High-performing teams: Is collective intelligence the answer?

BACKGROUND/OBJECTIVES: The concept of a general factor of collective intelligence, proposed by Woolley et al. in 2010, has spurred interest in understanding collective intelligence within small groups. This study aims to extend this investigation by examining the validity of a general collective intelligence factor, assessing its underlying factor structure, and evaluating its utility in predicting performance on future group problem-solving tasks and academic outcomes. METHODS: Employing a correlational study design, we engaged 85 university students in a series of complex cognitive tasks designed to measure collective intelligence through individual, group, and predictive phases. RESULTS: Contrary to the hypothesized single-factor model, our findings favor a two-factor model influenced by Cattell's theory of crystalized and fluid intelligence. These two factors accounted for substantial variance in group performance outcomes, challenging the prevailing single-factor model. Notably, the predictive validity of these factors on group assignments was statistically significant, with both individual and collective intelligence measures correlating moderately with group assignment scores (rs = .40 to .47, p < .05). CONCLUSIONS: Our research suggests that collective intelligence in small group settings may not be uniformly governed by a single factor but rather by multiple dimensions that reflect established theories of individual intelligence. This nuanced understanding of collective intelligence could have significant implications for enhancing group performance in both educational and organizational contexts. Future research should explore these dimensions and their independent contributions to group dynamics and outcomes.

Who Says You can't go FAST at Night? Use of a Novel Ultrasound-Capable Night Vision Device for Prehospital Medical Personnel to Identify Noncompressible Truncal Hemorrhage.

BACKGROUND: Early detection of abdominal hemorrhage via ultrasound has life-saving implications for military and civilian trauma. However, strict adherence to light discipline may prohibit the use of ultrasound devices in the deployed setting. Additionally, current night vision devices remain noncompatible with ultrasound technology. This study sought to assess an innovative night vision device with ultrasound capable picture-in-picture display via a intraabdominal hemorrhage model to identify noncompressible truncal hemorrhage in blackout conditions. METHODS: 8 post mortem fetal porcine specimens were used and divided into 2 groups: intrabdominal hemorrhage (n = 4) vs no hemorrhage (n = 4). Intrabdominal hemorrhage was modeled via direct injection of 200 mL of normal saline into the peritoneal cavity. Under blackout conditions, 5 participants performed a focused assessment with sonography for trauma (FAST) exam on each model using the prototype ultrasound-capable night vision device. RESULTS: Of the 40 FAST exams performed, 95% (N = 38) resulted in the correct identification of intraabdominal hemorrhage. Of the incorrectly identified exams, both were false positives resulting in a 100% sensitivity, 90% specificity, 91% positive predictive value, and a 100% negative predictive value. All participants noted the novel device was easy to use and provided superior visualization for performing FAST exams under blackout conditions. CONCLUSION: The ultrasound-enabled night vision prototype demonstrated promising results in identifying noncompressible truncal hemorrhage while maintaining strict light discipline in blackout conditions. Further research efforts should be directed at assessing the ability of providers to perform procedures in blackout conditions using the ultrasound-enabled prototype night vision device.

Academic Productivity of Applicant and Program as Predictors of a Future Academic Career in Neurosurgery.

BACKGROUND AND OBJECTIVES: Academic productivity is viewed as a critical objective factor for a neurosurgery residency applicant. There has been a consistent rise in academic productivity over the last decade, but a lack of consistent data on the utility of this in helping neurosurgery residency programs identify which applicants will enter academic neurosurgery. This cross-sectional study evaluates the predictiveness of academic productivity before and during residency on career choice, both independent and dependent of training environment. METHODS: The 116 accredited neurosurgery residency programs were split into 4 quartile groups based on their 2022 Doximity rankings. Six neurosurgery residency programs were randomly selected from each quartile. Publicly available information including number and type (before or during residency) of publication and type of employment (academic vs nonacademic) was collected on neurosurgeons who matriculated into residency in the year 2000 or later. Multivariable logistic regression was used to explore the associations among neurosurgeon and program characteristics, and an academic career. RESULTS: A total of 557 neurosurgeons were identified. Group 1 (n = 194) had the highest median publications during residency total (12) and first author (5), as well as the highest percentage of neurosurgeons who attended a top 20 medical school (38.7%), hold a higher educational degree (20.6%), and pursued an academic career (72.2%). Neither attending a top 20 medical school, holding a higher educational degree, nor publications were significant multivariable predictors of an academic career. Being in group 1 was the only significant predictor of entering an academic career across analyses. CONCLUSION: Only residency group ranking, not academic productivity, predicted a future academic career. For residency programs evaluating applicants as future academic neurosurgeons, this suggests that program environment is more predictive than traditionally valued characteristics such as research productivity. Additional work is needed to elucidate characteristics or practices by which future academic neurosurgeons can be identified.

