Abstract Background The potential role of Klebsiella pneumoniae (K.pn) in hypertension development has been emphasized, although the specific mechanisms have not been well understood. Bacterial extracellular vesicles (BEVs) released by Gram-negative bacteria modulate host cell functions by delivering bacterial components to host cells. Endothelial dysfunction is an important early event in the pathogenesis of hypertension, yet the impact of K.pn-secreted EVs (K.pn EVs) on endothelial function remains unclear. This study aimed to investigate the effects of K.pn EVs on endothelial function and to elucidate the underlying mechanisms. Methods K.pn EVs were purified from the bacterial suspension using ultracentrifugation and characterized by transmission electron microscopy nanoparticle tracking analysis, and EV marker expression. Endothelium-dependent relaxation was measured using a wire myograph after in vivo or ex vivo treatment with K.pn EVs. Superoxide anion production was measured by confocal microscopy and HUVEC senescence was assessed by SA-β-gal activity. SIRT1 overexpression or activator was utilized to investigate the underlying mechanisms. Results Our data showed that K.pn significantly impaired acetylcholine-induced endothelium-dependent relaxation and increased superoxide anion production in endothelial cells in vivo. Similarly, in vivo and ex vivo studies showed that K.pn EVs caused significant endothelial dysfunction, endothelial provocation, and increased blood pressure. Further examination revealed that K.pn EVs reduced the levels of SIRT1 and p-eNOS and increased the levels of NOX2, COX-2, ET-1, and p53 in endothelial cells. Notably, overexpression or activation of SIRT1 attenuated the adverse effects and protein changes induced by K.pn EVs on endothelial cells. Conclusion This study reveals a novel role of K.pn EVs in endothelial dysfunction and dissects the relevant mechanism involved in this process, which will help to establish a comprehensive understanding of K.pn EVs in endothelial dysfunction and hypertension from a new scope.

BACKGROUND AND AIMS:Secreted protein acidic and rich in cysteine (SPARC) is involved in the pathological processes of many metabolic diseases. However, studies on the relevance of SPARC to hypertension and its involvement in endothelial function are scarce. In this study, we aim to explore the relevance of SPARC to hypertension and investigate its role in endothelium-dependent relaxation (EDR). METHODS:110 patients who met the criteria were recruited as participants. Serum SPARC concentrations were determined by Luminex assay. The correlation between SPARC levels and hypertension was analyzed. After treatment with SPARC ex vivo or in vivo, endothelial-dependent relaxation (EDR) was measured by wire myography. Western blotting was performed to detect the expression of proteins relevant to endothelial function. RESULTS:Our results showed that serum SPARC levels were significantly higher in the hypertensive group and were positively associated with systolic blood pressure (SBP) and diastolic blood pressure (DBP). Functional results demonstrated that SPARC dramatically impaired EDR and induced the excess production of reactive oxygen species (ROS) in endothelial cells. Further experimental results confirmed that SPARC reduced angiotensin-converting enzyme 2 (ACE2) expression and ACE2 overexpression or activation completely abolished the impairing effect of SPARC on endothelial function. CONCLUSIONS:The present study reveals the correlation between elevated SPARC and hypertension and confirms its adverse effect on endothelial function, helping establish a comprehensive understanding of hypertension-related endothelial dysfunction in a new scope.

AimsMorphine, a commonly used drug for anesthesia, affects lipid metabolism in different tissues, but the mechanism is currently unclear. Adipose triglyceride lipase (ATGL) is the rate-limiting enzyme responsible for the first step of triglyceride (TG) hydrolysis. Here we aim to investigate whether ATGL phosphorylation is involved in morphine-induced TG accumulation.Main methodsOil red O staining and TG content analysis were used to detect the effect of morphine on lipid storage. A series of ATGL phosphoamino acid site mutant plasmids were constructed by gene synthesis and transfected to HL-1 cells to evaluate the phosphorylation levels of ATGL phosphoamino acid in morphine-treated HL-1 cells with immunoprecipitation and immunoblotting assay.Key findingsMorphine acute treatment induced excessive accumulation of TG and decreased the phosphorylation level of ATGL Ser406 in HL-1 cells. Of note, the phosphorylation positive mutation of ATGL Ser406 to aspartic acid effectively reversed morphine-induced excessive accumulation of TG in HL-1 cells.SignificanceThis discovery will help to fully understand the lipid regulation function of morphine in a new scope. In addition, it will expand the phosphorylation research of ATGL more comprehensively and provide powerful clues for lipid metabolism regulation.

