Objective To improve the level of diagnosis and treatment of the sharp injury in the back. Methods 47 cases which were treated from Jan 1991 to May 2000 were reviewed. ResultsAmong 37 cases who underwent the exploration, 5 cases died. Among 10 cases who underwent conservative treatment, 2 cases died. ConclusionThe condition of sharp injury in the back is very complicated,it is easy to be misdiagnosed, the mortality is high. Saving should be equalled with the diagnosis and treatment. The application of wound exploration, abdominal puncture, ultrasound examination and X-ray checking is valuable to the diagnosis. The patients with operation indications should be operated at once,while the others should be observed for some time to prevent the delayed clinical manifestation.

Hv1 is the only voltage-gated proton-selective channel in mammalian cells. It contains a conserved voltage-sensor domain, shared by a large class of voltage-gated ion channels, but lacks a pore domain. Its primary role is to extrude protons from the cytoplasm upon pH reduction and membrane depolarization. The best-known function of Hv1 is the regulation of cytosolic pH and the nicotinamide adenine dinucleotide phosphate oxidase-dependent production of reactive oxygen species. Accumulating evidence indicates that Hv1 is expressed in nervous systems, in addition to immune cells and others. Here, we summarize the molecular properties, distribution, and physiological functions of Hv1 in the peripheral and central nervous systems. We describe the recently discovered functions of Hv1 in various neurological diseases, including brain or spinal cord injury, ischemic stroke, demyelinating diseases, and pain. We also summarize the current advances in the discovery and application of Hv1-targeted small molecules in neurological diseases. Finally, we discuss the current limitations of our understanding of Hv1 and suggest future research directions.
Animals ; Protons ; Ion Channels/metabolism* ; Reactive Oxygen Species/metabolism* ; Brain/metabolism* ; NADPH Oxidases ; Mammals/metabolism*

Postoperative cognitive dysfunction (POCD) is one of the most common complications after surgery under general anesthesia and usually manifests as newly presented cognitive impairment. However, the mechanism of POCD is still unclear. In addition to neurons, glial cells including microglia, astrocytes and oligodendrocytes, represent a large cell population in the nervous system. The bi-directional communication between neurons and glia provides basis for neural circuit function. Recent studies suggest that glial dysfunctions may contribute to the occurrence and progress of POCD. In this paper, we review the relevant work on POCD, which may provide new insights into the mechanism and therapeutic strategy for POCD.
Anesthesia, General ; Humans ; Microglia ; Postoperative Cognitive Complications ; Postoperative Complications