Pulmonary Fibrosis Ferret Model Demonstrates Sustained Fibrosis, Restrictive Physiology, and Aberrant Repair.

Rationale: The role of MUC5B mucin expression in IPF pathogenesis is unknown. Bleomycin-exposed rodent models do not exhibit sustained fibrosis or airway remodeling. Unlike mice, ferrets have human-like distribution of MUC5B expressing cell types and natively express the risk-conferring variant that induces high MUC5B expression in humans. We hypothesized that ferrets would consequently exhibit aberrant repair to propagate fibrosis similar to human IPF. Methods: Bleomycin (5U/kg) or saline-control was micro-sprayed intratracheally then wild-type ferrets were evaluated through 22 wks. Clinical phenotype was assessed with lung function. Fibrosis was assessed with µCT imaging and comparative histology with Ashcroft scoring. Airway remodeling was assessed with histology and quantitative immunofluorescence. Results: Bleomycin ferrets exhibited sustained restrictive physiology including decreased inspiratory capacity, decreased compliance, and shifted Pressure-Volume loops through 22 wks. Volumetric µCT analysis revealed increased opacification of the lung bleomycin-ferrets. Histology showed extensive fibrotic injury that matured over time and MUC5B-positive cystic structures in the distal lung suggestive of honeycombing. Bleomycin ferrets had increased proportion of small airways that were double-positive for CCSP and alpha-tubulin compared to controls, indicating an aberrant 'proximalization' repair phenotype. Notably, this aberrant repair was associated with extent of fibrotic injury at the airway level. Conclusions: Bleomycin-exposed ferrets exhibit sustained fibrosis through 22 wks and have pathologic features of IPF not found in rodents. Ferrets exhibited proximalization of the distal airways and other pathologic features characteristic of human IPF. MUC5B expression through native cell types may play a key role in promoting airway remodeling and lung injury in IPF.

FGF receptors mediate cellular senescence in the cystic fibrosis airway epithelium.

The number of adults living with cystic fibrosis (CF) has already increased significantly because of drastic improvements in life expectancy attributable to advances in treatment, including the development of highly effective modulator therapy. Chronic airway inflammation in CF contributes to morbidity and mortality, and aging processes like inflammaging and cell senescence influence CF pathology. Our results show that single-cell RNA sequencing data, human primary bronchial epithelial cells from non-CF and CF donors, a CF bronchial epithelial cell line, and Cftr-knockout (Cftr-/-) rats all demonstrated increased cell senescence markers in the CF bronchial epithelium. This was associated with upregulation of fibroblast growth factor receptors (FGFRs) and mitogen-activated protein kinase (MAPK) p38. Inhibition of FGFRs, specifically FGFR4 and to some extent FGFR1, attenuated cell senescence and improved mucociliary clearance, which was associated with MAPK p38 signaling. Mucociliary dysfunction could also be improved using a combination of senolytics in a CF ex vivo model. In summary, FGFR/MAPK p38 signaling contributes to cell senescence in CF airways, which is associated with impaired mucociliary clearance. Therefore, attenuation of cell senescence in the CF airways might be a future therapeutic strategy improving mucociliary dysfunction and lung disease in an aging population with CF.

Reciprocal regulation of cardiac ß-oxidation and pyruvate dehydrogenase by insulin.

