IL-6/STAT3通路对THP-1单核细胞环氧化酶2表达的影响

目的探讨人THP-1单核细胞中白细胞介素6(IL-6)/信号转导与转录激活子3(STAT3)通路与环氧化酶2(COX-2)表达之间的关系。方法以人THP-1单核细胞株作为研究对象,分别设置0至48 h不同时间点,检测IL-6对STAT3磷酸化和COX-2表达的时效性影响。用100μmol/L S3I-201(STAT3通路选择性抑制剂)对THP-1单核细胞预处理24 h,再经10μg/L IL-6作用相应时间,将THP-1单核细胞分为4组:对照组、S3I-201组、IL-6组及IL-6+S3I-201组,检测STAT3磷酸化及COX-2表达水平变化。采用实时荧光定量PCR方法检测THP-1单核细胞COX-2的mRNA表达量,Western blot方法检测THP-1单核细胞STAT3磷酸化水平与COX-2的蛋白表达量。结果THP-1单核细胞经IL-6作用后STAT3的磷酸化及COX-2的表达均出现时效性激活,IL-6刺激5 min后STAT3磷酸化水平即显著增加(P0.001),同时COX-2 mRNA和蛋白水平均明显上调,分别于1 h和2 h达到峰值(P0.001)。与对照组相比,S3I-201组COX-2 mRNA及蛋白表达水平均降低(P0.01);与IL-6组相比,IL-6+S3I-201组STAT3磷酸化水平下降(P0.001),COX-2 mRNA表达水平降低(P0.001),同时COX-2蛋白表达受到明显抑制(P0.05)。结论 IL-6能够激活THP-1单核细胞STAT3通路,其可能通过催化下游COX-2的表达影响动脉粥样硬化性疾病进程。     

替米沙坦通过激活PPARγ而下调NF-κB通路抑制脂多糖诱导的单核细胞THP-1炎症反应

目的探讨替米沙坦（Telm）对脂多糖（LPS）诱导的人THP-1巨噬细胞炎症因子释放的影响及机制。方法体外培养人THP-1单核细胞随机分为对照组、脂多糖组和替米沙坦组（LPS+Telm）。替米沙坦组细胞予替米沙坦（10μmol/L）预孵育2h后与脂多糖组均加入脂多糖刺激24h。应用Westernblot检测各组细胞过氧化体增殖物激活型受体γ（PPARγ）、磷酸化过氧化体增殖物激活型受体γ（p-PPARγ）、IκBα、磷酸化IκBα（p-IκBα）、核因子κB（NF-κB）、磷酸化核因子κB（p-NF-κB）的蛋白表达,ELISA法检测各组细胞培养上清中单核细胞趋化蛋白1（MCP-1）、肿瘤坏死因子α（TNF-α）和白细胞介素6（IL-6）的表达水平,应用实时定量PCR（RT-PCR）检测各组细胞MCP-1、TNF-α和IL-6的mRNA表达水平。结果Westernblot检测发现,与对照组相比,脂多糖组p-PPARγ、p-NF-κB和p-IκBα蛋白表达水平明显升高（P<0.05）,IκBα表达明显下降（P<0.05）,PPARγ和NF-κB表达水平无显著差异（P>0.05）;RT-PCR和ELISA检测发现,与对照组相比,脂多糖组MCP-1、TNF-α和IL-6蛋白水平和mRNA表达水平均明显增高（P<0.05）。与脂多糖组相比,替米沙坦组p-NF-κB和p-IκBα蛋白水平表达明显下降,MCP-1、TNF-α及IL-6分泌水平和mRNA水平也均明显降低,p-PPARγ和IκBα蛋白表达水平明显增加（P<0.05）,但是NF-κB和PPARγ表达水平依然无显著差异（P>0.05）。结论替米沙坦预处理可通过激活PPARγ而下调NF-κB活化从而抑制脂多糖诱导单核细胞THP-1产生炎症反应。     

