力比泰治疗恶性肿瘤17例初步分析

目的:观察力比泰一、二线治疗恶性肿瘤的临床疗效和毒性反应。方法:17例患者均经病理或细胞学证实,其中复发性非小细胞肺癌5例,复发性乳腺癌4例,恶性间皮瘤3例,晚期原发性肝癌3例,复发性食管癌1例,复发性鼻咽癌1例。首次力比泰给药前7天开始口服叶酸600μg,1次/日,连服至末次力比泰给药后21天停药;Vit-B12 1000μg/次,首次力比泰给药前7天内肌肉注射1次,以后每3个周期肌注1次;力比泰500μg/m2,10min以上静脉滴注,21天为一周期。结果:总有效率(CR+PR)41.8%,白细胞减少11.76%,血小板减少5.88%,恶心呕吐31.76%,口腔炎11.76%,腹泻11.76%。结论:力比泰作为一、二线治疗药物治疗恶性肿瘤疗效明显,且毒性反应轻,耐受性好。     

急性心肌缺血监测方法与作用的现状分析与进展

从急性心肌缺血的临床监测和心电监护两方面概述急性心肌缺血监测的方法和作用,以及综述了其发展历史、现状及进展.     

结直肠癌IL-10和IL-12的检测及意义

目的 检测IL-10和IL-12在结直肠癌组织中含量及术前和术后3周血清浓度并探讨其意义.方法 采用ELISA法检测了46例结直肠癌IL-10和IL-12在癌组织和癌周组织中含量及术前和术后3周血清浓度,与24例良性结肠息肉患者资料为对照.结果 结直肠癌组织IL-10含量高于癌周组织,而癌组织IL-12含量低于癌周组织;Ⅲ、Ⅳ期患者癌组织和癌周组织中IL-10含量高于Ⅰ、Ⅱ期, 而Ⅰ、Ⅱ期癌组织和癌周组织中IL-12含量高于Ⅲ、Ⅳ.术前和术后1周血清IL-10升高而IL-12降低,术后3周血清IL-10和IL-12浓度接近对照组.癌组IL-10和IL-12呈明显负相关.结论 结直肠癌细胞可分泌IL-10抑制IL-12的产生,进而营造免疫抑制微环境,动态检测IL-10和IL-12可反映结直肠癌病期、判断疗效和估计预后.     

Streptozotocin induced activation of oxidative stress responsive splenic cell signaling pathways: Protective role of arjunolic acid

Present study investigates the beneficial role of arjunolic acid (AA) against the alteration in the cytokine levels and simultaneous activation of oxidative stress responsive signaling pathways in spleen under hyperglycemic condition. Diabetes was induced by injection of streptozotocin (STZ) (at a dose of 70 mg/kg body weight, injected in the tail vain). STZ administration elevated the levels of IL-2 as well as IFN-γ and attenuated the level of TNF-α in the sera of diabetic animals. In addition, hyperglycemia is also associated with the increased production of intracellular reactive intermediates resulting with the elevation in lipid peroxidation, protein carbonylation and reduction in intracellular antioxidant defense. Investigating the oxidative stress responsive cell signaling pathways, increased expressions (immunoreactive concentrations) of phosphorylated p65 as well as its inhibitor protein phospho IκBα and phosphorylated mitogen activated protein kinases (MAPKs) have been observed in diabetic spleen tissue. Studies on isolated splenocytes revealed that hyperglycemia caused disruption of mitochondrial membrane potential, elevation in the concentration of cytosolic cytochrome c as well as activation of caspase 3 leading to apoptotic cell death. Histological examination revealed that diabetic induction depleted the white pulp scoring which is in agreement with the reduced immunological response. Treatment with AA prevented the hyperglycemia and its associated pathogenesis in spleen tissue. Results suggest that AA might act as an anti-diabetic and immunomodulatory agent against hyperglycemia.     

Forgiveness and purpose in life as spiritual mechanisms of recovery from substance use disorders

Spirituality has often been associated with recovery from substance use disorders through its emphasis in faith-based rehabilitation programs. The purpose of this article is to describe some psychological dynamics that may explain how spirituality aids in the treatment of substance abuse and dependence. Forgiveness and purpose in life are proposed as “spiritual mechanisms” that partially mediate a spiritually directed recovery. Recent empirical studies on spirituality and recovery from substance use disorders are discussed in relation to 12-steps of Alcoholics Anonymous and Christian principles in order to describe how forgiveness and purpose in life interact with spiritual development in substance use disorder treatment programs. A theoretical model detailing the relationship between spirituality, forgiveness, purpose, and recovery is presented based on anecdotal and empirical literature.     

