Impaired Regulation Research Articles

Osteoimmune Interaction and TH-1/TH-2 Ratio in Jawbone Marrow Defects: An Underestimated Association - Original Research.

Osteoimmunology recognizes the relationship between bone cells and immune cells. Chronic osteoimmune dysregulation is present in bone marrow defects of the jaw (BMDJ) as fatty-degenerative osteonecrosis (FDOJ). In comparison to samples from healthy jaw bone, the cytokine analysis of samples of BMDJ/FDOJ from 128 patients showed downregulated TNF-α and IL-6 expression and the singular overexpression of the chemokine RANTES/CCL5. This paper raises the question of whether the osteoimmune defects due to incomplete wound healing in BMDJ/FDOJ in 128 patients are related to dysregulation of the Th1/Th2 ratio and regulatory T cell (T-reg) expression in a control group of 197 BMDJ/FDOJ patients, each presenting with BMDJ/FJOD and one of seven different immune disorders. In the control group, serum concentrations of the cytokines IFN-y and IL-4 were determined after stimulated cytokine release and displayed as Th1/Th2 ratios. Data show a shift in Th2 in more than 80% (n = 167) of the control cohort of 197 chronically ill patients with concomitant BMDJ/FDOJ. In these 167 subjects, the Th1/Th2 ratio was <6.1 demonstrating impaired immune regulation. Forty-seven subjects or 30% showed not only a shift in Th2 but also excessive T-reg overactivation with levels of >1.900 pg/mL, indicating strongly downregulated immune activity. BMDJ/FDOJ is characterized by a lack of Th1 cytokines and an excessive expression of RANTES/CCL5 and IL-1ra and, thus, the inversion of an acute inflammatory cytokine pattern. In contrast, abdominal fat contains a very high proportion of regulatory Th1 cells and produces an inflammatory immune response through the high overexpression of TNF-α and IL-6. The lack of Th1 activation in BMDJ/FDOJ areas inhibits normal wound healing and supports the persistence of BMDJ/FDOJ. The Th1/Th2 ratio requires greater consideration, especially with respect to wound healing following dental surgical interventions, such as jaw surgery, implantation and augmentation, to avoid the emergence of the osteoimmune situation that is characteristic of BMDJ/FDOJ.

Exosomal MicroRNAs: Biomarkers of moyamoya disease and involvement in vascular cytoskeleton reconstruction

Moyamoya disease currently lacks a suitable method for early clinical screening.This study aimed to identify a simple and feasible clinical screening index by investigating microRNAs carried by peripheral blood exosomes. Experimental subjects participated in venous blood collection, and exosomes were isolated using Exquick-related technology. Sequencing was performed on the extracted exosomal ribonucleic acids (RNAs) to identify differential microRNAs. Verification of the results involved selecting relevant samples from the genetic database. The study successfully pinpointed a potential marker for early screening, hsa-miR-328-3p + hsa-miR-200c-3p carried by peripheral blood exosomes. Enrichment analysis of target genes revealed associations with intercellular junctions, impaired cytoskeletal regulation, and increased fibroblast proliferation, leading to bilateral internal carotid artery neointimal expansion and progressive stenosis. These findings establish the diagnostic value of hsa-miR-328-3p+hsa-miR-200c-3p in screening moyamoya disease, while also contributing to a deeper understanding of its underlying pathophysiology. Significant differences in microRNA expressions derived from peripheral blood exosomes were observed between moyamoya disease patients and control subjects. Consequently, the utilization of peripheral blood exosomes, specifically hsa-miR-328-3p + hsa-miR-200c-3p, holds potential for diagnostic screening purposes.

Proteomic Landscape Associated with Cognitive Impairment in Individuals with Long-term Methamphetamine Dependence.

