系统论方法在糖尿病性视网膜病变危险因素及治疗研究中的应用

全球糖尿病患者人数在不断的增多,大约10％的Ⅰ型糖尿病患者在10年后可出现糖尿病性视网膜病变,而大约95％的Ⅱ型糖尿病患者在20年后可出现糖尿病性视网膜病变。目前,糖尿病性视网膜病的发病机制尚不明确,影响其发生发展的因素也很复杂,因此,对糖尿病性视网膜病的发病危险因素及其诊治的研究,具有相当重要的意义。系统论,研究各种物质运动形态所共有的系统联系和关系,具有普遍的方法论意义,为现代医学的进步提供了全新的思维方式和科学方法论原则。本文试用系统论的整体性、优化原理阐述糖尿病性视网膜病变发病的危险因素与治疗进展,为对其深入研究提供方法论依据。     

系统论方法在糖尿病性视网膜病变危险因素及治疗研究中的应用

全球糖尿病患者人数在不断的增多,大约10%的Ⅰ型糖尿病患者在10年后可出现糖尿病性视网膜病变,而大约95%的Ⅱ型糖尿病患者在20年后可出现糖尿病性视网膜病变.目前,糖尿病性视网膜病的发病机制尚不明确,影响其发生发展的因素也很复杂.因此,对糖尿病性视网膜病的发病危险因素及其诊治的研究,具有相当重要的意义.系统论,研究各种物质运动形态所共有的系统联系和关系,具有普遍的方法论意义,为现代医学的进步提供了全新的思维方式和科学方法论原则.本文试用系统论的整体性、优化原理阐述糖尿病性视网膜病变发病的危险因素与治疗进展,为对其深人研究提供方法论依据.     

糖尿病性黄斑水肿的诊疗思考

糖尿病性视网膜病变(diabetic retinopathy,DR)是糖尿病患者严重的眼部并发症之一,而黄斑水肿是导致糖尿病性视网膜病变患者视力下降的主要原因之一,其发病机制、诊断技术和治疗方法是一个辩证发展的过程。因此运用科学哲学方法来分析糖尿病性黄斑水肿(diabetic macular edema,DME)的诊断和治疗显得尤为重要。     

糖尿病性黄斑水肿的诊疗思考

糖尿病性视网膜病变(diabetic retinopathy,DR)是糖尿病患者严重的眼部并发症之一,而黄斑水肿是导致糖尿病性视网膜病变患者视力下降的主要原因之一,其发病机制、诊断技术和治疗方法是一个辩证发展的过程.因此运用科学哲学方法来分析糖尿病性黄斑水肿(diabetic macular edema,DME)的诊断和治疗显得尤为重要.     

糖尿病性视网膜病变的个体化治疗

糖尿病性视网膜病变(DRP)是糖尿病患者致盲的一个主要原因。其发病的多样性决定了对其治疗应该个体化。就其个体化治疗的依据、方法的研究及具体的措施运用哲学原理加以综述。     

糖尿病性视网膜病变的个体化治疗

糖尿病性视网膜病变(DRP)是糖尿病患者致盲的一个主要原因.其发病的多样性决定了对其治疗应该个体化.就其个体化治疗的依据、方法的研究及具体的措施运用哲学原理加以综述.     

糖尿病性视网膜病变综合治疗的策略

糖尿病性视网膜病变（diabetic retinopathy,DRP）是糖尿病的常见并发症,其发病率和致盲率呈逐年上升趋势。半个多世纪以来,已经认识到DRP各种治疗手段都有一定的优势和局限性,单纯依靠一种治疗方法难以取得理想效果。因此,多种手段相结合的综合治疗措施成为糖尿病视网膜病变的一种科学合理的治疗模式。     

基于利益相关者视角的糖尿病视网膜监测服务探析

糖尿病性致盲已成为成年人首要致盲因素之一,通过早期糖尿病视网膜监测和系统治疗可以有效地降低糖尿病视网膜病变发生的几率,因此有效的监测手段对于科学规范管理糖尿病是十分有必要的。由于血糖的正常值和糖代谢异常的诊断切点主要依据血糖值与糖尿病视网膜病变和糖尿病发生风险的关系来确定,因此糖尿病视网膜监测可能会更加精确地监测糖尿病的变化。本文应用利益相关者分析对糖尿病视网膜监测服务开展过程中涉及的各主体利益及存在问题进行探讨,为进一步有效管理糖尿病提供相关建议。     

视网膜手术的发展与思考

视网膜脱离是严重的致盲性眼病之一.视网膜玻璃体疾病的手术治疗是从20世纪开始,首先是Gonin面开辟的视网膜脱离的手术治疗,使得这一疾病从不治变为可治.20世纪70年代以后,玻璃体手术的出现,各种玻璃体替代物更新与临床应用,使视网膜脱离的手术进一步完善与提高.尤其是80年代以后,各种膨胀气体、硅油、全氟化碳液体的应用、眼内光凝、视网膜切开与切除技术的应用,对增生性玻璃体视网膜病变(PVR)的认识和研究不断地深入,尤其是前部PVR的研究等,使玻璃体手术适应症逐步拓宽,手术技术日新月异,视网膜玻璃体手术成功率大大提高.     

