228 results about "Normal cell" patented technology

The application discloses a cell detection method and system based on deep learning and machine vision, which comprises the following steps: cutting a cervical liquid-based cell pathology digital image into a plurality of sub-images to form a sub-image set; inputting the sub-image set into a normal cell detection model and a lesion cell detection model respectively, and identifying normal cells and lesion cells and their categories; selecting an overlapping area of the normal cells and the lesion cells, and performing secondary classification on the overlapping area through a classification model; performing threshold segmentation on granulocytes in the cervical liquid-based cell pathology digital image to obtain all possible granulocyte targets, filtering to determine final granulocyte targets, and counting and determining the number of the granulocytes. The application solves the problem that the detection model in the prior art has poor detection effect due to the imbalance of normal cell and lesion cell categories, improves the accuracy of cell identification, and realizes accurate detection and identification of cervical liquid-based cells in combination with accurately identified granulocytes.

A memory device includes a memory cell array including normal cell blocks and at least one error correction code (ECC) cell block, which include a plurality of rows; a scrub control circuit configured to perform an error check operation on each of the plurality of rows; and a write-back prevention circuit configured to store, based on local error signals for the normal cell blocks and the at least one ECC cell block during the error check operation, a severe address for a row in which a severe error occurs, and selectively perform a write-back operation on the row corresponding to the stored severe address during the error check operation or a read-modify-write (RMW) operation.

The embodiment of the present disclosure discloses a method for editing the layout of a frozen column of a table, creating a normal table in a webpage, setting a title row as a sticky layout to be fixed in the first row of the normal table, setting a first normal cell as a sticky layout to be fixed in the first column of the normal table, creating a floating row, setting the floating row as an absolute positioning, adding an additional element to a cell of the floating row, adjusting a top offset position of the floating row to be consistent with a top offset position of a second normal cell, adjusting a side offset position of the additional element to be consistent with a side offset position of the second normal cell, setting the additional element as a sticky positioning if the second normal cell is a sticky layout, which can realize code decoupling, reduce the development difficulty of the additional element, make the additional element more accurately attached to the second normal cell of the normal table, and correctly handle the hierarchical coverage relationship between the additional element and the frozen column of the normal table.

The invention relates to a bispecific antibody-cytokine fusion protein as well as a preparation method and application thereof. The fusion protein comprises a TAA binding unit, a T cell binding unit and a cytokine unit, the TAA binding unit comprises an anti-HER2 structural domain, the T cell binding unit comprises an anti-CD3 structural domain, and the cell factor unit comprises IL-2; the anti-CD3 structural domain and the IL-2 structural domain can act on T cells at the same time, further amplification of the T cells is promoted while the T cells are activated to generate cytotoxic killing, the anti-CD3 structural domain and the IL-2 structural domain can be directionally migrated to the periphery of HER2 positive tumor cells through the anti-HER2 structural domain, the efficiency of promoting proliferation and differentiation of tumor infiltrating T cells is improved, and the T cells can be effectively degraded. The effect of killing solid tumor cells by immune cells is greatly improved, the non-specific killing effect of the fusion protein on normal cells and the accompanying release of cytokines in peripheral blood can be reduced to the minimum, and the toxic and side effects of the fusion protein in clinical treatment are reduced.

This application relates to a method, apparatus, and memory for detecting memory failures. The memory failure detection method performs error detection on read data from the memory array to identify failed cells. When repair triggering conditions are met, a repair operation is performed on the failed cell. The success of the repair is verified. If successful, the failed cell is marked as a normal memory cell and continues to be used. If not, redundant cells are used to replace the failed cell. Performing repair operations on failed cells can repair soft-failure cells, avoiding the replacement of a large number of normal cells by redundant cells, thus consuming redundant resources. This allows limited redundant cells to replace unrepairable hard-failure cells, improving the effective utilization rate of redundant cells and preventing redundant resources from being prematurely consumed by repairable soft-failure cells, thus delaying the depletion rate of redundant resources and extending the working life of the memory.

