A pulsar in a binary with a compact object in the mass gap between neutron stars and black holes.

Some compact objects observed in gravitational wave events have masses in the gap between known neutron stars (NSs) and black holes (BHs). The nature of these mass gap objects is unknown, as is the formation of their host binary systems. We report pulsar timing observations made with the Karoo Array Telescope (MeerKAT) of PSR J0514-4002E, an eccentric binary millisecond pulsar in the globular cluster NGC 1851. We found a total binary mass of 3.887 ± 0.004 solar masses (M⊙), and multiwavelength observations show that the pulsar's binary companion is also a compact object. The companion's mass (2.09 to 2.71 M⊙, 95% confidence interval) is in the mass gap, indicating either a very massive NS or a low-mass BH. We propose that the companion formed in a merger between two earlier NSs.

Measurement of Direct-Photon Cross Section and Double-Helicity Asymmetry at sqrt[s]=510 GeV in p[over →]+p[over →] Collisions.

We present measurements of the cross section and double-helicity asymmetry A_{LL} of direct-photon production in p[over →]+p[over →] collisions at sqrt[s]=510 GeV. The measurements have been performed at midrapidity (|η|<0.25) with the PHENIX detector at the Relativistic Heavy Ion Collider. At relativistic energies, direct photons are dominantly produced from the initial quark-gluon hard scattering and do not interact via the strong force at leading order. Therefore, at sqrt[s]=510 GeV, where leading-order-effects dominate, these measurements provide clean and direct access to the gluon helicity in the polarized proton in the gluon-momentum-fraction range 0.02

Chondroitin Sulfate Enhances Proliferation and Migration via Inducing ß-Catenin and Intracellular ROS as Well as Suppressing Metalloproteinases through Akt/NF-κB Pathway Inhibition in Human Chondrocytes.

BACKGROUND: Chondroitin sulfate (CS) is found in humans' cartilage, bone, cornea, skin, and arterial wall. It consists of the foundation substance in the extracellular matrix (ECM) of connective tissue. The oral supplement form of CS is clinically used in treating osteoarthritis (OA). METHODS: Cell migration was observed by the transwell assay. The EMT, Akt/IKK/IκB pathways, TIMPs, collagen and MMPs in cell lysate were determined by Western blotting. The expression of MMP activity was determined by gelatin zymography. The production of reactive oxygen species (ROS) was determined by using a fluorescence spectrophotometer. RESULTS: In the current report, we demonstrated that CS can increase the cell proliferation and migration of chon-001 chondrocytes. Treatment with CS induced the epithelial-mesenchymal transition and increased the expression of type II collagen and TIMP-1/TIMP2 and inhibited the expressions and activities of metalloproteinase-9 (MMP-9) and metalloproteinase-2 (MMP-2). The phosphorylation of Akt, IκB kinase (IKK), IκB and p65 was decreased by CS. CS treatment resulted in ß-catenin production and XAV939, a ß-catenin inhibitor, and inhibited the cell proliferation by CS treatment. In addition, also significantly induced intracellular ROS generation. Treatment with antioxidant propyl gallate blocked cell migration induced by CS. CONCLUSION: We demonstrated that CS induced cell proliferation and migration of chondrocytes by inducing ß-catenin and enhancing ROS production. Moreover, our studies demonstrated that CS can increase the activity of chondrocytes and help patients with osteoarthritis to restore cartilage function.

Intravenous tissue plasminogen activator for acute ischemic stroke in patients with renal dysfunction.

OBJECTIVE: This study used the Taiwan Stroke Registry data to evaluate the efficacy and safety of intravenous tissue plasminogen activator (tPA) in treating acute ischemic stroke in patients with renal dysfunction. DESIGN: We identified 3525 ischemic stroke patients and classified them into two groups according to the estimated glomerular filtration rate (eGFR) at the emergency department: ≥60, and <60 ml/min/1.73 m2 or on dialysis and by the propensity score from August 2006 to May 2015. The odds ratio of poor functional outcome (modified Rankin Scale ≥2) was calculated for patients with tPA treatment (N = 705), compared to those without tPA treatment (N = 2820), by eGFR levels, at 1, 3 and 6 months after ischemic stroke. We also evaluated the risks of intracerebral hemorrhage, upper gastrointestinal bleeding, mortality, between the two groups by eGFR levels. RESULTS: Among patients with eGFR levels of <60 ml/min/1.73 m2, tPA therapy reduced the odds ratio of poor functional outcome to 0.60 (95% confidence interval = 0.42-0.87) at 6 months after ischemic stroke. The tPA therapy was not associated with increased overall risk of upper gastrointestinal bleeding, but with increased risk of intracerebral hemorrhage. The low eGFR was not a significant risk factor of intracerebral hemorrhage among ischemic stroke patients receiving tPA treatment. CONCLUSIONS: tPA for acute ischemic stroke could improve functional outcomes without increasing the risks of upper gastrointestinal bleeding for patients with or without renal dysfunction. The low eGFR was not a significant risk factor for intracerebral hemorrhage among patients receiving tPA treatment.

