Ling Chen

Bio: Ling Chen is an academic researcher from Applied Materials. The author has contributed to research in topics: Barrier layer & Chemical vapor deposition. The author has an hindex of 20, co-authored 36 publications receiving 2337 citations. Previous affiliations of Ling Chen include University of Texas Health Science Center at San Antonio.

Copper interconnect barrier layer structure and formation method

Abstract: A method for forming a tungsten-containing copper interconnect barrier layer (e.g., a tungsten [W] or tungsten-nitride [WxN] copper interconnect barrier layer) on a substrate with a high (e.g., greater than 30%) sidewall step coverage and ample adhesion to underlying dielectric layers. The method includes first depositing a thin titanium-nitride (TiN) or tantalum nitride (TaN) nucleation layer (12) on the substrate, followed by the formation of a tungsten-containing copper interconnect barrier layer (20) (e.g., a W orWxN copper interconnect barrier layer) overlying the substrate. The tungsten-containing copper interconnect barrier layer can, for example, be formed using a Chemical Vapor Deposition (CVD) technique that employs a fluorine-free tungsten-containing gas (e.g., tungsten hexacarbonyl [W(CO)6]) or a WF6-based Atomic Layer Deposition (ALD) technique. The presence of a thin TiN (or TaN) nucleation layer facilitates the formation of a tungsten-­containing copper interconnect barrier layer with a sidewall step coverage of greater than 30% and ample adhesion to dielectric layers. A copper interconnect barrier layer structure includes a thin titanium-nitride (TiN) (or tantalum nitride [TAN]) nucleation layer disposed directly on the dielectric substrate (e.g., a single or dual-damascene copper interconnect dielectric substrate). The copper interconnect barrier layer structure also includes a tungsten-­containing copper interconnect barrier layer (e.g., a W or WxN copper interconnect barrier layer) formed on the thin TiN (or TaN) nucleation layer using, for example, a CVD technique that employs a fluorine-free tungsten-containing gas (e.g., [W(CO)6]) or a WF6-based ALD technique.

Method and apparatus for providing gas to a processing chamber

Abstract: A method and apparatus for generating gas for a processing system is provided. In one embodiment, an apparatus for generating gas for a processing system includes a canister having at least one baffle disposed between two ports and containing a precursor material. The precursor material is adapted to produce a gas vapor when heated to a defined temperature at a defined pressure. The baffle forces a carrier gas to travel an extended mean path between the inlet and outlet ports. In another embodiment, an apparatus for generating gas includes a canister having a tube that directs a carrier gas flowing into the canister away from a precursor material disposed within the canister.

Method and apparatus for monitoring solid precursor delivery

Abstract: A method and apparatus for monitoring the delivery of a solid precursor from a vessel to a process chamber via a process gas produced by flowing a carrier gas into the vessel is provided. The precursor typically changes state from a solid to a gas (vapor) through a sublimation process within the chamber. The apparatus comprises a gas analyzer to generate a first signal indicative of a density of the precursor in the process gas and a controller. The controller receives the first signal and a second signal indicative of a volume flow rate of the process gas or the carrier gas and calculates a mass flow rate and/or a total amount consumed of the precursor based on the first and second signals. The controller may calculate an amount precursor remaining in the vessel based on the total amount consumed and an initial amount. The amount of precursor remaining in the vessel may be used by an operator to efficiently schedule replacement or replenishment of the precursor in an effort to minimize material waste and processing down time.

The Mechanism of Double-Strand DNA Break Repair by the Nonhomologous DNA End-Joining Pathway

Abstract: Double-strand DNA breaks are common events in eukaryotic cells, and there are two major pathways for repairing them: homologous recombination (HR) and nonhomologous DNA end joining (NHEJ). The various causes of double-strand breaks (DSBs) result in a diverse chemistry of DNA ends that must be repaired. Across NHEJ evolution, the enzymes of the NHEJ pathway exhibit a remarkable degree of structural tolerance in the range of DNA end substrate configurations upon which they can act. In vertebrate cells, the nuclease, DNA polymerases, and ligase of NHEJ are the most mechanistically flexible and multifunctional enzymes in each of their classes. Unlike repair pathways for more defined lesions, NHEJ repair enzymes act iteratively, act in any order, and can function independently of one another at each of the two DNA ends being joined. NHEJ is critical not only for the repair of pathologic DSBs as in chromosomal translocations, but also for the repair of physiologic DSBs created during variable (diversity) joining [V(D)J] recombination and class switch recombination (CSR). Therefore, patients lacking normal NHEJ are not only sensitive to ionizing radiation (IR), but also severely immunodeficient.

