The effects of obesity on venous thromboembolism: A review

Obesity has emerged as a global health issue that is associated with wide spectrum of disorders, including coronary artery disease, diabetes mellitus, hypertension, stroke, and venous thromboembolism (VTE). VTE is one of the most common vascular disorders in the United States and Europe and is associated with significant mortality. Although the association between obesity and VTE appears to be moderate, obesity can interact with other environmental or genetic factors and pose a significantly greater risk of VTE among individuals who are obese and who are exposed simultaneously to several other risk factors for VTE. Therefore, identification of potential interactions between obesity and certain VTE risk factors might offer some critical points for VTE interventions and thus minimize VTE morbidity and mortality among patients who are obese. However, current obesity measurements have limitations and can introduce contradictory results in the outcome of obesity. To overcome these limitations, this review proposes several future directions and suggests some avenues for prevention of VTE associated with obesity as well.

Physiological functions and clinical implications of fibrinogen-like 2:A review

Fibrinogen-like 2(FGL2) encompasses a transmembrane(m FGL2) and a soluble(s FGL2) form with differential tertiary structure and biological activities. Typically, m FGL2 functions as prothrombinase that is capable of initiating coagulation in tissue without activation of the blood clotting cascade, whereas s FGL2 largely acts as an immunosuppressor that can repress proliferation of alloreactive T lymphocytes and maturation of bone marrow dendritic cells. Protein sequences of FGL2 exhibit evolutionary conservation across wide variety of species, especially at the carboxyl terminus that contains fibrinogen related domain(FRED). The FRED of FGL2 confers specificity and complexity in the action of FGL2, including receptor recognition, calcium affiliation, and substrate binding. Constitutive expression of FGL2 during embryogenesis and in mature tissues suggests FGL2 might be physiologically important. However, excessive induction of FGL2 under certain medical conditions(e.g. pathogen invasion) could trigger complement activation, inflammatory response,cellular apoptosis, and immune dysfunctions. On the other hand, complete absence of FGL2 is also detrimental as lack of FGL2 can cause autoimmune glomerulonephritis and acute cellular rejection of xenografts. All these roles involve m FGL2, s FGL2, or their combination. Although it is not clear how m FGL2 is cleaved off its host cells and secreted into the blood, circulating s FGL2 has been found correlated with disease severity and viral loading among patients with human hepatitis B virus or hepatitis C virus infection. Further studies are warranted to understand how FGL2 expression is regulated under physiological and pathological conditions. Even more interesting is to determine whether m FGL2 can fulfill an immunoregulatory role through its FRED at carboxyl end of the molecule and, and vice versa, whether s FGL2 is procoagulant upon binding to a target cell. Knowledge in this area should shed light on development of s FGL2 as an alternative immunosuppressive agent for organ transplantation or as a biomarker for predicting disease progression, monitoring therapeutic effects, and targeting FGL2 for repression in ameliorating fulminant viral hepatitis.

Are neonatal morbidities associated with no prenatal care different from those associated with inadequate prenatal care?

Objective: Compare neonatal morbidities in women with no prenatal care, and women with inadequate prenatal care, to those with adequate prenatal care. Methods: Retrospective cohort study of neonatal morbidities of 3 exposure groups. Group 1: No prenatal care;Group 2: Inadequate prenatal care;Group 3: Intermediate/adequate prenatal care. Results: 2.5%, 23.3% and 74.1% of subjects (N = 264,138) were in Groups 1, 2 and 3 respectively. Severe neonatal morbidity was more common in Group 1, followed by Group 2, and least common in Group 3. After controlling for gestational age and birth weight, most of these differences were attenuated and not significant except for the following Group 1 vs Group 3 comparisons: meconium aspiration, odds ratio (OR) 2.15 and 95% confidence interval (CI) 1.39 - 3.33;suspected sepsis, OR 1.30 and CI 1.13 - 1.49;proven viral sepsis, OR 2.23 and CI 1.24 - 4.00. Conclusions: Severe neonatal morbidity was most common in those with no prenatal care followed by those with inadequate prenatal care. For most neonatal morbidities, this could largely be explained by gestational age and birth weight differences, but for some neonatal morbidities (meconium aspirations, viral sepsis and dysmorphic features) the impact of no prenatal care persisted after adjustment for these factors.