The heart alters the rate and relative oxidation of fatty acids and glucose based on availability and energetic demand. Insulin plays a crucial role in this process diminishing fatty acid and increasing glucose oxidation when glucose availability increases. Loss of insulin sensitivity and metabolic flexibility can result in cardiovascular disease. It is therefore important to identify mechanisms by which insulin regulates substrate utilization in the heart. Mitochondrial pyruvate dehydrogenase (PDH) is the key regulatory site for the oxidation of glucose for ATP production. Nevertheless, the impact of insulin on PDH activity has not been fully delineated, particularly in the heart. We sought in vivo evidence that insulin stimulates cardiac PDH and that this process is driven by the inhibition of fatty acid oxidation. Mice injected with insulin exhibited dephosphorylation and activation of cardiac PDH. This was accompanied by an increase in the content of malonyl-CoA, an inhibitor of carnitine palmitoyltransferase 1 (CPT1), and, thus, mitochondrial import of fatty acids. Administration of the CPT1 inhibitor oxfenicine was sufficient to activate PDH. Malonyl-CoA is produced by acetyl-CoA carboxylase (ACC). Pharmacologic inhibition or knockout of cardiac ACC diminished insulin-dependent production of malonyl-CoA and activation of PDH. Finally, circulating insulin and cardiac glucose utilization exhibit daily rhythms reflective of nutritional status. We demonstrate that time-of-day-dependent changes in PDH activity are mediated, in part, by ACC-dependent production of malonyl-CoA. Thus, by inhibiting fatty acid oxidation, insulin reciprocally activates PDH. These studies identify potential molecular targets to promote cardiac glucose oxidation and treat heart disease.

Thioredoxin-1 and its mimetic peptide improve systolic cardiac function and remodeling after myocardial infarction.

Myocardial infarction (MI) is characterized by a significant loss of cardiomyocytes (CMs), and it is suggested that reactive oxygen species (ROS) are involved in cell cycle arrest, leading to impaired CM renewal. Thioredoxin-1 (Trx-1) scavenges ROS and may play a role in restoring CM renewal. However, the truncated form of Trx-1, Trx-80, can compromise its efficacy by exerting antagonistic effects. Therefore, a Trx-1 mimetic peptide called CB3 was tested as an alternative way to restore CMs. This study aimed to investigate the effects of Trx-1, Trx-80, and CB3 on mice with experimental MI and study the underlying mechanism of CB3 on CMs. Mouse cardiac parameters were quantified by echocardiography, and infarction size and fibrosis determined using Trichrome and Picro-Sirius Red staining. The study found that Trx-1 and CB3 improved mouse cardiac function, reduced the size of cardiac infarct and fibrosis, and decreased the expression of cardiac inflammatory markers. Furthermore, CB3 polarized macrophages into M2 phenotype, reduced apoptosis and oxidative stress after MI, and increased CM proliferation in cell culture and in vivo. CB3 effectively protected against myocardial infarction and could represent a new class of compounds for treating MI.

Selection on plastic adherence leads to hyper-multicellular strains and incidental virulence in the budding yeast.

Many disease-causing microbes are not obligate pathogens; rather, they are environmental microbes taking advantage of an ecological opportunity. The existence of microbes whose life cycle does not require a host and are not normally pathogenic, yet are well-suited to host exploitation, is an evolutionary puzzle. One hypothesis posits that selection in the environment may favor traits that incidentally lead to pathogenicity and virulence, or serve as pre-adaptations for survival in a host. An example of such a trait is surface adherence. To experimentally test the idea of 'accidental virulence', replicate populations of Saccharomyces cerevisiae were evolved to attach to a plastic bead for hundreds of generations. Along with plastic adherence, two multicellular phenotypes- biofilm formation and flor formation- increased; another phenotype, pseudohyphal growth, responded to the nutrient limitation. Thus, experimental selection led to the evolution of highly-adherent, hyper-multicellular strains. Wax moth larvae injected with evolved hyper-multicellular strains were significantly more likely to die than those injected with evolved non-multicellular strains. Hence, selection on plastic adherence incidentally led to the evolution of enhanced multicellularity and increased virulence. Our results support the idea that selection for a trait beneficial in the open environment can inadvertently generate opportunistic, 'accidental' pathogens.