Protein kinase C signalling involved in prothoracicotropic hormone-stimulated prothoracic glands in the silkworm, Bombyx mori.

In the present study, the participation of protein kinase C (PKC) signalling in prothoracicotropic hormone (PTTH)-stimulated ecdysteroidogenesis in Bombyx prothoracic glands (PGs) is demonstrated and characterized. PTTH stimulated phosphorylation of a 37-kDa protein in Bombyx PGs both in vitro and in vivo, as recognized by a PKC substrate antibody. Treatment with either A23187 or thapsigargin also stimulated this 37-kDa protein phosphorylation. PTTH-stimulated phosphorylation of the 37-kDa protein was markedly attenuated in the absence of Ca2+ . The phospholipase C (PLC) inhibitor, U73122, greatly inhibited PTTH-stimulated phosphorylation of this protein, indicating the involvement of Ca2+ and PLC. A mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase (MEK) inhibitor (U0126), a phosphoinositide 3-kinase (PI3K) inhibitor (LY294002) and a chemical activator of adenosine 5'-monophosphate-activated protein kinase (AMPK) (5-aminoimidazole-4-carboxamide-1-ß-d-ribofuranoside) did not affect PTTH-stimulated phosphorylation of the 37-kDa protein, implying that ERK and PI3K/AMPK are not the upstream signalling pathways for PKC-dependent protein phosphorylation. The mitochondrial oxidative phosphorylation inhibitors (the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone and diphenylene iodonium) inhibited PTTH-stimulated phosphorylation of the 37-kDa protein, indicating its redox regulation. Treatment with PKC inhibitors (either calphostin C, chelerythrine C or rottlerin) reduced PTTH-stimulated phosphorylation of the 37-kDa protein. PTTH-stimulated ecdysteroidogenesis was also inhibited by treatment with rottlerin, thus further confirming participation of PKC-dependent phosphorylation in PTTH signalling. From these results, we demonstrated that redox-regulated PTTH-stimulated PKC signalling is involved in ecdysteroid secretion in Bombyx PGs.

Involvement of RSK phosphorylation in PTTH-stimulated ecdysone secretion in prothoracic glands of the silkworm, Bombyx mori.

It is well known that phosphorylation of extracellular signal-regulated kinase (ERK) is involved in prothoracicotropic hormone (PTTH)-stimulated ecdysteroidogenesis in insect prothoracic glands (PGs). In the present study, we further investigated the downstream signalling pathways. Our results showed that PTTH stimulated p90 ribosomal S6 kinase (RSK) phosphorylation at Thr573 in Bombyx mori PGs both in vitro and in vivo. The in vitro PTTH stimulation was stage- and dose-dependent. The absence of Ca2+ reduced PTTH-stimulated RSK phosphorylation. Stimulation of RSK phosphorylation was also observed after treatment with either A23187 or thapsigargin. A phospholipase C (PLC) inhibitor, U73122, blocked PTTH-stimulated RSK phosphorylation. These results indicate the involvement of Ca2+ and PLC. Treatment with diphenylene iodonium (DPI), a mitochondrial oxidative phosphorylation inhibitor, blocked PTTH-regulated RSK phosphorylation, indicating its redox regulation. A mitogen-activated protein kinase (MAPK)/ERK kinase (MEK) inhibitor, U0126, but not a phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, decreased PTTH-stimulated RSK phosphorylation, indicating that ERK is an upstream signalling. A protein kinase C (PKC) inhibitor, chelerythrine C, inhibited PTTH-stimulated RSK phosphorylation, and a PKC activator, phorbol 12-myristate acetate (PMA) stimulated RSK phosphorylation, indicating the involvement of PKC. BI-D1870, a specific RSK inhibitor, partly prevented PTTH-stimulated RSK phosphorylation and significantly inhibited PTTH-stimulated ecdysteroid secretion, indicating that PTTH-stimulated RSK phosphorylation is involved in ecdysteroidogenesis. Taken together, these data indicate that PTTH activates RSK phosphorylation which plays important roles in PTTH-stimulated ecdysteroidogenesis.