Methamphetamine (METH) is a highly addictive drug that directly affects the central nervous system. METH use not only harms the user's health but also poses risks and costs to society. Prolonged METH dependence has been shown to impair cognition, which may be the primary factor in impulsive drug-seeking behaviors and high relapse rates. However, the molecular mechanisms underlying METH addiction and METH-induced cognitive decline remain poorly understood. To illuminate the potential molecular mechanisms underpinning METH addiction, we compared serum protein expression levels between 12 long-term METH users and 12 healthy controls using label-free quantitative proteomics. Bioinformatic analyses were conducted to determine functional networks and protein-protein interactions. In total, 23 differentially expressed proteins were identified between the two groups. The differentially expressed proteins were related to cognitive dysfunction, neuroinflammation, immune impairment, metabolic disturbances, and calcium binding and regulation. These 23 proteins may underpin the multi-system damage induced by chronic METH exposure. Our findings provide novel insights into the molecular basis of METH addiction and inform potential prevention and treatment strategies for individuals with METH dependence.

Aberrant cerebral blood flow and functional connectivity in patients with vestibular migraine: a resting-state ASL and fMRI study

BackgroundPrior neuroimaging studies on vestibular migraine (VM) have extensively certified the functional and structural alterations in multiple brain regions and networks. However, few studies have assessed the cerebral blood flow (CBF) in VM patients using arterial spin labeling (ASL). The present study aimed to investigate CBF and functional connectivity (FC) alterations in VM patients during interictal periods.MethodsWe evaluated 52 VM patients and 46 healthy controls (HC) who received resting-state pseudo-continuous ASL and functional magnetic resonance imaging (fMRI) scanning. Comparisons of voxel-based CBF and seed-based FC were performed between the two groups. Brain regions showed significant group differences in CBF analyses were chosen as seeds in FC analyses. Additionally, the associations between abnormal imaging results and clinical features were explored.ResultsCompared with HC, VM patients showed higher normalized CBF in the right precentral gyrus (PreCG), left postcentral gyrus (PostCG), left superior frontal gyrus and bilateral insular (p < 0.05, FDR corrected). Furthermore, VM patients exhibited increased FC between the right PreCG and areas of the left PostCG, left cuneus and right lingual gyrus (p < 0.05, FDR corrected). In addition, we observed decreased FC between the left insular and regions of the left thalamus and right anterior cingulate cortex, as well as increased FC between the left insular and right fusiform gyrus in VM patients (p < 0.05, FDR corrected). Moreover, these variations in brain perfusion and FC were significantly correlated with multiple clinical features including frequency of migraine symptoms, frequency of vestibular symptoms and disease duration of VM (all p < 0.05).ConclusionsPatients with VM during interictal period showed hyperperfusion and abnormal resting-state FC in brain regions potentially contributed to disrupted multi-sensory and autonomic processing, as well as impaired ocular motor control, pain modulation and emotional regulation. Our study provided novel insights into the complex neuropathology of VM from a CBF perspective.

Effectiveness of a Web-Based Cognitive Behavioral Self-Help Intervention for Binge Eating Disorder: A Randomized Clinical Trial.

Binge eating disorder (BED) is one of the most frequent eating pathologies and imposes substantial emotional and physical distress, yet insufficient health care resources limit access to specialized treatment. Web-based self-help interventions emerge as a promising solution, offering more accessible care. To examine the effectiveness of a web-based cognitive behavioral self-help intervention for individuals with BED. This 2-arm, parallel-group randomized clinical trial conducted from January 15, 2021, to August 3, 2022, in Germany and other German-speaking countries enrolled patients aged 18 to 65 years who met the diagnostic criteria for BED (according to the Diagnostic and Statistical Manual of Mental Disorders [Fifth Edition]). Data analysis occurred between January 27 and September 4, 2023, following our statistical analysis plan. Participants were randomized to a web-based self-help intervention or a waiting-list control condition. The primary outcome was a change in objective binge eating episodes from baseline to after treatment. Secondary outcomes included global eating pathology, clinical impairment, work capacity, well-being, comorbid psychopathology, self-esteem, and emotion regulation. A total of 1602 patients were screened, of whom 154 (mean [SD] age, 35.93 [10.59] years; 148 female [96.10%]) fulfilled the criteria for BED and were randomized (77 each to the intervention and control groups). The web-based intervention led to significant improvements in binge eating episodes (Cohen d, -0.79 [95% CI, -1.17 to -0.42]; P < .001), global eating psychopathology (Cohen d, -0.71 [95% CI, -1.07 to -0.35]; P < .001), weekly binge eating (Cohen d, -0.49 [95% CI, -0.74 to -0.24]; P < .001), clinical impairment (Cohen d, -0.75 [95% CI, -1.13 to -0.37]; P < .001), well-being (Cohen d, 0.38 [95% CI, 0.01 to 0.75]; P = .047), depression (Cohen d, -0.49 [95% CI, -0.86 to -0.12]; P = .01), anxiety (Cohen d, -0.37 [95% CI, -0.67 to -0.07]; P = .02), self-esteem (Cohen d, 0.36 [95% CI, 0.13 to 0.59]; P = .003), and emotion regulation (difficulties: Cohen d, -0.36 [95% CI, -0.65 to -0.07]; P = .01 and repertoire: Cohen d, 0.52 [95% CI, 0.19 to 0.84]; P = .003). In this randomized clinical trial of a web-based self-help intervention for patients with BED, the findings confirmed its effectiveness in reducing binge eating episodes and improving various mental health outcomes, highlighting a scalable solution to bridge the treatment gap for this condition. ClinicalTrials.gov Identifier: NCT04876183.

