Background: and Purpose Guillain–Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS. Methods: This study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects. The demographic and clinical features at entry were collected. The serum levels of the SAA isoforms SAA1, SAA2, and SAA4 were determined in the patients with GBS and the controls using the enzyme-linked immunosorbent assay and analyzed for the associations between levels of different SAA isoforms and the clinical features of the patients. Results: The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (p<0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (p=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (p>0.05 for all). Conclusions Increased levels of SAA2 and SAA4 may only represent the acute inflammatory status and so cannot be utilized as biomarkers of the disease severity or demyelinating injury in patients with GBS.

Background: and Purpose Guillain–Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS. Methods: This study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects. The demographic and clinical features at entry were collected. The serum levels of the SAA isoforms SAA1, SAA2, and SAA4 were determined in the patients with GBS and the controls using the enzyme-linked immunosorbent assay and analyzed for the associations between levels of different SAA isoforms and the clinical features of the patients. Results: The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (p<0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (p=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (p>0.05 for all). Conclusions Increased levels of SAA2 and SAA4 may only represent the acute inflammatory status and so cannot be utilized as biomarkers of the disease severity or demyelinating injury in patients with GBS.

Background: and Purpose Guillain–Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by demyelinating or axonal injury of the peripheral nerve. Our aim is to determine whether serum amyloid A (SAA) is a biomarker of demyelinating injury and disease severity in patients with GBS. Methods: This study retrospectively enrolled 40 patients with either the demyelinating or axonal GBS and sex- and age-matched controls with other neurological diseases as well as healthy subjects. The demographic and clinical features at entry were collected. The serum levels of the SAA isoforms SAA1, SAA2, and SAA4 were determined in the patients with GBS and the controls using the enzyme-linked immunosorbent assay and analyzed for the associations between levels of different SAA isoforms and the clinical features of the patients. Results: The levels of SAA2 and SAA4 were significantly higher in patients with GBS than in both the other neurological disease controls and the healthy subjects (p<0.05 for all). The level of SAA1 did not differ between patients with GBS and the controls. The level of SAA2 was considerably higher in GBS patients with antecedent infection than in those without infection (p=0.020). The levels of different SAA isoforms were not associated with the disease severity or other clinical features of patients with GBS (p>0.05 for all). Conclusions Increased levels of SAA2 and SAA4 may only represent the acute inflammatory status and so cannot be utilized as biomarkers of the disease severity or demyelinating injury in patients with GBS.

Humans ; Tranexamic Acid/therapeutic use* ; Arthroplasty, Replacement, Knee ; Antifibrinolytic Agents/therapeutic use* ; Blood Loss, Surgical ; Postoperative Hemorrhage

BackgroundSibling relationships play a critical role in shaping anxiety symptoms in firstborn children. Anxiety symptoms often originate in early childhood and can persist into adolescence and adulthood. However， there is insufficient research on anxiety symptoms in preschool children， especially firstborn preschool children. ObjectiveTo explore the influencing factors of anxiety symptoms among firstborn preschool children， so as to provide references for the intervention of anxiety symptom for children in families with multiple children. MethodsFrom October to December 2021， a total of 8 449 children from 234 kindergartens in Longhua District of Shenzhen were included using a cluster sampling method. Sibling Inventory of Behavior （SIB） and Spence Preschool Anxiety Scale （SPAS） were used to investigate. Logistic regression analysis was used to identify influencing factors of anxiety symptoms in firstborn preschool children. ResultsA total of 8 419 （99.64%） valid questionnaires were collected. Anxiety symptoms were detected in 344（4.09%） firstborn preschool children. Statistically significant differences were observed between anxiety group and non-anxiety group in terms of household registration， monthly family income， maternal age， maternal education level， paternal education level， family living conditions and whether they are left-behind children （χ²/t=9.906， 33.490， 5.136， 13.485， 9.690， 17.332， 21.975， P<0.05 or 0.01）. Compared with non-anxiety group， children in the anxiety group scored higher on the SIB dimensions of rivalry， aggression and avoidance （t=165.322， 74.471， 286.419， P<0.01）， and lower on companionship， empathy and teaching （t=59.133， 42.417， 39.112， P<0.01）. Risk factors for anxiety symptoms in firstborn preschool children included left-behind children， as well as negative sibling relationships characterized by rivalry and avoidance （OR=1.195， 1.143， 1.260， P<0.05 or 0.01）. ConclusionFirstborn preschool children who are left-behind are more susceptible to anxiety symptoms. Negative sibling relationships， characterized by competition and avoidance， may also contribute to the emergence of anxiety symptoms in firstborn preschool children.