To safely reopen after a lockdown, masks are crucial: lessons from Taiwan.

Taiwan had been using many important public health management strategies to beat Coronavirus disease 2019 (COVID-19) without a lockdown. Mask wearing by the general public was thought to be the major factor for the success of Taiwan to stop the spread of COVID-19. We share our experience in Taiwan as an example for other countries to safely reopen from a lockdown.

Knowledge, attitudes and practices of neonatal professionals regarding pain management.

Pain management is an important issue which impacts the prognosis of neonates in neonatal intensive care units. Evidence has shown that professionals' knowledge and attitudes regarding pain management can impact the quality of their practice. The purpose of this study was to evaluate the knowledge, attitudes, and practices of neonatal professionals regarding neonatal pain management. A cross-sectional study was performed involving neonatal physicians and nurses, using a research questionnaire to investigate the knowledge and attitudes of professionals as well as to assess their practice of pain management. Research found an apparent discrepancy between the knowledge levels of neonatologists and nurses regarding pain assessment and management, with nurses displaying weaker professional knowledge and more negative attitudes toward pain management than did neonatologists. Additionally, research revealed a lack of knowledge and negative attitudes among participants regarding the provision of sufficient opioid analgesics to sick infants during invasive procedures and even for dying neonates. There is an urgent need for continuing education regarding neonatal pain management with the goal of empowering neonatal professionals; further research is needed into the question of how to translate education into more reliable practice.Conclusion: This research provides useful information regarding the knowledge, attitudes, and clinical practice of neonatal pain management among neonatologists and nurses and points out some differences in the knowledge levels of these two groups. What is Known: •Neonates can perceive and respond to pain stimuli by showing their biological signals similarly to children and adults. •Untreated or insufficient pain management for high-risk neonates has short-term. negative effects and may also induce long-term negative effects. What is New: •The level of knowledge, the attitudes, and the practices regarding neonatal pain in intensive care are different among neonatal professionals. •There is an urgent need to provide interdisciplinary continuing education to improve the knowledge of neonatal professionals and encourage them to more highly prioritize neonatal pain management.

MiR-155 affects proliferation and apoptosis of bladder cancer cells by regulating GSK-3ß/ß-catenin pathway.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "MiR-155 affects proliferation and apoptosis of bladder cancer cells by regulating GSK-3ß/ß-catenin pathway, by Z.-C. Dong, D. Zhang, X.-X. Zhang, Z.-Q. Yao, H. Wu, C.-H. Chen, J.-Q. Tian, published in Eur Rev Med Pharmacol Sci 2019; 23 (13): 5682-5690-DOI: 10.26355/eurrev_201907_18305-PMID: 31298320" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18305.

Circular RNA ZNF292 affects proliferation and apoptosis of hepatocellular carcinoma cells by regulating Wnt/ß-catenin pathway.

OBJECTIVE: The purpose of this study was to explore the function of circular ribonucleic acid (circRNA) zinc finger protein 292 (ZNF292) in hepatocellular carcinoma (HCC). MATERIALS AND METHODS: The expression of circRNA ZNF292 in Huh-7 cells was knocked down by small interfering RNAs (siRNAs), and the effect of circRNA ZNF292 knockdown on the proliferation of Huh-7 cells was analyzed by Cell Counting Kit-8 (CCK-8) assay and colony formation assay. Then, flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) were adopted to analyze the impacts of circRNA ZNF292 knockdown on the cycle distribution and apoptosis of Huh-7 cells. Besides, the influences of circRNA ZNF292 knockdown on Wnt/ß-catenin signaling pathway and its downstream molecules were detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting. RESULTS: Compared with those in siRNA-normal control (NC) group, the proliferation of Huh-7 cells was significantly inhibited and their cloning ability was remarkably weakened (p<0.05), the proportion of cells in S phase was decreased while that in G1 phase was increased (p<0.05), the apoptosis rate of Huh-7 cells was higher and the number of apoptosis was larger in siRNA-2# knockdown group (p<0.05). Besides, in Huh-7 cells with circRNA ZNF292 knockdown, the expressions of Axin, ß-catenin, phosphorylated signal transducer and activator of transcription 3 (p-STAT3), p-STAT5, Cyclin A and Cyclin-dependent kinase 2 (CDK2) were down-regulated, while the expressions of STAT3 and STAT5 did not change remarkably. CONCLUSIONS: Knock downing circRNA ZNF292 leads to cell cycle arrest in G1 phase, thus suppressing cell proliferation and promoting cell apoptosis. The regulatory mechanism of circRNA ZNF292 may involve the regulation of cell cycle and related genes.

