Character strengths and fluid intelligence.

OBJECTIVE: Research on the associations between cognitive and noncognitive personality traits has widely neglected character strengths, that means positively and morally valued personality traits that constitute good character. METHOD: The present study aimed to bridge this gap by studying the associations between character strengths and fluid intelligence using different operationalizations of character strengths (including self- and informant-reports) and fluid intelligence in children, adolescents, and adults. RESULTS: The results, based on four samples (N = 193/290/330/324), suggested that morally valued personality traits are independent of fluid intelligence, with the exception of love of learning, which showed small but robust positive relationships with fluid intelligence across all samples. CONCLUSIONS: Nonetheless, we argue for further research on the associations with other cognitive abilities and interactions between character strengths and intelligence when examining their relationships with external criteria.

Development and Linguistic Cue Analysis of the State-Trait Cheerfulness Inventory-Short Form.

The present study derived a short form of the State-Trait Cheerfulness Inventory-Trait Version (STCI-T30) using an item response theory framework. Latent trait test-retest correlations and reliability across the latent continuum in the STCI-T30 remained high. Moreover, the STCI-T30 showed external validity with criterion variables (e.g., playfulness) and a short writing task completed by these participants was rated by unacquainted judges to infer the author's cheerfulness, seriousness, and bad-mood. Results suggested significant self-other and inter-judge agreement of cheerfulness, seriousness, and bad-mood and linguistic cues analysis suggested cheerfulness and bad-mood manifested through writing in tone, social processes, and affect.

Sedimentation Velocity Analysis with Fluorescence Detection of Mutant Huntingtin Exon 1 Aggregation in Drosophila melanogaster and Caenorhabditis elegans.

At least nine neurodegenerative diseases that are caused by the aggregation induced by long tracts of glutamine sequences have been identified. One such polyglutamine-containing protein is huntingtin, which is the primary factor responsible for Huntington's disease. Sedimentation velocity with fluorescence detection is applied to perform a comparative study of the aggregation of the huntingtin exon 1 protein fragment upon transgenic expression in Drosophila melanogaster and Caenorhabditis elegans. This approach allows the detection of aggregation in complex mixtures under physiologically relevant conditions. Complementary methods used to support this biophysical approach included fluorescence microscopy and semidenaturing detergent agarose gel electrophoresis, as a point of comparison with earlier studies. New analysis tools developed for the analytical ultracentrifuge have made it possible to readily identify a wide range of aggregating species, including the monomer, a set of intermediate aggregates, and insoluble inclusion bodies. Differences in aggregation in the two animal model systems are noted, possibly because of differences in levels of expression of glutamine-rich sequences. An increased level of aggregation is shown to correlate with increased toxicity for both animal models. Co-expression of the human Hsp70 in D. melanogaster showed some mitigation of aggregation and toxicity, correlating best with inclusion body formation. The comparative study emphasizes the value of the analytical ultracentrifuge equipped with fluorescence detection as a useful and rigorous tool for in situ aggregation analysis to assess commonalities in aggregation across animal model systems.

Self-association motifs in the enteroaggregative Escherichia coli heat-resistant agglutinin 1.

The heat-resistant agglutinin 1 (Hra1) is an integral outer membrane protein found in strains of Escherichia coli that are exceptional colonizers. Hra1 from enteroaggregative E. coli strain 042 is sufficient to confer adherence to human epithelial cells and to cause bacterial autoaggregation. Hra1 is closely related to the Tia invasin, which also confers adherence, but not autoaggregation. Here, we have demonstrated that Hra1 mediates autoaggregation by self-association and we hypothesize that at least some surface-exposed amino acid sequences that are present in Hra1, but absent in Tia, represent autoaggregation motifs. We inserted FLAG tags along the length of Hra1 and used immune-dot blots to verify that four in silico-predicted outer loops were indeed surface exposed. In Hra1 we swapped nine candidate motifs in three of these loops, ranging from one to ten amino acids in length, to the corresponding sequences in Tia. Three of the motifs were required for Hra1-mediated autoaggregation. The database was searched for other surface proteins containing these motifs; the GGXWRDDXK motif was also present in a surface-exposed region of Rck, a Salmonella enterica serotype Typhimurium complement resistance protein. Cloning and site-specific mutagenesis demonstrated that Rck can confer weak, GGXWRDDXK-dependent autoaggregation by self-association. Hra1 and Rck appear to form heterologous associations and GGXWRDDXK is required on both molecules for Hra1-Rck association. However, a GGYWRDDLKE peptide was not sufficient to interfere with Hra1-mediated autoaggregation. In the present study, three autoaggregation motifs in an integral outer membrane protein have been identified and it was demonstrated that at least one of them works in the context of a different cell surface.

