BackgroundBecause the outcomes and sequelae after different types of brain injury (BI) are variable and difficult to predict, investigations on whether enhanced expressions of BI-associated biomarkers (BIABs), including transforming growth factor β1 (TGF-β1), S100B, glial fibrillary acidic protein (GFAP), neurofilament light chain (NF-L), tissue transglutaminases (tTGs), β-amyloid precursor proteins (AβPP), and tau are present as well as whether impairment of the ubiquitin-proteasome system (UPS) is present have been widely used to help delineate pathophysiological mechanisms in various BIs. Larvae of Toxocara canis can invade the brain and cause BI in humans and mice, leading to cerebral toxocariasis (CT). Because the parasitic burden is light in CT, it may be too cryptic to be detected in humans, making it difficult to clearly understand the pathogenesis of subtle BI in CT. Since the pathogenesis of murine toxocariasis is very similar to that in humans, it appears appropriate to use a murine model to investigate the pathogenesis of CT.MethodsBIAB expressions and UPS function in the brains of mice inoculated with a single dose of 250 T. canis embryonated eggs was investigated from 3 days (dpi) to 8 weeks post-infection (wpi) by Western blotting and RT-PCR.ResultsResults revealed that at 4 and 8 wpi, T. canis larvae were found to have invaded areas around the choroid plexus but without eliciting leukocyte infiltration in brains of infected mice; nevertheless, astrogliosis, an indicator of BI, with 78.9~142.0-fold increases in GFAP expression was present. Meanwhile, markedly increased levels of other BIAB proteins including TGF-β1, S100B, NF-L, tTG, AβPP, and tau, with increases ranging 2.0~12.0-fold were found, although their corresponding mRNA expressions were not found to be present at 8 wpi. Concomitantly, UPS impairment was evidenced by the overexpression of conjugated ubiquitin and ubiquitin in the brain.ConclusionFurther studies are needed to determine whether there is an increased risk of CT progression into neurodegenerative disease because neurodegeneration-associated AβPP and phosphorylated tau emerged in the brain.

No abstract

SUMMARY Infection by Toxocara canis in humans may cause cerebral toxocariasis (CT). Appreciable numbers of T. canis larvae cross the blood–brain barrier (BBB) to invade the brain thus causing CT. In the present studies, we evaluated the BBB permeability and BBB injury as assessed by the cerebral Evans blue (EB) concentration as well as by pathological changes and glial fibrillary acidic protein (GFAP) expression in T. canis‐infected mice monitored from 3 days (dpi) to 8 weeks post‐infection (wpi). The vasodilation neuropeptides, the expressions of substance P (SP) and its preferred binding neurokinin‐1 receptor (NK‐1R) as well as claudin‐5 of tight‐junction proteins associated with BBB impairment were also assessed by Western blotting and reverse‐transcriptase polymerase chain reaction. Results revealed that BBB permeability increased as evidenced by a significantly elevated EB concentration in brains of infected mice. BBB injury appeared due to enhanced GFAP protein and mRNA expressions from 4 to 8 wpi. Leukocytes might have been unrelated to BBB impairment because there was no inflammatory cell infiltration despite T. canis larvae having invaded the brain; whereas markedly elevated SP protein and NK‐1R mRNA expressions concomitant with enhanced claudin‐5 expression seemed to be associated with persistent BBB impairment in this experimental CT model.

A sero-epidemiological study of Toxocara canis infection was conducted among Atayal schoolchildren (aged 7-12 years) residing in the mountainous areas of north-eastern Taiwan. The 73 children investigated were each checked for anti-Toxocara IgG, in ELISA based on the larval excretory-secretory antigens of T. canis larvae. A short, self-administered questionnaire was then used to collect relevant information from each subject, including data on the keeping of dogs, playing in soil, eating raw vegetables, and whether the subjects normally washed their hands before eating. Once the seropositive children had been identified, odds ratios (OR), with their corresponding 95% confidence intervals (CI) and P-values, were calculated for each potential risk factor. When diluted 1:64, sera from 42 (57.5%) of the children gave a positive result in the ELISA, indicating that these 42 children were seropositive for T. canis infection. Seropositivity did not appear to be associated with the age or gender of the subject, the eating of raw vegetables, or the regular failure to wash hands prior to a meal. Compared with the other subjects, however, those who admitted living in a household where dogs were kept (OR = 3.79; CI = 1.23-11.69; P = 0.02) or playing in soil (OR = 3.00; CI = 1.10-8.16; P = 0.03) appeared at increased risk of seropositivity.

InrodudionVital statistics data is a readily available source of information on prenatal care usage in the United States. How to examine vital statistics and other types of data for the effect ofprenatal care on pregnancy outcome has generated a number of different methodologies.1-4 One of the difficulties encountered in using such data has been the problem of overcoming the preterm bias effect. The preterm bias effect is associated with observing better outcomes in women who receive prenatal care than in women who receive no care. This artifact occurs because women receiving no care may deliver prematurely and may not have an opportunity to enroll in prenatal care.5 By conditioning the effect of the age of entry into prenatal care on the gestational age of delivery, however, the preterm bias effect can be avoided. Nonetheless, other problems encountered in vital statistics data may invalidate the results of the conditional approach.In this study, we demonstrate the effect that the possible misclassification of gestational age in vital statistics data has on the interpretation of the conditional approach and discuss the problematic nature of the evaluation of prenatal care.Metods justed analyses and 374 244 (96.7%) were used for the adjusted analyses.The association of the gestational age of entry into prenatal care with pregnancy outcome was examined relative to the gestational age of delivery. Outcomes (stillbirths or infant deaths) are presented as death rates (percentage dead). We calculated odds ratios for stillbirths or infant deaths by logistic regression models adjusted for race (Black vs non-Black), multiple births (multiple vs single), (0 parity and parity greater than 3 compared with parity 1 through 3), maternal age (less than 18 and greater than 34 compared with 18 through 34 years), and matemal education (less than 12 compared with greater than 12 years). Mantel-Haenszel tests for linear trends were carried out for mortality rates over the gestational ages of entry into prenatal care.6 Furthermore, we adjusted our results by declaring newborns that exceeded the 90th percentile birth-weight standards for gestational age reported by Arbuckle7 as misclassified.All computations were carried out using SAS@88 ResultsBy conditional analysis, the risk (percentage of mortality) of stillbirth or infant death for those women who delivered at 25 weeks to 28 weeks ofgestation and who entered prenatal care between 1 and 4 weeks was greater than the risk of stillThe data for this analysis were obtained from linked birth and death certificates from Missouri for 1980 through 1984. The variables used in the analysis were the gestational age at which prenatal care was initiated (self-report and limited to the first 36 weeks of pregnancy), the gestational age at delivery (based on last menstrual period), the outcome (stillbirth, infant death, or alive at 1 year), race (Black or non-Black), birth number (multiple vs single), parity, maternal age, and maternal education. We used only those records that involved gestatio...