In this narrative, comprehensive, and updated review of the literature, we summarize evidence about the effectiveness of interventions aimed at reducing emotion dysregulation and improving emotion regulation in children, adolescents, and adults. After introducing emotion dysregulation and emotion regulation from a theoretical standpoint, we discuss the factors commonly associated with emotion regulation, including neurobiological and neuropsychological mechanisms, and the role of childhood adverse experiences and psycho-social factors in the onset of emotion dysregulation. We then present evidence about pharmacological and non-pharmacological interventions aiming at improving emotion dysregulation and promoting emotion regulation across the lifespan. Although our review was not intended as a traditional systematic review, and the search was only restricted to systematic reviews and meta-analyses, we highlighted important implications and provided recommendations for clinical practice and future research in this field.

Colorectal carcinoma (CRC) remains a significant contributor to cancer-related morbidity and mortality worldwide. MicroRNAs (miRNAs) have emerged as crucial regulators of gene expression and play critical roles in various biological processes, including carcinogenesis. This comprehensive review aims to elucidate the role of miRNAs in CRC by analyzing their expression patterns and functional implications. An extensive literature review identified dysregulated miRNAs associated with different stages of CRC progression, from initiation to metastasis. These miRNAs modulate key signaling pathways in tumor growth, invasion, and metastasis. Furthermore, we discuss the potential of miRNAs as diagnostic biomarkers and therapeutic targets in CRC management. Future research directions include elucidating the functional significance of dysregulated miRNAs using advanced experimental models and computational approaches and exploring the therapeutic potential of miRNA-based interventions in personalized treatment strategies for CRC patients. Collaboration among researchers, clinicians, and industry partners will be essential to translate these findings into clinically impactful interventions that improve patient outcomes in CRC.

Due to the lack of specific symptoms, characteristic diagnostic markers and effective comprehensive treatment, gallbladder cancer (GBC) is currently considered one of the most malignant abdominal tumors. With the rapid development of biological technologies, long non‑coding RNAs (lncRNAs), once regarded as transcriptional junk, have been demonstrated to participate in almost the whole process of the central dogma of molecular biology. The central dogma deals with the transfer of sequential information at the level of individual residues. LncRNAs have an effect on multiple cancer types. However, evidence of dysregulated lncRNA functions in GBC is limited. In the present review, the regulatory mechanisms of lncRNA function on gene expression were examined, including epigenetic modification, transcriptional regulation and post‑translational modulation. These mechanisms are strongly associated with tumor development and metastasis. Next, it was summarized how lncRNAs affect GBC diverse malignant phenotypes through various mechanisms. Moreover, predictions of lncRNA interactions with other functional molecules in malignancies were made using several valuable databases, including crosstalk between lncRNA and DNA, mRNA, microRNA, and protein. Additionally, several potential therapeutic methods targeting pathological lncRNAs in tumors were identified. Finally, perspectives about lncRNA research and applications in GBC were presented in the current study, including viewpoints of coding potential of lncRNAs and feasible usage of micropeptides encoded by lncRNAs; roles of lncRNAs in tumor cell metabolic reprogramming and tumor microenvironment; and function of lncRNAs as possible biomarkers and therapeutic targets for improving GBC diagnosis, treatment and prognosis.

Co-occurring regulatory problems in infancy, RPs, including excessive crying, feeding-eating and sleeping, have been found associated with mental health problems in school ages. Still, an overview is needed on trajectories of co-occurring or combined RPs, and mental health problems in early childhood. The aim of this review is to systematically review the literature on longitudinal community-based studies of combined RPs measuring mental health outcomes in early childhood. Following the PRISMA guideline, we systematically reviewed the literature published 2000-2020, in which combined RPs are assessed in infancy, and mental health is examined using standardised measures at ages 1-7 years. The search was performed in four databases MEDLINE, EMBASE, PsycINFO and Scopus. A protocol is published on PROSPERO. Based on 1978 screened articles, 42 papers were screened for eligibility, of which six were included, comprising data on two or more RPs investigated among a total of 20,675 children. Assessment of risk of bias in the studies showed overall good quality in five of the six papers. The literature reviewed suggests that combined RPs in infancy are early markers of mental health problems during early childhood, and highlights that community studies exploring the longitudinal associations of combined RP and mental health problems in preschool and early school age are still scarce. Overall, the review points to the need of research into preventive intervention targeting early manifestations of childhood dysregulation, such as RPs.