Impaired GABAergic regulation and developmental immaturity in interneurons derived from the medial ganglionic eminence in the tuberous sclerosis complex

GABAergic interneurons play a critical role in maintaining neural circuit balance, excitation–inhibition regulation, and cognitive function modulation. In tuberous sclerosis complex (TSC), GABAergic neuron dysfunction contributes to disrupted network activity and associated neurological symptoms, assumingly in a cell type-specific manner. This GABAergic centric study focuses on identifying specific interneuron subpopulations within TSC, emphasizing the unique characteristics of medial ganglionic eminence (MGE)- and caudal ganglionic eminence (CGE)-derived interneurons. Using single-nuclei RNA sequencing in TSC patient material, we identify somatostatin-expressing (SST+) interneurons as a unique and immature subpopulation in TSC. The disrupted maturation of SST+ interneurons may undergo an incomplete switch from excitatory to inhibitory GABAergic signaling during development, resulting in reduced inhibitory properties. Notably, this study reveals markers of immaturity specifically in SST+ interneurons, including an abnormal NKCC1/KCC2 ratio, indicating an imbalance in chloride homeostasis crucial for the postsynaptic consequences of GABAergic signaling as well as the downregulation of GABAA receptor subunits, GABRA1, and upregulation of GABRA2. Further exploration of SST+ interneurons revealed altered localization patterns of SST+ interneurons in TSC brain tissue, concentrated in deeper cortical layers, possibly linked to cortical dyslamination. In the epilepsy context, our research underscores the diverse cell type-specific roles of GABAergic interneurons in shaping seizures, advocating for precise therapeutic considerations. Moreover, this study illuminates the potential contribution of SST+ interneurons to TSC pathophysiology, offering insights for targeted therapeutic interventions.

Targeting programmed cell death in inflammatory bowel disease through natural products: New insights from molecular mechanisms to targeted therapies.

Inflammatory bowel disease (IBD) is an autoimmune disorder primarily characterized by intestinal inflammation and recurrent ulceration, leading to a compromised intestinal barrier and inflammatory infiltration. This disorder's pathogenesis is mainly attributed to extensive damage or death of intestinal epithelial cells, along with abnormal activation or impaired death regulation of immune cells and the release of various inflammatory factors, which contribute to the inflammatory environment in the intestines. Thus, maintaining intestinal homeostasis hinges on balancing the survival and functionality of various cell types. Programmed cell death (PCD) pathways, including apoptosis, pyroptosis, autophagy, ferroptosis, necroptosis, and neutrophil extracellular traps, are integral in the pathogenesis of IBD by mediating the death of intestinal epithelial and immune cells. Natural products derived from plants, fruits, and vegetables have shown potential in regulating PCD, offering preventive and therapeutic avenues for IBD. This article reviews the role of natural products in IBD treatment by focusing on targeting PCD pathways, opening new avenues for clinical IBD management.

