Objective To explore the susceptibility of epilepsy in rat with cerebral trauma. Methods An impact-acceleration head injury model was established with rats. After trauma, the electroencephalograph was recorded. Epileptic model wad established by injecting pentylenetetrazol (PTZ) intraperitoneally and the dosage of PTZ was recorded. Results The wave of delta and theta increased after trauma, alpha and beta decreased and there was significant difference among the power of delta, theta and alpha (P＜0.05). The dosage of rats with cerebral trauma was less than that in normal rats (P＜0.05). Conclusion The susceptibility of epilepsy in rat with cerebral trauma increases.

Objective:To investigate the clinical features, gene mutation and follow-up outcome of children with paroxysmal kinesigenic dyskinesia(PKD).Methods:Clinical data was collected at Beijing Tiantan Hospital Affiliated to Capital Medical University from November 2018 to November 2019.In total, seven children with PKD were recruited, and peripheral blood samples for gene study were collected from six patients and their parents.Mutation analysis of PRRT2 gene was performed by PCR sequencing in children and by Sanger sequencing in patients.Results:Of the seven patients, four were male and three were female, and the median age of onset was 11 years and 6 months, ranging from 5 to 14 years.Among them, two patients were family cases and the other five patients were sporadic cases.The presentation were abnormal involuntary movements provoked by sudden movements, without loss of consciousness.Five patients exhibited dystonia and two patients had dystonia and choreoathetosis.The duration of the attacks lasted for a few seconds to 40 seconds.The frequency ranged from 5 to 15 times per day.PRRT2 mutations, c.649_650insC(P.R217PfsX8), were found in two patients with PKD families and three sporadic PKD cases.Conclusion:The onset age of PKD is pre-school or school age.The attacks manifest as dystonia or mixed with dystonia and choreoathetosis.PRRT2 is the main pathogenic gene of PKD and mutation c. 649_650insC is the hotspot mutation.Low-dose Carbamazepine has good effects.

A 3-year-old girl was hospitalized for cough and asthma for 2 days, and fever and anuria for 1 day in Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology in January 2019.Retrospective analysis was used.She developed end-stage renal disease and received peritoneal dialysis 6 months ago.After admission, she was diagnosed as acute-on-chronic renal failure, respiratory failure, heart failure, severe influenza A (H1N1). The patient was rapidly recovered by the management of high-volume peritoneal dialysis, mechanical ventilation, and medications of Peramivir and Methylprednisolone.Through literature review, case report or cohort study about the treatment of acute kidney disease by high-volume peritoneal dialysis has not been previously reported.This case report suggested that high-volume peritoneal dialysis is able to effectively remove solutes and control volume without causing severe hypoproteinemia and hyperglycemia, which may become an effective renal replacement therapy for children with multi-organ dysfunction syndrome.

V-Raf murine sarcoma viral oncogene homolog B (BRAF) alteration is one of the most essential driver genes of non-small cell lung cancer (NSCLC). BRAF encodes serine/threonine protein kinases, and its mutations typically lead to protein compositional activation, thereby activating the mitogen-activated protein kinase kinase (MEK) signaling pathway. A promising new approach for the treatment of mutated BRAF and/or downstream MEK may provide customized treatment opportunities for BRAF driven NSCLC patients. However, combination therapy is necessary to overcome the difficulties such as short duration of benefit, poor therapeutic effect of non-V600 BRAF mutations and susceptibility to drug resistance. This article reviewed the progress in structural characteristics, related signaling pathways, mutation types of BRAF gene, and the clinical pathological relationship between BRAF mutations and NSCLC, as well as the therapy, in order to provide more evidences for clinical doctors to make treatment decisions.
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Animals ; Mice ; Humans ; Carcinoma, Non-Small-Cell Lung/pathology* ; Lung Neoplasms/pathology* ; Proto-Oncogene Proteins B-raf/genetics* ; Mutation ; Mitogen-Activated Protein Kinase Kinases/therapeutic use* ; Protein Kinase Inhibitors/therapeutic use*