自体输血与异体输血对创伤性颅脑损伤开颅手术患者凝血功能、细胞免疫功能和神经损伤标志物的影响

摘要 目的：探讨自体输血与异体输血对创伤性颅脑损伤（TBI）开颅手术患者凝血功能、细胞免疫功能和神经损伤标志物的影响。方法：回顾性分析2019年4月~2022年5月期间在本院行开颅手术的120例TBI患者的临床资料。根据输血方式的不同将患者分为异体输血组（n=58,异体输血）和自体输血组（n=62,自体输血）,观察两组临床指标、细胞免疫功能、凝血功能、神经损伤标志物和不良反应发生率情况。结果：两组患者手术出血量、输血量、输注含凝血成分血制品比例对比,差异无统计学意义（P>0.05）。自体输血组出院时CD3⁺、CD4⁺、CD4⁺/CD8⁺高于异体输血组,CD8⁺低于异体输血组（P<0.05）。两组出院时凝血酶原时间（PT）、凝血酶时间（TT）、纤维蛋白原（FIB）、活化部分凝血活酶时间（APTT）组间对比无统计学差异（P>0.05）。自体输血组出院时S100钙结合蛋白B（S100B）、神经胶质原纤维酸性蛋白（GFAP）、神经元特异性烯醇化酶（NSE）低于异体输血组（P<0.05）。两组不良反应发生率组间比较无差异（P>0.05）。结论：自体输血用于TBI开颅手术患者,对患者的凝血功能影响较小,同时还可改善机体细胞免疫功能,降低神经损伤标志物水平。     

Effect of modification of storage atmosphere on phospholipids and ultrastructure of cauliflower mitochondria

Differences in mitochondrial membrane composition and ultrastructure were studied after storage of cauliflower ( Brassica oleracea , L., Botrytis group) for 5 days at 25°C in air or under controlled atmospheres: 3% O₂, 21% O₂+ 15% CO₂ or 3% O₂+ 15% CO₂. In air, postharvest senescence involved a 20% decrease in mitochondrial phospholipid content. A large reduction in the relative abundance of phosphati-dylcholine (PC) and in the degree of unsaturation of PC and phosphatidyl ethanolamine (PE) was observed. However, the degree of unsaturation increased in cardiolipin (CL). Storage under 3% O₂ did not prevent phospholipid breakdown. Low O₂ prevented the relative decrease in PC observed during storage in air and the loss of linoleic acid from PC, but not from PE. This relative protection offered by the low O₂ atmosphere was lost under 3% O₂+ 15% CO₂. The high CO₂ atmospheres caused twice as much loss in phospholipids as that observed during storage in air. Extensive loss of mitochondrial protein, a marked decrease in phospholipid to protein ratio, and electron micrograph observations suggest structural alterations in the presence of high CO₂.     

Dynamic changes of mechanically activated channels and K+ channels at injury site of peripheral nerve in rat

Ectopic ion channels developed locally at the injury site after nerve damage by light ligation around common sciatic nerve of the rats. Different channel types have different processes of formation, accumulation and degeneration. During the first three days after injury, mechanically activated channels that are modulated by Ca++ channel activities first appeared. As the nerve fibers begin to be excited by TEA, a blocker of K+ channels, suggesting that the accumulation of K+ channels, the responsibility of mechanically activated channels was declining. Onset of K+ channels was from the 3rd postoperative day and lasted up to the fiftieth day. This time course of K+ channel development was closely related to allodynia and hyperalgesia of neuropathic animal behaviour. The results suggest that chronic contraction injury induces a dynamic change in the ectopic mechanically activated channels and K+ channels at the injury site of nerve and there is an interchange in the development time courses of the mechanic     

高氧预适应对大鼠心肌缺血─再灌注时自由基的影响

为了解决高氧预适应（ＨｙｐｅｒｏｘｉｃｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇＨＯＰ）对大鼠心肌缺血再灌注时自由基的影响,本实验将实验组大鼠放入高压氧舱内,每日吸８０－８５％氧气（１ａｔｍ）６ｈ,连续７ｄ。利用Ｌａｎｇｅｎｄｏｒｆ装置做成心肌缺血再灌注模型,采用电子自旋共振技术测定自由基含量。实验动物随机分为二组,第一组为对照组：缺血１０ｍｉｎ,再灌注６０ｍｉｎ。第二组为ＨＯＰ组：缺血１０ｍｉｎ,再灌注６０ｍｉｎ。实验观察冠脉回流液中自由基ＰＢＮ加合物含量。结果表明：在再灌注过程中,１、５、１０ｍｉｎ３个时间点,ＨＯＰ组ＰＢＮ加合物含量较对照组明显减少。提示：ＨＯＰ能减少缺血再灌注时自由基的产生。     

