“华光礁Ⅰ号”沉船出水瓷器“保护性损伤”量化评估的 ICP-AES 分析

目前,文物保护工作者已普遍认识到保护过程会对文物带来一定影响,产生'保护性损伤'。然而,关于'保护性损伤'的量化研究仍罕见报道。为探讨常用清洗试剂对'华光礁Ⅰ号'沉船出水瓷器的保护性损伤,本文利用ICP-AES测试了各步骤浸泡实验溶出液中的元素组成,发现浸泡液中Al,Fe,Mg三种元素的含量较高,且具有一定规律。利用这三种元素作为指标,对出水瓷器的保护性损伤进行了量化评估。研究结果表明,清洗能力强的试剂,对陶瓷本体的损伤也较大;保存较好的器物,所受'保护性损伤'更小;每种清洗剂都会对瓷器造成一定程度的损坏,连中性试剂(如H_2O)同样可以溶解出一定量胎体组分;而普遍认为的较为温和的清洗试剂在长时间浸泡陶瓷器时,对瓷器本体的损伤已非常接近强酸短时间浸泡的影响。故在此特别强调,在实际的文物保护过程中,应切实认识到各种清洗剂对陶瓷本体产生的损害,并同时考虑累积损伤。如此,方能安全有效的保护海洋出水瓷器。

急诊结肠手术患者行保护性回肠双造口的护理体会

目的：探讨急诊结肠手术患者行保护性回肠双造口的护理体会。方法：对49例急诊结肠手术行保护性回肠双造口的患者进行术前心理护理及准备工作，术后密切关注患者造口肠黏膜的血液循环状况、观察排泄物的量及性状、加强造口周围皮肤的护理、做好饮食护理及提供健康指导。结果：全部患者均在术后（1～3）天内出现造口内排气或肠液流出。术后49例中发生造口周围皮炎7例，伴有轻度造口回缩2例，经造口周围皮肤护理后均痊愈，其余病例术后恢复良好。结论：急诊结肠手术患者行保护性回肠双造口术，通过给予及时、有效的护理，可预防并治疗回肠造口并发症，使手术更安全。

Protective effect of Astragalus membranaceus on intestinal mucosa reperfusion injury after hemorrhagic shock in rats

AIM： To study the protective effect of Astragalus rnernbranaceus on intestinal mucosa reperfusion injury and its mechanism after hemorrhagic shock in rats. METHODS： A total of 32 SD rats were randomly divided into four groups （n = 8, each group）： normal group, model group, low dosage group （treated with 10 g/kg Astragalus membranaceus） and high dosage group （treated with 20 g/kg Astragalus membranaceus）. The model of hemorrhagic shock for 60 min and reperfusion for 90 min was established. Therapeutic solution （3 mL） was administrated before reperfusion. At the end of the study, the observed intestinal pathology was analyzed. The blood concentrations of lactic acid （LD）, nitric oxide （NO）, endothelin-1 （ET-1）, malondialdehyde （MDA） and the activity of superoxide dismutase （SOD）, glutathione peroxidase （GSH-PX） in intestinal mucosa were determined. RESULTS： The intestinal mucosa pathology showed severe damage in model group and low dosage group, slight damage in high dosage group and no obvious damage in normal group. The Chiu＇s score in low dose group and high dose group was significantly lower than that in model group. The content of MDA in model group was higher than that in low and high dose groups, while that in high dose group was almost the same as in normal group. The activity of SOD and GSH-PX was the lowest in model group and significantly higher in high dose group than in normal and low dose groups. The concentrations of LD and ET-1 in model group were the highest. The concentrations of NO in model group and low dose group were significantly lower than those in high dose group and normal group. CONCLUSION： High dose Astraga/us membranaeus has much better protective effect on hemorrhagic shockreperfusion injury of intestinal mucosa than low dose Astragalus membranaceus. The mechanism may be that Astragalus membranaceus can improve antioxidative effect and regulate NO/ET level during hemorrhagic reperfusion.

