Research progression on safety verification of diving decompression procedures / 中国职业医学

@#A diving decompression procedure is a specific rule that divers should follow when they ascend and get out of water. It comes from the decompression theory and algorithm and is designed for the prevention of decompression sickness. With the ， ， development of diving technology and diving medicine the decompression procedures are constantly innovated and the new ， decompression procedure can be used in diving practice after safety verification. In principle the safety verification of ， decompression procedures should be conducted on animal experiments before human experiments and the risks of ， decompression sickness and oxygen toxicity should be systematically assessed. However the assessment methods used in ， ， ， different studies differ greatly thus it is urgent to establish a standard and universal verification system. Traditionally the risk ， ， assessment of decompression sickness and oxygen toxicity is mainly carried out by observing the incidence detecting bubbles ， theoretical calculation and lung functional test. Furthermore biochemical indicators are increasingly becoming important ， ， supplements. Due to the special underwater environment the diving operation is prone to accidents. Therefore in addition to ， verifying the safety of the new decompression procedure exploring its safety decompression limit is of great significance for the formulation of emergency decompression procedures in emergency situations. The specific approach is to shorten the decompression time and assess the safety until the critical time for detecting bubbles without the occurrence of decompression ， ， sickness is found. Future studies should continue to optimize safety assessment methods explore sensitive biochemical markers ， clarify species associations and improve verification efficiency and reliability of results.

Effects of glucocorticoids on traumatic brain injury related critical illness-related corticosteroid insufficiency / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Traumatic brain injury (TBI) is a heterogeneous condition that can lead to critical LLLness-related corticosteroid insufficiency (CIRCI) causing a high mortality and morbidity. Glucocorticoids were widely used in the clinical management of TBI, but their benefit has been challenged in some studies and their efficacy, especially for treating CIRCI in TBI patients, remains unclear.</p><p><b>METHODS</b>We conducted a meta-analysis of published data to determine if the controversy is related to clinical dosing and timing of glucocorticoids (GCs) application. We analyzed published reports in four databases (MEDLINE, EMBASE, the Cochrane Controlled Trials Register, and CBMdisc). The published data were stratified into not only low- and high-dose GCs group but also short- and long-term GCs group to compare their effectiveness in improving TBI outcomes.</p><p><b>RESULTS</b>We totally identified 16 reports. For low-dose patients, the pooled relative risks (RRs) for two clinical outcomes of death or a combination of death and severe disability were 0.95 (95% confidence interval (CI): 0.80 to 1.13) and 0.95 (95% CI: 0.83 to 1.09), respectively. The risks for infection and gastrointestinal bleeding were 0.85 (95% CI: 0.50 to 1.45) and 0.64 (95% CI: 0.15 to 2.70), respectively. For high-dose group, the pooled RR of death is 1.14 (95% CI: 1.06 to 1.21). The pooled RRs for infection and gastrointestinal bleeding for the high-dose patients were 1.04 (95% CI: 0.93 to 1.15) and 1.26 (95% CI: 0.92 to 1.75), respectively. For long-term use group, the pooled RRs for two clinical outcomes of death or a combination of death and severe disability were 0.98 (95% CI: 0.87 to 1.12) and 1.00 (95% CI: 0.90 to 1.11), respectively. The risks for infection and gastrointestinal bleeding were 0.88 (95% CI: 0.71 to 1.11) and 0.96 (95% CI: 0.35 to 2.66), respectively. For short-term use group, the pooled RR of death is 1.15 (95% CI: 1.07 to 1.23), and importantly the effects on infections were beneficial in terms of TBI patients suffering from CIRCI.</p><p><b>CONCLUSIONS</b>This meta-analysis suggests an increased risk of death for TBI patients on a high dose and short term of glucocorticoids compared with those on a low dose and long term, for whom a trend towards clinical improvement is evident. In addition, stress-does of GCs further decrease the pneumonia incidence in TBI patients suffering from CIRCI. A large-scale multicenter randomized controlled trial is warranted for testing (1) the efficacy of stress-dose GCs treatment in the sub-acute phase of TBI (4-21 days after initial trauma), when CIRCI is most likely to occur; (2) the hypothesis that stress-dose GCs could boost patients' stress function and ensure survival.</p>

