Quantification of myocardial fibrosis using noninvasive T2-mapping magnetic resonance imaging: Preclinical models of aging and pressure overload

Noninvasive imaging of cardiac fibrosis is important for early diagnosis and intervention in chronic heart diseases. Here, we investigated whether noninvasive, contrast agent-free MRI T₂-mapping can quantify myocardial fibrosis in preclinical models of aging and pressure overload. Myocardial fibrosis and remodeling were analyzed in two animal models: (i) aging (15-month-old male CF-1 mice vs. young 6- to 8-week-old mice), and (ii) pressure overload (PO; by transverse aortic constriction in 4- to 5-month-old male C57BL/6 mice vs. sham-operated for 14 days). In vivo T₂-mapping was performed by acquiring data during the isovolumic and early diastolic phases, with a modified respiratory and ECG-triggered multiecho TurboRARE sequence on a 7-T MRI. Cine MRI provided cardiac morphology and function. A quantitative segmentation method was developed to analyze the in vivo T₂-maps of hearts at midventricle, apex, and basal regions. The cardiac fibrosis area was analyzed ex vivo by picro sirius red (PSR) staining. Both aged and pressure-overloaded hearts developed significant myocardial contractile dysfunction, cardiac hypertrophy, and interstitial fibrosis. The aged mice had two phenotypes, fibrotic and mild-fibrotic. Notably, the aged fibrotic subgroup and the PO mice showed a marked decrease in T₂ relaxation times (25.3 ± 0.6 in aged vs. 29.9 ± 0.7 ms in young mice, p = 0.002; and 24.3 ± 1.7 in PO vs. 28.7 ± 0.7 ms in shams, p = 0.05). However, no significant difference in T₂ was detected between the aged mild-fibrotic subgroup and the young mice. Accordingly, an inverse correlation between myocardial fibrosis percentage (FP) and T₂ relaxation time was derived (R² = 0.98): T₂ (ms) = 30.45 – 1.05 × FP. Thus, these results demonstrate a statistical agreement between T₂-map–quantified fibrosis and PSR staining in two different clinically relevant animal models. In conclusion, T₂-mapping MRI is a promising noninvasive contrast agent-free quantitative technique to characterize myocardial fibrosis.     

Treatment of thalassaemia: a review of the new approaches on transfusion safety and the novel therapeutics

Lifetime red cell concentrate (RCC) transfusions still account for significant iron overload‐related morbidity and mortality despite chelation therapy in thalassaemia. The cumulative risk of transfusion‐transmitted infections is substantial for thalassaemia patients. Pathogen reduction technologies for RCC may imply a proactive approach against new/re‐emerging pathogens and may be an ultimate safeguard for transfusion safety in the developing countries. Red cell alloimmunization may become a significant clinical challenge in thalassaemia. The availability of high‐throughput molecular blood group antigen typing in the donors may allow perfect match transfusion, beyond ABO‐D and CEK antigen‐matched transfusions. Allogeneic stem cell transplantation (A‐SCT) is the only available curative therapy in thalassaemia, but carries a substantial risk of serious adverse events and mortality. Gene addition therapy for correction of the α‐globin chain imbalance overcomes the problems of donor availability and immunological complications of A‐SCT. Gene editing by either gene disruption or correction emerged as a potential alternative to gene addition therapy in beta‐thalassaemia. A new era of novel therapeutics targeting α/β imbalance, ineffective erythropoiesis or iron dysregulation is unfolding in thalassaemia management, and a number of those now have agents in preclinical and clinical development. Hydroxyurea (HU) may improve globin chain imbalance and be beneficial for reducing or omitting transfusion requirement. Ruxolitinib has allowed steady decrease in spleen volume that may serve for avoiding splenectomy in beta‐thalassaemia. Luspatercept may restore normal erythroid differentiation and improve anaemia. Hepcidin mimetics or TMPRSS6 inhibitors may modulate ineffective erythropoiesis by iron restriction and improve anaemia and organ iron loading.     

