Renal Subcapsular Transplantation of 2'-Deoxyguanosine-Treated Murine Embryonic Thymus in Nude Mice

The thymus is an important central immune organ, which plays an essential role in the development and differentiation of T cells. Thymus transplantation ...

jinan university

&#x5730;&#x4E2D;&#x6D77;&#x8D2B;&#x8840;&#x4E2D;&#x95F4; (TI) &#x7684;&#x4E34;&#x5E8A;&#x7EFC;&#x5408;&#x5F81;&#x5F15;&#x8D77;&#x7684; &beta; &#x57FA;&#x56E0;&#x578B;&#x4E0E;&#x56E0;&#x7D20;&#x4EA7;&#x751F;&#x80CE;&#x513F;&#x8840;&#x7EA2;&#x86CB;&#x767D; (&#x534E;&#x90A6;&#xFF09; &#x548C; &#xFF08;&#x6216;&#xFF09; &#x5171;&#x540C;&#x7EE7;&#x627F;&#x7684; &alpha;-&#x5730;&#x4E2D;&#x6D77;&#x8D2B;&#x8840;&#x3002;&#x4F46;&#x662F;&#xFF0C;&#x5F88;&#x5C11;&#x662F;&#x76EE;&#x524D;&#x5DF2;&#x77E5;&#x7684;&#x4E2D;&#x56FD;&#x949B;&#x60A3;&#x8005;&#x7684;&#x5206;&#x5B50;&#x57FA;&#x7840;&#x3002;

&#x5728;&#x4E2D;&#x56FD;&#x5357;&#x65B9;&#x7684; &beta;-&#x5730;&#x4E2D;&#x6D77;&#x8D2B;&#x8840;&#x4E2D;&#x95F4;&#x4F53;&#x7684;&#x5206;&#x5B50;&#x57FA;&#x7840;&#xFF1A; &#x57FA;&#x56E0;&#x578B;&#x7684;&#x5F02;&#x8D28;&#x6027;&#x548C;&#x8868;&#x578B;&#x7684;&#x591A;&#x6837;&#x6027;&#x3002;

The clinical syndrome of thalassemia intermedia (TI) results from the beta-globin genotypes in combination with factors to produce fetal haemoglobin (HbF) and/or co-inheritance of alpha-thalassemia. However, very little is currently known of the molecular basis of Chinese TI patients.

The molecular basis of beta-thalassemia intermedia in southern China: genotypic heterogeneity and phenotypic diversity.

Le syndrome clinique de thalass&#xE9;mie interm&#xE9;diaire (TI) les r&#xE9;sultats des g&#xE9;notypes b&#xEA;ta-globine, en combinaison avec les facteurs pour produire l&#x26;#39;h&#xE9;moglobine f&#x153;tale (HbF) et / ou co-h&#xE9;ritage de l&#x26;#39;alpha-thalass&#xE9;mie. Cependant, tr&#xE8;s peu actuellement connue de la base mol&#xE9;culaire des patients TI chinois.

Les bases mol&#xE9;culaires de la b&#xEA;ta-thalass&#xE9;mie interm&#xE9;diaire dans le sud de la Chine: h&#xE9;t&#xE9;rog&#xE9;n&#xE9;it&#xE9; g&#xE9;notypique et ph&#xE9;notypique diversit&#xE9;

Das klinische Syndrom der Thalass&auml;mie Intermedia (TI) ergibt sich aus der Beta-Globin-Genotypen in Kombination mit Faktoren, fetalen H&auml;moglobins (HbF) und/oder Co-inheritance der Alpha-Thalass&auml;mie zu produzieren. Jedoch ist sehr wenig &uuml;ber die molekulare Grundlage der chinesischen TI Patienten bekannt.

Die molekulare Grundlage der Beta-Thalass&auml;mie Intermedia in S&uuml;dchina: Heterogenit&auml;t genotypische und ph&auml;notypische Vielfalt.

La sindrome clinica di talassemia intermedia (TI) risultati dai genotipi della beta-globina in combinazione con fattori per la produzione di emoglobina fetale (HbF) e/o co-inheritance di alfa-talassemia. Tuttavia, attualmente molto poco &egrave; conosciuto della base molecolare dei pazienti cinesi TI.

La base molecolare della beta-talassemia intermedia, nella Cina meridionale: eterogeneit&agrave; genotipica e fenotipica diversit&agrave;.