Diarrhoeagenic Escherichia coli in mother-child Pairs in Ile-Ife, South Western Nigeria.

BACKGROUND: Diarrhoeagenic Escherichia coli (DEC) pathotypes are among the most common bacterial causes of morbidity and mortality in young children. These pathogens are not sought routinely and capacity for their detection is limited in Africa. We investigated the distribution and dissemination of DEC in 126 children paired with their mothers in a Nigerian community. METHODS: A total of 861 E. coli were isolated from 126 children with diarrhoea and their mothers. Antimicrobial susceptibility of each isolate was determined by Kirby-Bauer disc diffusion technique. All the isolates were screened for DEC markers by multiplex PCR. Genetic relatedness of DEC strains was determined by flagellin typing and Insertion element 3 (IS3)-based PCR. RESULTS: DEC were identified from 35.7% of individuals with the most common pathotype being shiga toxin-producing E. coli (42, 16.7%). Identical pathotypes were found in 13 (10.3%) of the mother-child pairs and in three of these strains from mothers and their children showed identical genetic signatures. Over 90% of DEC isolates were resistant to ampicillin, sulphonamide, tetracycline, streptomycin or trimethoprim, but only 9 (7.2%) were ciprofloxacin resistant CONCLUSION: The data suggest that healthy mothers are asymptomatic reservoirs of multiply-resistant strains that are pathogenic in their children and there are instances in which identical strains are found in mother-child pairs.

Endothelial deletion of murine Jag1 leads to valve calcification and congenital heart defects associated with Alagille syndrome.

The Notch signaling pathway is an important contributor to the development and homeostasis of the cardiovascular system. Not surprisingly, mutations in Notch receptors and ligands have been linked to a variety of hereditary diseases that impact both the heart and the vasculature. In particular, mutations in the gene encoding the human Notch ligand jagged 1 result in a multisystem autosomal dominant disorder called Alagille syndrome, which includes tetralogy of Fallot among its more severe cardiac pathologies. Jagged 1 is expressed throughout the developing embryo, particularly in endothelial cells. Here, we demonstrate that endothelial-specific deletion of Jag1 leads to cardiovascular defects in both embryonic and adult mice that are reminiscent of those in Alagille syndrome. Mutant mice display right ventricular hypertrophy, overriding aorta, ventricular septal defects, coronary vessel abnormalities and valve defects. Examination of mid-gestational embryos revealed that the loss of Jag1, similar to the loss of Notch1, disrupts endothelial-to-mesenchymal transition during endocardial cushion formation. Furthermore, adult mutant mice exhibit cardiac valve calcifications associated with abnormal matrix remodeling and induction of bone morphogenesis. This work shows that the endothelium is responsible for the wide spectrum of cardiac phenotypes displayed in Alagille Syndrome and it demonstrates a crucial role for Jag1 in valve morphogenesis.

Notch1 regulates angio-supportive bone marrow-derived cells in mice: relevance to chemoresistance.

Host responses to chemotherapy can induce resistance mechanisms that facilitate tumor regrowth. To determine the contribution of bone marrow-derived cells (BMDCs), we exposed tumor-bearing mice to chemotherapeutic agents and evaluated the influx and contribution of a genetically traceable subpopulation of BMDCs (vascular endothelial-cadherin-Cre-enhanced yellow fluorescent protein [VE-Cad-Cre-EYFP]). Treatment of tumor-bearing mice with different chemotherapeutics resulted in a three- to 10-fold increase in the influx of VE-Cad-Cre-EYFP. This enhanced influx was accompanied by a significant increase in angiogenesis. Expression profile analysis revealed a progressive change in the EYFP population with loss of endothelial markers and an increase in mononuclear markers. In the tumor, 2 specific populations of VE-Cad-Cre-EYFP BMDCs were identified: Gr1⁺/CD11b⁺ and Tie2high/platelet endothelial cell adhesion moleculelow cells, both located in perivascular areas. A common signature of the EYFP population that exits the bone marrow is an increase in Notch. Inducible inactivation of Notch in the EYFP⁺ BMDCs impaired homing of these BMDCs to the tumor. Importantly, Notch deletion reduced therapy-enhanced angiogenesis, and was associated with an increased antitumor effect of the chemotherapy. These findings revealed the functional significance of a specific population of supportive BMDCs in response to chemotherapeutics and uncovered a new potential strategy to enhance anticancer therapy.

