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difficile after H. MC3 pylori eradication therapy.Paroxysmal kinesigenic dyskinesia is an episodic movement disorder caused by dominant mutations in the proline-rich transmembrane protein PRRT2, with onset in childhood and typically with improvement or resolution by middle age. Mutations in the same gene may also cause benign infantile seizures, which begin in the first year of life and typically remit by the age of 2 years. Many details of PRRT2 function at the synapse, and the effects of mutations on neuronal excitability in the pathophysiology of epilepsy and dyskinesia, have emerged through the work of several groups over the last decade. However, the age dependence of the phenotypes has not been explored in detail in transgenic models. Here, we report our findings in heterozygous and homozygous Prrt2 knockout mice that recapitulate the age dependence of dyskinesia seen in the human disease. We show that Prrt2 deletion reduces the levels of synaptic proteins in a dose-dependent manner that is most pronounced at postnatal day 5 (P5), attenuates at P60, and disappears by P180. In a test for foot slippage while crossing a balance beam, transient loss of coordination was most pronounced at P60 and less prominent at age extremes. Slower traverse time was noted in homozygous knockout mice only, consistent with the ataxia seen in rare individuals with biallelic loss of function mutations in Prrt2. We thus identify three age-dependent phenotypic windows in the mouse model, which recapitulate the pattern seen in humans with PRRT2-related diseases.
Reports of zinc and selenium deficiencies accompanying inflammatory bowel disease (IBD) mostly have originated from Western countries and concerned adult patients. Whether Japanese children with IBD have similar deficiencies remained unclear.
We aimed to elucidate differences in serum zinc and selenium concentrations in Japanese children between types of IBD.
Children under 17years old undergoing care at 12 Japanese pediatric centers were retrospectively enrolled between November 2016 and February 2018 to 3 groups representing Crohn's disease (CD), ulcerative colitis (UC), and normal controls (NC) with irritable bowel syndrome or no illnesses. Serum zinc and selenium were measured by atomic absorption spectrophotometry. Zinc and selenium deficiencies were defined by serum concentrations < 70μg/dL and < 9.5μg/dL, respectively.
Subjects included 98 patients with CD (median age, 13years), 118 with UC (11years), and 43 NC (11years). Serum zinc and selenium were significantly lower in CD (median, 64 and 12.6μg/dL respectively) than in UC (69 and 14.6; P < 0.05 and P < 0.001) or NC (77 and 15.7; P < 0.01 and P < 0.001). Zinc deficiency was significantly more prevalent in CD (60.2%) than in NC (37.2%; P < 0.05), but not than in UC (51.7%; P = 0.22). Selenium deficiency was significantly more prevalent in CD (15.3%) than in UC (5.9%; P < 0.05) or NC (0%; P < 0.01).
In Japanese children under 17years old, serum zinc and selenium were significantly lower in CD than in UC or NC. Zinc and selenium should be monitored, and supplemented when deficient, in children with IBD, especially CD.
In Japanese children under 17 years old, serum zinc and selenium were significantly lower in CD than in UC or NC. Zinc and selenium should be monitored, and supplemented when deficient, in children with IBD, especially CD.Facial expression stereotypes can affect the perception of other people's facial expressions. This study examined facial expression stereotypes of poor and rich adults and children. Experiment 1 found that the adult participants associated rich adults with positive emotions (i.e., happiness) and poor adults with negative emotions (i.e., sadness). In Experiments 2-4, adult participants still thought that rich 4-, 6-, and 10-year-old children would show positive facial expressions (happiness) but did not think that poor 4-, 6-, and 10-year-old children would show negative emotions (sadness). These finding have implications concerning how adults communicate with poor and rich adults and children.
Arteriovenous malformations (AVMs) are abnormal communications between arteries and veins without an intervening capillary system. The best endovascular treatment option for these is unclear and may involve multiple staged procedures using a variety of embolic materials. We report our initial experience using a modified version of a previously published neurointerventional technique to treat soft tissue AVMs with single-stage curative intent.
Soft tissue AVMs treated endovascularly using either sole arterial or combined arterial and venous balloon-assisted techniques with liquid embolic agents were retrospectively identified over a 3.5 year period (January 2017 to June 2020)) at two centres. Clinical, pre-operative radiological, procedural technical and post treatment details were recorded.
Seven patients were treated for symptomatic soft tissue arteriovenous malformations. These AVMs were located in the peripheral limbs (five), tongue (one) and uterus (one). Curative treatment was achieved in 6/7 patieieving durable occlusion for complex soft tissue AVMs.It is well established that natural killer (NK) cells are dysregulated in systemic lupus erythematosus (SLE) patients. However, the functions of NK cells and the mechanisms regulated by them in SLE remain incompletely understood. Patients with SLE were recruited from The First Affiliated Hospital of Nanchang University, and their clinical characteristics and treatments were recorded. The expression levels of T cell immunoglobulin mucin-3 (TIM-3) and programmed cell death protein 1 (PD-1) on NK cells were examined using flow cytometry. The correlations between the increase in TIM-3+PD-1+ NK cells in the SLE patients and clinical traits, including inflammatory markers, auto-antibodies, disease activity and severity of SLE, were examined. The TIM-3+NK cells, PD-1+NK cells and TIM-3+PD-1+ NK cells were significantly increased in the SLE patients. The increase in TIM-3+PD-1+ NK cells in the patients with SLE was associated with erythrocyte sedimentation rate, C-reactive protein, anti-double stranded DNA, anti-ribosomal P, SLE disease activity index and clinical features.
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