Yeast are microscopic fungi that are found on many plants, in the soil and in other environments around the world. But, when given the chance, some yeasts are also good at infecting human and other animals and causing disease. It has been proposed that some opportunistic microbes may have dual-use traits that evolved for one purpose in their natural environment but also incidentally allow them to infect animals. For example, a toxin that helps the opportunistic microbe compete against neighboring microbes may also weaken an animal. Or the ability of many individual microbe cells to clump together into structures known as biofilms on solid surfaces, or floating mats called flors on liquids, helps them to survive in harsh environments, whether in the soil or in the body of an animal. To investigate this possibility, Ekdahl, Salcedo et al. examined whether artificially selecting yeast with a specific trait ­ the ability to stick to plastic beads ­ in the absence of any host animals would inadvertently also select for yeast that were good at causing disease. This trait was selected because it has not been previously linked to opportunistic yeast infections. The team grew the yeast for 400 generations in tubes that each contained a plastic bead. At every generation, only yeast that stuck to the plastic bead were transferred to a fresh tube to grow the next generation. The experiments found that, not only did the ability of the yeast to stick to the plastic increase over time, but the yeast also evolved the ability to form biofilms and flors. Furthermore, the sticky yeast killed an insect host known as wax moth larvae more quickly than non-sticky yeast. Together, these findings demonstrate that when microbes evolve in an environment that is devoid of any host animals, selection can inadvertently favor dual-use traits that also help the yeast to infect animals. Opportunistic yeast infections are of increasing concern in human patients, particularly those with weakened immune systems. Understanding which yeast traits are dual-use will help guide future efforts in combatting yeast and other opportunistic microbes.

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during mouse fetal heart development.

Cardiomyocytes are highly metabolic cells responsible for generating the contractile force in the heart. During fetal development and regeneration, these cells actively divide but lose their proliferative activity in adulthood. The mechanisms that coordinate their metabolism and proliferation are not fully understood. Here, we study the role of the transcription factor NFYa in developing mouse hearts. Loss of NFYa alters cardiomyocyte composition, causing a decrease in immature regenerative cells and an increase in trabecular and mature cardiomyocytes, as identified by spatial and single-cell transcriptome analyses. NFYa-deleted cardiomyocytes exhibited reduced proliferation and impaired mitochondrial metabolism, leading to cardiac growth defects and embryonic death. NFYa, interacting with cofactor SP2, activates genes linking metabolism and proliferation at the transcription level. Our study identifies a nodal role of NFYa in regulating prenatal cardiac growth and a previously unrecognized transcriptional control mechanism of heart metabolism, highlighting the importance of mitochondrial metabolism during heart development and regeneration.

Inhibition of Pyruvate Dehydrogenase in the Heart as an Initiating Event in the Development of Diabetic Cardiomyopathy.

Obesity affects a growing fraction of the population and is a risk factor for type 2 diabetes and cardiovascular disease. Even in the absence of hypertension and coronary artery disease, type 2 diabetes can result in a heart disease termed diabetic cardiomyopathy. Diminished glucose oxidation, increased reliance on fatty acid oxidation for energy production, and oxidative stress are believed to play causal roles. However, the progression of metabolic changes and mechanisms by which these changes impact the heart have not been established. Cardiac pyruvate dehydrogenase (PDH), the central regulatory site for glucose oxidation, is rapidly inhibited in mice fed high dietary fat, a model of obesity and diabetes. Increased reliance on fatty acid oxidation for energy production, in turn, enhances mitochondrial pro-oxidant production. Inhibition of PDH may therefore initiate metabolic inflexibility and oxidative stress and precipitate diabetic cardiomyopathy. We discuss evidence from the literature that supports a role for PDH inhibition in loss in energy homeostasis and diastolic function in obese and diabetic humans and in rodent models. Finally, seemingly contradictory findings highlight the complexity of the disease and the need to delineate progressive changes in cardiac metabolism, the impact on myocardial structure and function, and the ability to intercede.