Role of Vitamin D in the Pathogenesis of Inflammatory Bowel Diseases: Literature Review

The pathogenesis of inflammatory bowel diseases still remains unclear nowadays. Genetic disposition, impaired immune regulation, disturbance in intestinal microbiota composition, exposure to environmental factors are associated with the development of inflammation in intestinal mucosa and increased epithelial penetrance that define disease's development and progression. There is a theory in scientific literature that vitamin D deficiency (among other environmental factors) increases the risk of inflammatory bowel disease. However, the role of vitamin D in the development of gastrointestinal tract diseases remains poorly studied. This article presents current data on the vitamin D effect on the intestinal mucosa barrier function, on the immune system and on the intestinal microbiota in the context of inflammatory bowel diseases pathogenesis.

Beyond the Nephron: Exploring Systemic Implications of Renal Tubular Acidosis

Renal Tubular Acidosis (RTA) is a complex renal disorder characterized by impaired acid-base regulation, leading to metabolic acidosis. While traditionally classified into several subtypes based on renal tubular dysfunction, emerging evidence highlights the systemic implications of RTA beyond nephron physiology. This article explores the multifaceted systemic manifestations of RTA, including cardiovascular, endocrine, neurological, and psychosocial implications, and discusses the importance of recognizing and addressing these systemic effects in patient care. Through interdisciplinary collaboration and personalized medicine approaches, tailored therapeutic strategies can be developed to mitigate renal and extrarenal manifestations of RTA, thereby improving overall patient well-being. Furthermore, future research directions aimed at elucidating the intricate interplay between acid-base disturbances and systemic organ systems hold promise for advancing our understanding and management of RTA, ultimately enhancing patient care outcomes

Chagas Cardiomyopathy and Myocardial Sympathetic Denervation.

More than a century since its discovery, the pathogenesis of Chagas heart disease (CHD) remains incompletely understood. The role of derangements in the autonomic control of the heart in triggering malignant arrhythmia before the appearance of contractile ventricular impairment was reviewed. Although previous investigations had demonstrated the anatomical and functional consequences of parasympathetic dysautonomia upon the heart rate control, only recently, coronary microvascular disturbances and sympathetic denervation at the ventricular level have been reported in patients and experimental models of CHD, exploring with nuclear medicine methods their impact on the progression of myocardial dysfunction and cardiac arrhythmias. More important than parasympathetic impaired sinus node regulation, recent evidence indicates that myocardial sympathetic denervation associated with coronary microvascular derangements is causally related to myocardial injury and arrhythmia in CHD. Additionally, 123I-MIBG imaging is a promising tool for risk stratification of progression of ventricular dysfunction and sudden death.

Impaired Emotional Regulation in Females with Post-Traumatic Stress Disorder after Experiencing Intimate Partner Violence

Impaired Emotional Regulation in Females with Post-Traumatic Stress Disorder after Experiencing Intimate Partner Violence

Effect of hypertension on muscle strength, balance, and mobility in older adults

Purpose: Hypertension (HT) can exacerbate impaired blood pressure regulation and thus increase the risk of falls. The higher incidence of HT and impaired balance in older adults may lead to the hypothesis of an association between HT and physical function in older individuals. The purpose of this study was to investigate the effects of HT on muscle strength, balance, and mobility in older adults and the relationship between them. Methods: Sixty-one older adults were included in the study and individuals with systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg formed the Hypertensive group (n=31), while the others formed the Normotensive group (n=30). Quadriceps Femoris (QF) muscle strength was evaluated with a hand-held dynamometer, mobility was evaluated with the Timed Up and Go Test (TUG), balance performance was evaluated with the Nintendo Wii Fit Balance Board (NWBB), and physiological age was evaluated with Wii Fit Age (WFA). The systolic and diastolic blood pressure were measured before the balance test. Results: TUG and NWBB scores between groups were significantly better in the Normotensive group (p&amp;lt;0.05). In both Hypertensive and Normotensive groups, there was a negative correlation between QF muscle strength and TUG score, and a positive correlation between QF muscle strength and NWBB score (p&amp;lt;0.05). Conclusion: HT may worsen mobility and balance in older adults. Further studies are required to better understand HT and establish better appropriate interventions for older hypertensive adults.

Assessment of Heart Rate Variability in Children with Mitral Valve Prolapse.

