Strain type for carrier mobility enhancement.
\r\n\tFinally, I want to emphasize that, in this book, I expect to have excellent contributons on the subjects other than muscle systems, so that the book will be widely read by people interested in non-muscle motile systems as well as by muscle researchers.
",isbn:null,printIsbn:null,pdfIsbn:null,doi:null,price:0,priceEur:null,priceUsd:null,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"862ba53997da17b644b918fe44e97d4a",bookSignature:"Emeritus Prof. Haruo Sugi",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/7021.jpg",keywords:"Musculo-skeletal system, Cardio-vascular system, Porter myosins, Cellular transport, Motile systems, cell division, Contractile ring formation, Mitotic apparatus, Ciliary Movement, Flagellar Movement, Amoeboid movement, Novel motile systems",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"August 13th 2018",dateEndSecondStepPublish:"September 3rd 2018",dateEndThirdStepPublish:"November 2nd 2018",dateEndFourthStepPublish:"January 21st 2019",dateEndFifthStepPublish:"March 22nd 2019",remainingDaysToSecondStep:"3 years",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"140827",title:"Emeritus Prof.",name:"Haruo",middleName:null,surname:"Sugi",slug:"haruo-sugi",fullName:"Haruo Sugi",profilePictureURL:"https://mts.intechopen.com/storage/users/140827/images/system/140827.jpg",biography:"Haruo Sugi was appointed instructor in the Depertment of Physiology of the University of Tokyoin 1962, and worked at Columbia University and the National Instututes of Health, USA, from 1965 to 1967. He was a professor and chairman of the Department of Physiology, Teikyo University Medical School from 1973 to 2004, when he became emeritus professor. Professor Sugi organized international symposia on muscle contraction seven times, each followed by publication of proceedings. He also edited 4 books. From 1995 to 2005, Sugi was Cairman of the Muscle Commission in the International Union of Physiological Sciences (IUPS).",institutionString:"Teikyo University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"University of Tokyo",institutionURL:null,country:{name:"Japan"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"6",title:"Biochemistry, Genetics and Molecular Biology",slug:"biochemistry-genetics-and-molecular-biology"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"220812",firstName:"Lada",lastName:"Bozic",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/220812/images/6021_n.jpg",email:"lada@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. Whether that be identifying an exceptional author and proposing an editorship collaboration, or contacting researchers who would like the opportunity to work with IntechOpen, I establish and help manage author and editor acquisition and contact."}},relatedBooks:[{type:"book",id:"2631",title:"Current Basic and Pathological Approaches to the Function of Muscle Cells and Tissues",subtitle:"From Molecules to Humans",isOpenForSubmission:!1,hash:"34fa138dc948d7121e2915ac84ea30cf",slug:"current-basic-and-pathological-approaches-to-the-function-of-muscle-cells-and-tissues-from-molecules-to-humans",bookSignature:"Haruo Sugi",coverURL:"https://cdn.intechopen.com/books/images_new/2631.jpg",editedByType:"Edited by",editors:[{id:"140827",title:"Emeritus Prof.",name:"Haruo",surname:"Sugi",slug:"haruo-sugi",fullName:"Haruo Sugi"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"6694",title:"New Trends in Ion Exchange Studies",subtitle:null,isOpenForSubmission:!1,hash:"3de8c8b090fd8faa7c11ec5b387c486a",slug:"new-trends-in-ion-exchange-studies",bookSignature:"Selcan Karakuş",coverURL:"https://cdn.intechopen.com/books/images_new/6694.jpg",editedByType:"Edited by",editors:[{id:"206110",title:"Dr.",name:"Selcan",surname:"Karakuş",slug:"selcan-karakus",fullName:"Selcan Karakuş"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1591",title:"Infrared Spectroscopy",subtitle:"Materials Science, Engineering and Technology",isOpenForSubmission:!1,hash:"99b4b7b71a8caeb693ed762b40b017f4",slug:"infrared-spectroscopy-materials-science-engineering-and-technology",bookSignature:"Theophile Theophanides",coverURL:"https://cdn.intechopen.com/books/images_new/1591.jpg",editedByType:"Edited by",editors:[{id:"37194",title:"Dr.",name:"Theophanides",surname:"Theophile",slug:"theophanides-theophile",fullName:"Theophanides Theophile"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3161",title:"Frontiers in Guided Wave Optics and Optoelectronics",subtitle:null,isOpenForSubmission:!1,hash:"deb44e9c99f82bbce1083abea743146c",slug:"frontiers-in-guided-wave-optics-and-optoelectronics",bookSignature:"Bishnu Pal",coverURL:"https://cdn.intechopen.com/books/images_new/3161.jpg",editedByType:"Edited by",editors:[{id:"4782",title:"Prof.",name:"Bishnu",surname:"Pal",slug:"bishnu-pal",fullName:"Bishnu Pal"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3092",title:"Anopheles mosquitoes",subtitle:"New insights into malaria vectors",isOpenForSubmission:!1,hash:"c9e622485316d5e296288bf24d2b0d64",slug:"anopheles-mosquitoes-new-insights-into-malaria-vectors",bookSignature:"Sylvie Manguin",coverURL:"https://cdn.intechopen.com/books/images_new/3092.jpg",editedByType:"Edited by",editors:[{id:"50017",title:"Prof.",name:"Sylvie",surname:"Manguin",slug:"sylvie-manguin",fullName:"Sylvie Manguin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"371",title:"Abiotic Stress in Plants",subtitle:"Mechanisms and Adaptations",isOpenForSubmission:!1,hash:"588466f487e307619849d72389178a74",slug:"abiotic-stress-in-plants-mechanisms-and-adaptations",bookSignature:"Arun Shanker and B. Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"72",title:"Ionic Liquids",subtitle:"Theory, Properties, New Approaches",isOpenForSubmission:!1,hash:"d94ffa3cfa10505e3b1d676d46fcd3f5",slug:"ionic-liquids-theory-properties-new-approaches",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/72.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"314",title:"Regenerative Medicine and Tissue Engineering",subtitle:"Cells and Biomaterials",isOpenForSubmission:!1,hash:"bb67e80e480c86bb8315458012d65686",slug:"regenerative-medicine-and-tissue-engineering-cells-and-biomaterials",bookSignature:"Daniel Eberli",coverURL:"https://cdn.intechopen.com/books/images_new/314.jpg",editedByType:"Edited by",editors:[{id:"6495",title:"Dr.",name:"Daniel",surname:"Eberli",slug:"daniel-eberli",fullName:"Daniel Eberli"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"57",title:"Physics and Applications of Graphene",subtitle:"Experiments",isOpenForSubmission:!1,hash:"0e6622a71cf4f02f45bfdd5691e1189a",slug:"physics-and-applications-of-graphene-experiments",bookSignature:"Sergey Mikhailov",coverURL:"https://cdn.intechopen.com/books/images_new/57.jpg",editedByType:"Edited by",editors:[{id:"16042",title:"Dr.",name:"Sergey",surname:"Mikhailov",slug:"sergey-mikhailov",fullName:"Sergey Mikhailov"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1373",title:"Ionic Liquids",subtitle:"Applications and Perspectives",isOpenForSubmission:!1,hash:"5e9ae5ae9167cde4b344e499a792c41c",slug:"ionic-liquids-applications-and-perspectives",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/1373.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"62046",title:"Advanced Transistor Process Technology from 22- to 14-nm Node",doi:"10.5772/intechopen.78655",slug:"advanced-transistor-process-technology-from-22-to-14-nm-node",body:'The metal-oxide-semiconductor field effect transistors (MOSFETs) are core switch devices of current large-scale complementary-metal-oxide-semiconductor integrated circuits (CMOS ICs). The performance of the transistor has a critical effect on the performance of IC. As the continuous scaling of the transistor CD for a higher IC performance and integration density, the fabrication process technologies and methods of the transistor are fast changing and becoming relatively complicated. To suppress the short-channel effect as well as the performance degradation of devices, three main new technologies, including strain engineering, high-k/metal gate (HKMG), and FinFET of MOSFETs, are implemented into state-of-art IC manufacture technology. The three technologies are quite important and firstly applied in the CMOS IC manufacturing process by Intel Corporation in the years 2003, 2007, and 2011 at 90-, 45-, and 22-nm node, respectively, which is developed into the industrial standards and widely adopted by other IC manufacturing corporations including TSMC, and Samsung. While the process node of CMOS IC scaling from 22- into 14-nm node, advanced technologies such as film growth, structure design, process optimization, and integration flow of them become more complicated, which often need elaborated process development with diversified knowledge and techniques from different fields.