Understanding the Interaction of Gluconamides and Gluconates with Amino Acids in Hair Care.

A hair care mixture formed from a gluconamide derivative and 3-hydroxypropyl ammonium gluconate is known to strengthen hair fibers; however, the mechanism by which the mixture affects hair is unknown. To give insight into the aggregation of the target gluconamide and potential interactions between the gluconate-derived mixture and hair fibers, a range of systems were characterized by X-ray crystallography namely two polymorphic forms of the target gluconamide and three salts of 3-hydroxypropylammonium with sulfuric acid, methane sulfonic acid, and oxalic acid. The gluconamide proves to aggregate and becomes a supramolecular gelator in aniline and benzyl alcohol solution. The resulting gels were characterized by rheology, scanning electron microscopy, proton nuclear magnetic resonance, Fourier transform infrared spectroscopy, and powder X-ray diffraction.

Stem cells: a comprehensive review of origins and emerging clinical roles in medical practice.

Stem cells are types of cells that have unique ability to self-renew and to differentiate into more than one cell lineage. They are considered building blocks of tissues and organs. Over recent decades, they have been studied and utilized for repair and regenerative medicine. One way to classify these cells is based on their differentiation capacity. Totipotent stem cells can give rise to any cell of an embryo but also to extra-embryonic tissue as well. Pluripotent stem cells are limited to any of the three embryonic germ layers; however, they cannot differentiate into extra-embryonic tissue. Multipotent stem cells can only differentiate into one germ line tissue. Oligopotent and unipotent stem cells are seen in adult organ tissues that have committed to a cell lineage. Another way to differentiate these cells is based on their origins. Stem cells can be extracted from different sources, including bone marrow, amniotic cells, adipose tissue, umbilical cord, and placental tissue. Stem cells began their role in modern regenerative medicine in the 1950's with the first bone marrow transplantation occurring in 1956. Stem cell therapies are at present indicated for a range of clinical conditions beyond traditional origins to treat genetic blood diseases and have seen substantial success. In this regard, emerging use for stem cells is their potential to treat pain states and neurodegenerative diseases such as Parkinson's and Alzheimer's disease. Stem cells offer hope in neurodegeneration to replace neurons damaged during certain disease states. This review compares stem cells arising from these different sources of origin and include clinical roles for stem cells in modern medical practice.

Prediction and Preparation of Coamorphous Phases of a Bislactam.

The effectiveness of a partial least squares-discriminant analysis coamorphous prediction model was tested using coamorphous screening data for a promising coamorphous former, the dimer of N-vinyl(caprolactam) (bisVCap) with a range of active pharmaceutical ingredients. The prediction model predicted 71% of the systems correctly. An experimental coamorphous screen was performed with this coformer with 13 different active pharmaceutical ingredients, and the results were compared to the predictions from the model. A total of 85% of the systems were correctly predicted. Stability assessments of three coamorphous systems showed that the prediction model score did not strongly correlate with the stability of the coamorphous material. The model performed well with small-molecule coformers, such as bisVCap, despite the difference in structure and properties compared to the amino-acid-based model training set.

Rural-Urban Differentials in Access to Behaviour Change Communication and Use of Long-Lasting Insecticide-Treated Nets and Artemisinin-Based Combination Therapy in Southeast Nigeria.

BACKGROUND: As Malaria continues to take a heavy toll on the life and economy of Nigerians, The National Malaria Elimination Programme uses behaviour change communication (BCC) to promote the use of Long-Lasting Insecticide-treated Nets (LLIN) and Artemisinin-based Combination Therapy (ACT) to combat malaria. This study examined the impact of BCC on the use of LLIN and ACT in Southeast Nigeria. METHODS: A structured questionnaire was used to gather data from 480 respondents in urban and rural communities across five states. Analysis of data was done using percentages, chi-square and logistic regression. RESULTS: Findings showed weak effect of BCC on LLIN and ACT use despite achieving high (93.75%) exposure. Only 45.1% and 45.7% of the respondents used LLIN and ACT respectively. Urban residents were found to sleep under LLINs and use ACTs more than rural dwellers. Regression results showed that newspapers (OR=1.341) and the Internet (OR=3.216) increased the odds of LLIN use in the rural areas and magazines (OR=1.837) in the urban areas. Television (OR=2.375; P=0.002) and the Internet (OR=6.063; P=0.001) increased the odds of ACT use in the urban areas. Education was found to be a positive predictor of LLIN use in the rural (OR=4.645; P=0.011) and urban areas (OR=6.102) as well as ACT use in the rural (OR=7.268; p=0.002) and urban areas (0R=6.145; P=0.009). CONCLUSION: Access to behaviour change communication though very high has not achieved the desired behaviour change. The National Malaria Elimination Programme should produce appropriate messages to address barriers to LLIN and ACT use.

