Partial Hepatectomy for the Resistant Fasciola Hepatica Infection in a Child.

Fascioliasis is an emerging and important chronic parasitic disease caused by two trematode liver fluke species: Fasciola hepatica (F. hepatica) and Fasciola gigantica (F. gigantica) infecting several herbivorous mammals including cattle, goats, sheep, and humans. We report a 9-year-old girl who suffered from F. hepatica infection and underwent right hepatectomy because of increasing abdominal pain resistant to anthelmintic chemotherapy. When anthelmintic drug treatment is not effective and abdominal pain persists, surgical resection including hepatectomy should be kept in mind for resistant F. hepatica infection

A Rare Pediatric Case of Neurocysticercosis Misdiagnosed As Brain Abscess

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Low-temperature, Inkjet-printed p-Type Copper(I) Iodide-based Thin-Film Transistors

Graduation date: 2016Inkjet-printed p-type copper(I) iodide-based TFTs were successfully fabricated. As-printed copper(I) halide semiconductor films, such as CuI, CuBrI, and CuClI, were used as p-type active channel layers for TFTs. The entire process of the TFTs fabrication was maintained under 150 °C, which is compatible with flexible plastic substrates and transparent glass substrate. Various printing temperatures, drop spacing, W/L ratios, and TFT structures were tested in order to find the optimum device properties for p-type copper(I) iodide-based TFT. In addition, inkjet-printed CuI, CuBrI, and CuClI films were characterized to study optical, electrical, and morphological properties. Furthermore, device performance of printed copper(I) iodide-based p-type TFTs was also investigated. Among them, CuI TFTs with SU-8 encapsulation exhibited outstanding p-type transistor behaviours with field-effect mobility as high as 4.36 cm² V⁻¹ s⁻¹ and Ion/Ioff ratio of 103.24 on the silicon substrate. Also, CuBrI TFTs resulted in successful p-type transistor behaviours with average\ud field-effect mobility of 2.4 cm² V⁻¹ s⁻¹ and I[subscript on]/I[subscript off] ratio of 101.9 on the glass substrates when the molar ratio of CuBr:CuI was 1:1. In addition, CuClI TFTs were successfully fabricated with field-effect mobility as high as 1.02 cm² V⁻¹ s⁻¹ and I[subscript on]/I[subscript off] ratio of 10⁰·⁷³ on the silicon substrates when the molar ratio of CuCl:CuI was 1:9. The device performances were comparable to reported p-type metal oxide TFTs. This study suggests promising candidates of low-temperature printed p-type TFTs that can be used for complementary inorganic circuits

Human genetic and immunological determinants of critical COVID-19 pneumonia

SARS-CoV-2 infection is benign in most individuals but, in around 10% of cases, it triggers hypoxaemic COVID-19 pneumonia, which leads to critical illness in around 3% of cases. The ensuing risk of death (approximately 1% across age and gender) doubles every five years from childhood onwards and is around 1.5 times greater in men than in women. Here we review the molecular and cellular determinants of critical COVID-19 pneumonia. Inborn errors of type I interferons (IFNs), including autosomal TLR3 and X-chromosome-linked TLR7 deficiencies, are found in around 1-5% of patients with critical pneumonia under 60 years old, and a lower proportion in older patients. Pre-existing auto-antibodies neutralizing IFN alpha, IFN beta and/or IFN omega, which are more common in men than in women, are found in approximately 15-20% of patients with critical pneumonia over 70 years old, and a lower proportion in younger patients. Thus, at least 15% of cases of critical COVID-19 pneumonia can be explained. The TLR3- and TLR7-dependent production of type I IFNs by respiratory epithelial cells and plasmacytoid dendritic cells, respectively, is essential for host defence against SARS-CoV-2. In ways that can depend on age and sex, insufficient type I IFN immunity in the respiratory tract during the first few days of infection may account for the spread of the virus, leading to pulmonary and systemic inflammation

Rare predicted loss-of-function variants of type I IFN immunity genes are associated with life-threatening COVID-19

BackgroundWe previously reported that impaired type I IFN activity, due to inborn errors of TLR3- and TLR7-dependent type I interferon (IFN) immunity or to autoantibodies against type I IFN, account for 15-20% of cases of life-threatening COVID-19 in unvaccinated patients. Therefore, the determinants of life-threatening COVID-19 remain to be identified in similar to 80% of cases.MethodsWe report here a genome-wide rare variant burden association analysis in 3269 unvaccinated patients with life-threatening COVID-19, and 1373 unvaccinated SARS-CoV-2-infected individuals without pneumonia. Among the 928 patients tested for autoantibodies against type I IFN, a quarter (234) were positive and were excluded.ResultsNo gene reached genome-wide significance. Under a recessive model, the most significant gene with at-risk variants was TLR7, with an OR of 27.68 (95%CI 1.5-528.7, P=1.1x10(-4)) for biochemically loss-of-function (bLOF) variants. We replicated the enrichment in rare predicted LOF (pLOF) variants at 13 influenza susceptibility loci involved in TLR3-dependent type I IFN immunity (OR=3.70[95%CI 1.3-8.2], P=2.1x10(-4)). This enrichment was further strengthened by (1) adding the recently reported TYK2 and TLR7 COVID-19 loci, particularly under a recessive model (OR=19.65[95%CI 2.1-2635.4], P=3.4x10(-3)), and (2) considering as pLOF branchpoint variants with potentially strong impacts on splicing among the 15 loci (OR=4.40[9%CI 2.3-8.4], P=7.7x10(-8)). Finally, the patients with pLOF/bLOF variants at these 15 loci were significantly younger (mean age [SD]=43.3 [20.3] years) than the other patients (56.0 [17.3] years; P=1.68x10(-5)).ConclusionsRare variants of TLR3- and TLR7-dependent type I IFN immunity genes can underlie life-threatening COVID-19, particularly with recessive inheritance, in patients under 60 years old