Lim domain binding 2: a key driver of transendothelial migration of leukocytes and atherosclerosis.

OBJECTIVE: Using a multi-tissue, genome-wide gene expression approach, we recently identified a gene module linked to the extent of human atherosclerosis. This atherosclerosis module was enriched with inherited risk for coronary and carotid artery disease (CAD) and overlapped with genes in the transendothelial migration of leukocyte (TEML) pathway. Among the atherosclerosis module genes, the transcription cofactor Lim domain binding 2 (LDB2) was the most connected in a CAD vascular wall regulatory gene network. Here, we used human genomics and atherosclerosis-prone mice to evaluate the possible role of LDB2 in TEML and atherosclerosis. APPROACH AND RESULTS: mRNA profiles generated from blood macrophages in patients with CAD were used to infer transcription factor regulatory gene networks; Ldlr(-/-)Apob(100/100) mice were used to study the effects of Ldb2 deficiency on TEML activity and atherogenesis. LDB2 was the most connected gene in a transcription factor regulatory network inferred from TEML and atherosclerosis module genes in CAD macrophages. In Ldlr(-/-)Apob(100/100) mice, loss of Ldb2 increased atherosclerotic lesion size ≈2-fold and decreased plaque stability. The exacerbated atherosclerosis was caused by increased TEML activity, as demonstrated in air-pouch and retinal vasculature models in vivo, by ex vivo perfusion of primary leukocytes, and by leukocyte migration in vitro. In THP1 cells, migration was increased by overexpression and decreased by small interfering RNA inhibition of LDB2. A functional LDB2 variant (rs10939673) was associated with the risk and extent of CAD across several cohorts. CONCLUSIONS: As a key driver of the TEML pathway in CAD macrophages, LDB2 is a novel candidate to target CAD by inhibiting the overall activity of TEML.

Notch promotes vascular maturation by inducing integrin-mediated smooth muscle cell adhesion to the endothelial basement membrane.

Vascular development and angiogenesis initially depend on endothelial tip cell invasion, which is followed by a series of maturation steps, including lumen formation and recruitment of perivascular cells. Notch ligands expressed on the endothelium and their cognate receptors expressed on perivascular cells are involved in blood vessel maturation, though little is known regarding the Notch-dependent effectors that facilitate perivascular coverage of nascent vessels. Here, we report that vascular smooth muscle cell (VSMC) recognition of the Notch ligand Jagged1 on endothelial cells leads to expression of integrin αvß3 on VSMCs. Once expressed, integrin αvß3 facilitates VSMC adhesion to VWF in the endothelial basement membrane of developing retinal arteries, leading to vessel maturation. Genetic or pharmacologic disruption of Jagged1, Notch, αvß3, or VWF suppresses VSMC coverage of nascent vessels and arterial maturation during vascular development. Therefore, we define a Notch-mediated interaction between the developing endothelium and VSMCs leading to adhesion of VSMCs to the endothelial basement membrane and arterial maturation.

Macromolecular interactions and geometrical confinement determine the 3D diffusion of ribosome-sized particles in live Escherichia coli cells.

The crowded bacterial cytoplasm is comprised of biomolecules that span several orders of magnitude in size and electrical charge. This complexity has been proposed as the source of the rich spatial organization and apparent anomalous diffusion of intracellular components, although this has not been tested directly. Here, we use biplane microscopy to track the 3D motion of self-assembled bacterial Genetically Encoded Multimeric nanoparticles (bGEMs) with tunable size (20 to 50 nm) and charge (-2160 to +1800 e) in live Escherichia coli cells. To probe intermolecular details at spatial and temporal resolutions beyond experimental limits, we also developed a colloidal whole-cell model that explicitly represents the size and charge of cytoplasmic macromolecules and the porous structure of the bacterial nucleoid. Combining these techniques, we show that bGEMs spatially segregate by size, with small 20-nm particles enriched inside the nucleoid, and larger and/or positively charged particles excluded from this region. Localization is driven by entropic and electrostatic forces arising from cytoplasmic polydispersity, nucleoid structure, geometrical confinement, and interactions with other biomolecules including ribosomes and DNA. We observe that at the timescales of traditional single molecule tracking experiments, motion appears sub-diffusive for all particle sizes and charges. However, using computer simulations with higher temporal resolution, we find that the apparent anomalous exponents are governed by the region of the cell in which bGEMs are located. Molecular motion does not display anomalous diffusion on short time scales and the apparent sub-diffusion arises from geometrical confinement within the nucleoid and by the cell boundary.

