Objectives:To investigate the feasibility of using bedside echocardiography on the evaluation of potential donors with different causes of brain death for adult heart transplantation. Methods:Bedside echocardiographic and clinical data of consecutive potential donors for adult heart transplantation evaluated by the team of our institution from February 2018 to December 2020 were retrospectively analyzed.Based on different causes of brain death,the potential donors were divided into stroke(ischemic or hemorrhagic,n=398)and non-stroke(head trauma,brain tumor,anoxia,n=272)groups.The clinical and echocardiographic features were compared between the two groups.A total of 350 donors were assigned to our hospital by the China Organ Transplant Response System and met the inclusion criteria for donor selection.There were 195 cases in the stroke group and 155 in the non-stroke group.Retrieval operations were performed and the retrieval rate of hearts for transplantation in stroke donors was compared to that in non-stroke donors. Results:(1)Among the 670 potential heart donors,compared with the non-stroke group,donors in the stroke group were significantly older,had higher body mass index,larger left ventricular end-diastolic diameter,thicker interventricular septum,higher rates of echocardiographic abnormalities,higher prevalence of hypertension(all P<0.001).Among the 670 potential heart donors,17.5%(117 cases)did not meet the echo selection criteria,the common causes were left ventricular hypertrophy(59 cases,50.4%),left ventricular ejection fraction<50%(27 cases,23.1%),wall motion abnormalities(21 cases,17.9%),and left ventricular dilation(14 cases,12.0%).(2)Among the 350 donors who had met the selection criteria and assigned to our hospital by the China Organ Transplant Response System and underwent retrieval operation,70.3%(246 cases)were successfully procured,110 cases(44.7%)in the stroke group and 136 cases(55.3%)in the non-stroke group.The retrieval rate of stroke donors(110/195,56.4%)was lower compared with that of non-stroke(136/155,87.7%,P<0.001),104 cases(29.7%)were not retrieved,and the leading cause of unsuccessful organ retrieval was the occlusion of at least one major coronary artery(91 cases,87.5%). Conclusions:Bedside echocardiography is of great value as a screening tool for cardiac donors.Cardiac structures of the potential donor with stroke as the cause of brain death were different from those with non-stroke causes.The retrieval rate of stroke donors was lower than that of non-stroke donors,even if the initial criteria for donor selection were fulfilled.

Objective:To explore the morbidity and risk factors of de novo malignancy after heart transplantation (HT).Methods:From June 2004 to August 2021, 995 patients undergoing HT were selected and followed up.The epidemiological characteristics, the morbidity of de novo malignancy (DNM) and its risk factors were examined.Kaplan-Meier survival analysis was performed for calculating the cumulative incidence and mortality of DNM.Log rank test was utilized for comparing the survival rate of each subgroup.Cox regression model was employed for examining the relationship between the included factors and the endpoint of DNM.Results:The median follow-up period was 6.36(3.64, 10.18) years.Thirty-six patients (3.6%) developed DNM during follow-up.Lung cancer accounted for 22.2%(8/36) of DNM while digestive system tumors accounted for 38.9% (including gastric cancer 6/36, 16.7%; liver cancer 3/36, 8.3%; colon cancer 2/36, 5.6%). The cumulative morbidity of DNM at Year 1/5/10/15 post-HT was 0.1%, 2.3%, 4.9% and 7.6% respectively.The median survival time of DNM recipients was 83.32 months.The mean survival time was significantly lower than those without DNM[(115.32±13.12) vs.(194.22±2.58), P<0.001]. The mortality of DNM recipients was around 6.57 folds higher ( HR=6.57, 95% CI: 4.06-10.64, P<0.01). Age was an independent risk factor for an occurrence of DNM.Hypertension and diabetes were also correlated with DNM. Conclusions:DNM after HT is associated with shorter survival time.And age is an independent risk factor for DNM after HT.