Erratum: Evolution of π

This corrects the article DOI: 10.1103/PhysRevLett.109.152301.

Insulin enhances and metformin reduces risk of colorectal carcinoma in type-2 diabetes.

BACKGROUND: Identifying colorectal cancer associated risks is important for conducting a program for the survey and prevention of colorectal cancer. AIM: To investigate the association between use of insulin or metformin with colorectal cancer (CRC) in type 2 diabetes (T2DM). DESIGN: Population-based cohort study. METHODS: Through analysis of National Health Insurance (NHI) database between 1998 and 2010 in Taiwan, we identified 66 324 T2DM patients aged ≥ 20 years and selected subjects without diabetes by 1: 1 randomly matching with the study cohort based on age, sex and index date. We followed up the participants until 31 December 2011 or when they withdrew from the NHI program. RESULTS: Compared with non-diabetic subjects, the T2DM patients exhibited an increased risk of CRC [adjusted HR (aHR) = 1.56, 95% confidence interval (CI) = 1.39-1.75], after adjustment for age, sex, urbanization level, comorbidities and examinations of colonoscopy, sigmoidoscopy, or stool occult blood test. Among the T2DM patients, insulin usage increased the risk of CRC (aHR = 1.86, 95% CI = 1.58-0-2.19) after adjustment for age, sex, urbanization level, comorbidities, metformin usage and examinations; nevertheless, metformin decreased the risk of CRC (aHR = 0.65, 95% CI = 0.54-0.77) after adjustment for age, sex, urbanization level, comorbidities, insulin usage and examinations. Compared with the non-insulin cohort, the risk of CRC tended to increase with the incremental dosage of insulin exposure. CONCLUSION: Our population-based cohort study demonstrated an association between T2DM and CRC. Among the T2DM patients, insulin use was associated with an increased risk of CRC and metformin use was associated with a decreased risk of CRC. Inability to obtain information on several potential confounding factors, such as lifestyle and dietary habits, is the major limitation of the study.

Limb salvage in antiphospholipid syndrome with repetitive arterial occlusions.

Outcomes of vascular surgery for patients with primary antiphospholipid syndrome (APS) presenting with acute limb ischaemia (ALI) are poor, with a high rate of postoperative arterial thrombosis and limb amputation. A primary antiphospholipid syndrome 42-year-old male patient presented with acute limb ischaemia. Timely endovascular thrombectomy successfully prevented irreversible tissue damage but failed to maintain this due to recurrent thrombosis. Intensive plasma exchange following repeated endovascular therapy (EVT) ameliorated this thrombotic event. Two weeks post-discharge, thrombotic arterial reocclusion led to readmission and repeated management. Following successful reperfusion, intensive immunosuppressive therapy and anticoagulant agents ensured that the patient was free from recurrent events during the next eight months. This case highlights the combination of endovascular thrombectomy and intensive plasma exchange for limb salvage in such cases.

STAT3-induced upregulation of lncRNA DUXAP8 functions as ceRNA for miR-577 to promote the migration and invasion in colorectal cancer through the regulation of RAB14.

OBJECTIVE: Previous reports have shown that long non-coding RNAs (lncRNAs) are involved in a series of biological processes and cancer in humans. Recently, lncRNA double homeobox A pseudogene 8 (DUXAP8) was frequently reported to be aberrantly expressed in multiple cancers and play a functional role. However, the exact expression, function, and mechanism of DUXAP8 in colorectal cancer (CRC) remain uncovered. PATIENTS AND METHODS: The expression levels of DUXAP8 were detected by Reverse Transcription-Polymerase Chain Reaction (RT-PCR). The clinical influence of DUXAP8 in HCC patients was statistically analyzed. Luciferase reporter and ChIP assays were carried out for the exploration of whether STAT3 was able to bind to the promoter of DUXAP8. Lost-of-function experiments were carried out for the determination of possible cellular function in CRC cells. The modulating associations between DUXAP8 and miR-577 and RAB14 were further studied in CRC cells. RESULTS: In this study, we first provided evidence that DUXAP8 was overexpressed in CRC and increasing expression of DUXAP8 indicates advanced clinical progression and poor survival of CRC patients. Then, transcription factor STAT3 was demonstrated to upregulate DUXAP8 in CRC cells. Functional assays via in vitro assays revealed that DUXAP8 knockdown through shRNA in HCT116 and LOVO cells inhibited cell proliferation, migration and invasion, and promoted apoptosis. Furthermore, an inverse relationship between DUXAP8 and miR-577 was found. In addition, we confirmed that DUXAP8 served as competing endogenous RNA to modulate miR-577, which can modulate RAB14, a well-studied oncogene. CONCLUSIONS: Our study revealed that the STAT3-induced up-regulation of DUXAP8 might provide a new perspective for CRC therapy.