The effective carrier mobility in the channel of the transistor is crucial to the device’s performance. With the gate length aggressively shrinking down, the electric field magnitude in the channel is strengthened with channel-doping concentration rising, resulting in obvious degradation in effective carrier mobility due to ionized impurity scattering. Mobility both for electron and for hole can be enhanced by changing the silicon atom arrangement of crystal lattice in the channel through the external stress. It is investigated that the tensile and compressive strain for silicon can improve the electron and hole mobility, respectively.
Mobility is closely dependent on the mean free time and the effective mass of the carrier. As we consider the simplified band structure of silicon, there are six equivalent minima at k = (x, 0, 0), (−x, 0, 0), (0, x, 0), (0, −x, 0), (0, 0, x), (0, 0, −x) with x = 5 nm−1 for the conduction band in Ref. [1]. There is one maximum containing two sub-bands at k = 0 for the valence band. These two sub-bands are referred to as the light and heavy hole bands with a light hole effective mass and a heavy hole effective mass. Therefore, the effective mass of these anisotropic minima is characterized by a longitudinal mass along the corresponding equivalent (1, 0, 0) direction and two transverse masses in the plane perpendicular to the longitudinal direction. For the electron in conduction band, the external stress can cause tensile or compressive strain in the silicon lattice. The longitudinal band valley will change. Thus, the corresponding longitudinal mass is changed leading to the mean free time increasing or decreasing for the carriers. For hole in the valence band, the strain effect on the light hole band and heavy hole band is familiar with electron.
For the device, several of strain types for the mobility enhancement are listed in Table 1. Different axial tensile and compressive strain can introduce different mobility enhancement or degradation for electron and hole. Therefore, strain technique is very practical and important for device’s performance promotion. In the point of IC process, this technique is called as strain engineering, which is divided into global strain stress and local strain stress. Global strain stress is less employed in the manufacturing process due to the application regime. Local strain stress can be targeted to enhance carrier’s mobility in the specified region and widely used in the modern IC process flow. Local strain stress can be induced and achieved by IC processes, such as selective epitaxy growth (SEG) of silicon-germanium (SiGe) source/drain, dielectric etch-stop layer (ESL), metal gate, and contact. For PMOS, the most important strain engineering technology is to use selective source/drain epitaxy of SiGe with large lattice constant in order to provide channel with axial compressive stress for hole mobility enhancement as shown in Figure 1.
Direction | NMOS | PMOS |
---|---|---|
Channel length | Tensile | Compressive |
Channel width | Tensile | Tensile |
Perpendicular to channel plane | Compressive | Tensile |
Strain type for carrier mobility enhancement.
(a) Homoepitaxy and (b) heteroepitaxy: SiGe with high stress growth on the Si substrate.
The embedded SiGe in source/drain (S/D) region has been widely used to induce uniaxial strain in the channel, especially for the sigma SD epitaxy in Ref. [2]. The strain engineering in 22-nm planar transistor is becoming more complicated. The film growth technique often requires relatively low temperature and the decreasing of pattern dependency. In 22-nm node, the SiGe layers need to be grown at 650°C in a reduced-pressure chemical vapor deposition (RPCVD) reactor and with a series of complicated steps. First, in situ cleaning is performed by annealing in the range of 740–825°C for 3–7 min. Then, dichlorosilane (SiH2Cl2), 10% germane (GeH4) in H2, and 1% diborane (B2H6) in H2 are used as Si, Ge, and B precursors, respectively. Moreover, HCl is utilized as Si etchant to obtain selectivity during the epitaxy. The SiGe growth rate can be denoted by an empirical model (Eq. (1)) in Refs. [3, 4], which considers the contribution of a variety of molecule fluxes coming from different directions toward Si planes during epitaxy in Ref. [5]:
where
where
For integrating SEG SiGe into 22-nm PMOSFET, a sacrificial epitaxy-block Si3N4 layer is deposited on whole wafer after the formation of dummy polysilicon gate and spacers. In the next step, the block layer is selectively opened and low-temperature epitaxy SiGe with high stress is performed at the source/drain region of PMOS.
The amount of strain induced by SiGe is dependent on the initial recess shape, interfacial quality of SiGe/Si, and defect density in the epilayers. Sigma-shaped recesses with (100) and {111} planes are very suitable shape for embedded SiGe in source/drain regions with the highest stress. Moreover, in such transistors, shorter distance between sigma-shaped recesses and channel region can generate a higher stress to the channel region. By applying dry etch together with wet etch in Si substrate, the sigma-shaped recesses turn more large and induce a stronger stress of embedded SiGe with a closer distance to the channel in Ref. [5].
For NMOS, PMD (pre-metal dielectric) layer is deposited as ESL, which can offer axial tensile stress to the channel for electron mobility enhancement [6]. In the modern IC manufacturing integrated process, more and more strain process is employed for the devices, which is of great significance to suppress the device’s performance degradation. However, the film thickness of ESL is limited due to the scaling of gate pitch between transistors. New techniques, such as metal gate and contact electrode stress of NMOS, are necessary. The TiN metal gate and the W plug often bring effective tensile stress into the channel of NMOSFET, resulting in the enhancement of motilities for electrons.
High-k/metal gate (HKMG) is a very important technique for modern CMOS IC manufacturing process. While the transistor CD scaling down, conventional oxide dielectric/polysilicon gate was formally replaced by high-k dielectric/metal gate, in order to suppress the unbearable leakage in the ultra-thin oxide dielectric film in Ref. [7]. HKMG technique has found a new effective path for equivalent oxide thickness (EOT) scaling tendency, which is of deep significance to continuous scaling of MOS transistors. However, HKMG brings about a series of challenges, including new high-k dielectric and metal gate materials, threshold voltage modulation, and process integration scheme. To some extent, the scaling of MOS transistor relies on the scaling of EOT of gate dielectric. When the conventional oxide film thickness shrinks to about 11–12 A, the transistor shrinking cannot be continued due to the extremely large leakage current from the gate to the substrate by the electron direct tunneling through the ultra-thin oxide film. EOT is defined as (Eq. (3)).
where
Many high-k materials have been investigated for CMOS devices including metal oxide (HfO2, ZrO2, Al2O3, etc.) as shown in Table 2. Among these metal-oxide materials, HfO2 has the advantages of the moderate relative permittivity value, the basically symmetrical energy band offset to silicon conduction band and valence band, and the uniformly amorphous structure. Therefore, HfO2 material is applied in the IC manufacturing production.