The invention provides a p53 fusion protein based on a targeted colorectal cancer marker CEA and application of the p53 fusion protein in preparation of medicines for inhibiting colorectal cancer, and relates to the field of biological medicines. The fusion protein comprises any one of the following components: p28-p53, MBP-TEV-p14ARF (1-63)-linker-p28, p28-p53-CEABP1, CEABP1-p28-p53, and CEABP2-p28-p53, and the fusion protein comprises any one component selected from the group consisting of the following components: a protein A, a protein B, a protein A, a protein B, a protein C and a protein B, according to the application, p53 and p14 ARF proteins for inhibiting cell proliferation in a human body, cell-penetrating peptide and designed protein CEABP1 or CEABP2 of a targeted binding colorectal cancer marker CEA are fused for the first time, and cell experiments and mouse experiments prove that the protein has a relatively high function of inhibiting growth of colorectal cancer cells, does not influence normal cell growth and has a wide application value.

Use of a BCL2 inhibitor in the preparation of a drug or medical instrument for treating giant congenital melanocytic nevi (GCMN). The use of the BCL2 inhibitor in GCMN has been validated to exert a therapeutic effect by means of reversing anti-apoptotic response of GCMN and inducing apoptosis of GCMN. In addition, good killing effects have been achieved in both primary GCMN cells from multiple patients and animal experiments, indicating that the BCL2 inhibitor has a strong and specific killing effect on giant nevus cells while exerting minimal impact on other normal cells, thereby achieving precise therapeutic and killing effects to address the predicament of the lack of effective treatment methods for GCMN.

The invention discloses a preparation method and application of programmable DNA hydrogel for inhibiting breast cancer tumor activity. The DNA hydrogel is composed of an RCA long chain AL containing a multivalent AS411 aptamer sequence and an RCA long chain CL hybridized with a cholesterol single chain ss-chol. Through reasonable DNA programming sequence design, a three-dimensional DNA structure can be formed on the surface of the cell. The DNA hydrogel specifically targets cancer cells with high expression of nucleolin receptors through the synergistic effect of multivalent AS1411 and chol, and is weak in targeting to normal cells with low expression of nucleolin, so that toxic and side effects on the normal cells are effectively avoided. The DNA hydrogel has excellent programmability, hydrogel with high, medium and low pore densities can be simply prepared through flexible DNA sequence design, and the breast cancer resistance activity of the DNA hydrogel is in positive correlation with the pore density of the DNA hydrogel. In animal in-vivo experiments, the DNA hydrogel under three-dimensional and high pore density significantly inhibits breast cancer activity, and a new strategy is provided for tumor treatment.

The invention relates to a preparation method and application of selenium-doped carbon quantum dots. The selenium-doped orange fluorescent carbon quantum dots are successfully prepared by treating a mixture of mangosteen peel, ethanol and sodium selenite through a hydrothermal method. Based on the excellent fluorescence property of the carbon quantum dots, the Cr < 2 + > can quench the fluorescence of the selenium-doped carbon quantum dots, so that the Cr < 2 + > can be detected. Meanwhile, the carbon quantum dot is found to be responsive to disease micromolecule glutathione, that is, glutathione can enhance fluorescence of the carbon quantum dot. By utilizing the concentration difference of glutathione in normal cells and cancer cells, the carbon quantum dots can realize the recognition of tumor cells. The orange fluorescent carbon quantum dot provided by the invention is prepared from easily available raw materials, and is safe and non-toxic. The prepared carbon quantum dot has stable fluorescent property, uniform particle size of 4.2 + / -0.5 nm, and relative quantum yield of 34.35%, can be imaged in cells, has GSH detection limit of 27.16 umol / L, and can identify tumor cells and normal cells.

The invention relates to the technical field of microalgae biology, in particular to a chlamydomonas reinhardtii strain with high yield of exosomes, which is named as Chlamydomonas reinhardtii YYAW026 and preserved in the China General Microbiological Culture Collection Center (CGMCC), the preservation number is CGMCC NO.46629, the preservation date is November 10, 2025, and the preservation address is No.3, Yard 1, Beichen West Road, Chaoyang District, Beijing. Compared with an original strain, the chlamydomonas reinhardtii cell provided by the invention cannot form a complete cell wall structure, so that the exosome can be quickly secreted into a culture solution; although the cell structure of the strain is incomplete, the strain can still perform normal cell activity, the growth curve is basically consistent with that of a wild type, the yield of the exosome of the strain is greater than that of the wild type when the strain reaches a plateau phase, and the particle size distribution width of the exosome is more concentrated. The chlamydomonas reinhardtii disclosed by the invention has a relatively good application prospect in the basic research fields of cosmetics, medical beauty industry and algae source exosomes.