Mitral valve prolapse (MVP) is a heart valve anomaly with specific electrocardiographic findings and arrhythmia. A predominant sympathetic tone and diminished vagal activity have been reported especially in symptomatic MVP patients. In the current study, we aim to review heart rate variability (HRV) parameters of MVP children in order to determine if there is an impaired autonomic regulation. The data of children with MVP were retrospectively analyzed. Demographic characteristics, body mass index, symptomatology, MVP type and mitral regurgitation, MVP-related electrocardiographic changes, arrhythmia, and HRV parameters in 24-h Holter monitoring were recorded. HRV parameters of the control group were obtained from children applying for sport participation. Statistical significance limit was accepted as p < 0.05. 154 of the patients (74.8%) were girls, the median age was 13.58 ± 2.99years. While MVP patients had shorter PR intervals, those who had syncope had longer PR intervals. Short PR distance may be a feature of MVP, long PR distance may be a condition associated with syncope with the underlying paroxysmal atrioventricular block. Moreover, the minimum heart rate was significantly lower in the MVP group compared to the control and there were no significant differences in terms of remaining parameters. The number of low LF values was higher in MVP patients than the control. Comparing HRV values of groups by gender, we found that overall HRV parameters were lower in girls with MVP while minimum, maximum, and average heart rate were lower in boys with MVP. Impaired HRV associated with MVP could be age, gender, and symptom related. In addition, low LF may indicate impaired baroreflex sensitivity in MVP patients.

Investigation of Zinc on hemorheological parameters in a rat model of diabetes

Diabetes mellitus (DM) is a complex, chronic metabolic disorder characterized by impaired regulation of blood glucose levels. Zinc (Zn) is an essential trace elements that plays a role in various physiological processes within the body, including those related to diabetes. The current study was investigated the effect of Zn supplementation on hemorheological parameters in a rat model of DM. After induction of DM, 32 male Wistar albino rats were divided into four groups: control, Zn, DM, and Zn+DM. Whole blood viscosity (WBV) was determined by using digital cone and plate viscometer and plasma viscosity (PV) was determined by a Coulter Harkness capillary viscometer. The rats in the DM Group showed a decrease in both Zn levels and body weight, as well as an increase in glucose levels when compared to the control group. Diabetic rats supplemented with Zn displayed lower blood glucose levels and higher concentrations of Zn compared to the DM Group. The higher PV and lower hematocrit level were measured in DM Group than control group and lower PV, higher hematocrit level were measured in Zn+DM group than DM Group. The WBV was measured at four different shear rates (57.6–115.2 - 172.8–230.4 s −1). A statistically significant increase was observed in the DM group compared to the control group. Additionally, a statistically significant decrease was observed in the Zn+DM Group compared to the DM Group at a shear rate of 230.4 s−1. Erythrocyte rigidity index (Tk) and oxygen delivery index (ODI) were computed under conditions of high shear rate. The rats in the DM group exhibited a reduction in ODI and an elevation in Tk in comparison to the control group. Conversely, the diabetic rats supplemented with Zn exhibited decreased Tk and increased ODI compared to the DM Group. Zn supplementation seems to have a potential beneficial effect for protecting adverse affect of diabetes on hemorheogical parameters and for maintaining vascular health.

POI-associated EIF4ENIF1 mutations exhibit impaired translation regulation abilities

Various genetic variants have been found to be associated with the clinical onset of premature ovarian insufficiency (POI). However, when measured in vitro, the functional influence of the variants can be difficult to determine. By whole-exome sequencing (WES) of 93 patients with sporadic POI, we found a missense variant c.623G > A;p.R208H in the EIF4ENIF1 gene. In silico prediction of the variant using different algorithms suggested it might be a damaging variant. We compared the property of EIF4ENIF1 R208H and Q842P, a POI-related mutant that we reported previously, with wildtype (WT) protein using 293FT cells in vitro. Surprisingly, a change in subcellular distribution and granule forming ability (Q842P) and nuclear import capacity (R208H) was not observed, despite domain prediction evidences. Since EIF4ENIF1 was reported to inhibit translation, we employed T&T-seq, a translation-transcription dual-omics sequencing method, to profile gene expression upon overexpression of EIF4ENIF1 WT and mutants. EIF4ENIF1 WT overexpression group exhibited significantly (P < 0.0001) lower translation efficiency (TE) than empty vector or GFP overexpression control group. Surprisingly, EIF4ENIF1 Q842P overexpression failed to repress global translation, showing an overall TE significantly higher than WT group. Overexpression R208H significantly (P < 0.0001) lowered the overall TE, whereas exhibiting a reduced translation inhibitory effect on high-TE genes (TE > 2 in GFP control group). Several fertility-associated genes, such as AMH in Q842P group and SERPINE1 and THBS1 in R208H group, was translationally up-regulated in mutant groups versus WT control, suggesting a potential mechanism of mutated EIF4ENIF1 causing POI via impaired translation repression. It is further proposed that T&T-seq can be a sensitive evaluation tool for the measurement of functional alteration by variants in many other translational regulator genes, not only EIF4ENIF1, helping to eliminate misinterpretation of clinical significance of genetic variants.