In some patients, the inflammatory-immune response to surgical injury progresses to a harmful, dysregulated state. We posit that postoperative systemic inflammatory dysregulation forms part of a pathophysiological response to surgical injury that places patients at increased risk of complications and subsequently prolongs hospital stay. In this narrative review, we have outlined the evolution, measurement and prediction of postoperative systemic inflammatory dysregulation, distinguishing it from a healthy and self-limiting host response. We reviewed the actions of glucocorticoids and the potential for heterogeneous responses to peri-operative corticosteroid supplementation. We have then appraised the evidence highlighting the safety of corticosteroid supplementation, and the potential benefits of high/repeated doses to reduce the risks of major complications and death. Finally, we addressed how clinical trials in the future should target patients at higher risk of peri-operative inflammatory complications, whereby corticosteroid regimes should be tailored to modify not only the a priori risk, but also further adjusted in response to markers of an evolving pathophysiological response.

Childhood irritability, operationalized as disproportionate and frequent temper tantrums and low frustration tolerance relative to peers, is a transdiagnostic symptom across many pediatric disorders. Studies using task-dependent functional magnetic resonance imaging (fMRI) to probe neural dysfunction in irritability have increased. However, an integrated review summarizing the published methods and synthesized fMRI results remains lacking.
We conducted a systematic search using irritability terms and task functional neuroimaging in key databases in March 2021, and identified 30 studies for our systematic review. Sample characteristics and fMRI methods were summarized. A subset of 28 studies met the criteria for extracting coordinate-based data for quantitative meta-analysis. Ten activation-likelihood estimations were performed to examine neural convergence across irritability measures and fMRI task domains.
Systematic review revealed small sample sizes (median = 58, mean age range = 8-16 years) with heterogeneous sample characteristics, irritability measures, tasks, and analytical procedures. Meta-analyses found no evidence for neural activation convergence of irritability across neurocognitive functions related to emotional reactivity, cognitive control, and reward processing, or within each domain. Sensitivity analyses partialing out variances driven by heterogeneous tasks, irritability measures, stimulus types, and developmental ages all yielded null findings. Results were compared with a review on irritability-related structural anomalies from 11 studies.
The lack of neural convergence suggests a need for common, standardized irritability assessments and more homogeneous fMRI tasks. Thoughtfully designed fMRI studies probing commonly defined neurocognitive functions may be more fruitful to elucidate the neural mechanisms of irritability. Open science practices, data mining in large neuroscience databases, and standardized analytical methods promote meaningful collaboration in irritability research.

Impairing emotional outbursts, defined by extreme anger or distress in response to relatively ordinary frustrations and disappointments, impact all mental health care systems, emergency departments, schools, and juvenile justice programs. However, the prevalence, outcome, and impact of outbursts are difficult to quantify because they are transdiagnostic and not explicitly defined by current diagnostic nosology. Research variably addresses outbursts under the rubrics of tantrums, anger, irritability, aggression, rage attacks, or emotional and behavioral dysregulation. Consistent methods for identifying and assessing impairing emotional outbursts across development or systems of care are lacking.
The American Academy of Child and Adolescent Psychiatry Presidential Task Force (2019-2021) conducted a narrative review addressing impairing emotional outbursts within the limitations of the existing literature and independent of diagnosis.
Extrapolating from the existing literature, best estimates suggest that outbursts occur in 4%-10% of community children (preschoolers through adolescents). Impairing emotional outbursts may respond to successful treatment of the primary disorder, especially for some children with attention-deficit/hyperactivity disorder whose medications have been optimized. However, outbursts are generally multi-determined and often represent maladaptive or deficient coping strategies and responses.
Evidence-based strategies are necessary to address factors that trigger, reinforce, or excuse the behaviors and to enhance problem-solving skills. Currently available interventions yield only modest effect sizes for treatment effect. More specific definitions and measures are needed to track and quantify outbursts and to design and assess the effectiveness of interventions. Better treatments are clearly needed.

