Genetic improvement of local rabbit breeds using modern approaches such as marker-assisted selection requires accurate and precise information about marker‒trait associations in animals with different genetic backgrounds. Therefore, this study was designed to estimate the association between two mutations located in the Neuropeptide Y (NPY, g.1778G > C) and Phosphoglycerate Mutase 2 (PGAM2, c.195 C > T) genes in New Zealand White (NZW), Baladi (BR), and V-line rabbits. The first mutation was genotyped using high-resolution melting, and the second mutation was genotyped using the PCR-RFLP method. The results revealed significant associations between the NPY mutation and body weight at 10 (V-line) and 12 weeks of age (NZW, BR, and V-line), body weight gain (BWG) from 10 to 12 weeks of age (BR), BWG from 6 to 12 weeks of age (NZW, BR, and V-line), average daily gain (NZW, BR, and V-line, and BR), growth rate (GR) from 8 to10 weeks (V-line), 10 to 12 weeks (BR), and GR from 6 to 12 weeks of age (BR, and V-line). The PGAM2 mutation was associated with body weight at 10 (V-line) and 12 (NZW, and V-line) weeks of age, with significant positive additive effects at 12 weeks of age in all breeds, and was associated with BWG from 8 to 10 and 10 to 12 in BR, and BWG from 6 to 12 weeks of age (NZW, and BR), and average daily gain (NZW, and BR), and was associated with GR form 8 to 10 weeks (BR), from10 to 12 weeks (BR, and V-line) and from 6 to 12 weeks (BR). The results highlighted the importance of the two mutations in growth development, and the possibility of considering them as candidate genes for late growth in rabbits.

(1) Background: We examined the effect of the acute administration of olive oil (EVOO), linseed oil (GLO), soybean oil (SO), and palm oil (PO) on gastric motility and appetite in rats. (2) Methods: We assessed food intake, gastric retention (GR), and gene expression in all groups. (3) Results: Both EVOO and GLO were found to enhance the rate of stomach retention, leading to a decrease in hunger. On the other hand, the reduction in food intake caused by SO was accompanied by delayed effects on stomach retention. PO caused an alteration in the mRNA expression of NPY, POMC, and CART. Although PO increased stomach retention after 180 min, it did not affect food intake. It was subsequently verified that the absence of an autonomic reaction did not nullify the influence of EVOO in reducing food consumption. Moreover, in the absence of parasympathetic responses, animals that received PO exhibited a significant decrease in food consumption, probably mediated by lower NPY expression. (4) Conclusions: This study discovered that different oils induce various effects on parameters related to food consumption. Specifically, EVOO reduces food consumption primarily through its impact on the gastrointestinal tract, making it a recommended adjunct for weight loss. Conversely, the intake of PO limits food consumption in the absence of an autonomic reaction, but it is not advised due to its contribution to the development of cardiometabolic disorders.

Neuropeptide Y (NPY), an endogenous peptide composed of 36 amino acids, has been investigated as a potential therapeutic agent for neurodegenerative diseases due to its neuroprotective attributes. This study investigated the neuroprotective effects of NPY in a mouse model of glaucoma characterized by elevated intraocular pressure (IOP) and progressive retinal ganglion cell degeneration. Elevated IOP in mice was induced through intracameral microbead injections, accompanied by intravitreal administration of NPY peptide. The results demonstrated that NPY treatment preserved both the structural and functional integrity of the inner retina and mitigated axonal damage and degenerative changes in the optic nerve under high IOP conditions. Further, NPY treatment effectively reduced inflammatory glial cell activation, as evidenced by decreased expression of glial fibrillary acidic protein and Iba-1. Notably, endogenous NPY expression and its receptors (NPY-Y1R and NPY-Y4R) levels were negatively affected in the retina under elevated IOP conditions. NPY treatment restored these changes to a significant extent. Molecular analysis revealed that NPY mediates its protective effects through the mitogen-activated protein kinase (MAPK) and PI3K/Akt signaling pathways. These findings highlight the therapeutic potential of NPY in glaucoma treatment, underscoring its capacity to preserve retinal health, modulate receptor expression under stress, reduce neuroinflammation, and impart protection against axonal impairment.