[Abstract] Dexmedetomidine (Dex) is a high affinity alpha2 ̄adrenergic receptor agonist. Studies have shown that Dex can alleviate ischemia and hypoxia injury of vital organs through anti ̄ sympatheticꎬ inhibition of inflammatory responseꎬ inhibition of oxidative stress and apoptosis. It also protects the vital organs through promotion of cell regenerationꎬ activation of cell protection signaling pathway and regulation of gene expression. In this articleꎬthe protective effects and mechanisms of Dex on heartꎬ kidneyꎬ brain and lung were reviewed. It also provides a theoretical basis for the safe and effective application of Dex in clinical practice. [Key words] Dexmedetomidine (Dex)ꎻ Ischemia ̄reperfusion injury (IRI)ꎻ Organ protection

目的 分析脊柱结核手术患者术中出现低体温的影响因素.方法 采用回顾性分析方法,选择2015年1月至2018年10月,北京胸科医院行脊柱结核手术的200例患者作为研究对象,包括前路病灶清除并植骨融合十内固定术52例,后路病灶清除并植骨融合十内固定术148例.根据患者术中否发生低体温将患者分为低体温组(91例)和非低体温组(109例).收集患者临床资料、术中液体总入量(含输血量)、麻醉时间和方式、手术持续时间和术式等资料.采用多因素logistic回归分析患者术中出现低体温的危险因素.结果 200例患者中有91例术中发生低体温,发生率为45.5％,体温最低为33.7℃.低体温组行开胸手术者31例(34.07％),非低体温组行开胸手术者18例(16.51％),两组比较差异有统计学意义.logistic回归分析显示,脊柱结核患者行开胸手术者术中出现低体温的风险是未行开胸手术者的2.17倍(95％CI:1.09～4.33).结论 开胸是脊柱结核手术患者术中低体温的危险因素.

Transforming growth factor (TGF)-β1, a main profibrogenic cytokine in the progression of idiopathic pulmonary fibrosis (IPF), induces differentiation of pulmonary fibroblasts to myofibroblasts that produce high levels of collagen, leading to concomitantly loss of lung elasticity and function. Recent studies implicate the importance of microRNAs (miRNAs) in IPF but their regulation and individual pathological roles remain largely unknown. We used both RNA sequencing and quantitative RT-PCR strategies to systematically study TGF-β1-induced alternations of miRNAs in human lung fibroblasts (HFL). Our data show that miR-133a was significantly upregulated by TGF-β1 in a time- and concentration-dependent manner. Surprisingly, miR-133a inhibits TGF-β1-induced myofibroblast differentiation whereas miR-133a inhibitor enhances TGF-β1-induced myofibroblast differentiation. Interestingly, quantitative proteomics analysis indicates that miR-133a attenuates myofibroblast differentiation via targeting multiple components of TGF-β1 profibrogenic pathways. Western blot analysis confirmed that miR-133a down-regulates TGF-β1-induced expression of classic myofibroblast differentiation markers such as ɑ-smooth muscle actin (ɑ-SMA), connective tissue growth factor (CTGF) and collagens. miRNA Target Searcher analysis and luciferase reporter assays indicate that TGF-β receptor 1, CTGF and collagen type 1-alpha1 (Col1a1) are direct targets of miR-133a. More importantly, miR-133a gene transferred into lung tissues ameliorated bleomycin-induced pulmonary fibrosis in mice. Together, our study identified TGF-β1-induced miR-133a as an anti-fibrotic factor. It functions as a feed-back negative regulator of TGF-β1 profibrogenic pathways. Thus, manipulations of miR-133a expression may provide a new therapeutic strategy to halt and perhaps even partially reverse the progression of IPF.