Material | Dielectric constant | Material | Dielectric constant |
---|---|---|---|
Al2O3 | 8–11.5 | NdAlO3 | 22.5 |
(Ba, Sr)TiO3 | 200–300 | PrAlO3 | 25 |
BeAl2O4 | 8.3–9.43 | Si3N4 | 7 |
CeO2 | 16.6–26 | SmAlO3 | 19 |
HfO2 | 26–30 | SrTiO3 | 150–250 |
Hf silicate | 11 | Ta2O5 | 25–45 |
La2O3 | 20.8 | TiO2 | 86–95 |
LaAlO3 | 23.8–27 | Y2O3 | 8–11.6 |
LaScO3 | 30 | ZrO2 | 22.2–28 |
High-k dielectric constant.
In the early 1990, it is reported that the integration of polysilicon gate with HfO2 dielectric results in serious Fermi Level Pinning (FLP) phenomenon, where the Fermi level of polysilicon gate is fixed at the poly/HfO2 interfacial energy level. Although some theories including oxygen vacancy model, and dipole formation, are put forward to explain the pinning effect, the process cannot successfully release the effect of FLP, which causes huge difficulties on the device’s threshold voltage modulation. Therefore, different metal gates with the high-k material are corresponded to different threshold voltage modulation regimes for PMOS and NMOS.
The introduction of high-k/metal gate provides great potential of transistor’s scaling down under 45-nm node. Metal gate can reduce oxide thickness by eliminating polysilicon gate depletion effect. Metal gate has a low gate resistance and can suppress boron penetration to the substrate in Refs. [8, 9, 10].
In 22-nm node, the main challenge and research hotpot for HKMG stack lie in the effective work function (EWF) modulation of metal gate. The EWF can be defined as the value between Fermi level of metal gate and vacuum level in the metal-oxide-semiconductor system. As shown in Figure 2, EWF is defined as (Eq. (4))
where
Illustration of band edge EWF of metal gate for PMOS.
Fermi level of metal gate can be shifted both upwards and downwards. The Fermi level (EF) of metal gate is set to be in the position of mid-gap in the substrate. When Fermi level shifts to the conduction band of Si substrate, the effective work function of metal gate decreases. On the other hand, when Fermi level shifts to the valence band of Si substrate, the effective work function of metal gate increases. The EWF movement behaviors can directly drive the threshold voltage (Vt) modulation for the MOS devices.
The most effective method to manipulate EWF is the selection of metal gate. For PMOS, a large EWF is preferred to achieve high Vt for low-power (LP) IC performance. Hence, Fermi level of PMOS metal gate is ideally near to the valence band maximum of silicon substrate, where the position in the valence band minima of silicon is the best choice for Fermi level of metal gate. For NMOS, a small EWF is preferred to achieve high Vt for LP IC performance, where the Fermi level of NMOS metal gate is ideally near to or at the conduction band minima of silicon substrate. Therefore, the demand of the large EWF for PMOS and small EWF for NMOS is selecting TiN with a high work function and TiAl with a low work function metals.
For the multi-Vt modulation of PMOS and NMOS, the most general method is to tune the gate-stack thickness control in Refs. [11, 12], in order to realize the regular, low, and high Vt levels. As shown in Figure 3, the metal gate stack can be divided into three layers: the first is the bottom-capping layer for the high-k dielectric, the second is exactly the work function layer, and the last is the top-capping layer for the contacted metal. Moreover, the etch-stop layer should be considered for the dual work function metal integration of PMOS and NMOS. Although the gate stack contains three parts, the effective work function of the entire gate electrode is dominated by the work function layer metal, where EWF sensitivity is strictly limited by the bottom-capping layer thickness, and the top-capping layer acts as the barrier layer for the contacted metal (tungsten). Therefore, the thickness control of metal gate-stack design is exactly of precision and significance.
HKMG gate stack.
The novel gate-stack structure of HKMG has been implemented for MOSFETs to promise conventional scaling of the high-performance CMOS process down to the 45/32-nm node. Two completely different integration schemes were proposed [13]. With the HKMG in the IC process flow, a big question arises that the module of HKMG structure formation is ahead of or after the module of source/drain process. Gate-first process integration scheme is familiar with poly-Si/SiO2 process flow. HKMG module is firstly deposited after the active-region formation module, and then source/drain module formation module is following until the end. However, with the source/drain formation later than HKMG formation module, the high annealing temperature for the S/D doping profile has a serious impact on HKMG characteristics and its reliability.
To overcome shortcoming caused by gate-first integration scheme, gate-last integration scheme is put forward. In the gate-last process, conventional poly-Si/SiO2 is still formed on the wafer substrate firstly. After poly-Si/SiO2 formation module, it is followed by the S/D impurity doping and its activation with annealing process at high temperature ambient. Then, PMD layer is deposited on the poly-Si dummy gate, where PMD is also called an inter-layer-dielectric zero layer (ILD0). With poly-Si-open planarization (POP) chemical mechanical polishing (CMP), poly-Si gate is exposed for the following removal of poly-Si/SiO2 process. Finally, HKMG is deposited in the position where poly-Si dummy gate previously existed, which is called gate-last process due to HKMG module later than the middle end of line (MEOL) process. The implement of gate-last integration scheme avoids the damage to devices by the high annealing temperature of S/D process. Therefore, gate-last integration scheme has obvious performance advantages for HKMG devices and becomes popular technique applied beyond 28 nodes.
In gate-last technique, it is divided into two integration schemes: high-k first/metal-gate last and high-k last/metal-gate last. In the first approach, the high-k layer is deposited together with the formation of dummy gate and before the annealing of source/drain, where only metal gate stack is formed with gate-last scheme. In the second approach, both high-k and metal gate are formed after the annealing of source/drain, which is also called all gate-last integration scheme. It has better film quality and process adjustment window than the former and is widely adopted for CMOS IC fabrication process in 22 nm and beyond node. In this integration scheme, multilayer HKMG stacks are IL/HfO2/TiN/TaN/TiN/W and IL/HfO2/TiN/TiAlC/TiN/W for PMOS and NMOS, respectively. IL layer is an interfacial layer between HK and substrate and is normally SiO2 forming by chemical oxidation method. All HKMG depositions are finished by atomic layer deposition (ALD) approach with a high conformality and a precise thickness control ability.
While process node scaling from 22 to 14 nm, the basic architecture of the transistor is changing from 2D planar device to 3D volume inversion device for a better control of SCE in channel with less leakage. The device design as well as the process techniques turns more complicated and needs a more elaborated technologies.
With feature size of CMOS IC shrinking to 20-nm node and beyond, the structure of the conventional planar MOSFET consisting of single-gate electrode to control channel potential distribution and the flow of current in the channel region is faced with the undesirable parasitic effects called short-channel effect (SCE) and drain-induced barrier lowering (DIBL) effect. Via voltage-doping transformation (VDT) model [14], the device’s structure and material parameters can be translated into electrical parameters with electrostatic integrity (EI) (Eq. (5)). SCE and DIBL can be derived as (Eqs. (6) and (7))
where
The threshold voltage of MOSFET can be denoted as (Eq. (8))
According to the above expression, SCE can be minimized by reducing the junction depth, gate oxide thickness, and depletion depth via increasing the doping concentration in the channel region. However, the limits on the reducing junction depth and gate oxide thickness have become very toughly serious in the practical device. Hence, SCE and DIBL values of the planar MOSFET are not controlled well in the ultra-short-channel length.
