Ultrastructure changes associated with brain death in the human donor heart

Abstract Electromicroscopic examinations were carried out on 30 myocardial biopsies taken from 22 human donor hearts immediately after excision (prestorage) or immediately before transplantation (post-storage). All electron micrographs were independently examined by two morphologists. Eleven structures were examined in each micrograph, and each structure was scored according to the degree of injury. A good interobserver correlation was obtained in 84 % of the structures scored. In the prestorage left ventricular biopsies ( n = 11), approximately 20 %-25 % showed moderate to severe ultrastructural injury. The ultrastructural injury observed in the poststorage left ventricular biopsies ( n = 15) was no different from that in the prestorage group, particularly injury to the sarcomere and mitochondria. A similar degree and pattern of injury was seen in the right ventricle ( n = 4). There was no evidence that an ischemic storage period of less than 6 h increased the degree of injury seen. However, there was a higher incidence of moderate to severe injury in those hearts excised from donors initially dependent on high inotropic support.     

Triiodothyronine accelerates and enhances the antipsychotic effect of risperidone in acute schizophrenia

In acute psychotic schizophrenia patients we investigated if the combination of triiodothyronine (T3) plus risperidone was more effective when compared to risperidone monotherapy. Thirty-two in-patients meeting the DSM-IV-TR diagnostic criteria for schizophrenia and without thyroid disease received risperidone (flexibly adjusted dose for tolerability) and were randomized to additionally receive either T3 (25 μg daily; risperidone plus T3 group) or placebo (risperidone plus placebo group). Treatment lasted until meeting the response to treatment criteria defined as score of ≤3 on the Clinical Global Impression Severity and Improvement scales. Acute psychotic episode symptom severity was evaluated using the Brief Psychiatric Rating Scale (BPRS) at treatment initiation and at the final study assessment. Fourteen patients were randomized to receive risperidone plus T3 and eighteen to receive risperidone plus placebo. The time until treatment response was shorter in the risperidone plus T3 group relative to the risperidone plus placebo group (25.5 ± 4.4 days vs 32.2 ± 8.2 days, respectively; p = 0.001). Moreover, there was a greater reduction of BPRS-total score (p = 0.01) in the risperidone plus T3 group relative to the risperidone plus placebo group. Treatment with T3 was associated with shorter time to treatment response (β = −0.440, p = 0.022) and with greater improvement in BPRS score (β = 0.240, p = 0.053), independent of patients' gender, age, baseline BPRS score and mean risperidone dose. The study confirms that addition of T3 to risperidone was associated with accelerated and enhanced treatment response in acutely psychotic schizophrenic patients.     

血清游离三甲碘状腺原氨酸水平预测HBV相关慢加急性肝衰竭患者预后的价值分析

目的探讨血清游离三甲碘状腺原氨酸（FT3）水平对HBV相关慢加急性肝衰竭（HBV-ACLF）患者90 d预后的预测价值。方法收集2018年9月—2020年1月在首都医科大学附属北京佑安医院住院的122例HBV-ACLF患者的临床资料,根据确诊后90 d预后分为生存组（n=77）和死亡组（n=45）。采用ELISA法测定血清FT3水平,比较FT3水平在两组间差异,应用logistic回归分析探索影响预后的危险因素并建立FT3相关预测模型,采用预测概率值的ROC曲线下面积（AUC）评估预测模型的区分度,采用线性回归分析评估校准度。采用AUC比较模型与MELD评分预测预后价值的差异。符合正态分布的计量资料两组间比较采用t检验;非正态分布的计量资料两组间比较采用Mann-Whitney U检验;计数资料两组间比较采用χ²检验;采用logistic回归分析预后影响因素。结果死亡组FT3显著低于生存组[（2.27±0.38） pmol/L vs （2.69±0.55） pmol/L,t=4.526,P<0.001],FT3（OR=0.534,95%CI:0.300～0....     