PPARγ激动剂抑制脂多糖诱导肾小管上皮细胞分泌趋化因子及机制

目的:探讨过氧化物酶体增殖物激活受体γ(PPARγ)激动剂15d-PGJ2对脂多糖(LPS)诱导的趋化因子表达的影响及可能机制。方法:用15d-PGJ2(5μM)预处理人近端肾小管上皮细胞2h后加入LPS(1μg/ml),与LPS组、15d-PGJ2组及未加任何刺激组进行比较。用Real-time PCR方法检测IL-8和单核细胞趋化蛋白1(MCP-1)mRNA表达水平;用ELISA法检测细胞上清中IL-8和MCP-1蛋白水平;通过RNAi技术沉默肾小管上皮细胞PPARγ,观察15d-PGJ2的作用是否依赖于PPARγ;用间接免疫荧光法观察NF-κB在细胞内的定位;用Western blot法检测胞质中IκB的磷酸化水平。结果:在HK-2细胞中,与对照组相比,LPS刺激4h使IL-8 mRNA及蛋白分别升高(5.67±1.83)和(1.62±0.12)倍,使MCP-1 mRNA及蛋白分别升高(5.24±1.33)和(2.25±0.40)倍,且胞质中IκBα磷酸化水平明显增加(P0.05)。与LPS组相比,15d-PGJ2+LPS组,IL-8和MCP-1表达在mRNA水平分别下降74.23%和79.42%,在蛋白水平分别下降69.03%和49.44%,差异有统计学意义;在PPARγ沉默的HK-2细胞中,与LPS刺激组相比,15d-PGJ2使IL-8和MCP-1表达在mRNA水平分别下降59.21%和44.08%,在蛋白水平分别下降47.11%和39.40%(均P0.05),并明显抑制LPS诱导NF-κB核易位,下调IκBα磷酸化水平。结论:15d-PGJ2可抑制LPS诱导的趋化因子表达,且不完全依赖于PPARγ,可能与抑制IκBα磷酸化有关。     

内脂素对人单核细胞株源性巨噬细胞ATP结合盒转运蛋白A1的调控

目的:观察过氧化物酶体增殖物激活受体γ(PPARγ)信号转导通路在内脂素调控人单核细胞株(THP-1)源性巨噬细胞ATP结合盒转运蛋白A1(ABCA1)表达中的作用,探讨内脂素诱导泡沫细胞形成的机制和途径。方法:THP-1单核细胞诱导分化为巨噬细胞,随机分组,给予不同浓度和不同作用时间的内脂素进行干预,分别运用油红O染色观察细胞浆脂滴变化,反转录聚合酶链反应(RT-PCR)法和蛋白免疫印迹(Westernblot)法检测各组细胞PPARγ及ABCA1mRNA和蛋白表达,酶荧光学法检测细胞内TC和游离胆固醇(FC)含量,TC与FC之差为胆固醇酯(CE)含量。结果:与对照组比较,内脂素干预组细胞浆脂滴明显增多,细胞内FC和CE含量增加(P<0.05),PPARγ及ABCA1mRNA和蛋白表达降低(P<0.05);相关分析显示,内脂素呈浓度和时间依赖性下调PPARγ及ABCA1mRNA和蛋白的表达。结论:内脂素可能通过PPARγ信号转导通路下调ABCA1表达,减少细胞内FC流出,使细胞内CE合成增加,从而诱导泡沫细胞形成。这可能为内脂素致动脉粥样硬化发病机制的研究提供了一个新的理论依据。     