The expression of various isoforms of aquaporins (AQPs) in different tissues and organs of the body makes it a viable candidate for being responsible for maintaining cell stability and integrity as their involvement has been well documented in a number of pathophysiological conditions of the human body. Any alteration in the cellular environment brought about by these AQPs creates severe downstream effects like changes in cellular osmolality, volume, ionic composition, signaling pathways and even in the levels of intracellular second messengers and, as such, facilitates the occurrence of diseases like cancer. The altered equilibrium of water, extracellular ions and amino acid neurotransmitters caused by neuronal destruction and oxidative stress in neurodegenerative diseases proposed the role of these AQPs in these diseased conditions as well. The association of AQPs in a variety of inflammatory processes like lung injury, brain edema, neuromyelitis optica, and colitis as manifested through their dysregulation both in animal and human diseases is truly an eye opener for their role in protection and reaction to various noxious stimuli including bacterial infection. Renal diseases like nephrogenic diabetes inspidus, autosomal dominant polycystic kidney disease and acute kidney injury are some of the pathophysiological conditions related to malfunctioning of aquaporins. Besides, the malfunctioning of aquaglyceroporins like AQP7 and AQP9 makes them responsible for disorders like obesity, nonalcoholic fatty liver disease and non-alcoholic steatohepatitis. In this review article, we present our current understanding of the role of AQPs in the causation of these metabolic disorders and how targeting them holds promising therapeutic potential for most of these diseases like cancer, renal diseases and even cardiovascular disorders.

BACKGROUND: Osteoarthritis (OA) is the most common chronic joint disease and it may progressively cause disability and compromise quality of life. Lately, the role of miRNAs in the pathogenesis of OA has drawn a lot of attention. miRNAs are small, single-stranded, non-coding molecules of RNA which regulate gene expression at post-transcriptional level. The dysregulation of the expression of several miRNAs affects pathways involved in OA pathogenesis.
OBJECTIVE: The purpose of this article is to review the literature on the involvement of miRNAs in the pathogenesis of OA and the implications on its diagnosis and treatment.
METHODS: An extensive electronic literature search was conducted by two researchers from January 2008 to August 2017. Titles and abstracts of papers were screened by the authors for further inclusion in the present work. Finally, full texts of the selected articles were retrieved.
RESULTS: Abnormally expressed miRNAs enhance the production of cartilage degrading enzymes, inhibit the expression of cartilage matrix components, increase the production of proinflammatory cytokines, facilitate chondrocyte apoptosis, suppress autophagy in chondrocytes and are involved in pain-related pathways. miRNAs are also incorporated in extra-cellular membranous vesicles such as exosomes and participate in the intercellular communication in osteoarthritic joints.
CONCLUSIONS: Ongoing research on miRNAs has potential implications in the diagnosis and treatment of OA. Their different levels in peripheral blood and synovial fluid between OA patients and healthy population makes them candidates for being used as biomarkers of the disease, while targeting miRNAs may be a novel therapeutic strategy in OA.

MicroRNAs (miRNAs) are proposed as a family of short noncoding molecules able to manage and control the expression of the gene targets at the posttranscriptional level. They contribute in several fundamental physiological mechanisms as well as a verity of human and animal diseases such as cancer progression. Among these tiny RNAs, miR-451 placed on chromosome 17 at 17q11.2 presents an essential role in many biological processes in health condition and also in pathogenesis of different diseases. Besides, it has been recently considered as a valuable biomarker for cancer detection, prognosis and treatment. Therefore, this review will provide the critical functions of miR-451 on biological mechanisms including cell cycle and proliferation, cell survival and apoptosis, differentiation and development as well as disease initiation and progression such as tumor formation, migration, invasion, and metastasis.