The outcome of the elderly patients with acute myeloid leukemia (AML) has not improved in the last three decades. Their clinical features limit the ability to tolerate intensive cytotoxic chemotherapy and result in greater early mortality. The AML seen in elderly patients is also more likely to have greater resistance to therapy. Attempts to improve outcome have generally been unsuccessful But further manipulation of standard cytotoxic chemotherapy alone is unlikely to improve the outcome for the majority of patients with AML.

For the minimized phase transtorming risk, the most stable polymorph is generally considered as the desirable solid form for pharmaceutical applications. However, occasionally, the stable form may have some shortcomings such as low solubility, dissolution rate and bioavailability, etc. In that case, the metastable form which is kinetically stable at room or lower temperature could be selected. Using metastable form may result in polymorph transformation in pharmaceutical manufacture and storage. Hence, the knowledge of the transformation between solid forms is essential to the development of the drug materials. In this paper, we will review the recent studies in the area of crystal conversion of polymorphs and hydrates, to illustrate some cases to introduce the types, conditions and mechanisms of the crystalline solid transformation.
Biological Availability ; Chemistry, Pharmaceutical ; methods ; Crystallization ; Drug Stability ; Kinetics ; Pharmaceutical Preparations ; chemistry ; Solubility

Animals ; DNA Damage ; DNA Repair ; DNA-Activated Protein Kinase ; Humans

China ; Metals, Heavy ; Research Support as Topic ; statistics & numerical data

Objective To observe the effect of estrogen on H2O2-induced apoptosis and to explore the mechanism of protection by estrogen.Methods Setting up the experimental model of apoptosis induced by H2O2 in PC12 cells. The viability of cells was assessed by MTT assay. The activity of lactate dehydrogenase was detected by colorimetry. Hoechst 33258 was used as indicator of apoptosis. Apoptotic cells were measured by flow cytometry (FCM) with propidium iodide stain. The activity of caspase-3 was detected by colorimetry. Results H2O2 significantly decreased the viability of cell, increased LDH release and promoted apoptosis as well as caspase-3 activity in PC12. Estrogen markedly reduced these changes. Conclusion Estrogen reduces apoptosis induced by H2O2, and its mechanisms may be explained by inhibition of activation of caspase-3.

ObjectiveTo observe the effects of the two kinds of rigid fixed bridge design on the stress of the alveolar bone of mandibular first molar after hemisection.MethodsThe normal mandibular first molars were selected as control group. The two-abutment teeth and three-abutment teeth rigidly fixed bridge designs were selected as trial group. Stress distributions in the remaining sections of the alveolar bone models were evaluated with photoelastic stress analysis method.ResultsThe stress values of two kinds of rigid fixed bridge design were higher than the control group but still below the twice. There was no significantly difference between two-abutment teeth rigidly fixed bridge design and three-abutment teeth rigidly fixed bridge design (P>0.05).ConclusionTwo-abutment teeth rigidly fixed bridge of mandibular first molar should be chosen after hemisection.

ObjectiveTo discuss the design and fabrication of the photoelastic model of mandibular first molar after hemisection.MethodsAccording to principles of similarity, different materials were used to manufacture the photoelastic model of mandibular first molar with hemisection, which included teeth, alveolar bone and pericementum.ResultsThe photoelastic modle of mandibular first molar with hemisection was manufactured, which was as similar as noumenon in appearance, parameter and boundary condition.ConclusionThe photoelastic model can be applied in qualitative analysis of the stress distribution in the periodontal supporting tissues of mandibular first molar with hemisection.

Aim To investigate the protective effect of RTP1,one of the polysaccharide isolated from Rheum tanguticum,on H2O2 induced apoptosis in IEC-6 cells and its possible mechanism.Methods H2O2(100 mmol?L~-1)was used to induce IEC-6 cell apoptosis.Different doses(10,30,100 mg?L~-1)of RTP1 were administrated before H2O2 was added into IEC-6 cell culture.Cell viability was observed by MTT assay.Reactive oxygen species were measured with laser scanning confocal microscopy(LSCM).DNA content and percentage of apoptosis were assayed by DNA agarose gel electrophoresis,acridine orange staining and flow cytometry.The activation of Caspase-3 was detected with Western blot analysis.Results Following treatment with H2O2 for 2 h,H2O2 induced a significant decrease in cell viability,while DNA ladder was observed and apoptosis percentage was as high as 31.3%.Accumulation of intracellular ROS and increase in Caspase-3 activity were also detected.Pretreatment with RTP1 for 24 h exhibited cytoprotective effects in a dose-dependent manner.RTP1 obviously enhanced cell viability,reduced formation of DNA ladder and significantly reduced the number of cells labeled with Annexin V.The percentage of apoptosis/necrosis cells was markedly decreased to 24.4% and 21.5%,respectively.LSCM showed that RTP1 attenuated the accumulation of ROS.The significant decrease in Caspase-3 activity was detected.Conclusion RTP1 has cytoprotective capacity to antagonize H2O2-induced IEC-6 cell apoptosis and injury,and this effect may be related to decrease ROS and inhibit Caspase-3 activity

AIM To study whether nitric oxide preconditioning induce early protection of neonatal rat cardiomyocytes. METHODS Cultured neonatal rat cardiomyocytes were divided into 6 groups. ①Normal group;②NO group: SNAP(500 ?mol?L -1 ) was added to cell medium 1 h before lethal hypoxia/reoxygenation (HR) injury (6 h hypoxia and 3 h reoxygenation); ③HP group: Cells were cultured for 60min hypoxia followed by 30 min reoxygenation to form hypoxia preconditioning before lethal HR injury;④ L NAME+HP group: Nitric oxide synthase antagonist L NAME was added during HP stage;⑤ L Arg group: L arginine was added to cell medium 1h before lethal HR injury;⑥ L NAME+ L Arg group: Both L NAME and L Arg were added to cell medium 1 h before lethal HR injury;⑦H/R group: Cells underwent lethal HR injury without any treatment. Cardiomyocytes injury was detected by lactate dehydrogenase(LDH) activity and cell viability. RESULTS Nitric oxide preconditioning can protect cardiomyocytes by reducing LDH activity and improving cell viability ( P