弓形虫ROP16蛋白在人白血病细胞THP-1表达及对其细胞增殖与凋亡的影响北大核心CSCD

目的探讨弓形虫Ⅱ型(Me49)ROP16蛋白在急性单核细胞白血病细胞株THP-1中的表达及其对THP-1细胞增殖与凋亡的影响。方法构建过表达ROP16(overExp-ROP16)和空载体(overExp-NC)慢病毒,通过转染THP-1细胞,72 h后观察荧光表达情况,采用PCR与Western blot验证ROP16在THP-1细胞中的表达。免疫荧光技术检测ROP16蛋白在THP-1细胞中的定位。CCK-8与流式细胞术检测细胞增殖及凋亡。采用qRT-PCR检测细胞凋亡相关因子Bcl-2、Bax、Caspase-3 mRNA相对表达水平。Western blot检测Bax、Bcl-2、Pro-Caspase-3和Cleaved-Caspase-3蛋白的表达变化。结果构建的过表达ROP16重组慢病毒转染到THP-1细胞后,可观察强荧光信号,ROP16蛋白在THP-1细胞中成功表达。免疫荧光结果表明ROP16蛋白定位于THP-1细胞核。CCK-8与流式细胞术证实ROP16蛋白抑制THP-1细胞的增殖并促进其凋亡(均P<0.05)。与对照组相比,过表达组促凋亡因子Bax、Caspase-3 mRNA高表达(P<0.05),抗凋亡因子Bcl-2 mRNA低表达(P<0.01),Bax与Cleaved-Caspase-3蛋白水平上调(P<0.01),Bcl-2与Pro-Caspase-3蛋白水平下调(P<0.01)。结论构建的慢病毒表达质粒overExp-ROP16可在急性单核细胞白血病细胞株THP-1中表达且通过入核调节凋亡蛋白Bcl-2、Bax、Caspase-3而抑制THP-1细胞增殖,促进其凋亡。     

葡萄糖和晚期糖基化终产物联合刺激对人单核细胞血红素加氧酶1表达的影响

目的 探讨葡萄糖和晚期糖基化终产物(AGE)联合刺激对人单核细胞THP-1血红素加氧酶1(HO-1)表达的影响. 方法 分别以15mmol/L葡萄糖、100μg/ml AGE和二者联合刺激THP-1,比较各组活性氧(ROS)产量,培养液丙二醛(MDA)、肿瘤坏死因子α(TNFα)水平和细胞HO-1mRNA及蛋白的表达量. 结果葡萄糖和AGE联合刺激的ROS产量、MDA、TNFα水平及HO-1mRNA和蛋白表达均明显高于单独刺激组. 结论 葡萄糖和AGE联合刺激可导致THP-1细胞氧化应激和HO-1表达增加.     

PPARδ基因过表达对RAW264.7细胞MCP-1及VCAM-1表达的影响

目的:观察过氧化物酶增殖体激活受体δ(PPARδ)基因转染对氧化型低密度脂蛋白(ox-LDL)诱导的鼠源性单核细胞RAW264.7中单核细胞趋化蛋白-1(MCP-1)及血管细胞间黏附分子-1(VCAM-1)基因和蛋白表达的影响。方法: 构建表达人PPARδ基因的复制缺陷型腺病毒表达载体(Ad-PPARδ),并培养RAW264.7细胞。实验分为未转染的对照组、PPARδ基因转染组及假转染组。将RAW264.7细胞与ox-LDL(50 mg/L)孵育24 h后,采用RT-PCR及蛋白免疫印迹法分别检测各组细胞MCP-1及VCAM-1 mRNA及其蛋白的表达。采用单核细胞趋化试验检测人外周血单核细胞在不同条件培养基中的趋化活性。结果: PPARδ基因转染组细胞中MCP-1及VCAM-1的表达明显低于对照组及假转染组(P<0.05);单核细胞移动的距离明显小于对照组及假转染组(P<0.05)。假转染组与对照组比较,MCP-1及VCAM-1的表达及单核细胞移动的距离无显著差异。结论: PPARδ基因转染能抑制ox-LDL诱导的MCP-1及VCAM-1表达,增加PPARδ的表达可能具有防治动脉粥样硬化的作用。     