目的 探讨小潮气量通气和呼气末正压通气(positive end expiratory pressure,PEEP)结合压力控制通气(pressure controlled ventilation,PCV)对结核性毁损肺(tuberculous destroyed lung,TDL)患者全肺切除术单肺通气(one-lung ventilation,OLV)呼吸力学、肺内分流(Qs/Qt)、PaO2和术后肺部感染等的影响.方法 经首都医科大学附属北京胸科医院医学伦理委员会批准,选取2016年8月至2018年3月在首都医科大学附属北京胸科医院接受择期开胸全肺切除手术的TDL患者为研究对象,共48例.采用随机数字表法将患者分为观察组和对照组,每组24例.观察组OLV期间潮气量6 ml/kg,OLV开始即刻给予PCV通气,然后给予7 cm H2O(1 cm H2O=0.0098 kPa)的PEEP通气;对照组OLV期间潮气量8 ml/kg.记录OLV前(T1)、OLV开始后30 min(T2)及全肺切除术后5 min (T3)时气道峰压(Ppeak)和平台压(Pplat);T1、T2、T3和术后6 h(T4)抽取动静脉血,测血气指标pH、PaCO2和PaO2,并计算Qs/Qt值;术后第1天、第7天行临床肺部感染评分.计量资料组间比较,若方差齐,采用t检验,若方差不齐采用t'检验;组内比较采用重复测量设计的方差分析;计数资料比较采用x2检验,均以P＜0.05为差异有统计学意义.结果 T2时与对照组比较,观察组Ppeak明显降低[观察组:(21.0±2.2) cm H2O;对照组:(22.4±2.2) cm H2O;t=-2.446,P=0.021];T2时与对照组比较,观察组Pplat明显降低[观察组:(19.7±2.2)cm H2O;对照组:(21.0±2.7) cm H2O;t=-3.610,P=0.001];T3时与对照组比较,观察组pH明显降低[观察组:7.3±0.053;对照组,7.37±0.047;t=-3.000,P=0.006];T2时与对照组比较,观察组PaCO2明显升高[观察组:(44.0±2.2) mmHg(1 mm Hg=0.133 kPa);对照组:(35.7±4.0)mm Hg;t=7.091,P=0.000];T2时与对照组比较,观察组Qs/Qt明显降低[观察组:(21.4±5.4)％;对照组:(25.4±6.8)％;t=-0.256,P=0.020];T4时与对照组比较,观察组PaO2/FiO2明显升高[观察组:(181.2±29.0) mm Hg;对照组:(159.1±25.2) mm Hg;t=2.938,P=0.009].术后第1天,与对照组比较,观察组肺部感染评分明显降低[观察组:(4.7±0.6)分;对照组:(5.2±0.9)分;t=-2.567,P=0.017].结论 小潮气量和PEEP结合PCV的通气模式,在TDL患者开胸全肺切除手术OLV中可以较好的降低OLV期间气道压力、降低Qs/Qt,改善术后PaO2,降低术后第1天肺部感染的评分.

认知是大脑获取、记忆和处理信息的过程,术后认知功能障碍(postoperative cognitive dysfunction,POCD)是麻醉手术后患者出现的认知功能障碍,是手术麻醉后一种常见的并发症.POCD患者临床表现个体差异较大,主要表为短期记忆和执行功能受损,尤其是短期记忆受损.近年来,POCD越来越受到临床医生的重视,尤其是幼年及老年患者经历大手术后POCD发生率极高.POCD影响患者术后的恢复,早期POCD可能会演变成长期的认知功能障碍,将严重影响患者的生活质量,并对家庭及社会造成严重经济负担.尽管麻醉药物不断更新,其性能不断优化,且麻醉手术中相关监测技术也日益提高,但临床POCD的发生率仍然较高.迄今为止,仍未见行之有效的预防POCD的方法.该文就各种主要麻醉药物对患者POCD的影响及机制进行综述,旨在为临床麻醉方案实施及POCD防治提供参考及新的思路.

目的 比较纤维支气管镜引导普通双腔气管导管插管和可视双腔气管导管插管用于开胸手术单肺通气麻醉的临床效果.方法 选择需行开胸手术的患者60例,随机均分为两组.分别使用纤维支气管镜引导普通双腔气管导管插管和可视双腔气管导管插管.比较两组双腔气管导管定位时间及观察插管应激的血流动力学反应.结果 可视双腔气管导管插管组气管导管定位时间比纤维支气管镜引导普通双腔气管导管插管组短,定位及术中管理便捷;可视双腔气管导管插管组插管引起的血流动力学反应与纤维支气管镜引导普通双腔气管导管插管组也没有差异.结论 可视双腔气管导管定位时间短,定位准确,易于术中管理.但是仅有左侧双腔一种类型,应用范围存在一定局限性.

