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This study investigated the causal relationship between mathematical creativity and mathematical intelligence. Four hundred thirty-nine 8th-grade students, age ranged from 11 to 14 years, were included in the sample of this study by random cluster technique on which mathematical creativity and Hindi adaptation of mathematical intelligence test were administered with 4-month time lag. Cross-lagged panel analysis was used to analyze the data. The uncorrected cross-lagged correlations appeared to show no causal relation between mathematical creativity and mathematical intelligence. But after the correction the difference in the cross-lagged correlations was found to be small and does not give guarantee of unidirectional causal relation between these two constructs. It revealed that there is a mutually reinforcing (symmetric) relationship between mathematical intelligence and mathematical creativity, i.e., mathematical intelligence causes mathematical creativity and vice-versa. [ABSTRACT FROM PUBLISHER]

Cross-lagged panel correlation (CLPC) analysis has been used to identify causal relationships between mathematical creativity and mathematical aptitude. For this study, 480 8th standard students were selected through a random cluster technique from 9 intermediate and high schools of Varanasi, India. Mathematical creativity and mathematical aptitude tests were administered twice, 4 months apart. The CLPC analysis uncovered a significant relationship between mathematical creativity and mathematical aptitude. It appears that mathematical creativity was a cause of mathematical aptitude, rather than the converse (i.e., higher mathematical creativity leading to higher mathematical aptitude). Limitations and future directions are outlined. [ABSTRACT FROM AUTHOR]

The relationship between mathematical creativity (MC) and mathematical problem-solving performance (MP) has often been studied but the causal relation between these two constructs has yet to be clearly reported. The main purpose of this study was to define the causal relationship between MC and MP. Data from a representative sample of 480 eighth-grade students were analysed using a cross-lagged panel correlation (CLPC) design. CLPC attempts to rule out plausible alternative explanation of a causal effect. The result suggests that significant predominant causal relationship was found between MC and MP. It indicates that MP was found to be a cause of MC than the converse. [ABSTRACT FROM PUBLISHER]

Cross-lagged panel analysis is found in the main stream of social, behavioral, medical, business and educational research. It is a form of quasi-experimental design used to determine whether the relationship between two variables is spurious i.e., due to a third variable and not due to causation. Cross-lagged panel analysis is a process used to determine which variable is the cause and which variable is the effect. It is an exploratory method of collecting information at two points in time i.e., time 1 and time 2, to clarify the causal relations between uncontrolled variables which could be tested more rigorously in an experimental setting. The Cross-lagged Panel Correlation (CLPC) is a low power test but better adapted than either multiple regression or factor analysis for answering many questions in longitudinal studies. It captures the dynamic relationship among the variables and allows the model to be controlled over time. This paper focuses on the 2w2v (two wave & two variable) design to describe a research method which can be used to explore the causal predominance relationship in the absence of a true experimental design, but only in a passive manner. [ABSTRACT FROM AUTHOR]

Oxygen-compromised environments, such as high altitude, air travel, and sports, and pathological conditions, such as solid tumors, have been suggested to be prothrombotic. Despite the indispensable role of platelets in thrombus formation, the studies linking hypoxia, platelet reactivity, and thrombus formation are limited. In the present study, platelet proteome/reactivity was analyzed to elucidate the acute hypoxia-induced prothrombotic phenotype. Rats exposed to acute simulated hypoxia (282 torr/8% oxygen) demonstrated a decreased bleeding propensity and increased platelet reactivity. Proteomic analysis of hypoxic platelets revealed 27 differentially expressed proteins, including those involved in coagulation. Among these proteins, calpain small subunit 1, a 28-kDa regulatory component for calpain function, was significantly upregulated under hypoxic conditions. Moreover, intraplatelet Ca2+ level and platelet calpain activity were also found to be in accordance with calpain small subunit 1 expression. The inhibition of calpain activity demonstrated reversal of hypoxia-induced platelet hyperreactivity. The prothrombotic role for calpain was further confirmed by an in vivo model of hypoxia-induced thrombosis. Interestingly, patients who developed thrombosis while at extreme altitude had elevated plasma calpain activities and increased soluble P-selectin level. In summary, this study suggests that augmented calpain activity is associated with increased incidence of thrombosis under hypoxic environments. [ABSTRACT FROM AUTHOR]

Venous malformations are low flow endothelial malformations with aberrant and ectatic venous channels. They are defects in vascular growth which causes functional and cosmetic impairment. Gradual growth in size of the lesion occurs due to venous congestion or thrombosis. Venous malformations in parapharyngeal space are a rare entity and are difficult to diagnose. Case Report. 13 year old boy presented with a history of hyposmia and progressive difficulty in breathing for a duration of 2.5 years. MRI face and neck with contrast showed a 4.5 × 4.3x3.6 cm lesion in the left parapharyngeal space. CT angiogram of brain and neck demonstrated a heterogeneously enhancing mass in the left parapharyngeal region. PET scan illustrated an ill-defined mass in the left pre styloid parapharyngeal space. Biopsy from the lesion showed features consistent with venolymphatic malformation. Flexible laryngoscopy showed a bulge over the left soft palate region with narrowing of nasopharyngeal lumen. Patient underwent transoral robotic surgery for complete excision of the mass. Post-operative period was uneventful. He has been on follow up for the past 1 year with no evidence of any residual or recurrent disease. Venolymphatic malformation is a rare lesion in the parapharyngeal space which is difficult to diagnose pre operatively. Surgical excision is the preferred modality of treatment for deep seated lesions in the parapharyngeal space. The advent of transoral robotic surgery have reduced the morbidity and improved clearance for such cases. [ABSTRACT FROM AUTHOR]

