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Crews Salomonsen posted an update 1 year, 6 months ago
4%). Patients who developed major depression had significantly more depressive symptoms in the acute and subacute stroke phase as assessed by both the PHQ-9 and MADRS. Patients with PHQ-9 scores ≥9 in the acute and subacute stroke phases were significantly more likely to develop major depression in a chronic phase of stroke.
The self-administered PHQ-9 can identify patients in the acute and subacute stroke periods who are at increased risk for developing major depression during the first year after stroke.
The self-administered PHQ-9 can identify patients in the acute and subacute stroke periods who are at increased risk for developing major depression during the first year after stroke.
There are increasing reports about the potential role of kynurenine pathway metabolites in autism spectrum disorder (ASD). Early childhood is a very crucial period of time for the etiopathogenesis of ASD and previous studies reported an age-dependent alteration in kynurenine metabolism. However, no study specifically examined kynurenine metabolites in very young children with ASD. This study aimed to investigate kynurenine pathway metabolite levels, kynurenine pathway enzyme activities and neuroprotective index (kynurenic acid/3-hydroxykynurenine ratio) in toddlers and preschool children with ASD.
A total of 68 children with ASD and 44 healthy controls aged between 18 and 60 months were included in this study. Serum levels of kynurenine pathway metabolites were determined by liquid chromatography-mass spectrometry/mass spectrometry system.
Serum 3-hydroxykynurenine and kynurenic acid concentrations were significantly higher in the ASD group than in the control group, whereas serum 3-hydroxyanthranilic acid concentrations were significantly lower.
These findings showed that the kynurenine pathway may play a role in the etiopathogenesis of ASD in early childhood.
These findings showed that the kynurenine pathway may play a role in the etiopathogenesis of ASD in early childhood.Although relatively few in number compared to astrocytes and neurons, microglia demonstrate multiple, varied neuroimmunological functions in the central nervous system during normal and pathological states. After injury to the brain or spinal cord, microglia express beneficial pro- and anti-inflammatory phenotypes at various stages of recovery. However, prolonged microglial activation following injury has been linked to impaired parenchymal healing and functional restoration. The nature and magnitude of microglial response to injury relates in part to peripheral immune cell invasion, extent of tissue damage, and the local microenvironment.Previous studies have investigated whether migraine is a circulatory disorder, as migraineurs are at heightened risk of cerebrovascular disease. However, in most cases, systemic vascular function was evaluated, which may not reflect abnormalities in the cerebral circulation. Therefore, we aimed to determine whether cerebrovascular function differs between migraineurs and controls. A systematic literature search was conducted across three electronic databases to search for studies that compared cerebrovascular function in migraineurs to controls. Where applicable, meta-analyses were used to determine standardised mean differences (SMD) between migraineurs and controls. Seventy articles were identified, 40 of which contained quantitative data. Meta-analyses showed pulsatility index (PI) was higher (SMD = 0.23; 95%CI = 0.05 to 0.42, P = 0.01) and cerebrovascular responsiveness (CVR) to hypercapnia was lower (SMD=-0.34; 95%CI=-0.67 to -0.01, P = 0.04) in the posterior circulation of migraineurs, particularly those without aura. see more The meta-analyses also indicated that migraineurs have higher resting mean blood flow velocity in both anterior (SMD = 0.14; 95%CI = 0.05 to 0.23, P = 0.003) and posterior circulations (SMD = 0.20; 95%CI = 0.05 to 0.34, P = 0.007). Compared to healthy controls, migraineurs have altered cerebrovascular function, evidenced by elevated PI (representing arterial stiffness) and impaired CVR to hypercapnia (representing cerebral vasodilator function). Future studies should investigate whether improvement of cerebrovascular function is able to alleviate migraine.
To investigate the profiles of anti-RPLP0, anti-galectin3 antibodies, interferon-α (IFN-α), interferon-λ1(IFN-λ1) and interleukin-17A/F(IL-17A/F) in the subtypes of cutaneous lupus erythematosus (CLE) including acute CLE (ACLE), subacute CLE (SCLE) and discoid lupus erythematosus (DLE).
Serum levels of autoantibodies and cytokines were determined by enzyme-linked immunoabsorbent assay (ELISA). Lupus lesions were evaluated by cutaneous lupus erythematosus disease area and severity index (CLASI).
Serum anti-RPLP0, anti-galectin3 antibodies and IFN-λ1 were higher in systemic lupus erythematosus (SLE) patients with skin lesions than those without skin lesions, compared to healthy controls. IFN-α, IL-17A and IL-17F was elevated in all patients regardless of skin lesions. The two antibodies, IFN-α and IL-17A were positively correlated with the CLASI score in all patients with CLE. In addition, serum IL-17A was positively correlated to the CLASI score of ACLE, SCLE and DLE, while anti-RPLP0 and anti-galectin3 antibodies were only correlated to the score of SCLE and IL-17F to DLE.
Serum anti-RPLP0, anti-galectin3 antibodies, IFN-α, IFN-λ1 and IL-17A/F are associated with the occurrence of lupus skin lesions regardless of the systemic complications, whereas the profiles of these inflammatory mediators vary with the subtypes of lupus skin lesions.
Serum anti-RPLP0, anti-galectin3 antibodies, IFN-α, IFN-λ1 and IL-17A/F are associated with the occurrence of lupus skin lesions regardless of the systemic complications, whereas the profiles of these inflammatory mediators vary with the subtypes of lupus skin lesions.Neonatal Antiphospholipid syndrome (APS) is a rare disease related to transplacental passage of antiphospholipid (aPL) antibodies from the mother or de novo production of aPL in a newborn. Neonatal aPL antibodies have rarely been associated with thrombosis. We describe a 5-week-old infant who developed fever, portal vein thrombosis and livedo reticularis like skin rash. Evaluation for thrombosis revealed high titers of antiphospholipid (aPL) antibodies (dual positive) in the child without any evidence of aPL antibodies in the mother, suggesting a de novo production in the child. Autopsy findings revealed umbilical vein sepsis with thrombosis of portal vein secondary to gram positive cocci which led to multiple liver and lung abscesses. Additionally, the baby had disseminated Cytomegalovirus (CMV) disease (acquired postnatally) involving walls of umbilical and portal vein, liver, lungs, adrenals, pancreas, thymus, and kidneys. Our case highlights the need for testing of aPL in every neonate with arterial or venous thrombosis even when the mother may have no features suggestive of an autoimmune disease.
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