Objective To identify the posttraumatic growth (PTG) level of cancer patients and to examine the effects of rumination on posttraumatic growth of cancer patients.Methods A total of 312 cancer patients were recruited by convenience sampling.A cross-sectional study was conducted in cancer patient by means of questionnaires that included demographic scale,Event Related Rumination Inventory and the Posttraumatic Growth Inventory (PTGI).Results A total score of event-related rumination in cancer patients was 25.13±11.11,and the total score of posttraumatic growth was 67,21±14.66.The PTG was positively correlated to event-related rumination in cancer patients (r=0.384,P ＜ 0.01).Multiple stepwise regressions indicated that the variables of deliberate of rumination,gender,age,degree of psychological distress,intrusive rumination and education level were main predictors of PTG.Among those deliberate of rumination positively predicts PTG,while intrusive rumination negatively predicts PTG.The level of PTG in female gender cancer patients were higher than male patients,younger age and high education level,less psychological distress patients related to higher PTG.Conclusions Cancer patients reported a lower level of rumination and PTG.Clinical healthcare providers should inspire and promote cancer patients' deliberate rumination,decrease their intrusive rumination,pay attention to male,more psychological distress,older age and lower education level patients,in order to facilitate patients' PTG and then improve their quality of life.

Objective:To explore the impact of cognitive evaluation, processing and social support on post-traumatic growth of patients with accidental trauma, and analyzed their impact path.Methods:Cognitive evaluation scale, event-related rumination meditation scale, social support scale and Chinese version of post-traumatic growth questionnaire were used to conduct a cross-sectional survey on 336 patients with accidental trauma.Results:The total score of post-traumatic growth (PTG) of patients with accidental trauma (58.74±13.53) and the total score of purposeful rumination and total rumination were positively correlated with the total score of post-traumatic growth and all dimensions ( r=0.578, 0.439, P<0.01); the total score of invasive rumination was negatively correlated with the total post-traumatic growth score ( r=-0.144, P<0.01); the social support was positively correlated with the total post-traumatic growth score ( r=0.492, P<0.01). Positive cognitive evaluation and purposeful rumination meditation played a partial mediating role between social support and post-traumatic growth. The mediating effect was 0.142, accounting for 13% of the total effect. Conclusion:Social support not only directly predicted the post-traumatic growth, but also indirectly affected the post-traumatic growth through social support positive cognitive evaluation, and purposeful rumination.

Aim To observe the effect of Ginkgo biloba extract 50(GBE50)on L-type calcium current and cytosolic[Ca~(2+)]_i in ischemic guinea pig ventricular myocytes.Methods Single ventricular myocytes were isolated by enzymatic dissociation. I Ca-L was recorded by whole-cell patch clamp technique in voltage clamp mode.[Ca~(2+)]_i was detected by laser confocal micros-copy and represented by relative fluorescent intensity (FI).Results During ischemia, the peak Ca~(2+) current was reduced, and the I-U curve of I Ca-L was shifted upward.50 mg·L~(-1) GBE50 reversed the change induced by ischemia(n =6, P >0.05).After perfusing ischemic solution for 12 min, intracellular calcium concentration was increased(n =10, P <0.01).After perfusion with ischemic solution containing 50 mg·L~(-1) GBE50, the increase of intracellular calcium concentration was markedly inhibited(n =10, P >0.05).Conclusion GBE50 can reverse the decrease of I Ca-L and partially inhibit calcium overloading during ischemia.

In recent years,the influence of endemic arsenic poisoning on immune system has caught people's attention.Changes in histone modification patterns may be one of the mechanisms of arsenic regulated gene expression,arsenic plays an important role in differentiation,proliferation and function of immune cells.Arsenic has a certain effect on the differentiation and function of T cells,and it is rarely studied whether the process is regulated by histone methylation.In this paper,the study of histone methylation in arsenic induced T cellular immune damage is reviewed.

Endemic arsenicosis is a disease with complex systemic damage,but the mechanism and its control strategy are mostly focused on a single organ or system damage caused by arsenic,and the systemic damage of arsenic exposure remains not fully understood.In recent years,considerable progress has been made in the field of immunology,which made an important contribution for the pathogenic mechanism of various complex diseases,and also brings a new dawn for its prevention and treatment.In consequence,a breakthrough progress is expected to make in aspects of the mechanism and its control strategy of arsenic caused systemic damage from the perspective of immunology.

Arsenic is a common environmental toxin,but also a carcinogen.Long-term exposure to inorganic arsenic can cause multi-system and multi-organ damage in the body,including cancerous and non-cancerous lesions.As one of the main target organs of arsenic exposure,skin damage is of great significance for the diagnosis and health assessment of arsenic poisoning in population threatened by the disease.From the perspective of arsenic exposure and skin cancer,the aim of this article is to summarize the epidemiology,pathogenesis and medical intervention of arsenic-induced skin cancer,and to provide reference for the pathogenesis and prevention of endemic arsenic poisoning related skin diseases.