甲状腺激素与癌症的相关性研究进展

肿瘤患者甲状腺激素(T3)的代谢会产生异常,在肿瘤浸润深、淋巴结受累多、分期晚、病情重的患者中T3会显著下降。同时肿瘤的治疗(手术、放疗、化疗、靶向治疗、免疫治疗)也会造成T3下降。肿瘤患者T3的改变可以作为判断病情及临床分期、监测疗效、维护生活质量的参考指标,受到临床医生越来越多的关注。     

Relationship between β-amyloid protein 1-42, thyroid hormone levels and the risk of cognitive impairment after ischemic stroke

BACKGROUND Post-stroke cognitive impairment(PSCI)is not only a common consequence of stroke but also an important factor for adverse prognosis of patients.Biochemical indicators such as blood lipids and blood pressure are affected by many factors,and the ability of evaluating the progress of patients with PSCI is insufficient.Therefore,it is necessary to find sensitive markers for predicting the progress of patients and avoiding PSCI.Recent studies have shown thatβ-amyloid protein 1-42(Aβ1-42)and thyroid hormone levels are closely related to PSCI,which may be the influencing factors of PSCI,but there are few related studies.AIM To investigate the relationship between serum levels of Aβand thyroid hormones in acute stage and PSCI and its predicted value.METHODS A total of 195 patients with acute cerebral infarction confirmed from June 2016 to January 2018 were enrolled in this study.Baseline data and serological indicators were recorded to assess cognitive function of patients.All patients were followed up for 1 year.Their cognitive functions were evaluated within 1 wk,3 mo,6 mo and 1 yr after stroke.At the end of follow-up,the patients were divided into PSCI and non-PSCI according to Montreal cognitive assessment score,and the relationship between biochemical indexes and the progression of PSCI was explored.RESULTS Compared with patients with non-PSCI,the levels of Aβ1-42,triiodothyronine(T3)and free thyroxin were lower in the patients with PSCI.Repeated measures analysis of variance showed that the overall content of Aβ1-42 and T3 in PSCI was also lower than that of the non-PSCI patients.Further analysis revealed that Aβ1-42(r=0.348),T3(r=0.273)and free thyroxin(r=0.214)were positively correlated with disease progression(P<0.05),suggesting that these indicators have the potential to predict disease progression and outcome.Cox regression analysis showed that Aβ1-42 and T3 were important factors of PSCI.Then stratified analysis showed that the lower the Aβ1-42 and T3,the higher risk of PSCI in patients who were aged over 70,female and illiterate.CONCLUSION Aβ1-42 and T3 have the ability to predict the progression of PSCI,which is expected to be applied clinically to reduce the incidence of PSCI and improve the quality of life of patients.     

Plasma triiodothyronine at the end of pregnancy,in the cord blood and in the first days of the newborn

Triiodothyronine (T₃) and Thyroxine (T₄) were measured in women after delivery, in the cord blood of their children and in the first days of life. Furthermore TSH was determined in the cord blood. Women immediately after delivery showed T₃ and T₄ concentrations in the upper normal range. In the cord blood T₄ was normal, TSH elevated (9.2±7.4 uU/ml) and T₃ in the hypothyroid range (0.5±0.17ng/ml). T₃ increased to normal concentrations in most cases within 24 hrs; possible explanations of the low T₃ levels under fetal conditions are discussed.Über Teile dieser Arbeit wurde am 19. Symposion der Deutschen Gesellschaft für Endokrinologie (Berlin 1973) vorgetragen.     

Triiodothyronine and Brain Excitability

We investigated mechanisms involved in thyroid hormone action on brain excitability. The effect of acute exposure of triiodothyronine (T3) to rat hippocampal slices in vitro was studied. No significant changes could be detected in prevolley, field excitatory postsynaptic potentials (fEPSP) and population spike amplitude, while there was a minor, nonsignificant trend toward shortening of the population spike latency time. T3 had no effect on penicillin-induced epileptiform activity. There was, however, an active accumulation of radioactively labeled T3 in the slices. A rat cervaux-isolé preparation was used to determine focal seizure thresholds in the visual cortex, and no acute (2-4 h) effects were demonstrated. No significant acute effects of T3 on brain excitability in the hippocampus and visual cortex was observed, despite an active accumulation of T3. Thus, the effect of T3 on brain excitability most likely is due to delayed effects.     