肝炎平对D－氨基半乳精所致肝损害保护作用的酶组织化学研究

本实验采用Ｄ－氨基半乳糖（Ｄ－ＧａｌＮ）诱导的大鼠急性肝损伤模型,观察大鼠肝脏组织化学的变化,探讨肝炎平对急性肝损伤的保护作用。实验分为四组,即正常对照组、模型组、肝炎平及肝得健保护组。结果表明：肝炎平对肝细胞膜系统有一定的保护作用。肝炎平组和肝得健组ＳＤＨ、ＣＣＯ及ＣｈＥ活性明显高于模型组,且与正常对照组相近。本实验模型组ＡＣＰ的活性明显高于正常组,而肝炎平组ＡＣＰ的活性明显低于模型组,与正常对照组无显著性差异。提示：肝炎平可显著改善因Ｄ－氨基半乳糖所致肝损害的作用。且其对肝细胞的保护作用与肝得健一致。     

The Second Messenger, Cyclic AMP, Is Not Sufficient for Myelin Gene Induction in the Peripheral Nervous System

Abstract: The adenylyl cyclase-cyclic AMP (cAMP) second messenger pathway has been proposed to regulate myelin gene expression; however, a clear correlation between endogenous cAMP levels and myelin-specific mRNA levels has never been demonstrated during the induction or maintenance of differentiation by the myelinating Schwann cell. Endogenous cAMP levels decreased to 8–10% of normal nerve by 3 days after crush or permanent transection injury of adult rat sciatic nerve. Whereas levels remained low after transection injury, cAMP levels reached only 27% of the normal values by 35 days after crush injury. Because P₀ mRNA levels were 60% of normal levels by 14 days and 100% by 21 days after crush injury, cAMP increased only well after P₀ gene induction. cAMP, therefore, does not appear to trigger myelin gene induction but may be involved in myelin assembly or maintenance. Forskolin, an activator of adenylyl cyclase, increased endoneurial cAMP levels only in the normal nerve, and in the crushed nerve beginning at 16 days after injury, but at no time in the transected nerve. Only by treating transected nerve with 3-isobutyl-1-methylxanthine (IBMX), an inhibitor of cAMP phosphodiesterases, in combination with forskolin was it possible to increase cAMP levels. No induction of myelin genes, however, was observed with short- or long-term treatment with IBMX and forskolin in the transected nerve. A three-fold increase in phosphodiesterase activity was observed at 35 days after both injuries, and a nonmyelinated nerve was shown to have even higher activity. These experiments, therefore, suggest an important role for phosphodiesterase in the inactivation of this second messenger-dependent stimuli when Schwann cells are non-myelinating, such as after sciatic nerve injury or in the nonmyelinated nerve, which again implies that cAMP may be required for the maintenance of the myelin sheath.     

Nerve Growth Factor Administration Attenuates Cognitive but Not Neurobehavioral Motor Dysfunction or Hippocampal Cell Loss Following Fluid-Percussion Brain Injury in Rats

Abstract: Lateral fluid-percussion brain injury in rats results in cognitive deficits, motor dysfunction, and selective hippocampal cell loss. Neurotrophic factors have been shown to have potential therapeutic applications in neurodegenerative diseases, and nerve growth factor (NGF) has been shown to be neuroprotective in models of excitotoxicity. This study evaluated the neuroprotective efficacy of intracerebral NGF infusion after traumatic brain injury. Male Sprague-Dawley rats received lateral fluid-percussion brain injury of moderate severity (2.1–2.3 atm). A miniosmotic pump was implanted 24 h after injury to infuse NGF (n = 34) or vehicle (n = 16) directly into the region of maximal cortical injury. Infusions of NGF continued until the animal was killed at 72 h, 1 week, or 2 weeks after injury. Animals were evaluated for cognitive dysfunction (Morris Water Maze) and regional neuronal cell loss (Nissl staining) at each of the three time points. Animals surviving for 1 or 2 weeks were also evaluated for neurobehavioral motor function. Although an improvement in memory scores was not observed at 72 h after injury, animals receiving NGF infusions showed significantly improved memory scores when tested at 1 or 2 weeks after injury compared with injured animals receiving vehicle infusions ( p < 0.05). Motor scores and CA3 hippocampal cell loss were not significantly different in any group of NGF-treated animals when compared with controls. These data suggest that NGF administration, in the acute, posttraumatic period following fluid-percussion brain injury, may have potential in improving post-traumatic cognitive deficits.     

