMP as well 8-Br-cAMP and forskolin stimulated PAK4 activation. Secretin/VIP activation of Na+,K+-ATPase, was inhibited by PAK4 inhibitors (PF-3758309, LCH-7749944). These results demonstrate PAK4 is activated in pancreatic acini by stimulation of both VIP-/secretin-preferring receptors, as is CREB. However, they differ in their signaling cascades. Furthermore, PAK4 activation is needed for Na+,K+ATPase activation, which mediates pancreatic fluid secretion. These results, coupled with recent studies reporting PAKs are involved in both pancreatitis/ pancreatic cancer growth/enzyme secretion, show that PAK4, similar to PAK2, likely plays an important role in both pancreatic physiological/ pathological responses. NEW & NOTEWORTHY Pancreatic acini possess only the group II p21-activated kinase, PAK4, which is activated by PLC-stimulating agents/growth factors and is important in enzyme-secretion/growth/ pancreatitis. Little information exists on cAMP-activating agents stimulating group II PAKs. We studied ability/effect of cyclic AMPstimulating agents [vasoactive intestinal polypeptide (VIP), secretin] on PAK4 activity in rat pancreatic-acini. Both VIP/secretin activated PAK4/CREB, but the cAMP signaling cascades differed for EPAC, MAPK, and PKA pathways. Both hormones require PAK4 activation to stimulate sodium-potassium adenosine triphosphatase activity. This study shows PAK4 plays an important role in VIP-/secretin-stimulated pancreatic fluid secretion and suggests it plays important roles in pancreatic acinar physiological/pathophysiological responses mediated by cAMP-activating agents. [ABSTRACT FROM AUTHOR]

Hippocampus-dependent learning processes are coordinated via a large diversity of GABAergic inhibitory mechanisms. The α5 subunit-containing GABAa receptor (α5-GABAAR) is abundantly expressed in the hippocampus populating primarily the extrasynaptic domain of CA1 pyramidal cells, where it mediates tonic inhibitory conductance and may cause functional deficits in synaptic plasticity and hippocampus-dependent memory. However, little is known about synaptic expression of the α5-GABAAR and, accordingly, its location site-specific function. We examined the cell- and synapse-specific distribution of the α5-GABAAR in the CA1 stratum oriens/alveus (O/A) using a combination of immunohistochemistry, whole-cell patch-clamp recordings and optogenetic stimulation in hippocampal slices obtained from mice of either sex. In addition, the input-specific role of the α5-GABAaR in spatial learning and anxiety-related behavior was studied using behavioral testing and chemogenetic manipulations. We demonstrate that α5-GABAAR is preferentially targeted to the inhibitory synapses made by the vasoactive intestinal peptide (VIP)- and calretinin-positive terminals onto dendrites of somatostatin-expressing interneurons. In contrast, synapses made by the parvalbumin-positive inhibitory inputs to O/A interneurons showed no or little α5-GABAAR. Inhibiting the α5-GABAAR in control mice in vivo improved spatial learning but also induced anxiety-like behavior. Inhibiting the α5-GABAAR in mice with inactivated CA1 VIP input could still improve spatial learning and was not associated with anxiety. Together, these data indicate that the α5-GABAAR-mediated phasic inhibition via VIP input to interneurons plays a predominant role in the regulation of anxiety while the α5-GABAAR tonic inhibition via this subunit may control spatial learning. [ABSTRACT FROM AUTHOR]