Objective To investigate the changes and clinical significance of the plasma cytokines and endothelium function in patients with chronic pulmonary heart failure disease at high altitude area.Methods Plasma levels of tumor necrosisfactor-alpha(TNF-?),interleukin-6(IL-6),endothelin-1(ET-1) were measured in 278 chronic pulmonary heart patients with various degrees of heart failure and in 48 healthy controls.Left ventricular ejection fraction(LVEF),Right ventricular ejection fraction(RVEF) and Pulmonary(PASP) were examined with echocardiography.Results Plasma levels of TNF-?,IL-6,ET-1 were elevated in patients of functional classes Ⅱto Ⅳ as compared with age-matched control subjects and were progressively elvated with the decreasing functional status of the patients.The levels of TNF-?,IL-6,ET-1 respectively were positively correlated with PASP but negtively correlated with LVEF and RVEF(P

Human organ donation has entered a high-quality development stage in China, which proposes new requirements for the operation and management of Organ Procurement Organization (OPO). Strengthening cost management of OPO contributes to maintaining healthy and sustainable development of organ donation and highlighting the public welfare and social responsibility of OPO. Therefore, in this article, cost management was taken as the breakthrough point and the concept of value chain cost management was introduced to comprehensively analyze the internal and external value activities of OPO from the aspects of excessively high cost hindering the development of organ donation, value chain cost management promoting high-quality development of organ donation and OPO cost management optimization strategies based on value chain theory, aiming to provide reference for lowering internal cost, expanding the range of cost management and improving industry supervision, thereby reasonably controlling the cost of different activities on the organ donation value chain, achieving the goal of restraining excessive increase of organ procurement cost and promoting healthy development of organ donation and transplantation in China.

High-quality development is the primary task of building a socialist modern country in an all-round way. Organ donation and transplantation in China are evolving from high-speed growth to high-quality development, which put forward new requirements for the safe, stable and healthy operation of Organ Procurement Organization (OPO). Safety is the foundation and prerequisite for achieving the goal of high-quality development. As an independent and comprehensive department, internal audit should create new achievements in the new era. The department should include OPO and organ donation into the scope of internal audit, shift the emphasis upon the overall development of organ donation. Besides, it should fully consider the actual situation in different places, conduct all-round, objective and fair evaluation, provide evaluation and consulting services for OPO to properly implement organ donation, and give full play to the supervision and prevention role of internal audit.

Objective:To investigate the effect of lateral hydraulic injury(LFPI)on the integrity of blood-brain bar-rier in rats and its molecular mechanism.Methods:The rat LFPI model was prepared.Neurological impairment of rats was assessed by neurological severity score(NSS).The integrity of blood-brain barrier was assessed by dry/wet ratio test and Evans blue penetration test.The expressions of zonula occludens-1(ZO-1),occludin,and aquaporin 4(AQP4)were detected by Western Blot.Results:LFPI resulted in neurological dysfunction,increased cerebral water content,increased Evans blue permeability,decreased occludin and ZO-1 expression,and increased AQP4 expression.Conclusion:LFPI can cause cerebral edema and damage the integrity of blood-brain barrier in rats.