The most efficient and direct way to suppress SCE is to strengthen the gate electric field control capability by double-gate (DG) or multi-gate (MG) structure. DG or MG structures on thin Si channel improve the electrostatic integrity of MOSFET (Eq. (9)) with the transistor working in a volume inversion mode due to a reduced device structure parameter, which decreases the SCE and DIBL effects on the device electric parameters, such as threshold voltage, sub-threshold slope (SS), and DIBL voltage. In the equation, since the thickness of Si is much smaller than that of depletion region in planar transistor, EI is obviously improved. The whole new structures of MOSFET extend the shrinking boundary of the ultra-short gate length
FinFET is a typical double-gate or multi-gate device with a three-dimensional channel structure, as shown in Figure 4. The FinFET is made of a tall and narrow silicon island. The 3D channel is standing above the silicon substrate, where the ultra-thin silicon body is familiar with the fin of the fish. The fin channel under the gate can be fully depleted by electrostatic potential, providing a strong ability of controlling the carriers’ behaviors in the channel. FinFET can really expand the limit of the shrinking size and is widely adopted for the 16/14-nm technology node and beyond. FinFET can effectively suppress the leakage of the sub-surface channel, which can obviously reduce the off-state current for the device’s current-voltage transfer characteristic. In the meantime, the fully depleted channel can obtain benefit of carriers’ mobility with less scattering. For the 3D fin structure, the transistor’s width can be doubled compared to the planar one in the projected plane, which can improve the driving current at on-state in the saturation regime. With the same drive current, the supply voltage of FinFET can be significantly reduced regardless of the planar transistor’s power limit, where the suppression of power consumption in modern integrated circuits emphasizes energy efficiency ratio.
FinFET from fin to whole device.
Since 22-nm technology node, FinFET has been utilized for several process nodes [15, 16, 17]. It is firstly introduced by Intel in 22-nm node and widely adopted by different companies in 16- or 14-nm process node. The process integration scheme of FinFET is compatible with that of the planar transistor. In a general way, the critical fabrication steps of FinFET transistor include silicon fin formation on the substrate by the spacer-transfer lithography (STL), shallow trench isolation (STI) formation and recess, 3D dummy gate formation and planarization, 3D spacer formation, source/drain with 3D selective SEG, 3D HKMG formation, and back-end-of-line (BEOL) metallization and contact techniques. It added a little extra process steps than those of planar transistor fabrication. It is very meaningful to understand the integration process of FinFET. In future, the next-generation devices, such as gate-all-around nanowire transistor or nanosheet FET, are still dependent on current FinFET integration flow [18, 19].
Oxide by plasma-enhanced CVD (PECVD), poly-Si by low-pressure CVD (LPCVD), and SiNx by PECVD are sequentially deposited in the substrate for the formation of etch-hard-mask (EHM). After etching EHM with pattern, another SiNx is deposited as the spacer of the core layer of oxide/poly-Si/SiNx structure. After spacer and Si dry etch, the 3D Si fin is formed and the Si fin width depends on the SiN spacer thickness, as shown in Figure 5. The fin width may be beyond the lithography resolution limit and often smaller than 10 nm.
STL for bulk fin formation (a) Hard mask deposition; (b) Hard mark etch; (c) SiN spacer deposition and etch; (d) Fin structure etch.
For adjacent fins isolation, high-aspect-ratio-process (HARP) oxide deposition is widely used with a good step coverage on 3D fins. The oxide for HARP STI is deposited by sub-atmospheric CVD (SACVD) with the reaction by tetraethoxysilane (TEOS) precursor and O3. After the isolation oxide annealing, chemical mechanical polishing is utilized for the planarization of deposited dielectric on 3D fins. In following steps, the oxide is precisely etched back and making the fin final formation with shallow trench isolation structures as shown in Figure 6.
STI formation and recess on 3D fins (a) Fin and STI structure after recessng; (b) SEM images for Fin and STI after recessing.
On 3D fins with STI, thin oxide is firstly formed on the surface. Then, amorphous-Si (α-Si) is deposited as dummy gate on the fin. However, the dummy gate etch is the most challenging, for which the top dummy gate needs to be protected during the etching and sidewall and the foot of the dummy gate needs strong etching capability to prevent the residue of Si and no process damage on the exposed fin tip (Figure 7).
3D dummy gate formation (a) PolySi deposition, planarization and dummy gate etch; (b) SEM image after dummy gate formation.
On 3D fin, it often needs SEG on source/drain regions for less contact resistance. Source/drain selective epitaxy growth normally employs SiH2Cl2, GeH4, and HCl gases. Especially, for PMOS source/drain, B2H6 is mixed into the carrier gas of the reaction. The selectivity of SiGe epitaxy is mainly due to the function of HCl gas, where the etch rate of polycrystalline SiGe is higher than that of single crystalline of SiGe by HCl. In the whole process, the dilution protective gas contains N2 or H2 all the time. Due to the slowest growth rate on Si (111) lattice plane, as shown in Figure 8, the final formed SiGe shape on 3D fin is more like a diamond. The film stress not only depends on the process conditions but also is strongly affected by the surface quality of fins.
SEG SiGe on 3D fin.
Advanced transistor technologies were extensively implemented into the CMOS IC manufacture with the process node scaling from 22 to 14 nm. They require new materials and novel structures as well as complicated process techniques and different device integration flow. This chapter presented a summary on the three important techniques, strain engineering, high-k/metal gate, and FinFET. Both the process theory related to the suppress on SCE for device’s shrinking and the detailed illustration on material choice, film growth method, architecture design, critical process definition, and integration are presented in a comprehensive and systematic manner. The process condition optimizations for suppressing stress release are key technologies of strain engineering. The high-k/metal gate needs multilayer structure for modulating Vt in a different manner for PMOS and NMOS, respectively. The integration scheme is also changed from gate-first to all-last integration. FinFET requires a sophisticated device integration structure and a flow design with less extra process cost. It also has some new fabrication techniques, such as ultra-thin fin formation with STL and improved process methods, including HKMG and SiGe SEG in 3D approach.
The reported work was supported by “16/14nm Basic Technology Research” of national 02 IC R&D projects in China (No. 2013ZX02303). The authors would like to thank all the colleagues in Integrated Circuit Advanced Process Center, IMECAS, for their kind and great support.
The authors declare that they have no competing interests.
Skeletal muscle is the most abundant tissue in human body. Skeletal muscle accounts for approximately 20% of our resting energy expenditure [1], and composes 30–40% of one’s body mass [2] depending on their fitness level [3]. As a part of the musculoskeletal system, skeletal muscle is connected to the skeleton to form part of the mechanical system that moves the limbs and other parts of the body. While skeletal muscle refers to multiple bundles of cells called muscle fibers, the composition of the individual fibers is different between muscle types. In this review, we describe how muscle fiber types are specified during embryonic myogenesis, what potential factors would be involved in the changes of fiber type composition, and how fiber type variations are influenced by specific disease conditions. Knowing the functional role of how muscle fibers contribute to and are affected by skeletal muscle diseases aids in our understanding of the disease and provides insight to mechanisms of prevention, treatment, or cure of these conditions.
