老年患者不同证型红外热象舌图温度负荷的变化

目的 :探讨老年不同中医辨证分型的红外热象舌图温度负荷变化。方法 :被测试者分为阴虚证、阳虚证、气滞血瘀证、气血两虚证、湿热证五组。施以冷负荷后 ,红外舌图分析选取七个点温为代表 ,以计算机图像处理系统确定纵横坐标位置 ,对采录的所有红外舌图进行分析、处理。结果 :阴虚组舌尖、舌前两侧点冷负荷前后变化值与正常组比较 P<0 .0 5 ;阳虚组各点冷负荷前后变化值均低于正常组 (除 M点 ) ,且 T点、TL 点、TR点、M点均大于气血两虚组及湿热组 P<0 .0 5 ;气滞血瘀组舌温变化值低于正常 (T点 P<0 .0 5 ) ;气血两虚组各点温变化值均显著低于正常组 (P<0 .0 5～ 0 .0 1)及其他证型组 ;湿热组舌尖、舌前两侧点冷负荷前后变化值与正常组比较 P<0 .0 5 ,且低于阴虚组、阳虚组、气滞血瘀组。结论 :老年不同中医辨证分型的红外热象舌图各有其特征 ,红外热象舌图直观、重复性强 ,可作为中医辨证分型和疗效判断的临床指标     

中医药学研究方法的解构与特性分析

将中医药学研究方法从观念理论、核心方法和技术手段3个方面进行解构，并对其内在特性进行详细分析。明确提出中医药学研究方法的范式特性、观念理论的思辨性、核心方法的主观性以及整体刚性和局部柔性的特性，揭示了中医药研究方法的优势与不足，为中医药研究方法论的创新提供理论依据。     

术中输注氨基酸对硬膜外阻滞复合全麻开胸手术患者围术期体温的影响

目的评价术中输注氨基酸对硬膜外阻滞复合全麻食管癌和贲门癌手术患者围术期深部体温和代谢的影响。方法择期食管癌和贲门癌手术患者21例,ASAⅠ或Ⅱ级,随机分为3组(n =7):从麻醉诱导开始至手术结束,分别静脉输注氨基酸混合液240kJ·h-1(AA组)、等容量乳酸钠林格氏液(LR组)、葡萄糖溶液240kJ·h-1(GLU组)。麻醉诱导前至术后2h每5分钟测定鼓膜温度,于麻醉诱导前即刻、手术开始后1h和术后1h检测指尖血糖,采用4分表法评价术后2h内寒战的发生情况,采用间接测热仪测定术前与术后氧耗。结果与麻醉诱导前即刻比较,术后30min LR组和GLU组氧耗降低,AA组氧耗升高(P<0.01),术后2h LR组、GLU组鼓膜温度降低(P<0.05),AA组差异无统计学意义(P>0.05);与LR组和GLU组比较,AA组术后2h内寒战发生例数减少(P< 0.05),术后30min氧耗增多(P<0.05),LR组与GLU组比较差异无统计学意义(P>0.05)。结论硬膜外阻滞复合全麻开胸手术患者术中静脉输注氨基酸可通过提高基础代谢率,缓解围术期深部体温降低,减少术后寒战发生,而输注葡萄糖不产生此效应。     

论中医病因、致病因素、邪气、邪之关系

邪是一切不正常、不正当的因素,邪气是邪的一部分,主要指六气异常以及疫疠之气等外感因素。两者可以独立于人体而存在,也可以进入人体,成为可能导致疾病的因素,即致病因素,邪(邪气)进入人体是致病因素,未进入人体不是致病因素。未导致疾痛的致病因素不是病因,已经引起疾病的致病因素是病因。     

大鼠创伤性肠粘连模型的制备及黄厚排气颗粒对其粘连程度的影响

为筛选出操作方法简便，结果稳定可控的大鼠创伤性肠粘连模型，观察中药复方黄厚排气颗粒对其粘连程度的影响，选用SD大鼠，手术造成肠粘连模型，用中药复方2．5、5．0、10．0g/kg连续治疗7d后观察肠粘连程度。结果表明，以盲肠型动物模型的制备较为理想，手术易于操作，结果稳定可控。用中药复方治疗后模型动物的肠粘连程度得到明显改善。提示黄厚排气颗粒对术后肠粘连有一定的预防作用。     