&#x80CE;&#x5150;&#x306E;&#x30D8;&#x30E2;&#x30B0;&#x30ED;&#x30D3;&#x30F3;&#xFF08;HBF&#xFF09;&#x304A;&#x3088;&#x3073;/&#x307E;&#x305F;&#x306F;&#x3B1;-&#x30B5;&#x30E9;&#x30BB;&#x30DF;&#x30A2;&#x306E;&#x5171;&#x540C;&#x76F8;&#x7D9A;&#x3092;&#x751F;&#x6210;&#x3059;&#x308B;&#x8981;&#x56E0;&#x3068;&#x306E;&#x7D44;&#x307F;&#x5408;&#x308F;&#x305B;&#x3067;&#x3B2;-&#x30B0;&#x30ED;&#x30D3;&#x30F3;&#x907A;&#x4F1D;&#x5B50;&#x304B;&#x3089;&#x30B5;&#x30E9;&#x30BB;&#x30DF;&#x30A2;intermedia&#x304C;&#xFF08;TI&#xFF09;&#x306E;&#x7D50;&#x679C;&#x306E;&#x81E8;&#x5E8A;&#x7684;&#x75C7;&#x5019;&#x7FA4;&#x3002;&#x3057;&#x304B;&#x3057;&#x3001;&#x307B;&#x3068;&#x3093;&#x3069;&#x306F;&#x73FE;&#x5728;&#x3001;&#x4E2D;&#x56FD;&#x306E;TI&#x306E;&#x60A3;&#x8005;&#x306E;&#x5206;&#x5B50;&#x57FA;&#x76E4;&#x306E;&#x77E5;&#x3089;&#x308C;&#x3066;&#x3044;&#x307E;&#x3059;&#x3002;

&#x4E2D;&#x56FD;&#x5357;&#x90E8;&#x306B;&#x304A;&#x3051;&#x308B;&#x3B2;-&#x30B5;&#x30E9;&#x30BB;&#x30DF;&#x30A2;intermedia&#x306E;&#x5206;&#x5B50;&#x7684;&#x57FA;&#x790E;&#xFF1A;&#x907A;&#x4F1D;&#x5B50;&#x578B;&#x3068;&#x8868;&#x73FE;&#x578B;&#x306E;&#x591A;&#x69D8;&#x6027;&#x7570;&#x8CEA;&#x6027;

Thalassemia &#xC778;&#xD130; (TI)&#xC758; &#xC784;&#xC0C1; &#xC99D;&#xD6C4;&#xAD70; &#xD0DC;&#xC544; &#xD5E4;&#xBAA8;&#xAE00;&#xB85C;&#xBE48; (HbF) &#xBC0F; &#xC54C;&#xD30C; thalassemia co-inheritance &#xC0DD;&#xC0B0; &#xC694;&#xC18C;&#xC640; &#xD568;&#xAED8;&#xC5D0;&#xC11C; beta globin genotypes&#xC5D0;&#xC11C; &#xC720;&#xB798;&#xD55C; &#xB2E4;. &#xADF8;&#xB7EC;&#xB098;, &#xC544;&#xC8FC; &#xC791;&#xC740; &#xD604;&#xC7AC; &#xC911;&#xAD6D; TI &#xD658;&#xC790;&#xC758; &#xBD84;&#xC790; &#xAE30;&#xC900;&#xC73C;&#xB85C; &#xC54C;&#xB824;&#xC838; &#xC788;&#xC2B5;&#xB2C8;&#xB2E4;.

&#xC911;&#xAD6D; &#xB0A8;&#xBD80;&#xC5D0; &#xC788;&#xB294; &#xBCA0;&#xD0C0;-thalassemia &#xC778;&#xD130;&#xC758; &#xBD84;&#xC790; &#xAE30;&#xC900;: genotypic &#xC774;&#xC885; &#xBC0F; phenotypic &#xB2E4;&#xC591;&#xC131;.

El s&#xED;ndrome cl&#xED;nico de la talasemia intermedia (TI), los resultados de los genotipos de beta-globina en combinaci&#xF3;n con los factores para la producci&#xF3;n de hemoglobina fetal (HbF) y / o co-herencia de la alfa-talasemia. Sin embargo, muy poco se sabe actualmente de la base molecular de los pacientes chinos de TI.

La base molecular de la beta-talasemia intermedia en el sur de China: La heterogeneidad genot&#xED;pica y fenot&#xED;pica de la Diversidad

Acute myeloid leukemia (AML) is initiated and maintained by a subset of self-renewing leukemia stem cells (LSCs), which contribute to the progression, recurrence and therapeutic resistance of leukemia. However, the mechanisms underlying the maintenance of LSCs drug resistance have not been fully defined. In this study, we attempted to elucidate the mechanisms of LSCs drug resistance.

Sp1 and c-Myc modulate drug resistance of leukemia stem cells by regulating survivin expression through the ERK-MSK MAPK signaling pathway.

Research related to type 2 diabetes mellitus (DM) and parameters of electrocardiography (ECG) was limited. Patients with and without DM (NDM) were randomly enrolled in a study to exploit the influence of DM on planar QRS and T vectors derived from the Virtual Holter process.