Objective To investigate the role of endoplasmic reticulum stress in skeletal muscle in surgery-induced insulin resistance in rats. Methods The rat models of open-chest surgery were created. Twenty-four rats were randomly divided into 4 groups (n=6):control group, 4-phenyl butyric acid (4-PBA) group, operation group and 4-PBA+operation group. Rats in each group were treated with hyperinsulinemic-euglycemic clamp test to assess insulin sensitivity 1 day after operation. Western blot assay was used for detecting the expression of binding immunoglobulin protein (BiP) in skeletal muscles. Results Compared with the control group, 4-PBA group and 4-PBA+operation group, the plasma free fatty acid level of the operation groups was elevated, while glucose infusion rate (GIR) was decreased, BiP was significantly increased in rat soleus samples (P<0.05). Conclusions Endoplasmic reticulum stress in skeletal muscles is involved in surgery-induced insulin resistance. 4-PBA, endoplasmic reticulum stress inhibitor, ameliorates surgery-induced insulin resistance in rats.

Ceramide accumulation in blood vessels has been attributed to vascular dysfunction in progressive vascular complications in metabolic diseases. The present study showed that ceramide pretreatment promoted PE-induced vasoconstriction in rat endothelium-denuded vascular rings in a time- and dose-dependent manner. Endoplasmic reticulum (ER) stress inhibitors, 4-PBA and TUDCA, COX-2 inhibitors, Celecoxib and NS398, as well as PGE(2) receptor antagonist AH-6809 attenuated ceramide-promoted vascular hyperreactivity. Ceramide promoted the transcriptional and translational expression of COX-2 and BiP in VSMCs, which were blocked by the ER stress inhibitors, 4-PBA and TUDCA. These findings show that ceramide enhances PE-induced vascular smooth muscle constriction by mediation of the ER stress/COX-2/PGE(2) pathway. Therapeutic strategies targeted to reducing ER stress and COX-2 activation might be beneficial in attenuating vascular complications. Chemical compounds: C-2-Ceramide (N-acetyl-n-erythro-sphingosine) CID:2662Tauroursodeoxycholic Acid Sodium (TUDCA) CID:9848818phenylephrine (PE) CID:6041.

Objective Differential expression and significance of microRNA were studied in the lung tissue of mice with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) induced by mechanical ventilation. Method 20 C57BL mice were divided into control group (10 mice) and ventilator-induced lung injury (VILI) group (10 mice) according to random number table. The mice in VILI group after endotracheal intubation were treated with 10 ml/kg tidal volume mechanical ventilation and muscle relaxant under anaesthetic, building (ALI/ARDS) model. The mice in control group were treated without muscle relaxant and mechanical ventilation but to spontaneous breathing. All mice were sacrificed 24 hours after operation, the left lung was excised to measure the wet-to-dry weight (W/D) ratio, and the right middle lobe was stained with hematoxylin and eosin (HE), the levels of TNF-α, IL-β were detected by ELISA. A microRNA mieroarray chip was used to profile microRNA expressions in the lung of mice in both groups. Predicted target genes among the different microRNA and analysed the pathway of the targets of microRNA in this study. Result Compared with the control group, the VILI group mice had obvious respiratory symptoms, the pathology was characterized with ALI/ARDS, W/D and the levels of TNF-α, IL-β had significantly increased (P < 0.01). The microarray chip results demonstrated that the expressions of 34 microRNA were significantly changed in the ALI/ARDS mice. Among these microRNA 19 cases were up-regulated, 15 cases were down-regulated. Conclusion Pathophysiology of VILI may be involved in the microRNA-regulated inflammation pathway et al.

Objective To investigate the effects of penequinine hydrochloride on TNF-α and inducible nitric oxide synthase (iNOS) expression in endotoxemia rats,and the effects on nuclear factor kappa B p65 (NF-κB p65) expression in the lung tissue of these rats.Methods Sixty healthy SD rats were randomly divided into 5 groups:control group (group C),LPS group and P1 groups-P3 groups.Endotoxemia was induced by intraperitoneal LPS 8 mg/kg in LPS group,penequinine hydrochloride was infused intraperitoneally 5 min before LPS administration in P1-P3 groups.The animals were sacrificed 6 h later.The level of TNF-α in blood samples was determined using ELISA,and the level of iNOS activity in blood samples was evaluated using colorimetry.The expression of NF-κB p65 in the fight lung tissue was detected using Western blotting.The morphological changes of lung were inspected by means of optical microscope.Results Compared with control group,TNF-α content were significantly increased,iNOS activity were significantly increased in rat serum samples,and NF-κB p65 protein expression in the lung tissue were significantly increased (P＜0.05).Compared with LPS group,the expression of TNF-α,iNOS activity,and NF-κB p65 protein expression were significantly reduced in group P2 and P3,but group 1 had no significant difference.There was no significant difference in the indices mentioned above among group P2 and group P3.The inflammatory responses was significantly ameliorated in group P2 and P3 compared to LPS group.Conclusions Penequinine hydrochloride can inhibit endotoxin-induced systemic inflammatory response by blocking TNF-α,NF-κB p65 uncontrolling release and reducing iNOS activity.

