RESUMEN
BACKGROUND: Critical patients with the coronavirus disease 2019 (COVID-19), even those whose nucleic acid test results had turned negative and those receiving maximal medical support, have been noted to progress to irreversible fatal respiratory failure. Lung transplantation (LT) as the sole therapy for end-stage pulmonary fibrosis related to acute respiratory distress syndrome has been considered as the ultimate rescue therapy for these patients. METHODS: From February 10 to March 10, 2020, three male patients were urgently assessed and listed for transplantation. After conducting a full ethical review and after obtaining assent from the family of the patients, we performed three LT procedures for COVID-19 patients with illness durations of more than one month and extremely high sequential organ failure assessment scores. RESULTS: Two of the three recipients survived post-LT and started participating in a rehabilitation program. Pearls of the LT team collaboration and perioperative logistics were summarized and continually improved. The pathological results of the explanted lungs were concordant with the critical clinical manifestation, and provided insight towards better understanding of the disease. Government health affair systems, virology detection tools, and modern communication technology all play key roles towards the survival of the patients and their rehabilitation. CONCLUSIONS: LT can be performed in end-stage patients with respiratory failure due to COVID-19-related pulmonary fibrosis. If confirmed positive-turned-negative virology status without organ dysfunction that could contraindicate LT, LT provided the final option for these patients to avoid certain death, with proper protection of transplant surgeons and medical staffs. By ensuring instant seamless care for both patients and medical teams, the goal of reducing the mortality rate and salvaging the lives of patients with COVID-19 can be attained.
Asunto(s)
Betacoronavirus , Infecciones por Coronavirus/complicaciones , Trasplante de Pulmón/métodos , Neumonía Viral/complicaciones , Fibrosis Pulmonar/cirugía , Síndrome de Dificultad Respiratoria/cirugía , Anciano , COVID-19 , Infecciones por Coronavirus/mortalidad , Oxigenación por Membrana Extracorpórea , Humanos , Masculino , Persona de Mediana Edad , Pandemias , Neumonía Viral/mortalidad , Fibrosis Pulmonar/mortalidad , Síndrome de Dificultad Respiratoria/mortalidad , SARS-CoV-2RESUMEN
Cardiac c-kit+ cells isolated from cardiac explant-derived cells modestly improve cardiac functions after myocardial infarction; however, their full potential has not yet been realized. The present study was undertaken to determine the isolation and culture of c-kit+ cardiac stem cells (CSCs), and the roles of myocardial injection of CSCs on the survival of rat cardiac allograft. Recipient Sprague-Dawley rats were transplanted with hearts from Wistar rats. In the in vitro experiment, c-kit+ cells were isolated from mouse heart fragment culture by magnetic cell sorting. CSCs expressed of cardiomyocyte specific protein cardiac troponin I, α smooth muscle actin and von Willebrand factor in conditioned culture. CSC injection increased graft survival of cardiac allograft rats. The effects of CSCs on increase in graft survival of cardiac allograft rats were blocked by stromal-derived factor-1 (SDF-1) knockdown. The expression of SDF-1 was increased after CSC injection into the cardiac of cardiac allograft rats. These results indicate that CSC injection into the cardiac prolongs graft survival of cardiac allograft rats. SDF-1 plays an important role in the effects of CSCs on the graft survival of cardiac allograft rats.
Asunto(s)
Trasplante de Corazón , Trasplante de Células Madre , Animales , Células Cultivadas , Quimiocina CXCL12/genética , Quimiocina CXCL12/metabolismo , Supervivencia de Injerto , Masculino , Miocardio/citología , Proteínas Proto-Oncogénicas c-kit , Ratas Sprague-Dawley , Ratas Wistar , Células Madre , Trasplante HomólogoRESUMEN
BACKGROUND: It has been reported that rs940494 and rs805296 SNPs of apolipoprotein M (apoM) gene may confer the risk in the development of type 2 diabetes (T2D) and coronary artery disease (CAD) in the Han Chinese. However, a recent study demonstrated that rs805297 polymorphism is significantly associated with reduced total high density lipoprotein (HDL) levels in rheumatoid arthritis patients. But the relationship between rs805297 SNP and CAD has not been explored. The aim of the present study was to elucidate whether the rs805297 mutant allele is implicated in CAD and links to changes in blood lipid levels in these patients. METHODS: Three hundred CAD patients and three hundred and twelve non-CAD patients were subjected in the present study. All subjects were confirmed by the angiography. Plasma concentrations of apoM were semi-quantitatively determined by dot-blotting analysis, and total serum lipid levels were quantified using an automated RA-1000 (Technician, USA). The genotyping of rs805297 of apoM was analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: Genotype and allele frequencies were not significant (P = 0.5798 and 0.3834, respectively) between cases and controls. Compared with the wild-type C/C genotype, carriers of the C/A and A/A genotypes did not have an increased risk of CAD, as determined by multiple logistic regression analysis, after adjustment for age, sex, BMI, history of smoking, hypertension and hypercholesterolemia. (CA, odds ratio = 0.49, 95% confidence interval 0.15-1.87, P = 0.462; AA, odds ratio = 0.51, 95% confidence interval 0.13-1.68, P = 0.534). The plasma concentration levels of apoM did not differ significantly among carriers of the three genotypes between two groups. Lastly, control subjects with A/A genotypes had lower total levels of HDL cholesterol than did those with C/C genotypes. CONCLUSIONS: The results presented here suggest that the rs805297 SNP is not associated with an increased risk of developing CAD, although it does independently correlate with dyslipidaemia in Han Chinese individuals.