The cardiac-enriched microprotein mitolamban regulates mitochondrial respiratory complex assembly and function in mice.

Emerging evidence indicates that a subset of RNA molecules annotated as noncoding contain short open reading frames that code for small functional proteins called microproteins, which have largely been overlooked due to their small size. To search for cardiac-expressed microproteins, we used a comparative genomics approach and identified mitolamban (Mtlbn) as a highly conserved 47-amino acid transmembrane protein that is abundantly expressed in the heart. Mtlbn localizes specifically to the inner mitochondrial membrane where it interacts with subunits of complex III of the electron transport chain and with mitochondrial respiratory supercomplexes. Genetic deletion of Mtlbn in mice altered complex III assembly dynamics and reduced complex III activity. Unbiased metabolomic analysis of heart tissue from Mtlbn knockout mice further revealed an altered metabolite profile consistent with deficiencies in complex III activity. Cardiac-specific Mtlbn overexpression in transgenic (TG) mice induced cardiomyopathy with histological, biochemical, and ultrastructural pathologic features that contributed to premature death. Metabolomic analysis and biochemical studies indicated that hearts from Mtlbn TG mice exhibited increased oxidative stress and mitochondrial dysfunction. These findings reveal Mtlbn as a cardiac-expressed inner mitochondrial membrane microprotein that contributes to mitochondrial electron transport chain activity through direct association with complex III and the regulation of its assembly and function.

Structure and hydration of polyvinylpyrrolidone-hydrogen peroxide.

The structure of the commercially important polyvinylpyrrolidone-hydrogen peroxide complex can be understood by reference to the co-crystal structure of a hydrogen peroxide complex and its mixed hydrates of a two-monomer unit model compound, bisVP·2H2O2. The mixed hydrates involve selective water substitution into one of the two independent hydrogen peroxide binding sites.

autopsych: An R Shiny tool for the reproducible Rasch analysis, differential item functioning, equating, and examination of group effects.

In this paper, we present autopsych, a novel online tool that allows school assessment experts, test developers, and researchers to perform routine psychometric analyses and equating of student test data and to examine the effect of student demographic and group conditions on student test performance. The app extends current open-source software by providing (1) extensive embedded result narration and summaries for written reports, (2) improved handling of partial credit data via customizable item-person Wright maps, (3) customizable item- and person-flagging systems, (4) item-response theory model constraints and controls, (5) many-facets Rasch analysis to examine item bias, (6) Rasch fixed item equating for mapping student ability across test forms, (7) tabbed spreadsheet outputs and immediate options for secondary data analysis, (8) customizable graphical color schemes, (9) extended ANOVA analysis for examining group differences, and (10) inter-rater reliability analyses for the verifying the consistency of rater scoring systems. We present the app's architecture and functionalities and test its performance with simulated and real-world small-, medium-, and large-scale assessment data. Implications and planned future developments are also discussed.

Mitochondrial fatty acid utilization increases chromatin oxidative stress in cardiomyocytes.