\nSkeletal muscle plays important roles in the body that are concerned with movement, posture, and balance under voluntary control. Skeletal muscles are one of three major muscle types, the others being cardiac muscle and smooth muscle, and it is the most common of the three types of muscle in the body. As one component of the musculoskeletal system, skeletal muscle is attached to bones by tendons, and they produce all the movements of body parts in relation to each other. Unlike smooth muscle and cardiac muscle, skeletal muscle is under voluntary control. Similar to cardiac muscle, however, skeletal muscle is striated; it has long, thin, multinucleated fibers (known as myofibers).
\nSkeletal muscle function seems to be maintained across mammals, but the composition of the individual fibers is different between muscle types [4]. Fiber type composition is initially defined in each muscle during embryonic myogenesis. In this section, we will go through the basic fundamentals of skeletal muscle development and fiber type specification (Figure 1).
\nSkeletal muscle differentiation and fiber type specification. The terminal differentiation starts when Pax3+ and/or Pax7+ progenitors begin to express Myf5 or MyoD as committed myoblasts. Theses myoblasts gradually express myogenin (MyoG) and form single-nucleated nascent myotubes and multi-nucleated myotubes with myosin heavy chain (MyHC+). Actin, myosin, and elastic myofilaments are arranged to form organized sarcomeres within the myotubes. Primary myofibers express four isoforms of MyHC: MyHC I/β, MyHC-α, MyHC-emb and MyHC-peri. Development of fiber type continues as satellite cells differentiate and the fibers become innervated, forming mature fiber types. Different isoforms of myosin, MyHC I/β. MyHC-α, MyHC 2A, and MyHC 2x, are expressed. This figure is modified from Jiwlawat et al. [
Studies investigating embryonic myogenesis have been extensively conducted in the embryos of zebrafish, chicken, and mice. After an embryo is generated, three germ layers (ectoderm, endoderm, and mesoderm) are formed. The mesoderm is characterized as paraxial, intermediate, and lateral mesoderm. The formation of skeletal muscle initiates from the paraxial mesoderm in early embryogenesis. In response to the signals from the notochord, neural tube, and surface ectoderm, the paraxial mesoderm forms segmented spheres termed somites. The somites are located as a pair on either side of the neural tube and the notochord and develop in a rostral-caudal direction. The somite is further specified as the dermomyotome, myotome, and sclerotome. The cells in the dermomyotome express the paired box transcription factors Pax3 and Pax7 [5, 6]. The cells in the dorsomedial and ventrolateral portions of the dermomyotome will give rise to the epaxial (primaxial) and hypaxial (abaxial) myotomes, respectively. Myf5-positive cells in the epaxial myotomes differentiate and form the trunk and back muscles. In contrast, MyoD-positive progenitors de-laminate and migrate from the hypaxial myotome into the developing limb as the source of limb muscles. MyoD and Myf5 are expressed in committed muscle cells, and are located in the myotome, which is form the maturation of dermomyotome lips [7, 8, 9]. The ventrolateral lip of the dermomyotome contributes to the hypaxial myotome, which is a source of precursor cells that form the trunk and thoracic vertebral column muscles. The dorsomedial lip of the dermomyotome contributes to the epaxial myotome, which is a source of muscles of the back. The process of myotome maturation originally initiates at the rostral part of the embryo and then extends to the tail [7].
\nThe terminal differentiation of progenitors and myoblasts initiates when myogenic progenitors in the dermomyotome stop dividing and exit the undifferentiated stage [10]. The progenitors differentiate into committed myoblasts, and form nascent myotubes following the maturation of the myotome [11]. More specifically, Pax3 and/or Pax7-positive proliferating progenitors are withdrawn from the cell cycle once the differentiation step is initiated (Figure 1). These progenitors become committed myoblasts expressing Myf5 and/or MyoD and then form the nascent myosin heavy chain-positive myotubes with myogenin-positive nuclei.
\nTwo waves of myotube formation occur during skeletal muscle development, and sequentially give rise to primary and secondary myotubes [12]. Primary myotubes are generated from fusion of early myoblasts, and then align between muscle tendons. Late-stage myoblasts proliferate on the surface of primary myotubes and fuse to form secondary myotubes, and motor axons initiate innervation to the myotubes [12]. At this point, primary and secondary myotubes express specific isoforms of myosin heavy chain (MyHC), which can be used to broadly define two distinct fiber types, slow-twitch Type I and fast-twitch Type II myofibers. Primary myotubes preferentially express Type I fibers [13, 14], while Type II fibers appear later during myogenesis [15, 16]. Single-nucleated myotubes then fuse with the nearby myotubes to form multi-nucleated myotubes. Thick-myosin and thin-actin filaments within the myotube begin organization and form a sarcomere structure, which is the functional unit of muscle contraction. Well-organized sarcomeric structure gives rise to a striation pattern in myotubes, representing many chains of myofibrils.
\nPrimary myogenesis starts during the embryonic stage, when somatic stem cells express the genes Pax3 and Pax7 (Figure 1). This transforms the cells into myogenic progenitors, which migrate from the dermomyotome to form myocytes and primary myofibers. At this point of embryonic myogenesis, three isoforms of myosin heavy chain are expressed; slow MyHC (MYH7), MyHC-emb (MYH3), and MyHC-peri (MYH8) [17]. These primary myofibers serve as a template for the skeletal muscle to mature and differentiate. Secondary myogenesis progresses as satellite cells differentiate, become innervated, and mature myofibers are formed. In whole, genetic influences and motor neuron innervation during developmental differentiation determines the fiber types that one is born with [17]. Fiber type ratios determined at birth are not concrete throughout one’s life however, as skeletal muscle chemical properties can change over time to meet physiological or pathological demands.
\nSkeletal muscle tissue in humans is heterogeneous, composed of a variety of molecules [4]. The main functional proteins and structures within the muscle are maintained, such as mitochondria network, myosin, actin and titin. Yet, the specific isoforms of the molecules and the concentration of each monomer differ between skeletal muscles all throughout the body. These heterogeneous tissues are a resultant factor of evolution which allows each muscle to have a specialized function. The size of each whole muscle is determined by both the number and the diameter of muscle fibers that compose it. Individual muscle fibers are multi-nucleated, with each nucleus controlling the protein type, myosin that is translated in its surrounding. This is known as a nuclear domain [18].
\nMyosin is the main protein within skeletal muscle, and the certain isoform that is expressed determines the rate at which the muscle contracts, as well as its physiological properties. Within a single sarcomere of a skeletal muscle fiber, myosin heads and actin interact to form cross bridges. ATP hydrolyzation via ATPase is responsible for the energy to cause cycling of the myosin head and actin connections, which ultimately causes the muscle contraction. The type of myosin expressed is one factor that ultimately determines the fiber type. There are 11 total isoforms of myosin known to mammals [4, 19], which when expressed in different ratios compose a fiber type with distinct physiological properties. As discussed above, there are two categories of adult muscle fiber types in humans; Type I and Type II fibers (Figure 1).
\nType I and Type II fibers are classified based on their myosin isoform, velocity of contraction and presence of physiological enzymes [3]. Type I fibers are also known as slow oxidative. Compared to Type II, they contain a higher number of oxidative enzymes and a lower number of glycolytic enzymes. They are rich in mitochondria and have a great capillary network to perfuse the fibers [20]. This contributes to their oxidative capacity. Type I muscle fibers predominantly contain myosin isoforms MyHC I/β or MyHC-α, encoded by the gene MYH7 [17] and they contract slower and are more resistant to fatigue than Type II fibers. Because of their endurance properties, Type I fibers are commonly found in muscles mainly involved in posture, such as erector spinae, hamstrings, and gastrocnemius muscles.