心钠素对心肌血管钙超载的影响

提要本研究是在大鼠VD_3+Nicotine引起的心血管钙超载模型上观察心钠素(ANF)治疗(10ug ·kg~-1/d),对钙超载的影响。结果发现,钙超载组动物主动脉、心肌组织钙含量较对照组分别增高24倍(54.4±2.2vs 2.3±0.04fumol/gww)和9倍(16.9±2.1vs1.8±0.1umol/gww)。ANF治疗能显著抑制钙超载的发生,主动脉和心肌组织钙含量较钙超载组分别降低92％(3.8±0.4 umol/gww)和66％(5.6±0.6umol/gww)。离体滋流的钙超载血管环较对照组对去甲肾上腺素收缩反应增强;对乙酰胆碱舒张反应减弱,对硝普钠舒张反应无影响。ANF能显著改善钙超载所致的血管反应性障碍。实验结果表明,ANF具有显著的防治心血管钙超载的作用。     

下半面部除皱术的综合设计

目的：中年人下半面部皮肤松弛整形时，对不同特点的患者进行不同的手术设计，使面部有明显且理想的改善。方法：通过23例就医者面部的综合设计，采用耳前耳屏切口下半面部SMAS筋膜提紧术，结合下颌吸脂、脂肪移植填充、祛眼袋术及隆鼻术，达到一个理想的面部除皱效果。结果：本组患者23例，年龄28~56岁，女性21例，男性2例，下半面部除皱术结合眼袋手术14例，下半面部除皱术结合下颌吸脂12例，其中有9例行脂肪移植术，下半面部除皱术结合隆鼻4例。通过23例患者面部的综合设计，将面部皮肤提紧术、吸脂术、脂肪移植术、隆鼻术、祛眼袋术结合进行，患者均达到满意的效果。结论：对面部松弛的患者，应综合考虑，发现患者的缺陷，精心设计，减少创伤，手术才能达到理想效果。     

胸大肌肌皮瓣脂肪液化的相关危险因素探讨

目的探讨胸大肌肌皮瓣术后发生脂肪液化的相关危险因素。方法对1998年5月至2005年12月采用胸大肌肌皮瓣修复口腔癌术后组织缺损的82例中10例术后发生不同程度脂肪液化的病例,进行Logistic回归分析。结果Logistic单因素回归分析结果表明：肥胖、电刀切开皮下组织、皮岛设计低于第7肋、吸烟等因素与胸大肌肌皮瓣术后发生脂肪液化有关;Logistic多因素回归分析结果表明：胸大肌肌皮瓣术后发生脂肪液化与肥胖、电刀切开皮下组织、皮岛设计低于第7肋等因素有关,而与吸烟无关。结论肥胖、电刀切开皮下组织、皮岛设计低于第7肋等因素是胸大肌肌皮瓣术后发生脂肪液化的危险因素。     

小针刀辅助自体脂肪颗粒移植在面部除皱及凹陷充填中的应用

目的探讨小针刀辅助自体脂肪颗粒注射除去额部、眉间、鼻唇沟等部位皱纹及充填面部凹陷的效果。方法利用自制小针刀,离断真皮与其下方的"纤维粘连",然后用自体脂肪颗粒注射除皱和充填凹陷部位。结果本组共68例。修复面积最大约10cm×8cm,最小约1.5cm×0.5cm。随访45例,随访时间3～18个月,效果满意或基本满意。结论小针刀辅助自体脂肪移植具有操作简单、快捷、价廉、安全、无排异、不留瘢痕、术后恢复快等优点,患者易于接受,是除去额部、眉间、鼻唇沟等部位皱纹及填充面部凹陷的有效方法。     

外科手术切口脂肪液化的诊疗体会

目的 探讨外科手术切口病因及预防措施.方法 回顾分析我科自2001年5月～2005年7月施行大、中手术后发生切口脂肪液化的60例病例.结果 肥胖,术中皮下脂肪层使用电刀,术中切口器械挤压时间长,大块组织钳夹,老年人、糖尿病等可引发切口脂肪液化.结论 手术切口脂肪液病因较多,肥胖、术中使用电刀、器械挤压时间长、老年人糖尿病均为重要影响因素.