The inability of adult mammalian cardiomyocytes to proliferate underpins the development of heart failure following myocardial injury. Although the newborn mammalian heart can spontaneously regenerate for a short period of time after birth, this ability is lost within the first week after birth in mice, partly due to increased mitochondrial reactive oxygen species (ROS) production which results in oxidative DNA damage and activation of DNA damage response. This increase in ROS levels coincides with a postnatal switch from anaerobic glycolysis to fatty acid (FA) oxidation by cardiac mitochondria. However, to date, a direct link between mitochondrial substrate utilization and oxidative DNA damage is lacking. Here, we generated ROS-sensitive fluorescent sensors targeted to different subnuclear compartments (chromatin, heterochromatin, telomeres, and nuclear lamin) in neonatal rat ventricular cardiomyocytes, which allowed us to determine the spatial localization of ROS in cardiomyocyte nuclei upon manipulation of mitochondrial respiration. Our results demonstrate that FA utilization by the mitochondria induces a significant increase in ROS detection at the chromatin level compared to other nuclear compartments. These results indicate that mitochondrial metabolic perturbations directly alter the nuclear redox status and that the chromatin appears to be particularly sensitive to the prooxidant effect of FA utilization by the mitochondria.

PKM1 Exerts Critical Roles in Cardiac Remodeling Under Pressure Overload in the Heart.

BACKGROUND: Metabolic remodeling precedes most alterations during cardiac hypertrophic growth under hemodynamic stress. The elevation of glucose utilization has been recognized as a hallmark of metabolic remodeling. However, its role in cardiac hypertrophic growth and heart failure in response to pressure overload remains to be fully illustrated. Here, we aimed to dissect the role of cardiac PKM1 (pyruvate kinase muscle isozyme 1) in glucose metabolic regulation and cardiac response under pressure overload. METHODS: Cardiac-specific deletion of PKM1 was achieved by crossing the floxed PKM1 mouse model with the cardiomyocyte-specific Cre transgenic mouse. PKM1 transgenic mice were generated under the control of tetracycline response elements, and cardiac-specific overexpression of PKM1 was induced by doxycycline administration in adult mice. Pressure overload was triggered by transverse aortic constriction. Primary neonatal rat ventricular myocytes were used to dissect molecular mechanisms. Moreover, metabolomics and nuclear magnetic resonance spectroscopy analyses were conducted to determine cardiac metabolic flux in response to pressure overload. RESULTS: We found that PKM1 expression is reduced in failing human and mouse hearts. It is important to note that cardiomyocyte-specific deletion of PKM1 exacerbates cardiac dysfunction and fibrosis in response to pressure overload. Inducible overexpression of PKM1 in cardiomyocytes protects the heart against transverse aortic constriction-induced cardiomyopathy and heart failure. At the mechanistic level, PKM1 is required for the augmentation of glycolytic flux, mitochondrial respiration, and ATP production under pressure overload. Furthermore, deficiency of PKM1 causes a defect in cardiomyocyte growth and a decrease in pyruvate dehydrogenase complex activity at both in vitro and in vivo levels. CONCLUSIONS: These findings suggest that PKM1 plays an essential role in maintaining a homeostatic response in the heart under hemodynamic stress.

g versus c: comparing individual and collective intelligence across two meta-analyses.

Collective intelligence (CI) is said to manifest in a group's domain general mental ability. It can be measured across a battery of group IQ tests and statistically reduced to a latent factor called the "c-factor." Advocates have found the c-factor predicts group performance better than individual IQ. We test this claim by meta-analyzing correlations between the c-factor and nine group performance criterion tasks generated by eight independent samples (N = 857 groups). Results indicated a moderate correlation, r, of .26 (95% CI .10, .40). All but four studies comprising five independent samples (N = 366 groups) failed to control for the intelligence of individual members using individual IQ scores or their statistically reduced equivalent (i.e., the g-factor). A meta-analysis of this subset of studies found the average IQ of the groups' members had little to no correlation with group performance (r = .06, 95% CI -.08, .20). Around 80% of studies did not have enough statistical power to reliably detect correlations between the primary predictor variables and the criterion tasks. Though some of our findings are consistent with claims that a general factor of group performance may exist and relate positively to group performance, limitations suggest alternative explanations cannot be dismissed. We caution against prematurely embracing notions of the c-factor unless it can be independently and robustly replicated and demonstrated to be incrementally valid beyond the g-factor in group performance contexts.