糖尿病性视网膜病变综合治疗的策略

糖尿病性视网膜病变(diabetic retinopathy,DRP)是糖尿病的常见并发症,其发病率和致盲率呈逐年上升趋势.半个多世纪以来,已经认识到DRP各种治疗手段都有一定的优势和局限性,单纯依靠一种治疗方法难以取得理想效果.因此,多种手段相结合的综合治疗措施成为糖尿病视网膜病变的一种科学合理的治疗模式.     

Ophthalmological problems of the premature infant

Preterm infants are more likely than term infants to have significant abnormalities of all parts of the visual system leading to reduced vision. The most common problem is retinopathy of prematurity (ROP). The frequency and severity of this disorder is inversely related to gestational age. Damage ranges from minor to catastrophic. Preterm infants also have higher rates of amblyopia, strabismus, refractive error, and cortical visual impairment. The later problem is largely associated with neonatal brain injury. Years later, these children may develop glaucoma and retinal detachments.     

糖尿病的免疫抑制治疗

淡化糖尿病的分型为我们提供了一个全新的思维空间。即传统的1型和至少部分2型糖尿病可能都是一种自身免疫性疾病,而目前流行的炎症学说可能是对认可免疫损伤是糖尿病发病理论的一个过渡,我们应该重新审视糖尿病的早期治疗和研究其慢性并发症的发病机理。我们则采用小别量、长时间的治疗理念,早期接受这种免疫治疗的患者出现低血糖的症状,遂减少胰岛素的剂量;再次出现低血糖,我们就继续减少胰岛素的剂量。结果,有部分患者完全摆脱了胰岛素。我们对糖尿病的再认识是建立在对多脏器活检的基础之上。我们的活检结果表明,糖尿病肾病存在着免疫损伤。糖尿病眼底病变是使患者致盲的主要病因,糖尿病患者的眼底病变是一种自身免疫损伤的结果。我们尝试用小剂量的免疫抑制剂环孢菌素A（25mgbid）治疗糖尿病眼底出血,取得了不错的疗效,也证实糖尿病眼底病变是一种血管炎,与自身免疫病变有关。其他的器官还包括垂体、大脑的血管、糖尿病足、冠心病、皮肤的病变和肌肉活检的免疫组化也均有证据表明,免疫损伤是导致多种慢性并发症的罪魁祸首,是一种多器官免疫损伤的结果无论是1型糖尿病,还是2型糖尿病,肌细胞表面或多或少均有免疫复合物沉积。这些免疫复合物的存在势必会影响胰岛素与肌肉细胞表面的胰岛素受体结合,即胰岛素抵抗的存在。为此,我们在临床上广泛采用了免疫抑制治疗的理念治疗糖尿病。应用小剂量胰岛素和小剂量环孢素A治疗早期发现的糖尿病取得了不错的疗效。唯一担心的副作用发生在肝脏,即部分糖尿病患者会出现总胆红素升高,而也有一部分患者总胆红素不升高。     

Inflammation, glutamate, and glia in depression: a literature review

Multiple lines of evidence suggest that inflammation and glutamate dysfunction contribute to the pathophysiology of depression. In this review we provide an overview of how these two systems may interact. Excess levels of inflammatory mediators occur in a subgroup of depressed patients. Studies of acute experimental activation of the immune system with endotoxin and of chronic activation during interferon-alpha treatment show that inflammation can cause depression. Peripheral inflammation leads to microglial activation which could interfere with excitatory amino acid metabolism leading to inappropriate glutamate receptor activation. Loss of astroglia, a feature of depression, upsets the balance of anti- and pro-inflammatory mediators and further impairs the removal of excitatory amino acids. Microglia activated by excess inflammation, astroglial loss, and inappropriate glutamate receptor activation ultimately disrupt the delicate balance of neuroprotective versus neurotoxic effects in the brain, potentially leading to depression.     