The invention discloses an enzyme-activated fluorescent molecular precursor as well as a preparation method and application thereof. The enzyme-activated fluorescent molecular precursor has a chemical structure as shown in a formula I which is described in the specification. The invention develops an enzyme-activated fluorescent molecular precursor which can be used for real-time imaging of tumors by targeting exogenous enzyme to the tumors and specifically activating a probe at the tumors; according to the invention, the exogenous enzyme is introduced as an activation trigger, and normal cells do not have the exogenous enzyme, so that the problem of co-expression of the endogenous enzyme in non-tumor tissues can be avoided, background fluorescence signals can be reduced to the greatest extent, and the imaging specificity and accuracy are remarkably improved.

A memory device includes a memory cell array including normal cells and per row activation count (PRAC) cells coupled with a plurality of word lines corresponding to a plurality of rows, a refresh control circuit configured to refresh the plurality of word lines corresponding to the plurality of rows based on a refresh command, and an activation generating circuit configured to generate a row activation signal based on an activation command. The row activation signal is configured to activate the plurality of word lines corresponding to a row address of the plurality of rows. Each of the PRAC cells is configured to store row activation information. Each of the normal cells is configured to store data.

A method and apparatus for selecting microsecond pulsed electric field parameters for killing senescent cells. The method includes: 1) obtaining biological tissue cells and culturing them to obtain n groups of cell reagents containing normal cells and n groups of cell reagents containing senescent cells; 2) setting n groups of pulsed electric field parameters for killing senescent cells; 3) placing the i-th group of cell reagents containing normal cells and the i-th group of cell reagents containing senescent cells between an electrode pair, and electrically stimulating the i-th group of cell reagents containing normal cells and the i-th group of cell reagents containing senescent cells using the i-th group of pulsed electric field parameters; 4) performing cell activity detection, PI positivity rate detection, and electrosensitivity detection on each group of cell reagents after electrical stimulation to determine the optimal pulsed electric field parameters. The apparatus includes an electrode pair and a pulse generator. Compared with traditional treatment methods for chronic wounds, this invention only requires an electric field to efficiently and accurately kill senescent cells, without thermal effects or side effects.

The invention relates to the technical field of pharmacy and biology, in particular to a high-content drug screening method and system based on ControlNet-PPO. The method comprises the following specific steps: according to a current cell state, adopting a PPO algorithm reinforcement learning strategy to generate a combined action instruction for controlling release of various drugs; applying drug disturbance to cells based on the combined action instruction, and obtaining a disturbed cell image; inputting the cell image as a condition into a pre-trained ControlNet, and generating an expected cell state image under the action instruction; calculating a composite reward value based on a state difference between the expected cell state image and a normal cell reference image; and updating the reinforcement learning strategy by using the composite reward value, and iteratively optimizing the drug combination action until the cell state is converged to be close to the normal state, thereby obtaining an optimal drug combination path. By adopting the method, the synergistic effect of multiple drugs can be effectively captured and utilized, and the method has the characteristic of high optimization capacity.

The invention provides an immortalized livestock precursor fat cell line and a preparation method thereof, and belongs to the technical field of biology. The invention provides a preparation method of an immortalized livestock precursor adipocyte line, which takes adipose tissues of livestock larvae as a cell source, the cell source contains a small amount of mature adipocytes, but a main cell population is precursor adipocytes, so that the purity of a starting material for subsequent immortalization is ensured; after immortalized induction, the monoclonal cell strain is screened by using a limited dilution method, the immortalized monoclonal cell strain still has the capability of being differentiated into mature adipocytes and forming lipid droplets after induced differentiation treatment, and the immortalized cell line can keep normal cell morphology and overcome replicative senescence. The immortalized cell strain disclosed by the invention can be efficiently differentiated into fat cells with mature functions after being induced, and has normal lipid synthesis and storage capabilities.

The invention discloses a chimeric antigen receptor targeting EGFRvIII and application of the chimeric antigen receptor. The chimeric antigen receptor sequentially comprises an EGFRvIII targeting nucleic acid aptamer, a transmembrane domain and an intracellular signal domain from an N end to a C end, the EGFRvIII targeted nucleic acid aptamer is an EGFRvIII specific DNA aptamer obtained on the basis of SELEX (systematic evolution of ligands by exponential enrichment) screening, can only be combined with an extracellular domain of the EGFRvIII, and is not combined with an EGFR (epidermal growth factor receptor) wild type; the intracellular signal domain comprises a costimulatory signal domain and an activation signal domain, the C end of the costimulatory signal domain is connected with the N end of the activation signal domain, and the EGFRvIII specific nucleic acid aptamer screened based on SELEX is adopted as a targeting domain, can only be specifically combined with the extracellular domain of EGFRvIII positive tumor cells, and is not subjected to cross combination with EGFR wild cells and normal cells, so that the EGFRvIII specific nucleic acid aptamer can be used for detecting EGFRvIII positive tumor cells, and the EGFRvIII specific nucleic acid aptamer can be used for detecting EGFRvIII positive tumor cells. The problem of off-target killing caused by the fact that a common antibody scFv fragment of a traditional chimeric antigen receptor (CAR) is easily combined with a wild type EGFR is fundamentally avoided.