Objective To investigate the effect of melatonin on mice with ischemia-reperfusion via a silent information regulator 1 (SIRT1) reducing mitochondrial oxidative stress mechanism. Methods A transient middle cerebral artery occlusion ( MCAO) cerebral ischemia-reperfusion ( IR) model in mice was established by the suture-occluded method. One hundred and ninety mice were injected with melatonin intraperitoneally or the SIRT1 inhibitor (EX527) intracerebroventricularly,30 dead and model failure mice were excluded. They were divided into IR,melatonin,melatonin +EX527,and EX527 groups (n =40 in each group ) according to the random number table. The cerebral infarct volume was detected by the triphenyltetrazolium chloride (TTC) method,the brain edema was measured by the wet and dry weight method and the neurological deficit scores were measured. Western blot was used to detect SIRT1,Ac-P53, acetylated-nuclear factorκB (Ac-NF-κB),BCl2,Bax proteins in the mitochondria and cytoplasm,as well as the cytochrome C protein expression. A single factor analysis of variance was used for comparison among the groups. Results ( 1 ) There were significant differences in cerebral infarction volume, neurological dysfunction scores and cerebral edema among the four groups ( F values,16. 452,23. 622,and 18. 786, respectively (all P<0. 05). There were significant differences in the expression levels of SIRT1,Ac-P53, Ac-NF-κB,BCl2, and Bax among the four groups ( F values, 2348. 158, 1434. 841, 7042. 563, 14627. 128,and 691. 475,respectively,all P<0. 05). There were significant differences in mitochondrial membrane potential,mitochondrial reactive oxygen species,and complex I activity in mice among the four groups (F value,28. 454,33. 728 and 29. 716,respectively,all P <0. 05). (2) Compared with the IR group,the infarct volume was reduced (32 ± 5 mm3 vs. 57 ± 5 mm3,P<0. 05),neurological deficit scores were decreased (2. 4 ± 0. 3 vs. 3. 5 ± 0. 3,P<0. 05);brain edema was reduced (80. 2 ± 0. 9% vs. 83. 9 ± 1. 2%,P<0. 05);the expression levels of SIRT1 and anti-apoptosis protein BCL2 were increased in the melatonin group (P<0. 05);the expression levels of pro-apoptotic protein BAX and Ac-P53,Ac-NF-κB were reduced ( P <0. 05 );the mitochondrial membrane potential, mitochondrial complex I activity and cytochrome C level were increased (P<0. 05);and the cytoplasmic reactive oxygen species and cytochrome C level were decreased (P < 0. 05). (3) Compared with the melatonin group,cerebral infarction volume were increased (42 ± 5 mm3 vs. 32 ± 5 mm3,P < 0. 05);nerve dysfunction scores were increased(3. 2 ± 0. 3 vs. 2. 4 ± 0. 3,P<0. 05);cerebral edema was aggravated (83. 4 ± 0. 8% vs. 80. 2 ± 0. 9%, P < 0. 05 );the expression levels of SIRT1 and anti-apoptotic protein BCL2 were reduced (P <0. 05);the pro-apoptotic protein BAX,Ac-P53,and Ac-NF-κB expression levels were increased (P<0. 05);the mitochondrial membrane potential and mitochondrial complex I activity and cytochrome C level were decreased (P<0. 05);and the cytoplasmic reactive oxygen species and cytoplasmic cytochrome C level were increased in the melatonin+EX527 group (P<0. 05). Conclusion In ischemic stroke model mice, melatonin plays a neuroprotective role by activating the SIRT1 signaling pathway and reducing oxidative stress injury and cell death in mitochondria,thus plays a role in cerebral protection.

Objective To determine the factors that influence the development of abnormal thyrotropin (TSH) level in an euthyroid population.Methods We conducted a follow-up study in 3 communities with different iodine status.Of the 3403 euthyroid subjects at baseline screened in 1999,80.1% ( n = 2727 ) was visited and sampled in 2004 for measuring TSH,thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb).Results Iodine status in the 3 communities were stable.Decreased TSH level( <0.3 mU/L) developed in 2.5% (n =68) of sampled subjects,while raised TSH level( > 4.8 mU/L) in 2.4% (n = 64).A logistic analysis showed that risk factors for developing decreased TSH level included positive conversion of TPOAb (OR = 5.5 ),positive TPOAb both in 1999 and in 2004 ( OR = 4.0),positive TgAb in 2004 ( OR = 3.7) and TSH < 1.0 mU/L in 1999 ( OR = 2.6).Risk factors involved in developing raised TSH level included iodine status of Zhangwu community ( OR = 4.1 ),iodine status of Huanghua community ( OR = 3.9),positive TgAb in 2004 ( OR = 3.7 ),positive TPOAb both in 1999 and 2004 (OR =3.6),positive conversion of TPOAb (OR =2.7) and TSH > 1.9 mU/L in 1999 (OR = 2.6 ).Conclusions Exposure to long-term iodine excess imposes danger of developing hypothyroidism.The risk will be even higher when exposing to iodine adequacy after correction of iodine deficiency.An interval between 1.0 and 1.9 mU/L of TSH level was optimul with the least probability of developing abnormal TSH level.