内脏脂肪素对巨噬细胞中EMMPRIN表达的影响及其机制的探讨

目的:研究内脏脂肪素(visfatin,Vis)对巨噬细胞细胞外基质金属蛋白酶诱导因子(EMMPRIN)表达的影响及其机制。方法:诱导THP-1单核细胞转化为巨噬细胞后,加入Vis,用RT-PCR和Western blot分别测定EMM-PRIN基因和其蛋白的表达。以丝裂原活化蛋白激酶(MAPK)信号通路抑制剂、视黄醛X受体(RXR)配体及过氧化物酶增殖体活化受体γ(PPARγ)配体预处理巨噬细胞后,加入Vis,检测上述抑制剂及配体对Vis刺激效果的作用。以Vis刺激巨噬细胞,检测Vis对MAPK通路激活及对PPARγ蛋白表达的作用。结果:Vis刺激组,EMMPRIN基因及其蛋白的水平均明显增高,与对照组相比具有统计学差异(P0.05,P0.01)。p38 MAPK、ERK1/2 MAPK通路抑制剂及RXR配体可抑制Vis对EMMPRIN表达的促进作用。Vis可促进38 MAPK及ERK1/2 MAPK的磷酸化。结论:Vis可增加巨噬细胞炎症因子的表达,该过程同p38 MAPK及ERK1/2 MAPK通路的磷酸化相关。RXR可能参与了该过程。     

单核细胞趋化蛋白-1对其表面淋巴细胞功能相关抗原-1、清道夫受体和载脂蛋白E表达的影响及雌二醇的干预作用

为研究单核细胞趋化蛋白-1对单核细胞表面淋巴细胞功能相关抗原-1、清道夫受体和载脂蛋白E表达的影响,采用培养人单核细胞株THP-1细胞,以间接免疫荧光法结合流式细胞术和激光共聚焦扫描显微镜分别检测淋巴细胞功能相关抗原-1 和清道夫受体蛋白的表达,用逆转录-多聚酶链反应检测清道夫受体和载脂蛋白E mRNA的表达水平.结果显示,在单核细胞趋化蛋白-1刺激组淋巴细胞功能相关抗原-1和清道夫受体蛋白的表达明显高于对照组(P<0.01);17-β-雌二醇可部分抑制单核细胞趋化蛋白-1对THP-1细胞表面淋巴细胞功能相关抗原-1表达的促进作用(P<0.05),但对单核细胞趋化蛋白-1促进清道夫受体表达的作用无明显影响;单核细胞趋化蛋白-1明显促进THP-1细胞清道夫受体mRNA的表达,而对载脂蛋白E mRNA的表达无明显影响.研究提示,单核细胞趋化蛋白-1可通过促进单核细胞表面粘附分子、淋巴细胞功能相关抗原-1以及清道夫受体的表达而促进动脉粥样硬化的发生,雌二醇还可能通过抑制单核细胞趋化蛋白-1对淋巴细胞功能相关抗原-1表达的促进而发挥抗动脉粥样硬化作用.     

锌指蛋白A20抑制Toll样受体4介导的人单核细胞炎症反应的实验研究

目的:观察锌指蛋白A20过度表达对人单核细胞膜Toll样受体(TLR4),下游促炎因子肿瘤坏死因子-α(TNF-α)与白细胞介素(IL)-12,以及抗炎因子IL-10表达的影响,探讨锌指蛋白A20对单核细胞炎症反应的抑制作用及可能的调节机制。方法:Ficoll细胞分离液分离人外周血单核细胞,随机分为对照组、脂多糖(LPS)组、A20转染组与LPS+A20转染组。荧光显微镜检测GFP报告基因,免疫组织化学检测A20蛋白的表达,RT-PCR检测A20及TLR4的mRNA表达,流式细胞检测技术检测TLR4的蛋白表达,ELISA方法检测上清液TNF-α、IL-12及IL-10表达水平。结果:LPS刺激后,单核细胞TLR4和内源性A20的mRNA和蛋白、TNF-α、IL-12和IL-10表达较对照组均明显升高(均P<0.01);TNF-α/IL-10和IL-12/IL-10均明显高于对照组(均P<0.01);转染A20基因的单核细胞,在无LPS刺激的条件下,上述指标与对照组相比均差异无统计学意义;转染A20基因的单核细胞在LPS刺激后,TLR4mRNA和蛋白、TNF-α、IL-12的表达以及TNF-α/IL-10和IL-12/IL-10均显著低于LPS组,而IL-10的表达明显高于对照组和LPS组(均P<0.01)。结论:TLR4激活介导单核细胞的炎症反应,且正反馈调节其自身受体TLR4和内源性A20的表达;A20参与单核细胞TLR4激活所介导的炎症反应,其表达增加与TLR4表达的增加有关;单纯提高A20表达对未被激活的单核细胞TLR4及其信号通路影响不大;A20过表达可抑制TLR4激活所介导的单核细胞的炎症反应。     