The invention belongs to the technical field of organic synthesis and medicinal chemistry, and particularly relates to a synthesis method of a novel polycyclic aromatic hydrocarbon derivate 2, 6-di-tert-butyl pyrene and indolizine phenothiazine compound and application of the compound in the aspect of anti-cancer drugs. The synthesis process is simple and convenient, conditions are mild, and the yield is ideal. Pharmacodynamic evaluation shows that the compound shows strong inhibitory activity on various human cancer cell lines, and the IC50 values are respectively cervical cancer Hela cells (0.17 mu M), lung cancer A549 cells (0.3 mu M), prostatic cancer PC-3 cells (0.42 mu M) and liver cancer HepG2 cells (10.79 mu M), which are respectively reduced by 109 times, 173 times, 35 times and 1.8 times compared with positive control drug cis-platinum. In addition to efficiently inhibiting cancer cells, the compound has low toxicity to normal cells, meets the basic requirements of excellent anti-cancer drugs, and shows important application value and potential in the field of research and development of novel anti-cancer drugs.

The utility model relates to an electric stimulation cell culture device which comprises, from top to bottom, a cover, a fence, a conductive glass plate and a fixing frame. The fence is open at the top and bottom and closed around. A pressing mechanism is arranged between the fence and the cover or the fixing frame. The pressing mechanism is used to fix the fence on the fixing frame. The conductive glass plate is arranged between the fence and the fixing frame. The bottom of the fence is in sealing contact with the conductive glass plate to form a cell culture chamber. The length of the conductive glass plate is longer than that of the fence at both ends to form an electrode connecting part for connecting with an electrode. The electric stimulation cell culture device provided by the utility model avoids direct contact between the electrode and the culture medium, effectively avoids the risk of cell contamination, and has a simple overall structure, which can simplify experimental operation and ensure normal cell culture environment while applying electric stimulation.

The MYC and NMYC transcription factors (TFs) play a key role in cell proliferation and are overexpressed in most cancer cells. However, in normal cells their overexpression triggers safeguard mechanisms promoting cell death and cellular senescence, which are bypassed in cancer cells. Here, the inventors reveal that in normal cells MYC binds to the Inositol 1,4,5-Trisphosphate Receptor type 1 (ITPR1) gene and upregulates its expression, triggering an ER-mitochondria calcium (Ca2+) transfer, which is involved in MYC-induced cell death and senescence. Supporting a tumor suppressive role of MYC / ITPR1 axis, ITPR1 expression is generally decreased in cancer and reactivation of this pathway induces cancer cell death. Nevertheless, some cancer cells, generally expressing high levels of MYCN and / or MYC, also express high level of ITPR1, which correlates with high expression of BCL2, encoding an inhibitor of ITPR1. Strikingly, in high-risk MYCN-amplified neuroblastoma, ITPR1 expression is controlled by NMYC and its level correlates with worse patient survival. In these cells, blocking the interaction between BCL2 and ITPR1, via an BCL2-BH4 domain inhibitor induces mitochondrial Ca2+ accumulation and cell death, and decreases tumor size. Thus, the present invention relates to a method for treating MYChigh cancer, and in particular NMYC--amplified neuroblastoma in a subject by administering an BCL2-BH4 domain inhibitor.

The application discloses preparation and application of a kind of antimony tungstate material with catalytic Fenton reaction activity, the molecular formula of the antimony tungstate material is H 11 [Ln2Sb2W7O 23 (OH)(DMF)2(SbW9O 33 )2]·xH2O, abbreviated as 1-Ln, wherein Ln=Dy, Ho, Er, Tm, Y, Yb or Lu;DMF=N or N-dimethylformamide;The crystal structure of the antimony tungstate material is that two three-defect {B-alpha-SbW9O 33} units sandwich one four-core heterometallic cluster {Sb2Ln2O 10 (DMF)2} and one {W7O 29 (OH)} cluster unit to form a high 1.9nm capsule-like isolated cluster structure, which has good water solubility and stability under physiological conditions.The antimony tungstate material with catalytic Fenton reaction activity can generate a large number of ·OH to kill cancer cells by catalyzing H2O2 decomposition and consuming glutathione through Fenton-like reaction, has high cytotoxicity and selectivity to various cancer cells, can significantly inhibit the growth of tumor in vivo, has small toxic and side effects to normal cells and organs, and can be used as an antitumor drug, applied to the field of biological medicine.