StaphyIococcus caprae is a coagulase-negative staphylococcus which has been originally isolated from goat and has been recognized as an important nosocomial pathogen. A patient with small B-cell lymphoma diagnosed with a brain abscess caused by Staphylococcus caprae infection was described in this paper. His prognosis was still poor after active treatment with meropenem, vancomycin and linezolid. The clinical characteristics of this patient and discussion of the possible pathogenesis were summarized, so as to provide information for clinicians′ understanding of Staphylococcus caprae infection.

Objective To establish a fluorescent assay for rapid detection of Plasmodium falciparum based on recombinaseaided amplification (RAA) and CRISPR-Cas12a system,and to preliminarily evaluate the diagnostic efficiency of this system.. Methods The 18S ribosomal RNA (rRNA) gene of P. falciparum was selected as the target sequence, and three pairs of RAA primers and CRISPR-derived RNA (crRNA) were designed and synthesized. The optimal combination of RAA primers and crRNA was screened and the reaction conditions of the system were optimized to create a fluorescent RAA/CRISPR-Cas12a system. The plasmid containing 18S rRNA gene of the P. falciparum strain 3D7 was generated, and diluted into concentrations of 1 000, 100, 10, 1 copy/μL for the fluorescent RAA/CRISPR-Cas12a assay, and its sensitivity was evaluated. The genomic DNA from P. vivax, P. malariae, P. ovum, hepatitis B virus, human immunodeficiency virus and Treponema pallidum was employed as templates for the fluorescent RAA/CRISPR-Cas12a assay, and its specificity was evaluated. Fifty malaria clinical samples were subjected to the fluorescent RAA/CRISPR-Cas12a assay and nested PCR assay, and the consistency between two assays was compared. In addition, P. falciparum strain 3D7 was cultured in vitro. Then, the culture was diluted into blood samples with parasite densities of 1 000, 500, 200, 50, 10 parasites/μL with healthy volunteers’ O-positive red blood cells for the RAA/CRISPR-Cas12a assay, and the detection efficiency was tested. Results The Pf-F3/Pf-R3/crRNA2 combination, 2.5 μL as the addition amount of B buffer, 40 min as the RAA reaction time, 37 °C as the reaction temperature of the CRISPR-Cas12a system were employed to establish the fluorescent RAA/CRISPR-Cas12a system. Such a system was effective to detect the plasmid containing 18S rRNA gene of the P. falciparum strain 3D7 at a concentration of 1 copy/μL, and presented fluorescent signals for detection of P. falciparum, but failed to detect P. ovum, P. malariae, P. vivax, T. pallidum, hepatitis B virus or human immunodeficiency virus. The fluorescent RAA/CRISPR-Cas12a system and nested PCR assay showed completely consistent results for detection of 50 malaria clinical samples (kappa = 1.0, P < 0.001). Following 6-day in vitro culture of the P. falciparum strain 3D7, 10 mL cultures were generated and the fluorescent RAA/CRISPR-Cas12a system showed the minimal detection limit of 50 parasites/μL. Conclusion The fluorescent RAA/CRISPR-Cas12a system is rapid, sensitive and specific for detection of P. falciparum, which shows promising value for rapid detection and risk monitoring of P. falciparum.

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a chronic autoimmune disease affecting the peripheral nervous system mediated by cellular and humoral immunity, characterized by limb weakness and sensory impairment. The main feature of CIDP by electrophysiological and pathological examinations is the demyelination of peripheral nerves. First-line treatment for CIDP includes glucocorticoids, intravenous immunoglobulins, and plasmapheresis. Some patients respond to current treatment not well and have a poor prognosis. Progress in the pathogenesis, diagnosis, and treatment of CIDP worldwide was reviewed in this article, aiming to provide references for the clinical diagnosis and treatment of CIDP.

Combined central and peripheral demyelination (CCPD) is a rare autoimmune disease and its action mechanism remains unknown. This article described a case of CCPD with anti-neurofascin 155 IgG4 antibodies after varicella-zoster virus (VZV) infection who was recovered after steroids and intravenous immunoglobulin treatments. The clinical characteristics of this patient were summarized and the possible pathogenesis was discussed, so as to provide information of CCPD after VZV infection for clinicians.