Protective effect of fufanghuangqiduogan against acute liver injury in mice

AIM: To study the effects and possible mechanisms of fufanghuangqiduogan (FFHQ) in mice with acute liver injury (ALI). METHODS: ALI was successfully induced by injecting carbon tetrachloride (CCl4) intra peritoneally and by tail vein injection of Bacillus Calmette Guerin (BCG) and lipopolysaccharide (LPS) in mice, respectively. Each of the two model groups was divided into normal group, model group, FFHQ (60, 120 and 240 mg/kg) treatment groups, and bifendate treatment group. At the end of the experiment, levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), content of malondialdehyde (MDA), activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) in liver homogenate were measured by biochemical methods. The activities of tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) were determined by radio-immunoassay. Hepatic tissue sections were stained with hematoxylin and eosin and examined under a light microscope. RESULTS: In the two models of ALI, FFHQ (60, 120, 240 mg/kg) was found to significantly decrease the serum transaminase (ALT, AST) activities. Meanwhile, FFHQ decreased MDA contents and upregulated the lower SOD and GSH-px levels in liver homogenate. Furthermore, in immunologic liver injury model, FFHQ decreased levels of TNF-α and IL-1 in serum. Histologic examination showed that FFHQ could attenuate the area and extent of necrosis, reduce the immigration of inflammatory cells. CONCLUSION: FFHQ had protective effect on liver injury induced by either CCl4 or BCG+LPS in mice, and its mechanisms were related to free radical scavenging, increasing SOD and GSH-px activities and inhibiting the production of proinflammatory mediators.

Protective Effects of Oyster Extract Against Hepatic Tissue Injury in Alcoholic Liver Diseases

Oyster extract is an effective bioactivity component. It has abundant nutritional value and antiviral, antitumor and im- mune defense fimctions. The role of oyster extract in treating liver injury has been paid more attention. We use Wistar rats to make alcoholic liver disease model through injecting alcohol into rats＇ stomachs. These rats were randomly divided into five groups： model group, control group, low-dose, middle-dose and high-dose experimental group with a dose of 0.12gkg-1, 0.40gkg-1, and 1.20gkg-1 alcoholic. After nine weeks, serum biomarkers （ALT, AST, TG and TCHO）, malondialdehyde （MDA）, glutathione （GSH）, C3a, CSa, IL-17, TNF-a, anti-MAA-HAS IgC~ CD3＋, CD4＋, CDS＋, NK cell activation and zinc content were assessed. The results showed that the serum biomarkers（ALT, AST, TG and TCHO）, MDA content, anti-MAA-HSA IgG, serum C3a, CSa IL-17 and TNF-a levels of oyster extract treatment groups were significantly decreased in comparison with model group. On the contrary, GSH showed ad- verse trend. Serum CD3＋, CD4＋ and NK cell activation were significantly increased in middle-dose group and high-dose group compared with model group, and there was decrease of CD8＋ activity in high-dose group. Plasma Zn level was decreased in model group compared with that in control group. Meanwhile, Mean plasma Zn levels increased dramatically following the dose increase of a given oyster extract.

Using the endocannabinoid system as a neuroprotective strategy in perinatal hypoxic-ischemic brain injury

One of the most important causes of brain injury in the neonatal period is a perinatal hypoxicischemic event.This devastating condition can lead to long-term neurological deficits or even death.After hypoxic-ischemic brain injury,a variety of specific cellular mechanisms are set in motion,triggering cell damage and finally producing cell death.Effective therapeutic treatments against this phenomenon are still unavailable because of complex molecular mechanisms underlying hypoxic-ischemic brain injury.After a thorough understanding of the mechanism underlying neural plasticity following hypoxic-ischemic brain injury,various neuroprotective therapies have been developed for alleviating brain injury and improving long-term outcomes.Among them,the endocannabinoid system emerges as a natural system of neuroprotection.The endocannabinoid system modulates a wide range of physiological processes in mammals and has demonstrated neuroprotective effects in different paradigms of acute brain injury,acting as a natural neuroprotectant.The aim of this review is to study the use of different therapies to induce long-term therapeutic effects after hypoxic-ischemic brain injury,and analyze the important role of the endocannabinoid system as a new neuroprotective strategy against perinatal hypoxic-ischemic brain injury.