Jagged1 in the portal vein mesenchyme regulates intrahepatic bile duct development: insights into Alagille syndrome.

Mutations in the human Notch ligand jagged 1 (JAG1) result in a multi-system disorder called Alagille syndrome (AGS). AGS is chiefly characterized by a paucity of intrahepatic bile ducts (IHBD), but also includes cardiac, ocular, skeletal, craniofacial and renal defects. The disease penetration and severity of the affected organs can vary significantly and the molecular basis for this broad spectrum of pathology is unclear. Here, we report that Jag1 inactivation in the portal vein mesenchyme (PVM), but not in the endothelium of mice, leads to the hepatic defects associated with AGS. Loss of Jag1 expression in SM22α-positive cells of the PVM leads to defective bile duct development beyond the initial formation of the ductal plate. Cytokeratin 19-positive cells are detected surrounding the portal vein, yet they are unable to form biliary tubes, revealing an instructive role of the vasculature in liver development. These findings uncover the cellular basis for the defining feature of AGS, identify mesenchymal Jag1-dependent and -independent stages of duct development, and provide mechanistic information for the role of Jag1 in IHBD formation.

Dll4 signalling through Notch1 regulates formation of tip cells during angiogenesis.

In sprouting angiogenesis, specialized endothelial tip cells lead the outgrowth of blood-vessel sprouts towards gradients of vascular endothelial growth factor (VEGF)-A. VEGF-A is also essential for the induction of endothelial tip cells, but it is not known how single tip cells are selected to lead each vessel sprout, and how tip-cell numbers are determined. Here we present evidence that delta-like 4 (Dll4)-Notch1 signalling regulates the formation of appropriate numbers of tip cells to control vessel sprouting and branching in the mouse retina. We show that inhibition of Notch signalling using gamma-secretase inhibitors, genetic inactivation of one allele of the endothelial Notch ligand Dll4, or endothelial-specific genetic deletion of Notch1, all promote increased numbers of tip cells. Conversely, activation of Notch by a soluble jagged1 peptide leads to fewer tip cells and vessel branches. Dll4 and reporters of Notch signalling are distributed in a mosaic pattern among endothelial cells of actively sprouting retinal vessels. At this location, Notch1-deleted endothelial cells preferentially assume tip-cell characteristics. Together, our results suggest that Dll4-Notch1 signalling between the endothelial cells within the angiogenic sprout serves to restrict tip-cell formation in response to VEGF, thereby establishing the adequate ratio between tip and stalk cells required for correct sprouting and branching patterns. This model offers an explanation for the dose-dependency and haploinsufficiency of the Dll4 gene, and indicates that modulators of Dll4 or Notch signalling, such as gamma-secretase inhibitors developed for Alzheimer's disease, might find usage as pharmacological regulators of angiogenesis.

Improving Scale Equivalence by Increasing Access to Scale-Specific Information.

Measures of the same phenomenon should produce the same results; this principle is fundamental because it allows for replication-the basis of science. Unfortunately, measures of a psychological construct in one language can often measure something a bit different in another language (i.e., low "scale equivalence"). Historically, the problem was thought to stem from insufficient knowledge of best-practice translation procedures. Yet solutions based on this diagnosis and their widespread adoption have not resolved the issue. In this article, we suggest that an additional problem might be insufficient information about the measure being translated. If so, low scale equivalence is a problem that translators and cross-cultural psychologists cannot solve on their own. We explore the possibility that measure-specific translation guides be created by original scale builders for the most widely used measures of important psychological constructs. We describe why such guides are needed, when they are needed, what they might look like, their feasibility, and next steps, providing a complete example guide and test case in a supplement concerning the Primals Inventory. In this article, we seek to spark discussion on translation practices happening behind the scenes and how greater transparency can improve scale equivalence, in the spirit of open science.