Microglia and inflammation: impact on developmental brain injuries

Inflammation during the perinatal period has become a recognized risk factor for developmental brain injuries over the past decade or more. To fully understand the relationship between inflammation and brain development, a comprehensive knowledge about the immune system within the brain is essential. Microglia are resident immune cells within the central nervous system and play a critical role in the development of an inflammatory response within the brain. Microglia are critically involved with both the innate and adaptive immune system, regulating inflammation and cell damage within the brain via activation of Toll-like receptors, production of cytokines, and a myriad of other intracellular and intercellular processes. In this article, microglial physiology is reviewed along with the role of microglia in developmental brain injuries in humans and animal models. Last, microglial functions within the innate and adaptive immune system will be summarized. Understanding the processes of inflammation and microglial activation is critical for formulating effective preventative and therapeutic strategies for developmental brain injuries.     

糖尿病分型与治疗：我们还需要走多远

由于糖尿病病因至今未明,虽然临床上多采用ADA糖尿病分型方法,但随着对糖尿病病因及发病机制的研究,出现了许多难以用传统的标准进行分类的疾病状态。有人提出淡化糖尿病分型的争论。笔者认为高血糖仅是一种表现,并不是疾病的本质,慢性低活度炎症状态可能是核心机制之一,机体的这种慢性低活度炎症状态可能与糖尿病肾病、抗感染免疫失控以及创伤愈合障碍有关。短时间内控制急性高血糖状态对挽救生命是关键的,但要实现长期是代谢紊乱控制、纠正不良生活习惯、减轻腹内脂肪堆积,进而降低改善机体的慢性炎症状态可能是最全面且安全的唯一措施。     

Models of white matter injury: comparison of infectious, hypoxic-ischemic, and excitotoxic insults

White matter damage (WMD) in preterm neonates is strongly associated with adverse outcome. The etiology of white matter injury is not known but clinical data suggest that ischemia-reperfusion and/or infection-inflammation are important factors. Furthermore, antenatal infection seems to be an important risk factor for brain injury in term infants. In order to explore the pathophysiological mechanisms of WMD and to better understand how infectious agents may affect the vulnerability of the immature brain to injury, numerous novel animal models have been developed over the past decade. WMD can be induced by antenatal or postnatal administration of microbes (E. coli or Gardnerella vaginalis), virus (border disease virus) or bacterial products (lipopolysaccharide, LPS). Alternatively, various hypoperfusion paradigms or administration of excitatory amino acid receptor agonists (excitotoxicity models) can be used. Irrespective of which insult is utilized, the maturational age of the CNS and choice of species seem critical. Generally, lesions with similarity to human WMD, with respect to distribution and morphological characteristics, are easier to induce in gyrencephalic species (rabbits, dogs, cats and sheep) than in rodents. Recently, however, models have been developed in rats (PND 1-7), using either bilateral carotid occlusion or combined hypoxia-ischemia, that produce predominantly white matter lesions. LPS is the infectious agent most often used to produce WMD in immature dogs, cats, or fetal sheep. The mechanism whereby LPS induces brain injury is not completely understood but involves activation of toll-like receptor 4 on immune cells with initiation of a generalized inflammatory response resulting in systemic hypoglycemia, perturbation of coagulation, cerebral hypoperfusion, and activation of inflammatory cells in the CNS. LPS and umbilical cord occlusion both produce WMD with quite similar distribution in 65% gestational sheep. The morphological appearance is different, however, with a more pronounced infiltration of inflammatory cells into the brain and focal microglia/macrophage ("inflammatory WMD") in response to LPS compared to hypoperfusion evoking a more diffuse microglial response usually devoid of cellular infiltrates ("ischemic WMD"). Furthermore, low doses of LPS that by themselves have no adverse effects in 7-day-old rats (maturation corresponding to the near term human fetus), dramatically increase brain injury to a subsequent hypoxic-ischemic challenge, implicating that bacterial products can sensitize the immature CNS. Contrary to this finding, other bacterial agents like lipoteichoic acid were recently shown to induce tolerance of the immature brain suggesting that the innate immune system may respond differently to various ligands, which needs to be further explored.     

The effect of retinal size on the perception of distance in photographs

The effect of the retinal size of a target on the perception of absolute distance to a single target and relative distance between near and far targets was examined with photographic displays including two persons. Retinal size was systematically varied by varying the focal length of the camera lens, the display size, and the viewing distance. The results showed that, although the relationship between the perceived absolute distance and retinal size was not inversely proportional, the perceived absolute distance decreased with an increase in retinal size. This was more evident when the retinal size was changed by varying the focal length. These results suggest that the determinants of the perceived absolute distance were not only the retinal size of the target but also its ratio to the overall display. The results also showed that the perceived relative distances were little influenced by retinal size, but were strongly dependent on the size ratio of the two targets in the display.