Asunto(s)
Apolipoproteínas/genética , Enfermedad de la Arteria Coronaria/genética , Dislipidemias/genética , Predisposición Genética a la Enfermedad , Lipocalinas/genética , Polimorfismo de Nucleótido Simple , Regiones Promotoras Genéticas , Anciano , Apolipoproteínas M , Pueblo Asiatico , Estudios de Casos y Controles , Enfermedad de la Arteria Coronaria/enzimología , Enfermedad de la Arteria Coronaria/patología , Dislipidemias/etnología , Dislipidemias/patología , Femenino , Humanos , Modelos Logísticos , Masculino , Persona de Mediana Edad , Reacción en Cadena de la Polimerasa , Polimorfismo de Longitud del Fragmento de Restricción , RiesgoRESUMEN
OBJECTIVES: Apolipoprotein M (apoM) is important for the formation of pre-beta-high-density lipoprotein (HDL) and cholesterol efflux in macrophages. It is demonstrated that single-nucleotide polymorphism (SNP) T-778C of apoM gene is related to type 2 diabetes in Han Chinese. In the present study, we investigated the possible association of apoM polymorphism in relation to coronary artery disease (CAD) in Han Chinese. DESIGN AND METHODS: This case-controlled study consisted of 118 CAD patients who were diagnosed angiographically to have at least 30% stenosis, and 255 unrelated subjects who were used as control. ApoM gene polymorphism in the proximal promoter region was analyzed by PCR-RFLP and serum lipid levels were also measured. RESULTS: It is indicated that CAD patients had increased frequency of C allele on apoM T-778C compared to the controls (14.8% vs. 6.9%, P=0.0008). Multivariable logistic regression analysis indicated that odds ratios (ORs) for all subjects with apoM CC+CT genotypes and C allele were 1.9 (95% CI=1.1-2.9, P<0.0001) and 1.9 (95% CI=1.3-3.2, P<0.0001), respectively. The plasma total cholesterol (TC) levels were significantly higher in individuals with CC or CT genotype than those with TT genotype in both CAD patients and controls. CONCLUSIONS: The present findings suggest that the C allele at nucleotide -778 in the apoM gene is a risk factor for genetic susceptibility to CAD and is also associated with TC levels in Han Chinese.
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Apolipoproteínas/genética , Enfermedad de la Arteria Coronaria/genética , Polimorfismo de Nucleótido Simple , Anciano , Apolipoproteínas M , Secuencia de Bases , Estudios de Casos y Controles , China , Colesterol/sangre , Colesterol/genética , Análisis Mutacional de ADN , Femenino , Predisposición Genética a la Enfermedad , Humanos , Lipocalinas , Masculino , Persona de Mediana EdadRESUMEN
Apolipoprotein M (apoM) is a recently discovered human apolipoprotein predominantly present in high-density lipoprotein (HDL), and in minor proportions in triglyceride-rich lipoprotein (TGRLP) and low-density lipoprotein (LDL). The gene encoding apoM is present in all mammalian genomes. The identity of the apoM gene of human, rat and mouse is over 80%. However, the (patho)physiological functions of apoM are unknown yet. In the present study, we investigated apoM expression patterns during mouse and human embryogenesis. ApoM transcripts were detectable in mouse embryos from day 7.5 to day 18.5. ApoM was expressed at low levels at day 7.5, its expression increased significantly at day 9.7, decreased at day 10.5, and then increased continually up to day 18.5. ApoM-positive cells appeared mainly in liver of day-12 embryos as detected by in situ hybridization. In day-15 embryos, apoM was expressed in both liver and kidney. During human embryogenesis, apoM was mainly expressed in liver and kidney and little was found in small intestine as determined by mRNA array of human fetal normal tissues. ApoM was also detected in stomach and skeletal muscle in early stages of embryogenesis (3-5 months).