Chronic effects of oligomeric Aβ(1-42) on hippocampal synaptic plasticity in vivo / 生理学报

Synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD), is widely considered as one of the major mechanisms underlying learning and memory. This study explored hippocampal synaptic plasticity and spatial memory formation of an Alzheimer's disease (AD) rat model established by intrahippocampal injection of oligomeric Aβ(1-42). Twenty four Sprague-Dawley rats at 2.5 months of age were randomly divided into AD and control groups, and were bilaterally injected with 5 μg oligomeric Aβ(1-42) or normal saline into dentate gyrus (DG) of hippocampus. Morris water maze test was used to observe the capability of learning and memory of two groups, 30 d after injection. To investigate the variations of paired-pulse facilitation (PPF) and range of synaptic plasticity, field potentials were recorded in the DG of the dorsal hippocampus by stimulating the perforant path (PP). The results showed that oligomeric Aβ(1-42) obviously impaired spatial memory formation in rats (P < 0.05). Furthermore, oligomeric Aβ(1-42) reduced the PPF ratio (P < 0.05) and hippocampal LTP formation (P < 0.05), while facilitated the hippocampal LTD formation (P < 0.05). These data suggest that chronic Aβ aggregation impairs synaptic plasticity of hippocampal PP-DG pathway, which may be involved in the spatial memory deficit in AD rats.

Traumatic brain injury impairs synaptic plasticity in hippocampus in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Traumatic brain injury (TBI) often causes cognitive deficits and remote symptomatic epilepsy. Hippocampal regional excitability is associated with the cognitive function. However, little is known about injury-induced neuronal loss and subsequent alterations of hippocampal regional excitability. The present study was designed to determine whether TBI may impair the cellular circuit in the hippocampus.</p><p><b>METHODS</b>Forty male Wistar rats were randomized into control (n = 20) and TBI groups (n = 20). Long-term potentiation, extracellular input/output curves, and hippocampal parvalbumin-immunoreactive and cholecystokinin-immunoreactive interneurons were compared between the two groups.</p><p><b>RESULTS</b>TBI resulted in a significantly increased excitability in the dentate gyrus (DG), but a significantly decreased excitability in the cornu ammonis 1 (CA1) area. Using design-based stereological injury procedures, we induced interneuronal loss in the DG and CA3 subregions in the hippocampus, but not in the CA1 area.</p><p><b>CONCLUSIONS</b>TBI leads to the impairment of hippocampus synaptic plasticity due to the changing of interneuronal interaction. The injury-induced disruption of synaptic efficacy within the hippocampal circuit may underlie the observed cognitive deficits and symptomatic epilepsy.</p>

Effect of low-intensity pulsed ultrasound on the enchondral bone formation in posterolateral lumbar fusion in rabbits / 中南大学学报(医学版)

OBJECTIVE@#To observe the effect of daily low-intensity pulsed ultrasound (LIPUs) therapy on improving the enchondral bone formation in lumbar fusion in rabbit models, and to explore its possible mechanism.@*METHODS@#Posterolateral noninstrumented bilateral fusions were performed at the L5 approximately L6 levels in 20 New Zealand rabbits. The autograft iliac bone was implanted on the left side, and the hydroxyapatite bioceramic artificial bone on the right. The rabbits were divided into a treatment group and a control group randomly. One week after the surgery, LIUPs was administered for 20 minutes per day for 4 weeks over the fusion site in the treatment group and false treatment was used in the control group. Post-anterior X-ray photographs were taken to determine the conditions of fusion area, and then, rabbits were killed and the fusion tissues were obtained. Chondrocytes were detected by histological and cytological methods.@*RESULTS@#Compared with the control group, the fusion rate of the treatment group was significantly up-regulated (P0.05).@*CONCLUSION@#Low-intensity pulsed ultrasound therapy improves the endochondral bone formation in the lumbar spine fusion in rabbit models.