Catheter ablation (CA) is an essential method for the interventional treatment of atrial fibrillation (AF), and it is very important to reduce long-term recurrence after CA. The mechanism of recurrence after CA is still unclear. We established a long-term model of beagle canines after circumferential pulmonary vein ablation (CPVA). The transcriptome and proteome were obtained using high-throughput sequencing and TMT-tagged LC-MS/LC analysis, respectively. Differentially expressed genes and proteins were screened and enriched, and the effect of fibrosis was found and verified in tissues. A downregulated protein, neuropeptide Y (NPY), was selected for validation and the results suggest that NPY may play a role in the long-term reinduction of AF after CPVA. Then, the molecular mechanism of NPY was further investigated. The results showed that the atrial effective refractory period (AERP) was shortened and fibrosis was increased after CPVA. Atrial myocyte apoptosis was alleviated by NPY intervention, and Akt activation was inhibited in cardiac fibroblasts. These results suggest that long-term suppression of NPY after CPVA may lead to induction of AF through promoting cardiomyocyte apoptosis and activating the Akt pathway in cardiac fibroblasts, which may make AF more likely to reinduce.

BACKGROUND: Neuropeptide Y is a neurotransmitter in the nervous system and belongs to the orexigenic system that increases appetite. Its excessive secretion leads to obesity. Leptin is a pro-inflammatory adipokine (produced in adipose tissue) induced in obesity and may mediate increased antitumor immunity in obesity (including the promotion of M1 macrophages). Leptin and neuropeptide Y gene polymorphisms, causing increased leptin levels and the occurrence of obesity, and lipid profile disorders, may increase the effectiveness of immunotherapy.
METHODS: In 121 patients with advanced NSCLC without mutations in the EGFR gene and rearrangements of the ALK and ROS1 genes, undergoing immunotherapy (1st and 2nd line of treatment) or chemoimmunotherapy (1st line of treatment), we assessed BMI, lipid profile, PD-L1 expression on cancer cells using the immunohistochemical method (clone SP263 antibody), leptin concentration in blood serum by ELISA, polymorphisms in the promoter region of the genes for leptin (LEP) and neuropeptide Y (NPY) by real-time PCR.
RESULTS: Leptin concentration was significantly higher in obese patients than in patients with normal or low weight (p = 0.00003) and in patients with disease stabilization compared to patients with progression observed during immunotherapy (p = 0.012). Disease control occurred significantly more often in patients with the GA or AA genotype than patients with the GG genotype in the rs779039 polymorphism of the LEP gene. The median PFS in the entire study group was five months (95% CI: 3-5.5), and the median OS was 12 months (95% CI: 8-16). Median PFS was highest in patients with TPS ≥ 50% (6.5 months) and in obese patients (6.6 months). Obese patients also had a slightly longer median OS compared to other patients (23.8 vs. 13 months). The multivariate Cox logistic regression test showed that the only factor reducing the risk of progression was TPS ≥ 50% (HR = 0.6068, 95% CI: 0.4001-0.9204, p = 0, 0187), and the only factor reducing the risk of death was high leptin concentration (HR = 0.6743, 95% CI: 0.4243-1.0715, p = 0.0953).
CONCLUSIONS: Assessment of nutritional status, serum leptin concentration and polymorphisms in the LEP gene may be of additional importance in predicting the effectiveness of immunotherapy and chemoimmunotherapy in patients with advanced NSCLC.

In this analysis, we aimed to investigate the effect of COVID-19 disease on eating behavior. A total of 55 right-handed adults, <50 years of age, without overweight or obesity, from two cross-sectional studies were included. The first one enrolled subjects between September 2018 and December 2019 (non-COVID-19 group). The second one included subjects enrolled between March 2022 and May 2023; for this analysis, 28 with a history of COVID-19 (COVID-19 group) were retained. Hunger, TFEQ-18, plasma ghrelin, neuropeptide Y (NPY) and resting-state fMRI were assessed during fasting. Intraregional neuronal synchronicity and connectivity were assessed by voxel-based regional homogeneity (ReHo) and degree of centrality (DC). Significantly higher ghrelin and NPY levels were observed in the COVID-19 group than in the non-COVID-19 group (ghrelin 197.5 pg/mL vs. 67.1 pg/mL, p < 0.001; NPY 128.0 pg/mL vs. 84.5 pg/mL, p = 0.005). The NPY levels positively correlated with the DC and ReHo in the left lingual (r = 0.67785 and r = 0.73604, respectively). Similar scores were noted for cognitive restraint, uncontrolled eating and emotional eating in both groups according to the TFEQ-18 questionnaire results (p > 0.05 for all). Our data showed increased levels of appetite-related hormones, correlated with activity in brain regions involved in appetite regulation, persisting long after COVID-19 infection.