Three layer functional model and energy exchange concept of aging process

Relying on a certain degree of abstraction, we can propose that no particular distinction exists between animate or living matter and inanimate matter. While focusing attention on some specifics, the dividing line between the two can be drawn. The most apparent distinction is in the level of structural and functional organization with the dissimilar streams of ‘energy flow’ between the observed entity and the surrounding environment. In essence, living matter is created from inanimate matter which is organized to contain internal intense energy processes and maintain lower intensity energy exchange processes with the environment. Taking internal and external energy processes into account, we contend in this paper that living matter can be referred to as matter of dissipative structure, with this structure assumed to be a common quality of all living creatures and living matter in general. Interruption of internal energy conversion processes and terminating the controlled energy exchange with the environment leads to degeneration of dissipative structure and reduction of the same to inanimate matter, (gas, liquid and/or solid inanimate substances), and ultimately what can be called ‘death.’ This concept of what we call dissipative nature can be extended from living organisms to social groups of animals, to mankind. An analogy based on the organization of matter provides a basis for a functional model of living entities. The models relies on the parallels among the three central structures of any cell (nucleus, cytoplasm and outer membrane) and the human body (central organs, body fluids along with the connective tissues, and external skin integument). This three-part structural organization may be observed almost universally in nature. It can be observed from the atomic structure to the planetary and intergalactic organizations. This similarity is corroborated by the membrane theory applied to living organisms. According to the energy nature of living matter and the proposed functional model, the decreased integrity of a human body's external envelope membrane is a first cause of the structural degradation and aging of the entire organism. The aging process than progresses externally to internally, as in single cell organisms, suggesting that much of the efforts towards the restoration and maintenance of the mechanisms responsible for structural development should be focused accordingly, on the membrane, i.e., the skin. Numerous reports indicate that all parts of the human body, like: bones, blood with blood vessels, muscles, skin, and so on, have some ability for restoration. Therefore, actual revival of not only aging tissue of the human body's membrane, but the entire human body enclosed within, with all internal organs, might be expected. We assess several aging theories within the context of our model and provide suggestions on how to activate the body's own anti-aging mechanisms and increase longevity. This paper presents some analogies and some distinctions that exist between the living dissipative structure matter and inanimate matter, discusses the aging process and proposes certain aging reversal solutions.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Unusual responses of nocturnal pineal melatonin synthesis and secretion to swimming: Attempts to define mechanisms

Abstract: The effect of swimming at night on rat pineal melatonin synthesis was compared with that of light exposure at night. Rats were forced to swim at 0030 hr (lights out at 2000 hr) and sacrificed by decapitation 15 and 30 min later, immediately after swimming. Other groups of animals were exposed to white light (650μW/cm²) for 15 and 30 min at same time. Swimming caused a rapid and highly significant drop in the melatonin content in the pineal gland; however, the activity of N-acetyltransferase (NAT), the supposed rate limiting enzyme in the melatonin production, was not changed. Despite the drop in pineal melatonin levels, serum concentrations of the indole remained elevated in the rats that swam. In contrast, melatonin levels in the pineal and serum of light exposed rats fell precipitously, accompanied by a significant suppression of NAT activity. Since we anticipated that the strenuous exercise associated with swimming may induce release of artrial natriuretic peptide (ANP) from the heart, which in turn could cause the release of pineal melatonin, in a second study we injected physiological saline intravenously to stretch the cardiac muscle and release ANP. Three milliliters of normal saline was injected during the day into the jugular vein of anesthetized rats that were pretreated with isoproterenol to stimulate pineal melatonin production. Animals were killed 15 min after the saline injection, and pineal NAT activity and pineal melatonin levels were measured. The saline injections caused no alteration in the elevated levels of either NAT or melatonin. These data suggest that the disparity in pineal NAT activity (which was high) and pineal melatonin (which was low), in animals swum at night, may not be caused by ANP which is released during strenuous exercise such as swimming.     