Vascular remodeling of the vitelline artery initiates extravascular emergence of hematopoietic clusters.

The vitelline artery is a temporary structure that undergoes extensive remodeling during midgestation to eventually become the superior mesenteric artery (also called the cranial mesenteric artery, in the mouse). Here we show that, during this remodeling process, large clusters of hematopoietic progenitors emerge via extravascular budding and form structures that resemble previously described mesenteric blood islands. We demonstrate through fate mapping of vascular endothelium that these mesenteric blood islands are derived from the endothelium of the vitelline artery. We further show that the vitelline arterial endothelium and subsequent blood island structures originate from a lateral plate mesodermal population. Lineage tracing of the lateral plate mesoderm demonstrates contribution to all hemogenic vascular beds in the embryo, and eventually, all hematopoietic cells in the adult. The intraembryonic hematopoietic cell clusters contain viable, proliferative cells that exhibit hematopoietic stem cell markers and are able to further differentiate into myeloid and erythroid lineages. Vitelline artery-derived hematopoietic progenitor clusters appear between embryonic day 10 and embryonic day 10.75 in the caudal half of the midgut mesentery, but by embryonic day 11.0 are sporadically found on the cranial side of the midgut, thus suggesting possible extravascular migration aided by midgut rotation.

Character Strengths: Person-Environment Fit and Relationships With Job and Life Satisfaction.

Several studies demonstrated the relevance of character strengths in the workplace. For example, it has been shown that they positively relate to performance and are strong predictors of job satisfaction. Furthermore, it was demonstrated that occupational groups differ in their average levels of character strengths. However, little is known about the effects of the congruence between a person's strengths profile with the average profile within an occupational group (environmental congruence) on well-being. In a nationally representative sample (N = 870) of employed adults, we analyzed data on character strengths (t1), and measures of job and life satisfaction at three different time points (t1-t3; separated by 1 year). We studied (1) whether employees in different occupational groups differ with regard to their levels and configurations of character strengths, (2) how levels and configurations of character strengths relate to concurrent and predictive job and life satisfaction, and (3) whether a fit between strengths of a person and the environment goes along with current and future job and life satisfaction. Results confirmed previous findings that small, but meaningful, differences in character strengths among employees in different occupational groups can be found and that character strengths positively relate to current and prospective job and life satisfaction. Furthermore, results suggested that a better person-environment fit goes along with higher job and life satisfaction. These results suggest character strengths and could play an important role in vocational and career counseling.

Drosophila melanogaster as a model for arbovirus infection of adult salivary glands.

Arboviruses are an emerging threat to public health. Arbovirus transmission to vertebrates hinges on dissemination from the arthropod gastrointestinal tract, and ultimately infection of the arthropod salivary glands. Therefore, salivary gland immunity impacts arbovirus transmission; however, these immune responses are poorly understood. Here, we describe the utility of Drosophila melanogaster as a salivary gland infection model. First, we describe the use of a salivary gland-specific driver to launch RNA interference or virus replicon transgenes. Next, we infect flies with an arbovirus panel and find multiple viruses that infect Drosophila salivary glands, albeit inefficiently. We find that this infection is not controlled by antiviral RNA silencing; thus, we silence a panel of immune genes in the salivary glands, but do not observe changes in infection. These data suggest that Drosophila may be used to study salivary gland infection, and that there are likely unexplored pathways controlling infection of this tissue.

The Not so Good, the Bad and the Ugly: Differential Bacterial Adhesion and Invasion Mediated by Salmonella PagN Allelic Variants.

While advances in genomic sequencing have highlighted significant strain variability between and within Salmonella serovars, only a few protein variants have been directly related to evolutionary adaptation for survival, such as host specificity or differential virulence. The current study investigated whether allelic variation of the Salmonella adhesin/invasin PagN influences bacterial interaction with their receptors. The Salmonella enterica, subspecies enterica serovar Typhi (S. Typhi) allelic variant of PagN was found to bind significantly better to different enterocytes as well as to the extracellular matrix protein laminin than did the major Salmonella enterica, subspecies enterica serovar Typhimurium (S. Typhimurium) allele. The two alleles differed at amino acid residues 49 and 109 in two of the four predicted PagN surface loops, and residue substitution analysis revealed that a glutamic acid at residue 49 increased the adhesive and invasive properties of S. Typhi PagN. PagN sequence comparisons from 542 Salmonella strains for six representative S. enterica serovars and S. diarizonae further supported the role of glutamic acid at residues 49 and 109 in optimizing adhesion to cells and laminin, as well as for cell invasion. In summary, this study characterized unique residues in allelic variants of a virulence factor that participates in the colonization and invasive properties of different Salmonella stains, subspecies and serovars.