Objective:To explore the clinical and imaging characteristics of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) caused by mitochondrial DNA 14453G>A (m.14453G>A) mutation.Methods:A case of MELAS caused by m.14453G>A mutation in the First Affiliated Hospital of Harbin Medical University on October 12, 2021 was reported. At the same time, the reported cases of MELAS and Leigh syndrome (LS) caused by the m.14453G>A mutation were reviewed. This enabled a comprehensive summarization, analysis, and comparison of these cases.Results:The patient was a female. She has suffered from the disease since 13-year old with seizures, accompanied by the disturbance of mood and the loss of memory. Brain magnetic resonance imaging findings consisted of lesions in frontal, parietal, occipital, temporal lobe and cerebellar. The patient was initially considered with autoimmune encephalitis and posterior reversible encephalopathy syndrome. Since direct sequencing of the complete mitochondrial genome from blood of the patient revealed m.14453G>A mutation in ND6 gene, and the mutation rate was 17.0%, the patient eventually diagnosed with MELAS based on clinical manifestations, imaging examinations, and genetic testing results. Using "m.14453G>A" as the search term, the relevant literature in China and abroad was retrieved and those with complete clinical data were identified. A total of 11 cases of m.14453G>A mutation including this case were reported, of whom 5 patients were diagnosed as MELAS, and 6 patients were diagnosed as LS. Among the 11 patients, those being adolescent or adult and with lesions in the cortex and subcortical white matter were probably be MELAS; those being infant or young child and with lesions in basal ganglia, thalamus and brainstem could be LS. Conclusions:Mitochondrial disease caused by m.14453G>A gene mutation shows a great heterogeneity, which can cause MELAS and LS. The clinical phenotype of the m.14453G>A mutation may be related to the age of onset and lesion′ s location.

Objective:To analyze the case characteristics and outcomes of 12 idiopathic giant cell myocarditis(IGCM)cases after heart transplantation(HT).Methods:From June 2004 to May 2022, clinical data were retrospectively reviewed for 12 cases with pathologically confirm IGCM after HT at Fuwai Hospital.General characteristics, clinical manifestations, pathological examinations and postoperative follow-ups are recorded.Results:From June 2004 to May 2022, a total of 1 143 HT operations are performed at Fuwai Hospital and 12 cases of IGCM(1.05%)are confirmed by postoperative pathology.The age is(47.6±7.3)years.There are 5 boys and 7 girls.Initial presenting manifestations are congestive heart failure(7 cases, 58.3%)and arrhythmia(4 cases, 33.3%). Median time from symptom onset to HT is 6 months.All of them are undiagnosed pre-operation.And dilated cardiomyopathy(5 cases, 41.7%)and arrhythmogenic right ventricular cardiomyopathy(3 cases, 25%)are confirmed.The follow-up period is(4~142)months post-HT.One death occurred during perioperative period and another is due to heart failure at 68 months post-HT.Only 1 case of grade 1R transplant heart rejection occurrs at 9 years post-HT and there is no case of recurrence.According to Kaplan-Meier survival analysis, cumulative survival rates of 1/5/10 years post-HT in IGCM patients are 91.7%, 91.7% and 73.3% respectively.No significant difference exist in survival rate for other etiologies post-HT(Log-rank P=0.265). Conclusions:HT is efficacious for end-stage IGCM.Regular and sufficient postoperative immunosuppression is vital for preventing heart transplant rejection and recurrent IGCM.Most IGCM patients have a decent prognosis post-HT.

As an effective anticancer drug, the clinical limitation of doxorubicin (Dox) is the time- and dose-dependent cardiotoxicity. Yes-associated protein 1 (YAP1) interacts with transcription factor TEA domain 1 (TEAD1) and plays an important role in cell proliferation and survival. However, the role of YAP1 in Dox-induced cardiomyopathy has not been reported. In this study, the expression of YAP1 was reduced in clinical human failing hearts with dilated cardiomyopathy and Dox-induced

Objective To explore the treatment experience of acute paraquat poisoning,thus to explore the prognostic factors and treatment measures.Methods The clinical data of 87 patients with paraquat poisoning who were treated with combined therapy in our hospital emergency department 2014-2015 were retrospectively analyzed.Results 49 cases survived and 38 cases were died in 87 paraquat poisoning patients,the survival rate was 56.32％.The average paraquat of the death group was 65.3mL,which was significantly higher than 41.2mL of the survival group(t =16.65,P ＜ 0.01).Conclusion Amount of poisoning is the key to the prognosis,white blood cells were significantly increased,early or large areas of lung disease is an important factor in poor prognosis;early gastric lavage,cathartic and timely blood purification,application of adrenal cortex hormones,antioxidant and other comprehensive treatment can reduce mortality.