A patient with the inability to maintain in vivo levels of bound cobalamin (Cbl) and manifestations of tissue deficiency of Cbl

A 39-year-old woman presented with mild anemia, glossitis, an increased MCV, a low serum cobalamin (Cbl) (vitamin B12), mild tissue deficiency of Cbl, but with neither malabsorption of Cbl, impaired intake, nor deficiency of or inactivity of transcobalamin II (TC II). Because of a persistently low holo-TC II (TC II carrying Cbl as the circulating complex of TC II-Cbl), much of the evaluation was focused on the patient's TC II. Her TC II promoted the uptake of Cbl, reacted with anti-TC II, and bound Cbl in vitro. A test dose of 200 micrograms of cyanocobalamin (CN-Cbl) i.m. increased her holo TC II to levels higher than those in healthy persons, but with a much more abrupt fall to a subnormal level. Two milligrams of CN-Cbl i.m. followed by 100 micrograms i.m. monthly failed to maintain normal amounts of circulating TC II-Cbl or to overcome the tissue deficiency of Cbl. One milligram i.m. weekly or daily p.o. corrected both. The low holo TC II was considered to be responsible for the clinical expression and may have been primary to the reduced amounts of total and holo R binder of Cbl in the circulation. This study of a newly recognized defect points out the need for circulating holo TC II, a rational use of pharmacologic amounts of Cbl, and a possible interrelationship between TC II and the R binder of Cbl.     

体内药物累积法研究白血康的表观药物动力学

采用体内药物累积法测定小鼠 ip 白血康后的体内过程和药动学参数,白血康在小鼠体内的过程符合二室开放模型,模型方程为:体存率%=87.1711e~(-1.0952t) 138.1771e~(-0.0272t),t_(1/2)α=0.6328h,t_1/2β=25.48h,k_(21):0.6821h~(-1),k_(12)=0.3966h~(-1),k_(10)=0.0437h~(-1),Vc=3.55L/kg.     

Prevention of abnormal calcium accumulation in postischemic gerbil brain by vinconate

We investigated the effect of vinconate on ischemia-induced calcium accumulation in the gerbil brain. The animals were allowed to survive for 7 days after 10 min of ischemia. Abnormal calcium accumulation was evaluated in the gerbil brain after ischemia. Following 10 min ischemia, abnormal calcium accumulation was found in the neocortex, the striatum, the hippocampus, the thalamus, the substantia nigra and the inferior colliculus. Intraperitoneal administration of vinconate (100 mg/kg) immediately after 10 min of ischemia significantly reduced the areas of abnormal calcium accumulation only in the striatum. However, the application of vinconate (100 and 300 mg/kg) 10 min before ischemia dose-dependently decreased the areas of abnormal calcium accumulation in the striatum, the thalamus and the substantia nigra. Morphological observation revealed neuronal damage in the identical sites of the abnormal calcium accumulation. Furthermore, a autoradiographic study using 14C-vinconate showed that this drug easily penetrates the blood-brain barrier and especially localizes in the striatum and the thalamus after 5 min ischemia. The result suggests that vinconate reduces the areas of abnormal calcium accumulation in the postischemic gerbil brain. This effect seems to be mediated via the height distribution in the brain following ischemia.     

Restoration of decreased suppressor cells by vitamin B12 therapy in a patient with pernicious anemia

A unique case of pernicious anemia is described. Initially, the percentage of OKT8-positive blood cells was markedly decreased, resulting in an increase in the OKT4/OKT8 ratio. The level of OKT8-positive blood cells was, however, returned to normal after vitamin B12 therapy. The finding may propose a possible role of the imbalance of blood lymphocyte subpopulations on the pathogenesis of pernicious anemia and also a responsibility of vitamin B12 for such a selective reduction in the OKT8-positive blood cells.     

各种分化诱导剂对人白血病HL-60细胞内中性糖脂合成的影响

作者采用[~(14)C]-标记的半乳糖研究HL-60细胞分化过程中中性糖脂的合成,以了解佛波酯(TPA)、二甲基亚砜(DMSO]、GM3(NeuAc-Gal-Glc-Cer)、GMI[Gal-GalNAc-(NeuAc)Gal-Glc-Cer]和硫脂对其生物合成的影响。TPA、GM3不但能诱导HL-60细胞分化为单核细胞,而且明显地增加[~(14)C]-半乳糖的掺入。TPAGM3在不同程度上促进[~(14)C]-标记的中性糖脂合成,其中主要促进二己糖基神经酰胺(GL2)合成。DMSO诱导HL-60细胞分化为粒细胞,不仅显著地抑制了[~(14)C]-半乳糖掺入,而且抑制了[~(14)C]-标记的中性糖脂的合成,但是促进-已糖基神经酰胺[GL1]的合成。这些结果提示中性糖脂的生物合成与HL-60细胞的分化有关。