目的 观察腰丛-坐骨神经阻滞与蛛网膜下腔阻滞用于膝关节结核手术的效果.方法 选择我院2014年4月至2015年2月择期行膝关节结核手术的患者40例,按随机数字表法分为腰丛-坐骨神经阻滞组(A组)与蛛网膜下腔阻滞组(B组),每组20例.记录两组术中不同时间点,即阻滞前(T0)、阻滞后5 min(T1)、15 min(T2)、30 min(T3)血压变化、心率情况,感觉神经和运动神经阻滞起效和持续时间.采用SPSS 11.0统计学软件进行分析,计量资料以“x±s”表示,组内各时点参数比较采用单因素方差分析,组间参数采用两独立样本t检验,计数资料采用x2检验.P＜0.05为差异有统计学意义.结果 阻滞后,B组患者收缩压(SBP)、舒张压(DBP)均下降[SBP:T0为(133±14)mm Hg(1 mm Hg=0.133 kPa),T1为(108±9)mm Hg,T2为(113±15)mm Hg,T3为(116±15)mm Hg(F=13.442,P=0.000);DBP:T0为(77±8)mm Hg,T1为(68±5)mm Hg,T2为(67±9)mm Hg,T3为(66±8)mm Hg(F=8.264,P=0.000)].阻滞后,A组患者各时间点SBP、DBP均高于B组,两组比较差异有统计学意义[A组T1时SBP为(134±20)mm Hg(与B组比较,t=5.519,P=0.000),DBP为(78±10)mm Hg(与B组比较,t=3.848,P=0.000);T2时SBP为(133±19)mm Hg(与B组比较,t=3.701,P=0.001),DBP为(79±10)mm Hg(与B组比较,t=3.101,P=0.004);T3时SBP为(130±23)mm Hg(与B组比较,t=2.398,P=0.022),DBP为(80±10)mm Hg(与B组比较,t=4.898,P=0.000)].阻滞前后,两组心率(HR)比较差异均无统计学意义[A组:T0为(74±9)次/min,T1为(73±10)次/min,T2为(74±6)次/min,T3为(74±14)次/min (F=0.015,P=0.998);B组:T0为(73±9)次/min,T1为(73±9)次/min,T2为(72±5)次/min,T3为(74±13)次/min(F=0.093,P=0.964)].A组感觉神经阻滞起效时间慢于B组[A组平均起效时间为(14±2)min,B组为(5±2)min(t=12.802,P=0.000)];A组感觉神经阻滞持续时间长于B组,两组比较差异有统计学意义[A组平均持续时间为(523±23) min,B组为(377±17)min(t=22.425,P=0.000)].A组运动神经阻滞起效时间慢于B组[A组平均起效时间为(16±2)min,B组为(5±1)min(t=26.323,P=0.000)];A组运动神经阻滞持续时间长于B组,两组比较差异有统计学意义[A组平均持续时间为(410±41)min,B组为(294±19)min(t=11.280,P=0.000)].B组有3例恶心、呕吐,5例尿潴留;A组无不良反应,两组不良反应比较差异有统计学意义(x2=10.000,P=0.003).结论 腰丛-坐骨神经阻滞用于膝关节结核手术,与蛛网膜下腔阻滞相比,对血压、心率影响小,镇痛时间长,不良反应少.

Despite the dramatically expanding of biological data, insights into human health and disease from these data have not kept pace. The concept of precision medicine as a new disease management model is now emerging. It is about the customization of healthcare, with decisions and practices being tailored to the individual patient based on intrinsic biology in addition to traditional physical “signs and symptoms.” Building a standardized model for the integration of omics data from various platforms is the central mission, which is helpful for the development of new taxonomy of diseases to identify diseases subtypes and personalize therapy based on patients' genetic proifles. So, as a new medicine model, the implement of precision medicine will influence the advanced medical education in the future, including the promotion of the genetic research, the generation of new subject group, the production of new medical textbooks, and the conifguration of current education resource.