\nType II fibers on the other hand are fast to fatigue, as they have low oxidative capacity. These fiber types are recruited in short bursts of movement or power [3]. This is due to their greater maximal velocity of shortening, and abundance of glycolytic enzymes [3]. This in turn allows for quick energy utilization due to increased ATPase activity. There are two subcategories in human Type II fibers; Type IIa and Type IIx. Type IIa are classified as fast-oxidative glycolytic, a sort of combination between fast and slow contraction rates. Type IIx are fast glycolytic, having the fastest rate of contraction of all the human fiber types, yet the shortest time to fatigue. MyHC isoform genes MYH2 and MYH1 are expressed respectively in Type IIa and Type IIx fibers. The myosin protein isoforms present in each subtype are termed MyHC-2A and MyHC-2X [17].
\nSkeletal muscles are innervated by motor neurons which are responsible for the initiation of muscle contraction. Motor units are formed, consisting of a single alpha motor neuron that originates in the spinal cord that innervates a group of skeletal muscle fibers, all of the same fiber type. Changes in motor unit innervation of the skeletal muscle has shown to change the properties of fiber types innervated, therefore motor units too are contributors to the determinants of fiber type [21].
\nSkeletal muscles have the property of plasticity. This means the composition of fiber types within a given skeletal muscle can change when under the influence of physiological changes such as mechanical stress and unloading. Further, abnormal health conditions caused by diseases and injuries also triggers significant changes of muscle fiber types [22]. The size and functional capacity of the muscle can be decreased upon injury, disease, or excess weight. As a result, scar tissue, connective tissue, or fat can take up mass that was once occupied by functional muscle [18]. When muscles become denervated, there is a tendency for slow to fast fiber transition [3]. This carries heavy implications for training status and disease state in humans [3, 23, 24].
\nThe physiological and pathological changes influence the levels of trophic factors, hormones, and nerve signaling associated with the muscle, which result in adaptive changes in muscle fibers. The relative amounts of these factors and the extent of the changes that they can make are ultimately determined by genomic background and epigenetic control in individuals. The genes that one inherits controls and determines 40–50% of the ratio of Type I fibers within a muscle [3]. This means that physiological stressors can impact the plasticity of the muscles to a point, but in the end one’s genetic make-up determines the extent to which the fiber types within the muscle can switch [3]. Like all cells in the body, the different fiber types contain the same genomic DNA sequence. MYH genes have been hypothesized to be clustered in a manner to facilitate temporal and spatial expression of these related genes [23]. Slow MyHC isoforms are located on chromosome 14, while chromosome 17 contains the fast and embryonic MYH genes in a cluster. The difference in gene expression, and resultant protein levels in a specific cell, are controlled by epigenetic mechanisms. As fiber types shift within a lifetime, the epigenetic profile within the cell is also affected, specifically in the amount of acetylation or deacetylation within the genome. This change is mostly seen within differentiating satellite cells, which are not fully mature [23]. Further, variations in expression levels of genes controlling systems such as mitochondrial biogenesis, glucose/lipid metabolism, cytoskeletal function, hypoxia, angiogenesis, and circulatory homeostasis would influence muscle fiber type. The frequency of alleles within a genome also impact the fiber type development [3]. Overall, there are many genetic factors at play such as single gene effects, gene–gene interactions and gene–environment interactions [3].
\nNeuromuscular diseases are caused by functional defects of skeletal muscles, directly via muscle pathology or indirectly via disruption of the nervous system. Most of these diseases are multi-facetted, and terminally result in wasting and atrophy of skeletal muscles. These abnormal conditions often lead to disabilities and complete loss of muscle function, with little to no cure. Pathology is best understood at the cellular level, and here we explore how the progression of the disease is involved in the changes of muscle fiber types, and how changes in fiber type may serve as a protective mechanism. Diseases covered in this chapter are mainly genetic in nature, having an uncontrollable disruption in cellular function that results in disease. This can either be inherited from previous ancestors or be sporadic in nature. This section will introduce several names of muscle and motor neuron diseases; however, this is not an exhaustive list.
\nSarcopenia is a term that refers to the loss of lean body mass, particularly skeletal muscle, with an increase in aging [25]. This can be diagnosed through weakness within the body, difficulties walking, or dual-energy absorptiometry, which is a machine that tells the exact body composition of fat, bone mass and tissue. Sarcopenia at the individual fiber level is characterized by a loss of satellite cells associated with Type II fibers [18]. Organelles affected in the myofibers include a decreased amount of mitochondria, an alteration in the sarcoplasmic reticulum, and hindered excitation-contraction coupling. Both Type I and II fibers have shown to be affected by losing their maximal force in both men and women. This is attributed to a loss of myosin expression within the cell, or oxidation of the myosin protein which inhibits the formation of crosslinks [18]. Surprisingly, the expression levels of myosin isoform MYH7, that of slow muscle fibers, are not affected [26].
\nMuscular dystrophies are a group of muscle diseases that result in the wasting of skeletal muscles, caused by muscle fiber necrosis [27]. The dystrophies involve mutations in genes that encode functional proteins involved in dystrophin or enzymes that modify the dystrophin proteins [18]. These mutations affect velocity of cross bridge cycling of actin filaments on myosin and of particular interest, they change the quality and force production of Type I and Type II fibers [18]. Apoptosis and necrosis in fiber types are a trademark of the disease, with caspase 3 being a known apoptotic gene that is upregulated in muscular dystrophies compared to unaffected individuals [27].
\nIn Duchenne Muscular Dystrophy, Type II muscle fibers are the first to be affected with Type I muscle fibers following late in the disease progression [26]. Remaining Type I fibers are not similar to those found in healthy muscle. Degeneration and regeneration of diseased fibers is hypothesized to take place, due to coexpression of fetal MYH and slow MYH genes in adult muscle fibers [28]. Since Type II fibers are the most commonly affected in Duchenne Muscular Dystrophy, it is thought that inducing the expression of Type I fibers will alleviate both the symptoms and progression of Duchenne Muscular Dystrophy. A similar trend was found in another type of muscular dystrophy, Facioscapulohumeral Muscular Dystrophy, as there is an early decrease in Type II fibers and an overall increase in the number of Type I fibers [29]. On the contrary, in myotonic dystrophy, Type I fibers are affected, as they atrophy more frequently and they lose a greater amount of force generation compared to Type II fibers [30, 31, 32]. One hypothesis for this fiber type susceptibility to disease states is variation to transcriptional control of muscle fiber type. Genetic manipulations and pharmacological interventions have shown the effect of fiber type switching on disease sates in mice [26]. For example, over expression of the transcriptional coactivator PPARGC1A rescues the cellular defects cause by the Dmdmdx mutation via increased expression of Type I fiber contractile machinery and oxidative enzymes [26].
\nMotor neuron diseases are characterized by the progressive degeneration of motor neurons with subsequent functional loss. In the motor system, motor neuron axons carry the motor impulses from the spinal cord to the voluntary muscles. Innervation of alpha motor neurons from the central nervous system has a large part in determining the fiber type that is expressed within muscles. Motor units innervate muscle fibers in an “all or none” fashion, meaning a single motor unit innervates Type I and each subcategory of Type II fibers individually, and all the fibers that the motor unit innervate are of the same fiber type.