Melatonin and photoperiodic time measurement: Seasonal breeding in the sheep

Abstract: Well-established circadian physiology supports the view that photoperiodic time measurement utilizes the coincidence between the presence of light and a photosensitive phase of a 'biological clock' to alter reproductive status—the so-called external coincidence model of seasonal breeding. In this review, we examine the mechanism whereby photoperiod interacts with presumed suprachiasmatic nuclei activity to allow endogenous melatonin to normally synchronize reproductive activity to the optimal time of year. The Romney Marsh sheep is particularly explored as an experimental model. It is suggested that the on/off activity of seasonal reproduction may be a robust mechanism able to be predictably manipulated by the judicious use of the light/dark cycle and exogenous melatonin, but firmly based on circadian principles.     

Response of rat pineal melatonin to calcium, magnesium, and lithium is circadian stage dependent

Abstract: Herein we documented the response of pineal melatonin production to electrolytes known to be effective on pineal function in view of a possible circadian stage dependence. We studied the release of melatonin by perifused rat pineal glands at 2 different circadian stages corresponding to the middle of the light and dark periods, i.e., respectively, 7 and 19 HALO (Hours After Light Onset, L:D = 12:12). The initial efflux rates were, as expected, much higher in the perifusates of glands removed from rats sacrificed during the dark phase than of those removed during the light phase. After 3 hr of perifusion, melatonin release reached similar levels which were found constant up to the 8th hr of perifusion, whatever the circadian stage. Perifusion of the glands with physiological concentrations for the rat of calcium (5.2 mmol/1) and magnesium (1.34 mmol/1) resulted in a stimulatory effect on the pineal glands removed from rats sacrificed in the middle of the dark period (19 HALO), whereas no effects were observed on the pineal glands removed from rats sacrificed during the light (7 HALO). Lithium (0.28 and 0.55 mmol/1) was ineffective on melatonin release in pineal glands removed 7 and 19 HALO. Our results show differences in the initial efflux rates of melatonin and in the response of perifused pineal glands to calcium and magnesium according to the circadian stage.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.     

Changes in connexin43, the gap junction protein of astrocytes, during development of the rat pineal gland

Abstract: The abundance of gap junctions between rat pineal astrocytes formed by connexin43 (Cx43) was studied during development. Levels and distribution of Cx43 were measured by immunoblotting and indirect immunofluorescence, respectively. The amount of Cx43 in cells located within the gland was low until about the 7th postnatal day and increased to adult values between the 14th and 21st days postpartum. Although astrocytes, recognized by their vimentin immunoreactivity, were scarce before birth, they were abundant by the 7th postnatal day suggesting that the low levels of Cx43 found at this age corresponded to a low expression of this protein. Localization of the immunoreactivity to Cx43 and vimentin showed a close correlation, indicating that mature or immature pineal astrocytes form gap junctions made of Cx43. Since Cx43 levels attained their adult values at about the time the innervation and the functional state of the gland reached maturity (2–3 weeks after birth), it is proposed that astrocyte gap junctions are involved in the function of the adult rat pineal gland.     

Language of CTO interventions – Focus on hardware

The knowledge of variety of chronic total occlusion (CTO) hardware and the ability to use them represents the key to success of any CTO interventions. However, the multiplicity of CTO hardware and their physical character and the terminology used by experts create confusion in the mind of an average interventional cardiologist, particularly a beginner in this field. This knowledge is available but is scattered. We aim to classify and compare the currently used devices based on their properties focusing on how physical character of each device can be utilized in a specific situation, thus clarifying and simplifying the technical discourse.