BackgroundHookworms are important pathogens of humans. To date, Necator americanus is the sole, known species of the genus Necator infecting humans. In contrast, several Necator species have been described in African great apes and other primates. It has not yet been determined whether primate-originating Necator species are also parasitic in humans.Methodology/Principal FindingsThe infective larvae of Necator spp. were developed using modified Harada-Mori filter-paper cultures from faeces of humans and great apes inhabiting Dzanga-Sangha Protected Areas, Central African Republic. The first and second internal transcribed spacers (ITS-1 and ITS-2) of nuclear ribosomal DNA and partial cytochrome c oxidase subunit 1 (cox1) gene of mtDNA obtained from the hookworm larvae were sequenced and compared. Three sequence types (I–III) were recognized in the ITS region, and 34 cox1 haplotypes represented three phylogenetic groups (A–C). The combinations determined were I-A, II-B, II-C, III-B and III-C. Combination I-A, corresponding to N. americanus, was demonstrated in humans and western lowland gorillas; II-B and II-C were observed in humans, western lowland gorillas and chimpanzees; III-B and III-C were found only in humans. Pairwise nucleotide difference in the cox1 haplotypes between the groups was more than 8%, while the difference within each group was less than 2.1%.Conclusions/SignificanceThe distinctness of ITS sequence variants and high number of pairwise nucleotide differences among cox1 variants indicate the possible presence of several species of Necator in both humans and great apes. We conclude that Necator hookworms are shared by humans and great apes co-habiting the same tropical forest ecosystems.
We studied the mechanisms underlying calpain inhibition-mediated human neutrophil migration. MAPKs, including ERK, p38, and JNK, MEK1/2, MAPK kinase 3/6 (MKK3/6), PI-3K/Akt, c-Raf, and p21-activated kinase (PAK; an effector molecule of Rac) were rapidly (within 30 s) activated in neutrophils upon exposure to calpain inhibitors (PD150606 and N-acetyl-Leu-Leu-Nle-CHO) but not PD145305 (inactive analog of PD150606). Following activation of these pathways, neutrophils displayed active migration (chemotaxis), which was sustained for more than 45 min. The studies with pharmacological inhibitors suggest that calpain inhibition-mediated neutrophil migration is mediated by activation of MEK/ERK, p38, JNK, PI-3K/Akt, and Rac. NSC23766 (Rac inhibitor) and pertussis toxin (PTX) suppressed calpain inhibitor-induced phosphorylation of distinct signaling molecules (PAK, c-Raf, MEK1/2, ERK, MKK3/6, p38, JNK, and Akt) as well as cell migration, suggesting that the PTX-sensitive G protein and Rac axis may be a possible key target of calpain inhibitors. Differentiated neutrophil-like HL-60 cells but not undifferentiated cells displayed cell migration and activation of MAPKs and PI-3K/Akt on calpain inhibition. These findings suggest that constitutively active calpain negatively regulates activation of the distinct signaling pathways and cell migration in resting neutrophils, and this regulatory system develops during differentiation into mature neutrophils.
These observations suggest that the expression of XB130 in ESCC cells may affect cell cycle progression and impact prognosis of patients with ESCC. A deeper understanding of XB130 as a mediator and/or biomarker in ESCC is needed.
BackgroundAcetabular dysplasia (AD) is a well-known cause of osteoarthritis (OA) of the hip, with its prevalence previously determined on plain radiography. The prevalence of preexisting AD was reported as 7.3% in a patient-based Asian population. Although computed tomography (CT) could evaluate AD in multiple planes, its prevalence using multiplanar CT images has not been reported. We investigated its prevalence with CT on coronal, axial, and sagittal planes and then determined if adding the axial and sagittal planes enhanced the investigation.MethodsWe retrospectively examined 52 consecutive Japanese individuals (mean age 59.4 years) who had undergone CT for conditions unrelated to hip disorders. The inclusion criteria of CT images were (1) reconstructed axial slice thickness of ≤1 mm and (2) normal pelvic rotations and tilt. Exclusion criteria were (1) age <20 years, (2) neither hip center could be clearly detected, (3) evidence of hip OA. The parameters used to define AD on the coronal plane were the center–edge angle, Sharp angle, acetabular index, acetabular depth ratio, and acetabulum head index. The anterior and posterior acetabular sector angles were used as axial parameters and the vertical-center-anterior margin angle as the sagittal parameter. AD prevalence was calculated using multiplanar images and then compared with the previously reported Asian prevalence using 95% confidence intervals (CI). In this study, we defined “prevalence” as the proportion of subjects who had AD in at least one hip.ResultsThe mean prevalence of AD on coronal, axial, and sagittal planes was 16.9, 15.4, and 7.7%, respectively. The lowest prevalence found by combining the three planes was 25.0% (95% CI 15.2–38.2%). This prevalence was significantly higher than that in the previously reported Asian population (7.3%).ConclusionsAt the lowest estimate, the prevalence of AD evaluated in three planes was more than twice as high as the previously reported prevalence in Asians when we investigated its prevalence using multiplanar images. The prevalence of AD in the axial and sagittal planes was not negligible. We therefore suggest that it is important to add axial and sagittal planes’ data when investigating the prevalence of AD.
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