Nephrolithiasis in Renal Tubular Acidosis: Pathophysiology, Diagnosis, and Management Strategies

Renal tubular acidosis (RTA) encompasses a group of disorders characterized by impaired kidney acid-base regulation, resulting in metabolic acidosis. Nephrolithiasis, the formation of kidney stones, represents a significant complication of RTA. Despite its clinical importance, the relationship between RTA and nephrolithiasis remains complex and poorly understood. This review provides a comprehensive overview of nephrolithiasis in RTA, focusing on its pathophysiology, diagnostic challenges, and management strategies. Mechanisms underlying kidney stone formation in RTA, including altered urinary pH, electrolyte abnormalities, and mineral metabolism disturbances, are explored in detail. Clinical manifestations and diagnostic considerations specific to nephrolithiasis in RTA patients are discussed, emphasizing the importance of a comprehensive metabolic evaluation and imaging procedures for accurate diagnosis. Current therapeutic approaches for treating kidney stones in RTA patients, including dietary modifications, pharmacological interventions, and surgical interventions, are reviewed. By elucidating the intricate interplay between RTA and nephrolithiasis, this review aims to enhance clinical understanding and guide optimal management strategies for patients with this challenging renal disorder.

Connection of molecular and cellular components of the immune system in endogenous psychoses with depressive-delusional symptoms

IntroductionThe data of current research indicate the participation of systemic inflammation in the pathogenesis of endogenous psychoses. Changes in the level of peripheral immune markers are associated with the development of neuroinflammation and correlate with the severity of psychopathological symptoms detected in patients. However, the association between individual components of the immune system involved in the development of endogenous psychosis remains poorly understood.ObjectivesTo study the connection between molecular and cellular components of the immune system in women with endogenous psychoses with depressive-delusional symptoms.Methods32 female patients aged 23 [17; 36] years with endogenous psychoses within different nosologies (F20, F21, F31, depressive-delusional conditions) and 17 women without clinical signs of psychiatric pathology were examined. The activity of leukocyte elastase (LE), α1-proteinase inhibitor (α1-PI), the proportion of four subpopulations of monocytes (classical CD14++CD16-, intermediate CD14++CD16+, nonclassical CD14+CD16+ and transitional CD14+CD16-) in plasma, activity of cytochrome-c oxidase (COX), glutamate dehydrogenase (GDH), glutathione s-transferase (GST) and glutathione reductase (GR) in platelets and functional activity of complement system (faCS) in serum were determined. The PANSS scale was used to assess the severity of psychopathological symptoms.ResultsIncreased activity of the inflammatory markers LE (p=0.033) and α1-PI (p=0.02) was found in the plasma of the patients. Increased percentage of pro-inflammatory monocytes (intermediate and transient) in plasma (p=0.003) was confirmed by negative correlations between CD14++CD16- and CD14++CD16+ (R=-0.685, p=0.00002), CD14++CD16- and CD14+CD16- (R=-0.608, p=0.0002), CD14++CD16- and CD14+CD16+ (R=-0.424, p=0.002). A decrease in GDH activity (p=0.0079), GST activity (p=0.002) and GR activity (p=0.0006) was observed in patient platelets, which can reflect changes in the activity of intracellular metabolic pathways. A positive correlation was found between COX activity and α1-PI (R=0.51, p=0.025). A significant decrease in faCS compared to control (p=0.0003) and a negative correlation between faCS and GST activity (R=-0.496, p=0.011) were observed. faCS was positively correlated with the degree of reduction in the PANSS score (R=0.416, p=0.038).ConclusionsThe revealed connection between molecular and cellular components of the immune system in patients with endogenous psychoses reflect activation of the systemic inflammatory response accompanied by changes in the ratio of monocyte subpopulations and impaired regulation of the complement system. The data obtained can be used to develop methods of monitoring patients taking into account their immunological features.Disclosure of InterestNone Declared