The invention discloses a method for inducing cell copper death based on GK921 and application of the GK921, and relates to the technical field of biological medicine. The invention discloses a brand new function of inducing copper death by a known compound GK921 for the first time, and provides a brand new strategy for solving the problems of drug resistance and relapse of multiple myeloma. According to the method, target cells are treated with an effective amount of GK921, expression of copper ion transporter ATP7A in the cells is specifically reduced, copper ions are accumulated, and then typical copper death events such as iron-sulfur cluster protein reduction and DLAT protein oligomerization are caused. Experiments show that the GK921 can efficiently inhibit the activity of multiple myeloma cell lines and primary cells, and the IC50 value and the low toxicity to normal cells show excellent selectivity. On the basis, GK921 can be used for preparing a pharmaceutical composition for inducing copper death, and particularly has an important application prospect in treatment of multiple myeloma.

The application discloses a near-infrared distinguishing and iron-apoptosis-enhancing functional fluorescent probe and a preparation method and application thereof. The structural formula of the near-infrared distinguishing and iron-apoptosis-enhancing functional fluorescent probe is as follows: firstly, the traditional boronic acid ether trigger unit is improved to be a cyclic diboronic acid ester, N-methyl imidodicarboxylic acid is introduced above the phenylboronic acid to improve the response threshold, and the benzyl ether structure is abandoned and replaced by a phenyl ether structure, which also plays a role in further increasing the oxidation threshold; secondly, the response threshold is adjusted, and in combination with the strong coordination function of the released Fe(III), the cancer environment selectively triggers and releases the functional probe for iron-apoptosis enhancement. The probe disclosed by the application increases the difference in the reaction threshold between the cancer cell environment and the normal cell environment, and through twice adjustment, the fluorescence trigger difference is increased, the iron-apoptosis intermediate is released at the same time of fluorescence triggering, the cancer cells are caused to undergo iron-apoptosis, and the probe is applied to the detection of tumor cells.

A method and system of sensitization of cancerous cells in a volume is disclosed. A plasma tube including a pair of electrodes coupled to a power supply is provided. The plasma tube generates a plasma jet between the electrodes. A controller is coupled to a power supply to control a discharge voltage to the electrodes to generate the plasma jet and direct an electro-magnetic field at the volume having cancerous cells and normal cells for a sufficient time to sensitize the cancer cells. A treatment device applies a treatment such as TMZ to the sensitized cancer cells after the cancer cells are sensitized by the electro-magnetic field.

The present disclosure provides novel compositions and methods suitable for specifically eliminating target cells (e.g., cancer cells) without affecting non-target cells (e.g., non-cancer cells). For example, CRISPR system and the compositions of the present disclosure can be employed to specifically introduce a suicidal gene into a cancer cell in the loci of a cancer-specific target sequence, which as a result of chromosomal re-arrangement or translocation in a cancer cell presents a cancer specific sequence for a guide RNA and CAS to be recognized and such sequence is absent in a non-cancer cell. Consequently, the specific introduction of the composition(s) to cancer-specific site(s) and integration of suicide gene in the target genome, which is inapplicable to normal cells for lack of the site(s), leads to selective elimination of cancer cells but not non-cancer cells, and therefore render novel therapeutic methods and compositions for cancer treatment.

This invention belongs to the field of fluorescent probe technology, specifically relating to a nitroreductase fluorescent probe, its preparation method, and its application. To develop an NTR fluorescent probe with high selectivity, high sensitivity, short response time, and long excitation and emission wavelengths, this invention utilizes pentamethine cyanine dye and a "ester group → carboxyl group" conversion strategy at the central site of this dye to develop a nitroreductase fluorescent probe, Cy5-NTR. In the presence of NADPH, the nitro group of the probe is first catalyzed by the overexpression of NTR by cancer cells, resulting in a single-electron transfer and the generation of a nitro anion radical. This radical is then further reduced to an amino group, followed by a 1,6-rearrangement and elimination reaction, releasing the strongly fluorescent centrally carboxyl-substituted pentamethine cyanine dye Cy5-COO. This probe can not only distinguish cancer cells / tissues from normal cells / tissues with high contrast under hypoxic conditions, but also provide in situ real-time imaging of tumors in tumor-bearing mice.