\nCo-expression of fiber types within a single muscle fiber has been seen in motor neuron diseases such as Amyotrophic Lateral Sclerosis (ALS) and Spinal Muscular Atrophy [33]. In these diseases, specifically ALS, studying disease influence on skeletal muscles would provide valuable insight to the mechanisms of disease progression. Changes in muscle fiber types may occur at the early stage of diseases by reduced inputs from motor neurons, as disconnections between muscle and axon terminals have been observed in animal models of motor neuron diseases before symptom onset. Studying the disease onset in skeletal muscles has the potential to reveal the catastrophic pathology influence and the body’s compensatory mechanisms to counteract disease progression [34].
\nSwitches in muscle fiber type has been observed in patients in motor neuron diseases, however the switches cannot prevent the ultimate outcome: apoptosis and necrosis of individual muscle fibers [27]. Often, motor neuron diseases are diagnosed clinically via histochemical staining of muscle biopsies. Necrosis can be easily seen as fat or scar tissue under the microscope, but apoptosis is harder to identify due to the lack of inflammatory response from the body [27]. Denervation of the muscle results in upregulation of pro-apoptotic genes, such as bax and anti bcl-2, which are upregulated due to intrinsic cell stress. Muscle fiber atrophy is hypothesized to be caused by apoptosis induced degradation of a fiber’s nuclei. This includes destruction of the nuclear lamina, the nuclear envelope, and DNA destruction [27].
\nAmyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s disease, is a fatal neurodegenerative disease caused by the selective loss of motor neurons in the spinal cord and brain stem. Motor neuron degeneration and neuromuscular junction denervation rapidly result in decreased motor function. Death typically results 3–5 years after diagnosis due to respiratory failure after loss of diaphragm control. About 90% of ALS cases occur sporadically; the remaining 10% are familial components. Approximately 70–80% of familial ALS have mutations of the Cn2+/Zn2+ superoxide dismutase 1 (
Although a disease cause of sporadic ALS has not been specified, this disease is generally regarded as resulting from factors involving environment, lifestyle, aging, and genetic predisposition [36]. Several proposed pathological mechanisms of disease include protein misfolding and aggregation, glutamate excitotoxicity, oxidative stress, mitochondrial dysfunction, glial cell activation and related inflammatory processes, and axonal transport defects [37].
\nALS causes motor neuron death and gradual denervation of skeletal muscles over time. This denervation causes loss of muscle function and muscular atrophy within affected cells, ultimately resulting in cellular death due to apoptosis. While many of existing ALS therapies are expected to promote motor neuron survival in the spinal cord or motor cortex [38], looking at the pathologies within skeletal muscle gives support for the “dying-back” hypothesis. This hypothesis states that irregularities within the skeletal muscle are the primary cause of ALS, denervating muscle and motor neuron [39]. Based on this hypothesis, possible contributions of skeletal muscles and neuromuscular junctions in ALS pathology have been proposed in recent studies. Specifically, our research group also reported that using stem cells to deliver growth factors directly into the skeletal muscle could restore motor function in a rat model of familial ALS [40, 41, 42]. Our approach can sufficiently protect motor neurons by preventing the “dying back” of these cells from the skeletal muscle in ALS.
\nWhile the majority of ALS patients have limb onset, about 25% of cases eventually diagnosed with ALS have bulbar onset which strikes the corticobulbar area in the brain stem. This section controls muscles in the face, neck and head. Bulbar onset usually affects voice and swallowing first. Patients with bulbar onset have a correlation between the age of death and the loss of slow tonic fibers, although there is neither correlation seen in spinal onset ALS nor controls [34].
\nALS pathology affects skeletal muscle in many ways, which seems to influence muscle fiber type changes. Autopsies show fiber atrophy, fiber grouping, fiber splitting, with increased fatty tissue and connective tissue [43]. Interestingly, unlike atrophy from exercise, ALS shows a fast to slow fiber type switch [39, 44]. In the hindlimb muscle (tibialis anterior muscle) of pre-symptomatic ALS model mice, there is denervation of the most forceful and fast to fatigue fibers Type IIB (only found in mice). This results in transitions to fast motor units with intermediate fatigue and fatigue resistant fibers. Although this transition is present, it is not a sudden change nor a complete loss of Type IIB fibers [44]. Biopsies taken from atrophied skeletal muscles in patients with ALS have shown that individual muscle fibers contain myosin isoforms corresponding to both fiber Types I and II, termed a mixed fiber type. An early pattern of denervation can be detected and has the potential to be used for diagnostic purposes. This pattern is individual fibers with a mixed fiber type and little fiber type grouping, all within an atrophying muscle [45].
\nIt has been reported that specific muscle groups such as extraocular muscles are relatively spared from the disease phenotype in ALS [46]. Motility of the eye is often maintained in ALS patients [47] and autopsies have shown the extraocular muscles do have some muscle fiber pathology compared to control, but in relation to other ALS affected skeletal muscles in the body, the extraocular muscles were well preserved [43]. The pathology that was seen include change in fiber type composition, the cellular architecture, and decreased overall MyHC content. Embryonic MyHC was almost nonexistent in the extraocular muscles in those affected by ALS [43].
\nThis preservation of extraocular skeletal muscle is accredited to the distinct fiber type composition within the extraocular muscles. Extraocular muscles have a unique myosin expression that is not found in skeletal muscles located other places of the body. Along with Type I and Type II fibers, a special myosin isoform, MyHC extraocular, is present and Type I fibers seem to express two separate forms of MyHC, of specific interest MyHC α cardiac. [43]. Embryonic MyHC has notable expression in the extraocular muscles, as healthy human controls show co-expression of embryonic MyHC in Type II fibers, while ALS patients had no embryonic MyHC expression [43, 48].
\nAlthough there is great speculation, the exact mechanism of why extraocular muscles are spared in ALS is unknown. However, one interesting hypothesis is the multiple innervations of slow tonic fibers serve as a protective mechanism against the neurodegenerative disease [48]. It has also been found that the motor neurons of the extraocular muscles have different surface markers than motor neurons found elsewhere in the body, suggesting they have properties that make the neurons less susceptible to disease [49]. As an additional note, similar specific insusceptibility in the extraocular muscles has also been observed in Duchenne Muscular Dystrophy [50].
\nAnother question is how sex influences fiber type specification in the muscle during ALS pathology. The exact etiology of ALS is still uncertain, but most epidemiological studies have shown a higher incidence of ALS in men than women. Interestingly, sexual dimorphism in disease onset and progression is also observed in rodent models of familial ALS [51, 52]. Although it is still uncertain whether such sexual differences are originated from the intrinsic difference in individual cells [53], further studies would be required to answer this question.
\nSpinal Muscular Atrophy (SMA) is a group of motor neuron diseases, which are autosomal recessive in nature. Each SMA type has a different clinical outcome, however all SMA types commonly demonstrate motor neuron degeneration caused by insufficient expression of a specific protein named Survival of motor neuron (SMN) [54]. The clinical severity of SMA ranges from I–IV, with IV being the least severe. I is infantile SMA that causes death early in childhood and IV involves some motor neuron loss, but allows for a normal life expectancy [55].
\nAll cases of SMA result from reductions in levels of the SMN protein. Specifically, SMA is caused by deletion or mutation of the survival motor neuron gene (SMN1). The SMA disease is present in a spectrum of disease severities ranging from infant mortality, in the most severe cases, to minor motor impairment, in the mildest cases. The variability of disease severity inversely correlates with the copy number, and thus expression of a second, partially functional survival motor neuron gene, SMN2.