BACKGROUND: Apoprotein A-I (ApoA-I) and Apoprotein B (ApoB) have emerged as novel cardiovascular risk biomarkers influenced by feeding behavior. Hypothalamic appetite peptides regulate feeding behavior and impact lipoprotein levels, which effects vary in different weight states. This study explores the intricate relationship between body mass index (BMI), hypothalamic appetite peptides, and apolipoproteins with emphasis on the moderating role of body weight in the association between neuropeptide Y (NPY), ghrelin, orexin A (OXA), oxytocin in cerebrospinal fluid (CSF) and peripheral ApoA-I and ApoB.
METHODS: In this cross-sectional study, we included participants with a mean age of 31.77 ± 10.25 years, categorized into a normal weight (NW) (n = 73) and an overweight/obese (OW/OB) (n = 117) group based on BMI. NPY, ghrelin, OXA, and oxytocin levels in CSF were measured.
RESULTS: In the NW group, peripheral ApoA-I levels were higher, while ApoB levels were lower than in the OW/OB group (all p < 0.05). CSF NPY exhibited a positive correlation with peripheral ApoA-I in the NW group (r = 0.39, p = 0.001). Notably, participants with higher CSF NPY levels had higher peripheral ApoA-I levels in the NW group and lower peripheral ApoA-I levels in the OW/OB group, showing the significant moderating effect of BMI on this association (R2 = 0.144, β=-0.54, p < 0.001). The correlation between ghrelin, OXA and oxytocin in CSF and peripheral ApoB in both groups exhibited opposing trends (Ghrelin: r = -0.03 and r = 0.04; OXA: r = 0.23 and r=-0.01; Oxytocin: r=-0.09 and r = 0.04).
CONCLUSIONS: This study provides hitherto undocumented evidence that BMI moderates the relationship between CSF NPY and peripheral ApoA-I levels. It also reveals the protective role of NPY in the NW population, contrasting with its risk factor role in the OW/OB population, which was associated with the at-risk for cardiovascular disease.

