近年来，光动力治疗的研究已经取得了令人瞩目的成绩。光动力治疗诱导白血病细胞发生凋亡主要从光敏剂的定位、应用条件、对线粒体和细胞膜的损伤、引起细胞色素c的释放和半胱氨酸蛋白酶（caspase）。3的活化等方面发挥作用。在诸多因素引起凋亡的同时，Bd.2发挥着抗凋亡的作用。除此之外，离子通道的变化也参与凋亡的发生。

The formation of calcium potassium sodium orthophosphate (Ca2KNa(PO4)2) from sodium dihydrogen phosphate dihydrate (NaH2PO4 2H2O), potassium dihydrogen phosphate (KH2PO4) and calcium carbonate (CaCO3) was investigated using differential thermal analysis (DTA), thermal gravimetric analysis (TGA) and powder X-ray diffraction (XRD). DTA showed five distinct thermal events attributed to dehydration of NaH2PO4 2H2O, dehydration of NaH2PO4 and KH2PO4, the transition of amorphous calcium sodium phosphate to-CaNaPO4, the decomposition of CaCO3 to CaO, and the crystallization of Ca2KNa(PO4)2. TGA showed 5.6% weight loss between 70 and 170℃ due to the dehydration of NaH2PO4 2H2O to NaH2PO4; the 7.3% weight loss between 170 and 280℃ is due to the dehydration of NaH2PO4 and KH2PO4; a continuous weight loss over 280-760℃ due to the reaction of melted alkali metal phosphates with CaCO3 and an approximate 8% weight loss between 670 and 840℃ due to the calcination of residual CaCO3. XRD analysis, as a function of temperature, supported the evolution of these events and phases, showed the formation of other intermediates: -CaKPO4 and calcium potassium pyrophosphate (CaK2P2O7). The proposed mechanism of the reaction to Ca2KNa(PO4)2 involves the formation and consumption of these intermediates: acid alkali metal pyrophosphate, metaphosphate, CaK2P2O7 and β-CaNaPO4.

The formation of tricalcium phosphate (TCP) from dicalcium phosphate and calcium carbonate was investigated using differential thermal analysis (DTA), thermogravimetric analysis (TGA), and powder X-ray diffraction (XRD). DTA showed three distinct thermal events attributed to dehydration of dicalcium phosphate dihydrate (brushite, DCPD) to dicalcium phosphate anhydrous (monetite, DCPA), the formation of beta-calcium pyrophosphate (b-Ca2P2O7), and the calcination of calcium carbonate. TGA showed three weight losses corresponding to the three thermal events, respectively. XRD analysis showed that b-TCP formed, beginning at about 900°C, by the reaction of b-Ca2P2O7 with CaO and b-TCP changed to a-TCP above 1200℃. Further examination of the formation of TCP from calcium hydroxide (Ca(OH)2) and DCPA showed that b-TCP would form only after the decomposition of Ca(OH)2 to CaO and from the reaction of CaO with b-Ca2P2O7 at a fairly low temperature of 800℃. In addition, by naturally cooling a-TCP, formed at 1300℃ within the heating furnace, to room temperature, it was difficult to obtain a pure phase of b-TCP. The proposed mechanism of the reaction to form TCP may include the dehydration of brushite to monetite, dehydration of monetite to beta-calcium pyrophosphate, decomposition of calcium carbonate, the formation of b-TCP, and phase transition.

激光微手术的精度通常受到热作用或者热机械效应间接损伤的限制。把激光脉宽调整到与吸收颗粒的热弛豫时间一致可以避免热副作用，可对所选细胞产生选择性处理。这里胶体金与牛肠硷性磷酸脂酶（Alkaline phosphatase，AP）结合物作为分析强吸收颗粒附近的蛋白质变性的模型系统，利用皮秒和纳秒激光对结合体进行照射，在一定的条件下可以使蛋白质失活，并可以使细胞膜的通透性提高。通过计算可知，采用脉宽为皮秒或者纳秒级的激光照射纳米吸收物（胶体金）时，颗粒很容易被加热到几百开，而且热效应仅限于几十纳米的空间范围内。利用纳米吸收颗粒进行激光微手术的方法，在蛋白质失活的情况下对其机理进行了分析。

The underlying ionic mechanisms of ischemic-induced arrhythmia were studied by the computer simulation method. To approximate the real situation, ischemic cells were simulated by considering the three major component conditions of acute ischemia (elevated extracellular K+ concentration, acidosis and anoxia) at the level of ionic currents and ionic concentrations, and a round ischemic zone was introduced into a homogeneous healthy sheet to avoid sharp angle of the ischemic tissue. The constructed models were solved using the operator splitting and adaptive time step methods, and the perturbation finite difference (PFD) scheme was first used to integrate the partial differential equations (PDEs) in the model. The numerical experiments showed that the action potential durations (APDs) of ischemic cells did not exhibited rate adaptation characteristic, resulting in flattening of the APD restitution curve. With reduction of sodium channel availability and long recovery of excitability, refractory period of the ischemic tissue was significantly prolonged, and could no longer be considered as same as APD. Slope of the conduction velocity (CV) restitution curve increased both in normal and ischemic region when pacing cycle length (PCL) was short, and refractory period dispersion increased with shortening of PCL as well. Therefore, dynamic changes of CV and dispersion of refractory period rather than APD were suggested to be the fundamental mechanisms of arrhythmia in regional ischemic myocardium.