Endemic arsenicosis is one of the national key endemic diseases in our country. However, due to obscure mechanism of arsenic poisoning, lack of early diagnostic indicators and specific validated therapy, the ideal control of endemic arsenicosis has not yet been obtained. To date, considerable progress has been made to address endemic arsenic poising and also formed various hypotheses, whereas simultaneously there are some problems and the insufficiency such as unclear relationship among those hypotheses and the gap between mechanism studies and translational application. In consequence, enhancing the interactive effects among various mechanisms of arsenic poising and improving its translational application could have more realistic significance for scientific prevention and control of endemic arsenicosis.

Henoch-Sch(o)nlein purpura (HSP) is the common form of systemic vasculitis in children,which characterized by the deposition of immunoglobulin E within the small vessels.The long-term prognosis of HSP depends on the severity of renal involvement.Renal involvement in HSP affects 10％-100％ patients and the clinical manifestations vary from microscopic hematuria to nephritic/nephritic syndrome even renal dysfunction.Early diagnosis,early treatment and long-term follow-up affect the prognosis of HSP patients.As for the treatment of HSP nephritis (HSPN),there have been many reports dealing with the immunosuppressive agents.Now glucocorticoid is the first-line treatment for HSPN,and other immunosuppressive agents offer more choices to treat HSPN especially for severe HSPN.But,the use of immunosuppressive agents still needs large sample multicenter randomized controlled trials and evidence-based study.

Laboratory animal science, as a supporting discipline in life science research, has been set up courses in many universities, especially in medical schools.However, due to the curriculum design was too rigidly attached to tradition, emphasis on theory and cannot adapt to the development of natural science.In this paper, aiming to enhance the teaching effect, we focus on the practice, advance with the times, combine with customized teaching reform of laboratory animal science curriculum, teaching content and teaching forms.

OBJECTIVE To investigate the apoptosis of hepatocytes in arsenic poisoning rats caused by coal-burning and explore the effects of p53-induced mitochondrial apoptotic pathway on arsenic liver injury.METHODS Wistar rats were fed with 164.74 pp m arsenic conta minated grain at the levels of 15%,30% and 60% (arsenic contents were 25,50 and 100 mg·kg -1 ,respectively)for 90 d. The arsenic contents of urine and hair,apoptosis of hepatocytes and mRNA expression of p53,Bax and Bcl2 in peripheral blood and hepatocytes were evaluated.At the sa me ti me,protein expression of p53, Bax and Bcl2 in hepatocytes were analyzed.RESULTS The arsenic contents of urine and hair increased with the elevation of arsenic dose.The apoptotic rate of hepatocytes in arsenic 50 and 100 mg·kg -1 group were 16.49 ±2.06 and 15.83 ±1 .28,respectively which were significantly higher than the control group and arsenic 25 mg·kg -1 group (9.00 ±0.59 and 9.27 ±0.36,respectively,P <0.05).p53 mRNA expression of peripheral blood in arsenic 100 mg·kg -1 group was 2.69 ±1 .84 while p53 mRNA expression of hepatocytes in arsenic 25,50 and 100 mg·kg -1 group were 1 .63 ±0.28, 1 .91 ±0.38 and 1 .71 ±0.18,respectively which were significantly higher than the control group (0.86 ± 0.15 and 1 .22 ±0.12,respectively,P<0.05).Bax mRNA expression of peripheral blood in arsenic 50 and 100 mg·kg -1 group were 1 .36 ±0.30 and 1 .94 ±0.65 while Bax mRNA expression of hepatocytes in arsenic 100 mg·kg -1 group was 1 .34 ±0.23 which were significantly higher than the control group (0.77 ±0.15 and 0.84 ±0.34,respectively,P<0.05).Bcl2 mRNA expression of hepatocytes in arse-nic 100 mg·kg -1 group was 0.98 ±0.50 which was significantly lower than the control group (2.14 ± 1 .15,P<0.05).p53 protein expression of hepatocytes in arsenic 25,50 and 100 mg·kg -1 group were 1 .06 ±0.56,1 .15 ±0.77 and 0.74 ±0.27,respectively while Bax protein expression of hepatocytes in arsenic 50 and 100 mg·kg -1 group were 0.74 ±0.43 and 0.69 ±0.37 which were significantly higher than the control group (0.36 ±0.1 9 and 0.25 ±0.09,respectively,P<0.05).CONCLUSION Arsenic can induce hepatocytes apoptosis and p53-mediated mitochondrial apoptotic pathway may be involved in the develop ment of rat liver injury in arsenic poisoning rats caused by coal-burning.