BACKGROUND: Depression is one of the most common mental illnesses. Impaired neurogenesis is observed in depression. Biomarkers of impaired neurogenesis in depression can act as a useful objective and diagnostic and prognostic tool to determine the severity of depression.
OBJECTIVE: To study the concentration of biochemical indicators in the blood that may be involved in the pathogenesis of depression and their intercorrelations, and to determine any associations between the concentrations of biochemical indicators and severity of depressive symptoms.
METHODS: We determined the plasma concentrations of serotonin, dopamine, and neurotrophic factors involved in neurogenesis (BDNF, CDNF and neuropeptide Y) using enzyme immunoassay and mass spectrometry in depressed patients (n=22) and healthy controls (n=16) matched by socio-demographic parameters. All participants were assessed using the Hamilton Depression Scale (HAMD), the Generalized Anxiety Disorder Questionnaire (GAD-7), and the Center for Epidemiologic Studies Depression Scale (CES-D) to enter the study. The standard cut-offs for the CES-D and GAD-7 scales were used to confirm the presence or absence of depression and anxiety.
RESULTS: The concentrations of serotonin, dopamine, BDNF, CDNF, and neuropeptide Y in plasma did not differ between the groups and was not found to be associated with the scores on the scales. Positive correlations were found between the concentration of neuropeptide Y and serotonin, BDNF, and CDNF in blood plasma.
CONCLUSIONS: Plasma concentrations of biomarkers related to the pathophysiology of depression did not correlate with the severity of its symptoms.
UNASSIGNED: Изучение концентрации биохимических показателей в крови, принимающих возможное участие в патогенезе депрессии, поиск ассоциаций с тяжестью депрессивной симптоматики может быть полезным в качестве объективной диагностики заболевания и прогнозирования тяжести течения патологии.
UNASSIGNED: Изучение биохимических показателей крови, которые могут быть связаны с депрессией. Определения корреляционной взаимосвязи этих показателей при депрессивных расстройствах.
UNASSIGNED: В работе определяли концентрацию в плазме крови моноаминовых нейромедиаторов серотонина и дофамина, и нейротрофических факторов, участвующих в нейрогенезе (BDNF, CDNF и нейропептид Y) у пациентов с депрессией и здоровых добровольцев с одинаковыми социо-демографическими параметрами, используя методы иммуноферментного анализа и масс-спектрометрии. Все участники исследования были опрошены по шкале депрессии Гамильтона (HAMD), опроснику генерализованного тревожного расстройства (GAD-7) и опроснику депрессии центра эпидемиологических исследований (CES-D). Показатели шкал CES-D и GAD-7 использовались для подтверждения наличия или отсутствия депрессии и тревоги у участников исследования.
UNASSIGNED: Суммарный балл по трем исследованным шкалам у пациентов с депрессией существенно выше, чем в контрольной группе. Содержание серотонина, дофамина, BDNF, CDNF и нейропептида Y в плазме крови не отличалось в группах испытуемых и не было ассоциировано с баллами по шкалам. Обнаружены положительные корреляции содержания нейропептида Y с серотонином, и BDNF с CDNF в плазме крови.
UNASSIGNED: Исследованные маркеры хоть и связаны с патофизиологией депрессии, не коррелируют с тяжестью симптоматики и содержание их в плазме крови не отражает процессы, происходящие в мозге.

Neuropeptide Y (NPY) and related peptides have been proposed as promising biomarkers for the diagnosis of prostate cancer by previous immunoassays and immunohistochemical studies. In this study, we evaluated the additional value of NPY and related peptides compared with prostate-specific antigen (PSA). We performed a comprehensive analysis of NPY, its precursors, and metabolite concentrations in both plasma and tissue samples from 181 patients using a highly specific liquid chromatography tandem mass spectrometry method. Compared with PSA, NPY and related peptides (NPYs) were less accurate at diagnosing significant prostate cancer. Combinations of NPYs in a stepwise approach did not improve a model that would be beneficial for patients. NPY may be beneficial for patients presenting with a PSA concentration in the gray area between 4 and 9 ng/ml, but the strength of this conclusion is limited. Thus, the use of NPYs as standalone or in combination with other variables, such as PSA, prostate volume, or age, to improve the diagnosis is not supported by our study.
UNASSIGNED: This study evaluated neuropeptide Y (NPY) of the family of endogenous peptides as a new biomarker to diagnose prostate cancer. We found that NPY in a patient\'s blood was not more helpful at diagnosing prostate cancer than the standard prostate-specific antigen blood test. Further research is needed to explore the potential of NPY and related peptides in specific subgroups of patients.

Observed and recorded in various forms since ancient times, \'syncope\' is often popularly called \'fainting\', such that the two terms are used synonymously. Syncope/fainting can be caused by a variety of conditions, including but not limited to head injuries, vertigo, and oxygen deficiency. Here, we draw on a large body of literature on syncope, including the role of a recently discovered set of specialized mammalian neurons. Although the etiology of syncope still remains a mystery, we have attempted to provide a comprehensive account of what is known and what still needs to be performed. Much of our understanding of syncope is owing to studies in the laboratory mouse, whereas evidence from human patients remains scarce. Interestingly, the cardioinhibitory Bezold-Jarisch reflex, recognized in the early 1900s, has an intriguing similarity to-and forms the basis of-syncope. In this review, we have integrated this minimal model into the modern view of the brain-neuron-heart signaling loop of syncope, to which several signaling events contribute. Molecular signaling is our major focus here, presented in terms of a normal heart, and thus, syncope due to abnormal or weak heart activity is not discussed in detail. In addition, we have offered possible directions for clinical intervention based on this model. Overall, this article is expected to generate interest in chronic vertigo and syncope/fainting, an enigmatic condition that affects most humans at some point in life; it is also hoped that this may lead to a mechanism-based clinical intervention in the future.