Venous thromboembolism (VTE), caused by altered hemostasis, remains the third most common cause of mortality among all cardiovascular conditions. In addition to established genetic and acquired risk factors, low-oxygen environments also predispose otherwise healthy individuals to VTE. Although disease etiology appears to entail perturbation of hemostasis pathways, the key molecular determinants during immediate early response remain elusive. Using an established model of venous thrombosis, we here show that systemic hypoxia accelerates thromboembolic events, functionally stimulated by the activation of nucleotide binding domain, leucine-rich-containing family, pyrin domain containing 3 (NLRP3) inflammasome complex and increased IL-1β secretion. Interestingly, we also show that the expression of NLRP3 is mediated by hypoxia-inducible factor 1-alpha (HIF-1α) during these conditions. The pharmacological inhibition of caspase-1, in vivo knockdown of NLRP3, or HIF-1α other than IL-1β-neutralizing antibodies attenuated inflammasome activation and curtailed thrombosis under hypoxic conditions. We extend the significance of these preclinical findings by studying modulation of this pathway in patients with altitude-induced venous thrombosis. Our results demonstrate distinctive, increased expression of NLRP3, caspase-1, and IL-1β in individuals with clinically established venous thrombosis. We therefore propose that an early proinflammatory state in the venous milieu, orchestrated by the HIF-induced NLRP3 inflammasome complex, is a key determinant of acute thrombotic events during hypoxic conditions. [ABSTRACT FROM AUTHOR]

Physiological hemostatic balance is a coordinated outcome of counteracting coagulation and fibrinolytic systems. An imbalance of procoagulant and anticoagulant factors may result in life threatening thromboembolism. Presently, anticoagulant administration is the first line of therapy for the treatment of these conditions and several anticoagulants have been approved, including various forms of heparin. However, the polyanionic nature and multispecificity of heparin pose several complications. Generally, the polysulfated compounds with antithrombotic potential are thought to have feasible synthetic procedures with much less bleeding, thus having favourable safety profiles. Here we report the synthesis of a novel compound, trehalose octasulfate and the assessment of its anticoagulation potential. Molecular docking of trehalose and trehalose octasulfate with antithrombin showed a specificity switch in binding affinity on sulfation, where trehalose octasulfate interacts with critical residues of AT that are either directly involved in heparin binding or in the conformational rearrangement of AT on heparin binding. An in vitro analysis of trehalose octasulfate demonstrated prolonged clotting time. Lead compound when intravenously injected in occlusion induced thrombotic rats showed remarkable reduction in the size and weight of the clot at a low dose. Delay in coagulation time was observed by analysing blood plasma isolated from rats preinjected with trehalose octasulfate. A decrease in Adenosine 5′-Diphosphate (ADP) induced platelet aggregation indicated a probable dual anticoagulant and antiplatelet mechanism of action. To summarize, this study presents trehalose octasulfate as a novel, effective, dual acting antithrombotic agent. [ABSTRACT FROM AUTHOR]

The genetic variants linked with the susceptibility of individuals to VTE are well known; however, the studies explaining the ethnicity based difference in susceptibility to VTE are limited. Present study assesses mutations in six candidate genes contributing to the etiology of VTE in Indian subjects. The study comprised 93 VTE patients and 102 healthy controls. A PCRRFLP based analysis was performed for nine mutations in the following genes associated with VTE: favtor V Leiden (FVL), prothrombin, tissue factor pathway inhibitor (TFPI), fibrinogen-beta, plasminogen activator inhibitor 1 (PAI-1), and methylene tetrahydrofolatereductase (MTHFR). All the subjectswere found to bemonomorphic for FVL 1691G/A, prothrombin 20210G/A and TFPI -536C/Tmutations. Themutation in the MTHFR gene (677C/T) was observed only in patients. Contrarily, higher frequency ofmutation in the PAI-1 -844G/A and the fibrinogen-β -455G/Awas observed in controls in comparison to the patients. This study suggests that the PAI-1 -844G/A and fibrinogen-β -455G/A could be protective variants against VTE in Indians. While MTHFR 677C/T mutation was found to be associated, in contrast to other populations, the established genetic variants FVL 1691G/A, prothrombin 20210G/A, and TFPI -536C/T may not be associated with VTE in Indians thus revealing the basis of ethnicity related differences in susceptibility of Indians to VTE. [ABSTRACT FROM AUTHOR]