Objective:To investigate the effects of melatonin(MLT)on hypothalamic-pituitary-adrenal(HPA)axis in posttraumatic stress disorder(PTSD)rats induced by foot shocks.Methods:The rat model of PTSD was prepared by plantar electroshock,and MLT was given by intraperitoneal injection.The behavioral changes of rats were detected by rejection reaction test,the mRNA expression of corticotropin-releasing hormone(CRH)in hypothalamus was detected by real time RT-PCR,and the contents of adrenocorticotropin hormone(ACTH),epinephrine(EPI)and glucocorticoid(GC)in serum were detected by enzyme-linked immunosorbent assay(ELISA).Results:In the PTSD group,the rejection reaction was obvious,the expression of CRH mRNA in hypothalamus was increased(P＜0.05),the serum ACTH and EPI were increased(P＜0.05),but the GC level was decreased(P＜0.05).After MLT treatment,the rejection reaction of PTSD rats was significantly alleviated,CRH mRNA expression in hypothalamus was decreased(P＜0.05),serum ACTH and EPI levels were decreased(P＜0.05),and GC levels were increased(P＜0.05).Conclusion:MLT treatment can relieve the symptoms of PTSD and restore the neuroendocrine balance of HPA axis in rats.

Objective:To investigate the effect of minocycline on neuroinflammation of rats with post-traumatic stress disorder(PTSD).Methods:The rat model of PTSD was prepared by a single prolonged stress(SPS)method,and the rats were treated with minocycline(PTSD+Mino group)or normal saline(PTSD group)by gavage.The behavioral changes of rats were detected by light-dark box test.The expression of ionized calcium-binding adapter molecule 1(Iba-1)in hippocampus was detected by immunohistochemical staining.The contents of IL-1β and TNF-α in hippocampus were detected by ELISA,and the expression levels of IL-1β and TNF-α mRNA in hippocampus were detected by real-time RT-PCR(qRT-PCR).Results:After 3 days of SPS stimulation,the anxiety-like behavior of rats was obvious,the expression of Iba-1 in hippocampus was increased,and the contents of IL-1β and TNF-α in hippocampus were in-creased.Minocycline treatment significantly reduced anxiety-like behavior and decreased the expression of Iba-1 in the hippocampus of PTSD rats.Meanwhile,minocycline treatment also decreased the levels of IL-1β and TNF-α mRNA and protein in the hippocampus.Conclusion:Minocycline can improve the anxiety-like behavior of PTSD rats by inhibiting the activation of microglia.

Objective:To study the role of DDX3X/NF-κB pathway in early neuronal apoptosis in subarachnoid hemorrhage(SAH)mice.Methods:The mouse model of SAH was established by internal carotid artery puncture,and the neurological function score of the mice was evaluated.The DDX3X expression was knocked down using recombinant lentivirus expressing DDX3X targeted shRNA(Lv-shDDX3X),or the NF-κB pathway was inhibited by NF-κB-IN-1(IN-1).Western Blot was used to detect the expression of DDX3X and NF-κB(p65)in mouse cortex.TUNEL/NeuN staining was used to detect the apoptosis of cerebral cortex neurons.Results:Twenty-four hours after SAH operation,the neurological function of mice was significantly impaired(P＜0.05).While the expression of DDX3X was signifi-cantly increased and the expression of NF-κB(p65)was significantly decreased in the cortex(P＜0.05).When the DDX3X expression is knocked down firstly,then SAH surgery is performed.The neurological function of mice was sig-nificantly recovered,and the expression of NF-κB(p65)protein was significantly higher than that in SAH group(P＜0.05);If the NF-κB activity was inhibited by IN-1 while DDX3X knockdown,there is no significant recovery of neuro-logical function in SAH mice.TUNEL/NeuN staining showed that the number of TUNEL-positive neurons in the brain tissue after DDX3X knockdown was less than that in the SAH group(P＜0.05),while the number of TUNEL-positive neurons was not significantly reduced when IN-1 was used to inhibit NF-κB activity at the same time of DDX3X knock-down.Conclusion:DDX3X/NF-κB mediated cell death in mice with early brain injury after SAH.

Donation after death is the most important ethical principle to carry out organ donation after citizens’ death. The newly-revised Regulations on Human Organ Donation and Transplantation does not define death, and avoids the key question of “whether to recognize brain death”. Certain legal risks or damages to the rights and interests of donors may exist in organ donation. Death is an inevitable part of human life. It is necessary to establish specific criteria, which is also the only approach, to define death in any era. Death criteria are established based on the view of death, and restricted by the development level of productive forces and other social factors. The determination of death criteria hugely varies between China and the West. To standardize organ donation and transplantation and promote high-quality development of organ donation, medical staff must adhere to the principle of pure motivation, take informed consents as the premise, respect the donors' and their close relatives' rights to choose their own death criteria, strictly follow the death judgment procedures and operating norms, and ensure the scientificity, accuracy and fairness of death determination.