Effect of glycyrrhizin on traumatic brain injury in rats and its mechanism

Objective： To investigate the neuropro- tective effects of glycyrrhizin （Gly） as well as its effect on expression of high-mobility group box 1 （HMGB1） in rats after traumatic brain injury （TBI）. Methods： Male Sprague-Dawley rats were randomly divided into three groups： sham group, TBI group, and TBI＋Gly group （n=36 per group）. Rat TBI model was made by using the modified Feeney＇s method. In TBI＋Gly group, Gly was administered intravenously at a dosage of l0 mg/kg 30 min after TBI. At 24 h after TBI, motor function and brain water content were evaluated. Meanwhile, HMGB 1/HMGB 1 receptors including toll-like receptor 4 （TLR4） and receptor for advanced glycation end products （RAGE）/nuclear fac- tor-κ B（NF- κ B） signaling pathway and inflammatory cytokines in the injured brain tissues were detected using quantitative real-time polymerase chain reaction, western blot, electrophoretic mobility shift assay and enzyme-linked immunosorbent assay. Furthermore, HMGB l, RAGE and TLR4 immunohistochemistry and apoptosis were analyzed. Results： Beam walking performance impairment and brain edema were significantly reduced in TBI＋Gly group compared with TBI group; meanwhile, the over-expressions of HMGB 1PHMGB 1 receptors （TLR4 and RAGE）/NF- κB DNA-binding activity and inflammatory cytokines were inhibited. The percentages of HMGB 1, RAGE and TLR4- positive cells and apoptotic cells were respectively 58.37%±5.06%, 54.15%±4.65%, 65.50%± 4.83%, 52.02%±4.63% in TBI group and 39.99%±4.99%, 34.87%±5.02%, 43.33%±4.54%, 37.84%±5.16% in TBI＋Gly group （all P〈0.01 compared with TBI group）. Conclusion： Gly can reduce secondary brain injury and improve outcomes in rat following TBI by down-regula- tion of HMGB 1/HMGB 1 receptors （TLR4 and RAGE）/NF- κB - mediated inflammatory responses in the injured rat brain.

Protective effect of albumin on lung injury in traumatic/hemorrhagic shock in rats

Objective. To determine the effect of albumin administration on lung injury in traumatic/hemorrhagic shock （T/HS） rats. Methods： Forty-eight adult Sprague-Dawley rats were divided into three groups randomly （ n = 16 in each group） ： Group A, Group B, Group C. In Group A, rats underwent laparotomy without shock. In Group B, rats undergoing T/HS were resuscitated with their blood plus lactated Ringer＇s （twice the volume of shed blood ）. In Group C, rats undergoing T/HS were resuscitated with their shed blood plus additional 3 ml of 5% human albumin. The expression of polymorphonuclear neutrophils CD18/CD11b in jugular vein blood was evaluated. The main lung injury indexes （the activity of myeloperoxidase and lung injury score） were measured. Results： Significant differences of the expression of CD18/11b and the severity degree of lung injury were found between the three groups. （P〈0.05）. The expression of CD18/CD11b and the main lung injury indexes in Group B and Goup C incresed significantly compared with those in Group A （P 〈0.05）. At the same time, the expression of CD18/CD11b and the main lung injury indexes in Group C decreased dramatically, compared with those in Group B （ P 〈0.05 ）. Conclusions ： The infusion of albumin during resuscitation period can protect lungs from injury and decrease the expression of CD18/CD11b in T/HS rats.