The Influence of Benthik Traditional Gameson the Level of Sibling Rivalry among Children: A Quasi-Experimental Study

Abstract.Children's relationships with their siblings encompass a spectrum of experiences, ranging from positive connections to negative interactions. A notable negative facet that can emerge within sibling dynamics is the phenomenon of sibling rivalry. This phenomenon entails the manifestation of competition, jealousy, and animosity among siblings, often arising following the birth of a younger brother or sister.The prevalence of sibling rivalry is associated with adverse outcomes, including heightened anxiety and impaired emotional regulation in children. To address the intricate issue of sibling rivalry, fostering cooperative interactions among siblings has been proposed as a potential solution. This research aims to describe whether the modification of the traditional game "Benthik" from East Java can reduce siblingrivalry in children. Additionally, this study also elucidates how the concept of modifying the Benthik game can mitigate sibling rivalry in children. Employing a quasi-experimental methodology, the study was conducted at SD Negeri 1 Sumberjo, Bojonegoro, and involved 30 children aged 8 to 12, each of whom had at least one sibling. The paired sample t-test analysis results reveal a significant influence ofthe Benthik game on sibling rivalry conditions in children, with a p-value of 0.035 (&lt;0.05) denoting statistical significance, thereby indicating that the modified Benthik game holds promise as an effective intervention for addressing sibling rivalry. In conclusion, the research contributes not only to the realm of addressing sibling dynamics but also to the preservation and utilization of traditional regional gamesamid the pervasive influence of digital engagement.

Gut microbiota and prospects for probiotics in paediatric celiac disease

Celiac disease is a chronic disease, with predominant damage to the small intestine and provoked by gluten consumption in genetically predisposed individuals. Previous large-scale studies suggest a possible role of the gut microbiota in the pathogenesis of this disease. Changes in the qualitative and quantitative characteristics of microbiota of different genesis can lead to impaired regulation of immune response, which, in turn, may contribute to the development of gluten intolerance. In this context, it is relevant to analyse the data on changes in the intestinal microbiota in celiac disease and the possibility of its correction with probiotics as one of the strategies for the treatment of children with celiac disease, suffering from celiac disease.

Daily stress encounters: Positive emotion upregulation and depressive symptoms.

When it comes to coping with stress, positive emotion upregulation is of utmost importance. Positive emotions have been suggested to be an important resource during stressful times since people try to create and upregulate pleasant emotional states when feeling stressed. Accordingly, individual differences in the ability to generate and savor positive emotional states could also affect one's skills in dealing with stress. In this regard, an important factor might be depression, which is associated with impaired positive emotion regulation. To disentangle the reciprocal influence between perceived stress and positive emotion upregulation, we conducted an Ecological Momentary Assessment study (n = 92) in which we assessed participants' stress levels and use of positive upregulating strategies (attentional deployment, cognitive change, and response modulation) three times a day over 2 weeks. Results from linear mixed-effects models showed that higher levels of perceived stress at one point predicted increased use of positive upregulating strategies from this point to the next which, in turn, resulted in subsequent diminished stress levels. Interaction analyses indicated that participants with higher depressive symptoms implemented upregulating strategies to a lower extent when experiencing intense stress. Furthermore, attentional deployment was less effective in decreasing stress in individuals higher in depression, whereas the other strategies showed comparable or even higher efficacy. Overall, positive emotion upregulation might be regarded as an adaptive tool that helps cope with stress. This mechanism might be altered in people higher in depression, who specifically struggle to implement positive upregulating strategies during times of stress. (PsycInfo Database Record (c) 2024 APA, all rights reserved).