Lipid changes in mature-green bell pepper fruit during chilling at 2°C and after transfer to 20°C subsequent to chilling

Lipid composition and pigment content in bell pepper ( Capsicum annuum L. cv. Bell Tower) fruit that were freshly harvested, chilled 14 days at 2° C. or chilled and then transferred to 20 °C for 3 days ("rewarmed") were determined. There was slight to moderate loss of membrane glycerolipids during chilling, with much greater losses after chilled fruit was rewarmed. Galactolipid (GL) loss exceeded that of phospholipid (PL). The ratio of monogalactosyl -to digalactosyl-diacylglycerol did not change in chilled or in rewarmed fruit, and there was no chlorophyll loss, but the amount of neutral carotenes declined during chilling and dropped further alter rewarming. Only minor changes in total membrane sterols (TMS = free sterols + steryl glycosides + acylated steryl glycosides) were noted in chilled and in rewarmed fruit (a small increase followed by a small decrease), but major changes occurred in sterol glycosylation and esterification. The ratio of stigmasterol to sitosterol increased during chilling and rose further after rewarming. Due to PL loss, the ratios of TMS and free sterols to PL increased in rewarmed fruit. The ratio of linolenate (18:3) to linoleate (18:2) rose during chilling and after rewarming in all fatty-acyl lipids (GL. PL. and acylated steryl glycosides), but the unsaturation index increased only in GL. These results indicate that most membrane damage occurs after rewarming of chilled fruit and that the chloroplasts are especially chilling sensitive.     

Synthesis of Serotonin in Traumatized Rat Brain

Abstract: Previous studies have demonstrated that focal freezing lesions in rats cause a widespread decrease of cortical glucose use in the lesioned hemisphere and this was interpreted as a reflection of depression of cortical activity. The serotonergic neurotransmitter system was implicated in these alterations when it was shown that (1) cortical serotonin metabolism was increased widely in focally injured brain and (2) inhibition of serotonin synthesis prevented the development of cortical hypometabolism. In the present studies we applied an autoradiographic method that uses the accumulation of the ¹⁴C-labeled analogue of serotonin α-methylserotonin to assess changes in the rate of serotonin synthesis in injured brain. The results confirmed that 3 days after the lesion was made, at the time of greatest depression of glucose use, serotonin synthesis was significantly increased in cortical areas throughout the injured hemisphere. The increase was also seen in the dorsal hippocampus and area CA3, as well as in the medial geniculate and dorsal raphe, but not in any other subcortical structures including median raphe. Present results suggest that the functional changes in the cortex of the lesioned hemisphere are associated with an increased rate of serotonin synthesis mediated by activation of the dorsal raphe. We also documented by α-[¹⁴C]aminoisobutyric acid autoradiography that there was increased permeability of the blood-brain barrier, but this was restricted to the rim of the lesion.     

Phosphorylation of Myristoylated Alanine-Rich C Kinase Substrate (MARCKS) by Proline-Directed Protein Kinases and Its Dephosphorylation

Abstract: Excitatory amino acid (EAA) neurotransmitters may play a role in the pathophysiology of traumatic injury to the CNS. Although NMDA receptor antagonists have been reported to have therapeutic efficacy in animal models of brain injury, these compounds may have unacceptable toxicity for clinical use. One alternative approach is to inhibit the release of EAAs following traumatic injury. The present study examined the effects of administration of a novel sodium channel blocker and EAA release inhibitor, BW1003C87, or the NMDA receptor-associated ion channel blocker magnesium chloride on cerebral edema formation following experimental brain injury in the rat. Animals (n = 33) were subjected to fluid percussion brain injury of moderate severity (2.3 atm) over the left parietal cortex. Fifteen minutes after injury, the animals received a constant infusion of BW1003C87 (10 mg/kg, i.v.), magnesium chloride (300 µmol/kg, i.v.), or saline over 15 min (2.75 ml/kg/15 min). In all animals, regional tissue water content in brain was assessed at 48 h after injury, using the wet weight/dry weight technique. In saline-treated control animals, fluid percussion brain injury produced significant regional brain edema in injured left parietal cortex ( p < 0.001), the cortical area adjacent to the site of maximal injury ( p < 0.001), left hippocampus ( p < 0.001), and left thalamus ( p = 0.02) at 48 h after brain injury. Administration of BW1003C87 15 min postinjury significantly reduced focal brain edema in the cortical area adjacent to the site of maximal injury ( p < 0.02) and left hippocampus ( p < 0.01), whereas magnesium chloride attenuated edema in left hippocampus ( p = 0.02). These results suggest that excitatory neurotransmission may play an important role in the pathogenesis of posttraumatic brain edema and that pre- or post-synaptic blockade of glutamate receptor systems may attenuate part of the deleterious sequelae of traumatic brain injury.