MiR-155 affects proliferation and apoptosis of bladder cancer cells by regulating GSK-3ß/ß-catenin pathway.

OBJECTIVE: GSK-3ß negatively regulates Wnt/ß-catenin signaling pathway. The abnormal miR-155 expression is associated with bladder cancer. Bioinformatics analysis revealed a complementary binding site between miR-155 and GSK-3ß mRNA. This study investigated the role of miR-155 in the proliferation and apoptosis of bladder cancer cells. PATIENTS AND METHODS: The dual luciferase reporter gene assay validated the targeted regulation between miR-155 and GSK-3ß. Tumor tissues and adjacent tissues were collected from bladder cancer patients and the expression of miR-155 and GSK-3ß mRNA was detected by RT-PCR. Bladder cancer cell line BIU-87 cells were cultured in vitro and divided into miR-NC group and miR-155 inhibitor group. The expressions of miR-155, GSK-3ß and ß-catenin were compared, cell apoptosis was detected by flow cytometry, and cell proliferation was detected by EdU staining. RESULTS: Compared with adjacent tissues, miR-155 expression was significantly increased in bladder cancer tissues, and GSK-3ß mRNA expression was significantly decreased. There was a targeted regulatory relationship between miR-155 and GSK-3ß. Compared with SV-HUC-1 cells, miR-155 expression in bladder cancer BIU-87 and 5637 cells was significantly increased, and GSK-3ß expression was significantly decreased. Transfection of miR-155 inhibitor significantly increased GSK-3ß expression in BIU-87 and 5637 cells, decreased ß-catenin expression, increased cell apoptosis, and decreased cell proliferation. CONCLUSIONS: The increased expression of miR-155 plays a role in reducing the expression of GSK-3ß and in promoting the pathogenesis of bladder cancer. Inhibition of miR-155 can up-regulate the expression of GSK-3ß, inhibit the activity of Wnt/ß-catenin pathway, attenuate proliferation and promote apoptosis of bladder cancer cells.

Effects of miR-221 on the apoptosis of non-small cell lung cancer cells by lncRNA HOTAIR.

OBJECTIVE: The aim of this study was to investigate the effects of miR-221 on the proliferation of non-small cell lung cancer (NSCLC) cells through long non-coding RNA (lncRNA) HOX transcript antisense RNA (HO-TAIR), and to explore the possible underlying mechanism. PATIENTS AND METHODS: Reverse Transcription-Polymerase Chain Reaction (RT-PCR) was applied to detect the expression level of HOTAIR in 38 NSCLC patients. The correlations of HOTAIR expression with clinic-pathological features, as well as the correlation between HOTAIR expression and miR-221 expression was analyzed by RT-PCR. Furthermore, NSCLC cell lines were cultured in vitro, and the expressions of HOTAIR and miR-221 in NSCLC cells were also detected. A549 cells were transfected with miR-221 mimics, miR-221 inhibitors, HOTAIR-small interfering RNAs (siRNAs) and plasmid cytomegalovirus deoxyribonucleic acid (pcDNA)3.1-HOTAIR. The interaction between miR-221 and HOTAIR in transfected cells was analyzed via RT-PCR and Northern blotting. Ultimately, flow cytometry was adopted to analyze the effects of miR-221 on the apoptosis of NSCLC cells through HOTAIR. RESULTS: The expression of HOTAIR in tissues of clinical patients only exhibited a correlation with the stage of cancer. The expressions of HOTAIR in patients with stage I and II were remarkably lower than those with stage III and IV. Additionally, the expression of HOTAIR was negatively correlated with the expression of miR-221 (r=-0.7651, p<0.0001). Further studies revealed that there was a negatively regulatory interaction between miR-221 expression and HOTAIR expression. Apoptosis assay results manifested that miR-221 significantly promoted the apoptosis of NSCLC cells by negatively regulating HOTAIR expression. CONCLUSIONS: MiR-221 promotes the apoptosis of NSCLC cells through negative regulation of lncRNA HOTAIR, which can be used in the treatment of NSCLC.