This invention discloses a type of click-type covalent drug, its regionally selective delivery system, and its applications. The invention comprises two parts: a click-type covalent drug and a tumor regionally selective delivery system. The click-type covalent drug consists of three parts: an azacyclic alkyne (DBCO), a small molecule drug, and a linker, having the structure of Formula 1. Optionally, the small molecule drug is a membrane protein inhibitor, an immunomodulator, or a chemotherapeutic drug. The click-type covalent drug reacts with azide-labeled target cells via a click reaction, forming a covalent bond that binds to the cell membrane, increasing the local drug concentration and prolonging the drug retention time, thereby enhancing selective inhibition of the target cells. The regionally selective delivery system is co-assembled from an amphiphilic block polymer and the click-type covalent drug for regionally selective delivery. This invention achieves covalent binding to azide-labeled tumor cells through the click-type covalent drug, while having no effect on unlabeled normal cells, reducing toxic side effects on normal tissues.

The present invention relates to a Fab-arm (Fab-arm) exchange prevention Fc variant, the effector function of which is reduced due to elimination of binding force with Fc [gamma] Rs and C1q, and the human antibody Fc domain variant of the present invention is a novel variant different from the conventional Fab-arm exchange prevention variant, which can overcome the Fab arm exchange phenomenon, which is the disadvantage of IgG4, and which does not bind to all human Fc [gamma] Rs and C1q, and which can be used as a novel human antibody Fc domain variant having a reduced effector function due to elimination of binding force with Fc [gamma] Rs and C1q. The compound does not bind to mouse and monkey Fc [gamma] Rs, has excellent blood half-life and thermal stability, and thus can be used for preventing immune cell / normal cell death (toxicity) caused by a therapeutic antibody or an antibody Fc region of an Fc-fusion protein drug.

A memory device and a method of operating the memory device are provided. The memory device may include a memory cell array, a write driver, and a sensing circuit. A memory cell array may include a normal cell connected to a bit line and a one-time programmable (OTP) cell connected to the bit line. The programming state of the normal cell may be determined by a first reference resistance, and the programming state of the OTP cell may be determined by a second reference resistance that is less than the first reference resistance. The write driver may perform a first OTP write operation on the OTP cell, and the sensing circuit may determine whether the first OTP write operation on the OTP cell is passed. The write driver may perform a second OTP write operation on the failed OTP cell undergoing the first OTP write operation.

The present application relates to a kind of triplex-forming oligonucleotides (TFOs) sequence and its pharmaceutical application, especially to a kind of triplex-forming oligonucleotides sequence and its pharmaceutical application for inhibiting MDM2 and MDM4 gene amplification.The triplex-forming oligonucleotides sequence provided by the present application can form triplex structure locally in the amplified MDM2 / MDM4 gene of tumor cell, cause its replication stress, finally lead to the apoptosis of tumor cell.The triplex-forming oligonucleotides sequence provided by the present application and the medicine prepared using the sequence are aimed at the MDM2 / MDM4 amplification gene sequence of tumor rather than protein, have good drug resistance, and have no effect on normal cell without MDM2 / MDM4 gene amplification, have excellent safety, thus have good therapeutic effect on the tumor with MDM2 / MDM4 gene amplification.

The application discloses a battery cell fault diagnosis method and device, and relates to the technical field of batteries. According to the charging voltage of a battery cell, the sum of the absolute values of MN of a to-be-tested cell and the Euclidean distance are calculated, the sample entropy-scale factor curve slope of the to-be-tested cell is calculated according to the sampling time of the charging voltage, the first Hamming closeness of the sum of the absolute values of MN, the Euclidean distance and the sample entropy-scale factor curve slope of the to-be-tested cell to the normal cell clustering center is calculated, the second Hamming closeness of the sum of the absolute values of MN, the Euclidean distance and the sample entropy-scale factor curve slope of the to-be-tested cell to the fault cell clustering center is calculated, and if the second Hamming closeness is greater than the first Hamming closeness, the to-be-tested cell is judged to be faulty. The battery cell fault is comprehensively diagnosed from three dimensions.