Muscle atrophy caused by nerve injury is a common and difficult clinical problem. The development of stem cell researches has opened up a new way for the treatment of nerve injury-induced muscle atrophy. The induced pluripotent stem cells(iPSCs)can differentiate into various types of cells and have more advantages than embryonic stem cells (ESCs). After being transplanted into the damaged area, iPSCs are guided by neurogenic signals to the lesion sites, to repair the damaged nerve, promote generation of axon myelination, rebuild neural circuits and restore physiological function. Meanwhile, iPSCs can also differentiate into muscle cells and promote muscle tissue regeneration. Therefore, it would be possible to attenuate muscle atrophy caused by nerve injury with iPSCs treatment.
Animals ; Disease Models, Animal ; Embryonic Stem Cells ; Humans ; Induced Pluripotent Stem Cells ; cytology ; transplantation ; Muscular Atrophy ; therapy

Acute Disease ; Humans ; Nervous System Diseases ; diagnosis ; therapy ; Organophosphate Poisoning ; diagnosis ; therapy

BACKGROUND:Microtubule-associated protein-2 is a kind of important regulatory factor in regulating tubulin assembly. As one of the main members of microtubule-associated proteins, microtubule-associated protein-2 plays an important role in the repairing and development of the nervous system function. It has been found that microtubule-associated protein-2 can promote the repair and rebuilding of injured nerves. OBJECTIVE:To summarize the relationship between microtubule-associated protein-2 and nerve injury as wel as the mechanism of action. METHODS:The PubMed database and CNKI database were retrieved by the fist author for the articles related to microtubule-associated protein-2 published from January 1976 to January 2015. The key words were“microtubule-associated protein-2 (MAP-2), nerve injury, progress”in English and Chinese, respectively. In the same field, articles published recently or in authorized journals were preferred. Repetitive or old articles were excluded, and final y 82 articles were included in result analysis. RESULTS AND CONCLUSION:Microtubule-associated protein-2 is involved in nerve repair, and plays a promoting role in neuronal morphology and plasticity. To increase the concentration of microtubule-associated protein-2 contributes to the recovery of neurologic function in the early stage after nerve injury.

Objective To investigate the effects of hydrogen sulfide on autophagy and the apoptosis after acute spinal cord injury in rats. Methods Thirty-six adult male SD rats (250-300 g) were randomly divided into three groups (n=12 for each group):sham operation group (Sham group), spinal cord injury group (Model group) and hydrogen sulfide pre-treatment group (H2S group). Allen’s method was used to establish the rat model of spinal cord injury. Rats of sham operation group re?ceived only laminectomy. Rats of H2S group received sodium hydrosulphide injection intraperitoneally (50μmol/kg) 1h after spinal cord injury, and Model group was given the same amount of saline solution. Rats in the three groups were sacrificed 24 h after spinal cord injury, then the spinal cord was removed. The expressions of LC3, p70S6K and Cleaved caspase-3 were detected by Western blot assay. The expression of LC3 was also detected by immunofluorescence. The cell apoptosis was as?sessed by TUNEL stain. Results Compared with Sham group, the expression levels of LC3Ⅱ/LC3Ⅰand Cleaved caspase-3 were increased in Model group, but the expression of p70S6K decreased and cell apoptosis increased in Model group (P<0.01). Compared with Model group, the expression levels of LC3Ⅱ/LC3Ⅰand Cleaved caspase-3 were decreased significant?ly, while the expression of p70S6K increased and cell apoptosis decreased significantly in H2S group (P < 0.01). Conclu?sion Hydrogen sulfide can inhibit autophagy and reduce cell apoptosis after acute spinal cord injury in rats.