Reference intervals for free thyroxine, total triiodothyronine, thyrotropin and thyroglobulin for Quebec newborns, children and teenagers

OBJECTIVE: Paediatric reference values, although essential for interpreting patients' results, are scarce. Moreover, they are often population- and instrument-dependent. We have measured free thyroxine (Free T(4)), total triiodothyronine (Total T(3)), thyroglobulin (Tg) and thyrotropin (TSH) in samples obtained from groups of newborns, children and adolescents. SUBJECTS AND METHODS: Blood samples collected from healthy children and teenagers (100 girls and 100 boys) of age groups ranging between 9-10, 11-14 and 15-17 years and selected randomly from a cohort representative of the Quebec population, were used. Samples from infants of age ranging between 1 day and 2 years (n = 99) were obtained from a hospital-based population with benign conditions unlikely to affect thyroid function. Variables were measured on the Access 2 immunosystem. RESULTS: Free T(4), Tg and TSH levels declined significantly with age. However, Total T(3) level presented a nonlinear variation with age, being lower in the first month of life.     

Developing forebrain astrocytes are sensitive to thyroid hormone

Previous studies have shown that developing neurons of the basal forebrain and hippocampus are sensitive to thyroid hormone (Gould and Butcher: J. Neurosci., 9:3347-3358, 1989; Rami et al: Neuroscience, 19:1217-1226, 1986). In order to determine whether or not thyroid hormone influences the development of astrocytes in brain regions where neurons are affected, we performed vimentin and glial fibrillary acidic protein (GFAP) immunocytochemical and single-section Golgi-impregnation analyses on the basal forebrain and hippocampus of control and neonatally thyroid hormone treated rats. For purposes of comparison, glial cells of the pontomesencephalotegmental (PMT) region, a region where developing neurons are not morphologically affected by thyroid hormone imbalances (Gould and Butcher, op. cit.), were also examined. Neonatal thyroid hormone treatment resulted in a premature disappearance of vimentin-immunoreactive radial glia in the basal forebrain and hippocampus. In addition, a premature appearance of GFAP-immunoreactive astrocytes with mature morphological characteristics was observed in the basal forebrain and hippocampus of thyroid hormone treated animals. Quantitative analyses revealed significant increases in the density of GFAP-immunostained astrocytes and in the cross-sectional cell body area and the number of primary processes in Golgi-impregnated astrocytes of the basal forebrain and hippocampus of animals treated neonatally with thyroid hormone. In contrast, no changes in any of these parameters were observed in glial cells of the PMT region with neonatal thyroid hormone treatment.     

Triiodothyronine, a Regulator of Osteoblastic Differentiation: Depression of Histone H4, Attenuation of c-fos/c-jun, and Induction of Osteocalcin Expression

Thyroid hormones influence growth and differentiation of bone cells. In vivo and in vitro data indicate their importance for development and maintenance of the skeleton. Triiodothyronine (T3) inhibits proliferation and accelerates differentiation of osteoblasts. We studied the regulatory effect of T3 on markers of proliferation as well as on specific markers of the osteoblastic phenotype in cultured MC3T3-E1 cells at different time points. In parallel to the inhibitory effect on proliferation, T3 down-regulated histone H4 mRNA expression. Early genes (c-fos/c-jun) are highly expressed in proliferating cells and are down-regulated when the cells switch to differentiation. When MC3T3-E1 cells are cultured under serum-free conditions, basal c-fos/c-jun expressions are nearly undetectable. Under these conditions, c-fos/c-jun mRNAs can be stimulated by EGF, the effect of which is attenuated to about 46% by T3. In addition, T3 stimulated the expression at the mRNA and protein level of osteocalcin, a marker of mature osteoblasts and alkaline phosphatase activity. All these effects were more pronounced when cells were cultured for more than 6 days. These data indicate that T3 acts as a differentiation factor in osteoblasts by influencing the expression of cell cycle–regulated, of cell growth–regulated, and of phenotypic genes. Received: 10 May 1996 / Accepted: 5 June 1997