Changes of Virtual Planar QRS and T Vectors Derived from Holter in the Populations with and without Diabetes Mellitus.

Glucocorticoid treatment represents a standard palliative treatment for Duchenne muscular dystrophy (DMD) patients, but various adverse effects have limited this treatment. In an effort to understand the mechanism(s) by which glucocorticoids impart their effects on the dystrophic muscle, and potentially reduce the adverse effects, we have studied the effect of prednisolone treatment in dystrophin/utrophin double knockout (dKO) mice, which exhibit a severe dystrophic phenotype due to rapid muscle stem cell depletion. Our results indicate that muscle stem cell depletion in dKO muscle is related to upregulation of mTOR, and that prednisolone treatment reduces the expression of mTOR and other pro-inflammatory mediators, consequently slowing down muscle stem cell depletion. However, prednisolone treatment was unable to improve the myogenesis of stem cells and reduce fibrosis in dKO muscle. We then studied whether glucocorticoid treatment can be improved by co-administration of an inhibitor of RhoA/ROCK signaling, which can be activated by glucocorticoids and was found in our previous work to be over-activated in dystrophic muscle. Our results indicate that the combination of RhoA/ROCK inhibition and glucocorticoid treatment in dystrophic muscle have a synergistic effect in alleviating the dystrophic phenotype. Taken together, our study not only shed light on the mechanism by which glucocorticoid imparts its beneficial effect on dystrophic muscle, but also revealed the synergistic effect of RhoA/ROCK inhibition and glucocorticoid treatment, which could lead to the development of more efficient therapeutic approaches for treating DMD patients.

RhoA/ROCK inhibition improves the beneficial effects of glucocorticoid treatment in dystrophic muscle: implications for stem cell depletion.

Digoxin is widely used to treat various heart conditions. In order to clarify the association between digoxin and anemia adverse reaction, we inspected case reports submitted to the FDA Adverse Event Reporting System (FAERS) between January 2004 and December 2015. These reports involved 75618 atrial fibrillation patients and 15699 heart failure patients. Compared to other therapies, digoxin treatment was significantly more likely to be concurrent with anemia adverse reaction among both atrial fibrillation patients (pooled OR = 1.38, 95% CI 1.14-1.68, P-value = 0.001) and heart failure patients (pooled OR =1.50, 95% CI 1.33-1.59-, P =4.27×10). We further explored previously published evidences and found 821 human genes directly or indirectly interacting with digoxin. Functional analysis indicated that these genes were significantly enriched in the biological processes of iron transport, which are closely related to iron deficiency anemia. Taken together, our retrospective analysis demonstrated the significant association between digoxin treatment and anemia adverse reaction, which should be seriously considered in clinical practice. Functional enrichment analysis on digoxin-related genes warranted subsequent research on the underlying toxicological mechanisms.

Digoxin-induced anemia among patients with atrial fibrillation and heart failure: clinical data analysis and drug-gene interaction network.

Baseline β-cell mass is established during the early postnatal period when β-cells expand. In this study, we show that heterozygous ablation of  decreases baseline β-cell mass and subsequently impairs glucose tolerance. When exposed to a high-fat diet or on an  background, glucose intolerance was more severe in  mice compared with  mice, although no further decrease in the β-cell mass was detected. In islets of early postnatal  mice, the cell cycle was prolonged in β-cells due to downregulation of the cell cycle gene  Although Insm1 had a low affinity for the  promoter compared with other binding sites, binding affinity was strongly dependent on Insm1 levels. We observed dramatically decreased binding of Insm1 to the  promoter after downregulation of  expression. Furthermore, downregulation of  resulted in a prolonged cell cycle, and overexpression of Ccnd1 rescued cell cycle abnormalities observed in Insm1-deficient β-cells. We conclude that decreases in Insm1 interfere with β-cell specification during the early postnatal period and impair glucose homeostasis during metabolic stress in adults. Insm1 levels are therefore a factor that can influence the development of diabetes.

Wanqun Chen

Department of Biochemistry and Molecular Biology,
School of Basic Medical Science,
Department of Biochemistry and Molecular Biology, School of Basic Medical Science

jinan university

Renal Subcapsular Transplantation of 2'-Deoxyguanosine-Treated Murine Embryonic Thymus in Nude Mice

Wanqun Chen

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Biochemistry and Molecular Biology,School of Basic Medical Science,Department of Biochemistry and Molecular Biology, School of Basic Medical Science

jinan university

Renal Subcapsular Transplantation of 2'-Deoxyguanosine-Treated Murine Embryonic Thymus in Nude Mice

Department of Biochemistry and Molecular Biology,
School of Basic Medical Science,
Department of Biochemistry and Molecular Biology, School of Basic Medical Science