Excessive retention of neutral lipids in cardiac lipid droplets (LDs) is a common observation in cardiomyopathy. Thus, the systematic investigation of the cardiac LD proteome will help to dissect the underlying mechanisms linking cardiac steatosis and myocardial dysfunction. Here, after isolation of LDs from normal and dysfunctional Sprague-Dawley rat hearts, we identified 752 heart-associated LD proteins using iTRAQ quantitative proteomic method, including 451 proteins previously unreported on LDs. The most noteworthy finding was the identification of the membrane resealing protein, dysferlin. An analysis of dysferlin truncation mutants indicated that its C2 domain was responsible for its LD localization. Quantitative proteomic results further determined that 27 proteins were increased and 16 proteins were decreased in LDs from post pressure overload-induced dysfunctional hearts, compared with normal hearts. Notably, adipose triacylglycerol lipase (ATGL) was dramatically decreased and dysferlin was substantially increased on dysfunctional cardiac LDs. This study for the first time reveals the dataset of the heart LD proteome in healthy tissue and the variation of it under cardiac dysfunction. These findings highlight an association between the altered LD protein localization of dysferlin and ATGL and myocardial dysfunction.

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Brown adipose tissue (BAT) maintains animal body temperature by non-shivering thermogenesis, which is through uncoupling protein 1 (UCP1) that uncouples oxidative phosphorylation and utilizes β-oxidation of fatty acids released from triacylglycerol (TAG) in lipid droplets (LDs). Increasing BAT activity and “browning” other tissues such as white adipose tissue (WAT) can enhance the expenditure of excess stored energy, and in turn reduce prevalence of metabolic diseases. Although many studies have characterized the biology of BAT and brown adipocytes, BAT LDs especially their activation induced by cold exposure remain to be explored. We have isolated LDs from mouse interscapular BAT and characterized the full proteome using mass spectrometry. Both morphological and biochemical experiments showed that the LDs could tightly associate with mitochondria. Under cold treatment mouse BAT started expressing LD structure protein PLIN-2/ADRP and increased expression of PLIN1. Both hormone sensitive lipase (HSL) and adipose TAG lipase (ATGL) were increased in LDs. In addition, isolated BAT LDs showed increased levels of the mitochondrial protein UCP1, and prolonged cold exposure could stimulate BAT mitochondrial cristae biogenesis. These changes were in agreement with the data from transcriptional analysis. Our results provide the BAT LD proteome for the first time and show that BAT LDs facilitate heat production by coupling increasing TAG hydrolysis through recruitment of ATGL and HSL to the organelle and expression of another LD resident protein PLIN2/ADRP, as well as by tightly associating with activated mitochondria. These findings will benefit the study of BAT activation and the interaction between LDs and mitochondria.

Testicular Leydig cells contain abundant cytoplasmic lipid droplets (LDs) as a cholesteryl-ester store for releasing cholesterols as the precursor substrate for testosterone biosynthesis. Here, we identified the protein composition of testicular LDs purified from adult mice by using mass spectrometry and immunodetection. Among 337 proteins identified, 144 were previously detected in LD proteomes; 44 were confirmed by microscopy. Testicular LDs contained multiple Rab GTPases, chaperones, and proteins involved in glucuronidation, ubiquination and transport, many known to modulate LD formation and LD-related cellular functions. In particular, testicular LDs contained many members of both the perilipin family and classical lipase/esterase superfamily assembled predominately in adipocyte LDs. Thus, testicular LDs might be regulated similar to adipocyte LDs. Remarkably, testicular LDs contained a large number of classical enzymes for biosynthesis and metabolism of cholesterol and hormonal steroids, so steroidogenic reactions might occur on testicular LDs or the steroidogenic enzymes and products could be transferred through testicular LDs. These characteristics differ from the LDs in most other types of cells, so testicular LDs could be an active organelle functionally involved in steroidogenesis.

Excessive retention of neutral lipids in cardiac lipid droplets (LDs) is a common observation in cardiomyopathy. We anticipate that the systematic investigation of the cardiac LD proteome will help to dissect the underlying mechanisms linking cardiac steatosis and myocardial dysfunction. LDs