Objective To analyze the massive explosions and burn at Tianjin Port in 2015 resulted in a mass casualty event,and the entire course of response of a hospital to deal with such major sudden accident in order to find a rational strategy for optimal use of medical resources and reduce the critical mortality.Methods This study was done by a retrospective analysis of data from one trauma center at an academic hospital.Data including outcome,triage,severity and pattern of injuries,patient flow,and medical resources used were obtained by the review of hospital records.Results This disaster caused 165 deaths,8 missing contact,and 797 non-fatal casualties.The Pingjin Hospital admitted 298 casualties,and 29 of them were seriously injured referred to by Tianjin Emergency Medical Center.Excessive triage rate made after transfer to another hospital was 62.07% with 11 of the 29 severely injured patients.Maximum (also the first)surge had 147 injured patients arrived around one hour after incident,the second surge had 31 seriously injured patients occurred around 4 hours after incident.Of them,17 patients needed surgery and 17 patients were admitted to the intensive care unit.Conclusions These data showed that the number of casualties in the first surge was substantially larger than predicted and those casualties had less severe trauma,whereas the number of the injured in the second surge was less but the trauma was more severe.In order to maintain the hospital surge capacity,an effective re-triage and a hospital-wide damage control principle can be used to deal with.

Extranodal natural killer/T-cell lymphoma (ENKTCL) is the subtype of non-Hodgkin lymphoma with high heterogeneity and invasiveness. Though most ENKTCL patients are present as early-stage at diagnosis, clinical prognosis significantly differs due to the limitations of clinical staging. Radiotherapy (RT) and chemotherapy (CT) are the first-line treatments for early ENKTCL patients. However, there is no consensus on the combined modalities of RT and CT, and their optimal strategy. With the continuous renewal of clinical staging and prognostic models, early-stage ENKTCL patients tend to accept risk-adapted treatment with proper stratification. In this review, the latest research progresses on clinical staging, prognostic models and treatment were retrospectively analyzed, aiming to provide references for clinical decision-making.

Many people affected by fragile X syndrome (FXS) and autism spectrum disorders have sensory processing deficits, such as hypersensitivity to auditory, tactile, and visual stimuli. Like FXS in humans, loss of Fmr1 in rodents also cause sensory, behavioral, and cognitive deficits. However, the neural mechanisms underlying sensory impairment, especially vision impairment, remain unclear. It remains elusive whether the visual processing deficits originate from corrupted inputs, impaired perception in the primary sensory cortex, or altered integration in the higher cortex, and there is no effective treatment. In this study, we used a genetic knockout mouse model (Fmr1^KO), in vivo imaging, and behavioral measurements to show that the loss of Fmr1 impaired signal processing in the primary visual cortex (V1). Specifically, Fmr1^KO mice showed enhanced responses to low-intensity stimuli but normal responses to high-intensity stimuli. This abnormality was accompanied by enhancements in local network connectivity in V1 microcircuits and increased dendritic complexity of V1 neurons. These effects were ameliorated by the acute application of GABA_A receptor activators, which enhanced the activity of inhibitory neurons, or by reintroducing Fmr1 gene expression in knockout V1 neurons in both juvenile and young-adult mice. Overall, V1 plays an important role in the visual abnormalities of Fmr1^KO mice and it could be possible to rescue the sensory disturbances in developed FXS and autism patients.
Animals ; Disease Models, Animal ; Fragile X Mental Retardation Protein/metabolism* ; Fragile X Syndrome/metabolism* ; Humans ; Mice ; Mice, Knockout ; Neurons/metabolism*