\nIn type III SMA-induced mice, muscle atrophy resulted in a transition to slower, oxidative phenotype. This meaning that there were more Type I fibers in the soleus muscle and Type II fibers in fast twitch muscles transitioned to a more oxidative fiber type [54]. These same mice also had smaller motor neurons units than controls and the Type I motor neurons decreased in size as the disease progressed. Other studies that have used type III SMA-induced mice have shown to have increased fiber type grouping compared to wild type [56].
\nThere has been evidence that these pathological changes in muscle fiber types can be reversed. Swimming aided the mice to regain more glycolytic fast twitch fibers, and restore Type I motor unit size close to wild type levels [54]. Running produced more Type I fibers compared to sedentary SMA mouse control [54] and was able to restore SMA fast fiber types. Upon completion of exercise intervention by type III SMA-induced mice, their structure and number of the Type I fibers were comparable to controls [54].
\nIn humans, it has been shown that innervation of fibers in children with SMA (specifically Werdnig-Hoffmann disease) is incomplete. This results in atrophy of fibers and the inability of fetal MyHC to switch to adult Type I and Type II myosin. When this observation was tracked through childhood it showed that in infancy, there is a large increase in the number of Type I fibers, and no detectable Type II fibers by 20 months. This further emphasizes the need for motor neuron innervation for Type II fibers to prevail [4, 57].
\nMuscle fiber type composition is primarily determined during development but will be altered by physiological and pathological conditions. Significant changes of fiber type composition have been identified in the muscles with a background of major neuromuscular diseases. To further understand the roles of muscle fiber composition in skeletal muscle development and diseases, additional studies using new research approaches may help us understand how muscle fiber type specification occurs during development and disease conditions. For instance, skeletal muscle cell culture derived from human pluripotent cell resources can provide a new tool to study how human skeletal myocytes differentiate into myotubes with specific fiber types in culture [58, 59]. These studies could highlight what specific mechanisms are involved in the significant changes of fiber type composition and ratio in the skeletal muscle during embryonic myogenesis and under disease conditions, and how these changes of muscle fiber types impact on muscle physiology and pathology.
\nThis work was supported by grants from the ALS Association (15-IIP-201, Masatoshi Suzuki), NIH/NINDS (R01NS091540, Masatoshi Suzuki), and the University of Wisconsin Foundation (Masatoshi Suzuki).
\nThe authors declare that there is no conflict of interest regarding the publication of this paper.
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",metaTitle:"Team",metaDescription:"Advancing discovery in Open Access for the scientists by the scientist",metaKeywords:null,canonicalURL:"page/team",contentRaw:'[{"type":"htmlEditorComponent","content":"Our business values are based on those any scientist applies to their research. We have created a culture of respect and collaboration within a relaxed, friendly and progressive atmosphere, while maintaining academic rigour.
\\n\\nCo-founded by Alex Lazinica and Vedran Kordic: “We are passionate about the advancement of science. As Ph.D. researchers in Vienna, we found it difficult to access the scholarly research we needed. We created IntechOpen with the specific aim of putting the academic needs of the global research community before the business interests of publishers. Our Team is now a global one and includes highly-renowned scientists and publishers, as well as experts in disseminating your research.”
\\n\\nBut, one thing we have in common is -- we are all scientists at heart!
\\n\\nSara Uhac, COO
\\n\\nSara Uhac was appointed Managing Director of IntechOpen at the beginning of 2014. She directs and controls the company’s operations. Sara joined IntechOpen in 2010 as Head of Journal Publishing, a new strategically underdeveloped department at that time. After obtaining a Master's degree in Media Management, she completed her Ph.D. at the University of Lugano, Switzerland. She holds a BA in Financial Market Management from the Bocconi University in Milan, Italy, where she started her career in the American publishing house Condé Nast and further collaborated with the UK-based publishing company Time Out. Sara was awarded a professional degree in Publishing from Yale University (2012). She is a member of the professional branch association of "Publishers, Designers and Graphic Artists" at the Croatian Chamber of Commerce.
\\n\\nAdrian Assad De Marco
\\n\\nAdrian Assad De Marco joined the company as a Director in 2017. With his extensive experience in management, acquired while working for regional and global leaders, he took over direction and control of all the company's publishing processes. Adrian holds a degree in Economy and Management from the University of Zagreb, School of Economics, Croatia. A former sportsman, he continually strives to develop his skills through professional courses and specializations such as NLP (Neuro-linguistic programming).
\\n\\nDr Alex Lazinica
\\n\\nAlex Lazinica is co-founder and Board member of IntechOpen. After obtaining a Master's degree in Mechanical Engineering, he continued his Ph.D. in Robotics at the Vienna University of Technology. There, he worked as a robotics researcher with the university's Intelligent Manufacturing Systems Group, as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and, most importantly, co-founded and built the International Journal of Advanced Robotic Systems, the world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career since it proved to be the pathway to the foundation of IntechOpen with its focus on addressing academic researchers’ needs. Alex personifies many of IntechOpen´s key values, including the commitment to developing mutual trust, openness, and a spirit of entrepreneurialism. Today, his focus is on defining the growth and development strategy for the company.
\\n"}]'},components:[{type:"htmlEditorComponent",content:"Our business values are based on those any scientist applies to their research. We have created a culture of respect and collaboration within a relaxed, friendly and progressive atmosphere, while maintaining academic rigour.
\n\nCo-founded by Alex Lazinica and Vedran Kordic: “We are passionate about the advancement of science. As Ph.D. researchers in Vienna, we found it difficult to access the scholarly research we needed. We created IntechOpen with the specific aim of putting the academic needs of the global research community before the business interests of publishers. Our Team is now a global one and includes highly-renowned scientists and publishers, as well as experts in disseminating your research.”
\n\nBut, one thing we have in common is -- we are all scientists at heart!
\n\nSara Uhac, COO
\n\nSara Uhac was appointed Managing Director of IntechOpen at the beginning of 2014. She directs and controls the company’s operations. Sara joined IntechOpen in 2010 as Head of Journal Publishing, a new strategically underdeveloped department at that time. After obtaining a Master's degree in Media Management, she completed her Ph.D. at the University of Lugano, Switzerland. She holds a BA in Financial Market Management from the Bocconi University in Milan, Italy, where she started her career in the American publishing house Condé Nast and further collaborated with the UK-based publishing company Time Out. Sara was awarded a professional degree in Publishing from Yale University (2012). She is a member of the professional branch association of "Publishers, Designers and Graphic Artists" at the Croatian Chamber of Commerce.
\n\nAdrian Assad De Marco
\n\nAdrian Assad De Marco joined the company as a Director in 2017. With his extensive experience in management, acquired while working for regional and global leaders, he took over direction and control of all the company's publishing processes. Adrian holds a degree in Economy and Management from the University of Zagreb, School of Economics, Croatia. A former sportsman, he continually strives to develop his skills through professional courses and specializations such as NLP (Neuro-linguistic programming).
\n\nDr Alex Lazinica
\n\nAlex Lazinica is co-founder and Board member of IntechOpen. After obtaining a Master's degree in Mechanical Engineering, he continued his Ph.D. in Robotics at the Vienna University of Technology. There, he worked as a robotics researcher with the university's Intelligent Manufacturing Systems Group, as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and, most importantly, co-founded and built the International Journal of Advanced Robotic Systems, the world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career since it proved to be the pathway to the foundation of IntechOpen with its focus on addressing academic researchers’ needs. Alex personifies many of IntechOpen´s key values, including the commitment to developing mutual trust, openness, and a spirit of entrepreneurialism. Today, his focus is on defining the growth and development strategy for the company.
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