Notch signaling in blood vessels: who is talking to whom about what?

It has become increasingly clear that the Notch signaling pathway plays a critical role in the development and homeostasis of the cardiovascular system. This notion has emerged from loss- and gain-of-function analysis and from the realization that several hereditary cardiovascular disorders originate from gene mutations that have a direct impact on Notch signaling. Current research efforts are focused on determining the specific cellular and molecular effects of Notch signaling. The rationale for this has stemmed from the clinical importance and therapeutic potential of modulating vascular formation during various disease states. A more complete appreciation of Notch signaling, as it relates to vascular morphogenesis, requires an in-depth knowledge of expression patterns of the various signaling components and a comprehensive understanding of downstream targets. The goal of this review is to summarize current knowledge regarding Notch signaling during vascular development and within the adult vascular wall. Our focus is on the genetic analysis and cellular experiments that have been performed with Notch ligands, receptors, and downstream targets. We also highlight questions and controversies regarding the contribution of this pathway to vascular development.

Breast milk as the "water that supports and preserves life"--socio-cultural constructions of breastfeeding and their implications for the prevention of mother to child transmission of HIV in sub-Saharan Africa.

OBJECTIVES: Complementary breastfeeding represents an important source of risk of HIV infection for infants born to HIV positive mothers. The World Health Organisation recommends that infants born to HIV positive mothers receive either replacement feeding or exclusive breastfeeding (EBF) followed by early weaning. Beyond the clinical and epidemiological debate, it remains unclear how acceptable and feasible the two options are for rural populations in sub-Saharan Africa. This qualitative study aims to fill this gap in knowledge by exploring both the socio-cultural construction and the practice of breastfeeding in the Nouna Health District, rural Burkina Faso. METHODS: Information was collected through 32 individual interviews and 3 focus group discussions with women of all ages, and 6 interviews with local guérisseurs. RESULTS: The findings highlight that breastfeeding is perceived as central to motherhood, but that women practice complementary, rather than exclusive, breastfeeding. The findings also indicate that women recognise both the nutritional value of breast milk and its potential to act as a source of disease transmission. CONCLUSIONS: The findings suggest that given the socio-cultural importance attributed to breastfeeding and the prevailing poverty, it may be more acceptable and more feasible to promote EBF followed by early weaning than replacement feeding. A set of operational strategies are proposed to favour the prevention of mother to child transmission of HIV in the respect of the local socio-cultural setting.

Laughing away the pain: A narrative review of humour, sense of humour and pain.

BACKGROUND AND OBJECTIVE: The link between humour and sense of humour with pain has been a topic of research for decades. The purpose of the present article was to review the different studies that have been conducted to date on the association between humour and sense of humour with pain. DATABASES AND DATA TREATMENT: The literature search was conducted using the PubMed, Science Direct and ProQuest databases. Forty-one studies were reviewed, and the results are summarized and structured into three sections: experimental pain, chronic pain and pain in children. RESULTS: For experimental pain, the findings support the idea that humorous distractions, such as watching a comedy clip, increase pain tolerance, although most of the studies indicate that other non-humorous distractions produce similar effects. Regarding chronic pain, humour has been studied as a way of coping with pain and the emotional distress produced by chronic pain conditions. The results of correlational studies show significant associations between the use of humour and main variables such as anxiety and catastrophizing. Finally, concerning pain in children, similar findings to those described for the previous sections have been reported, with a notable presence of studies on clinic clown interventions, which promote emotional well-being among children and their parents, although their effectiveness in pain reduction is controversial. CONCLUSIONS: The study of the link between humour and pain is still on an early stage, and overcoming the limitations of previous studies is required to strengthen the promising results that have been observed up to date. SIGNIFICANCE: This review summarizes all main findings regarding humour, sense of humour and pain up until the first half of 2018 and offers a list of aspects to be considered in further studies regarding the link of humour and pain to contribute to a more systematic research.