Semiconductor device, and manufacturing method thereof

Abstract: An object is to provide a semiconductor device of which a manufacturing process is not complicated and by which cost can be suppressed, by forming a thin film transistor using an oxide semiconductor film typified by zinc oxide, and a manufacturing method thereof. For the semiconductor device, a gate electrode is formed over a substrate; a gate insulating film is formed covering the gate electrode; an oxide semiconductor film is formed over the gate insulating film; and a first conductive film and a second conductive film are formed over the oxide semiconductor film. The oxide semiconductor film has at least a crystallized region in a channel region.

Molecular and evolutionary basis of the cellular stress response

Abstract: The cellular stress response is a universal mechanism of extraordinary physiological/pathophysiological significance. It represents a defense reaction of cells to damage that environmental forces inflict on macromolecules. Many aspects of the cellular stress response are not stressor specific because cells monitor stress based on macromolecular damage without regard to the type of stress that causes such damage. Cellular mechanisms activated by DNA damage and protein damage are interconnected and share common elements. Other cellular responses directed at re-establishing homeostasis are stressor specific and often activated in parallel to the cellular stress response. All organisms have stress proteins, and universally conserved stress proteins can be regarded as the minimal stress proteome. Functional analysis of the minimal stress proteome yields information about key aspects of the cellular stress response, including physiological mechanisms of sensing membrane lipid, protein, and DNA damage; redox sensing and regulation; cell cycle control; macromolecular stabilization/repair; and control of energy metabolism. In addition, cells can quantify stress and activate a death program (apoptosis) when tolerance limits are exceeded.

Sensing and repairing DNA double-strand breaks.

Abstract: The DNA double-strand break (DSB) is the principle cytotoxic lesion for ionizing radiation and radio-mimetic chemicals but can also be caused by mechanical stress on chromosomes or when a replicative DNA polymerase encounters a DNA single-strand break or other type of DNA lesion. DSBs also occur as intermediates in various biological events, such as V(D)J recombination in developing lymphoid cells. Inaccurate repair or lack of repair of a DSB can lead to mutations or to larger-scale genomic instability through the generation of dicentric or acentric chromosomal fragments. Such genome changes may have tumourigenic potential. In other instances, DSBs can be sufficient to induce apoptosis. Because of the threats posed by DSBs, eukaryotic cells have evolved complex and highly conserved systems to rapidly and efficiently detect these lesions, signal their presence and bring about their repair. Here, I provide an overview of these systems, with particular emphasis on the two major pathways of DSB repair: non-homologous end-joining and homologous recombination. Inherited or acquired defects in these pathways may lead to cancer or to other human diseases, and may affect the sensitivity of patients or tumour cells to radiotherapy and certain chemotherapies. An increased knowledge of DSB repair and of other DNA DSB responses may therefore provide opportunities for developing more effective treatments for cancer.

Mechanism and regulation of class switch recombination.

Abstract: Antibody class switching occurs in mature B cells in response to antigen stimulation and costimulatory signals. It occurs by a unique type of intrachromosomal deletional recombination within special G-rich tandem repeated DNA sequences [called switch, or S, regions located upstream of each of the heavy chain constant (C(H)) region genes, except Cdelta]. The recombination is initiated by the B cell-specific activation-induced cytidine deaminase (AID), which deaminates cytosines in both the donor and acceptor S regions. AID activity converts several dC bases to dU bases in each S region, and the dU bases are then excised by the uracil DNA glycosylase UNG; the resulting abasic sites are nicked by apurinic/apyrimidinic endonuclease (APE). AID attacks both strands of transcriptionally active S regions, but how transcription promotes AID targeting is not entirely clear. Mismatch repair proteins are then involved in converting the resulting single-strand DNA breaks to double-strand breaks with DNA ends appropriate for end-joining recombination. Proteins required for the subsequent S-S recombination include DNA-PK, ATM, Mre11-Rad50-Nbs1, gammaH2AX, 53BP1, Mdc1, and XRCC4-ligase IV. These proteins are important for faithful joining of S regions, and in their absence aberrant recombination and chromosomal translocations involving S regions occur.