清热中药对大鼠下丘脑组织中AVP含量的影响

选用典型的清热中药黄芩、银花、连翘组成清热方,从体温调节中枢神经介质方面来探讨清热类中药的解热作用机制。实验表明影响体温调节中枢解热介质AVP代谢,增加其含量,从而抑制体温调定点上移是清热中药作用机理之一。     

Regulation of major histocompatibility complex (MHC) products in fresh and cultured human fetal pancreata aged 9–16 gestational weeks by gamma-interferon

Immunological data on the human fetal pancreas (HFP) are mainly confined to its constitutive expression of the MHC antigens. However, cytokines, such as gamma-interferon (g-IFN), released by lymphocytes during immune reactions, can induce or upregulate the expression of MHC products in allografts and alter their immunological behaviour. We investigated the effects of g-IFN on fresh and cultured HFPs aged 9–16 gestational weeks (gw). Following g-IFN stimulation of fresh HFPs, there was class I hyperexpression by the ductal cells, and some of the ductal, endothelial and islet cells also became class II⁺. Conventional tissue culture (5% CO₂ in air at 37°C) reduced the number of interstitial class II⁺ cells within the HFP after 1 week but was associated with de novo class I expression by some of the ductal cells. Remarkably, the changes in major histocompatibility complex (MHC) antigen expression by the ductal cells occurred earlier and were markedly enhanced when the HFPs were cultured beforehand. The number of interstitial class II⁺ cells in fresh and cultured HFPs was not influenced by g-IFN. The significance of these observations with regard to clinical HFP transplantation is discussed.     

Specific response to adrenaline in arterial hypertension induced by exogenous calcium deficiency

Injection of a synthetic analog of parathyroid hypertensive factor to WKY rats considerably increases and prolongs pressor response to adrenaline. Synthetic analog injected after adrenaline induces a short-term (3–4 min) and potent (to 250%) rise of arterial pressure. Each subsequent injection of the synthetic analog induces a less pronounced in the amplitude and duration pressor response. The α-adrenoblocker phentolamine completely abolishes the effects of the parathyroid hypertensive factor analog. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 8, pp. 148–150, August, 1997     

Hypothesis: association of the critical region of trisomy 18 and 18q2—syndrome with dermatoglyphic findings and a growth suppressor (deleted in colon cancer) locus

Evidence from the literature is reviewed to suggest that when fingertip dermal ridge patterns in chromosomal deletion syndromes are characteristic of the opposite spectrum of the developmental scale from patterns found in cases trisomic for the same chromosomal region, the association may be a consequence of loci with growth regulatory functions. Evidence is presented that DNA markers at 18q21 should be the first candidate sequences to be used to test this hypothesis in families with fingertip arches segregating in an apparent autosomal dominant fashion.     

Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: II

Cerebral cell volume regulatory mechanisms are activated by sustained disturbances in plasma osmolality. Acute hypernatremia causes a predictable shrinkage of brain cells due to the sudden imposition of a plasma-to-cell osmolal gradient. However, during chronic hypernatremia cerebral cell volume is maintained close to the normal range as a result of the accumulation of electrolytes and organic osmolytes including myo-inositol, taurine, glutamine, glycerophosphorylcholine, and betaine. The increased cytosolic level of these molecules is generally accomplished via increased activity of sodium (Na⁺)-dependent cotransport systems. The slow dissipation of these additional osmotically active solutes from the cell during treatment of hypernatremia necessitates gradual correction of this electrolyte abnormality. Acute hyponatremia leads to cerebral cell swelling and severe neurological dysfunction. However, prolonged hyponatremia is associated with significant reductions in brain cell electrolyte and organic osmolyte content so that cerebral cell volume is restored to normal. While acute hyponatremia can be treated with the administration of moderate doses of hypertonic saline in order to control seizure activity, chronic hyponatremia should be corrected slowly in order to prevent subsequent neurological deterioration. If the rate of correction exceeds 0.5 mmol/l per hour, or if the total increment in serum [Na⁺] exceeds 25 mmol/l in the first 48 h of therapy, then there is an increased risk of the development of cerebral demyelinating lesions. Chronic hyperglycemia activates the brain cell volume regulatory adaptations in the same manner as hypernatremia. Therefore, during the treatment of diabetic ketoacidosis, it is imperative to restore normoglycemia gradually in order to prevent the occurrence of cerebral edema. It is possible that excessive administration of electrolyte-free solutions and high doses of insulin may increase the risk of this complication. While there are some data to suggest that brain cell size is disturbed during acute uremia, additional work is necessary to clarify the role of cerebral cell volume regulation during acute and chronic uremia.