Overexpression of lncRNA GAS5 attenuates cardiac fibrosis through regulating PTEN/MMP-2 signal pathway in mice.

OBJECTIVE: The present study aimed at investigating the effect and mechanism of lncRNA Growth Arrest-Specific 5 (GAS5) in cardiac fibrosis induced by isoproterenol (ISO) in vivo. MATERIALS AND METHODS: The C57BL/6 mice were injected subcutaneously with ISO to induce cardiac fibrosis and injected intracoronary with lentivirus pcDNA-GAS5. After 3 weeks, cardiac function was detected by echocardiography. The interstitial collagen volume was stained by Masson trichrome. The expression of GAS5 was measured by Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR). The expressions of phosphatase and tensin homologue (PTEN), matrix metalloprotease-2 (MMP-2), α-smooth muscle actin (α-SMA), and collagen I protein were measured by Western blot. RESULTS: Our results indicated that the expression of GAS5 was significantly down-regulated in the fibrotic myocardium. Overexpression of GAS5 after injection with pcDNA-GAS5 could attenuate cardiac fibrosis and improve cardiac function through increasing the expression of PTEN and decreasing the expression of MMP-2, α-SMA, and collagen I. CONCLUSIONS: Overexpression of GAS5 could attenuate cardiac fibrosis induced by ISO. The molecular mechanism was associated with the regulation of PTEN/MMP-2 signaling pathway.

Chondrosarcoma in a paediatric population: a study of 247 cases.

PURPOSE: The aims of present study are to clarify the follow questions: 1) what constitutes paediatric chondrosarcoma?; 2) what are the effects of the demographic and tumour characteristics on survival in patients with paediatric chondrosarcoma?; 3) which prognostic factors of paediatric chondrosarcoma differ from those of the adult population, which have been reported previously? METHODS: Paediatric patients who were diagnosed with chondrosarcoma were searched for using the case listing session protocol of the National Cancer Institute's Surveillance, Epidemiology, and End Results 18 databases (1973 to 2014). The extracted demographic information includes: age, race, gender, year of diagnosis, tumour sites, tumour histological subtype, grade, stage and treatment. RESULTS: A total of 247 paediatric chondrosarcoma patients were extracted and included in our present study. We find that the paediatric patients have significantly better survival rates than the adult patients. The year of diagnosis, tumour sites, tumour histological subtype, grade, stage and surgery received are independent prognostic factors for the survival rate of paediatric chondrosarcoma patients, but race, gender and age are not. CONCLUSION: The paediatric chondrosarcoma patients have better survival rates than the adults. Paediatric patients with a diagnosis at an early age, tumour site at the vertebral column and pelvis/sacrococcyx, myxoid variants, high grade, distant stage and who did not have surgery have a poorer prognosis than patients with a diagnosis at a later age, tumour site at limbs, head and base, chondrosarcoma not otherwise specified, lower grade, localized stage and who received surgery. LEVEL OF EVIDENCE: II -Prognostic Study.

Polygenic risk for psychiatric disorders correlates with executive function in typical development.

Executive functions are a diverse and critical suite of cognitive abilities that are often disrupted in individuals with psychiatric disorders. Despite their moderate to high heritability, little is known about the molecular genetic factors that contribute to variability in executive functions and how these factors may be related to those that predispose to psychiatric disorders. We examined the relationship between polygenic risk scores built from large genome-wide association studies of psychiatric disorders and executive functioning in typically developing children. In our discovery sample (N = 417), consistent with previous reports on general cognitive abilities, polygenic risk for autism spectrum disorder was associated with better performance on the Dimensional Change Card Sort test from the NIH Cognition Toolbox, with the largest effect in the youngest children. Polygenic risk for major depressive disorder was associated with poorer performance on the Flanker test in the same sample. This second association replicated for performance on the Penn Conditional Exclusion Test in an independent cohort (N = 3681). Our results suggest that the molecular genetic factors contributing to variability in executive function during typical development are at least partially overlapping with those associated with psychiatric disorders, although larger studies and further replication are needed.