306 results about "Normal cell" patented technology

The invention relates to the field of molecular targeted therapy, and discloses an application of an SLC16A5 (MCT6) small-molecule inhibitor MCT6-Ai7-2 in preparation of a medicine for treating acute myeloid leukemia (AML). The inhibitor takes an SLC16A5 protein structure predicted by Alphafold as a target spot, and is obtained through compound database screening, molecular docking and druggability optimization. An in-vitro experiment proves that MCT6-Ai7-2 can remarkably inhibit proliferation of AML cell lines such as U937 and MOLM-13, induce cell apoptosis and retard a cell cycle, has an inhibiting effect on a primary AML patient specimen and is relatively low in toxicity to normal cells; in-vivo experiments show that the compound is effective and has good safety in AML model mice. In addition, the MCT6-Ai7-2 and the vinca can be combined to synergistically enhance the inhibition effect on vinca drug-resistant cells, and by reducing the expression of anti-apoptotic protein MCL-1, the activation of pro-apoptotic factors BIM and tBID is promoted to play a role. The invention provides a novel targeting drug and strategy for treatment of AML (especially drug-resistant or recurrent patients).

The invention discloses an early diagnosis marker for B-cell lymphoma, a cross-species screening method based on lamprey and application, and relates to the technical field of molecular diagnosis. In the prior art, tissue biopsy is strong in invasiveness, and a traditional marker is low in early detection rate; in order to solve the problems that a large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large-scale large- When the expression quantity of the gene in a sample is greater than or equal to 1.8 times of that of a normal B cell (HMY2. CIR), the lymphoma is judged to be positive, and the minimally invasive early diagnosis efficiency is remarkably improved.

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 invention relates to a memory including a sense amplifier and a method of operating the memory. The operating method of the memory may include: receiving a first activation command and a first row address; initiating a first mismatch compensation operation in a sense amplifier array for a normal cell array corresponding to the first row address and in a redundant sense amplifier array for a redundant cell array corresponding to the normal cell array; determining whether to access the normal cell array based on the first row address and the repair information; in response to a determination to access the normal cell array, deactivating the redundant sense amplifier array for the redundant cell array; activating a word line of the normal cell array corresponding to the first row address; and sensing and amplifying data of a memory cell corresponding to the activated word line by a sense amplifier array for the normal cell array.

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.

The invention relates to a nano AIE probe as well as a preparation method and application thereof. The probe is synthesized by taking a compound A as a raw material and F-127 as a surfactant through a nano precipitation method; the structural general formula of the compound A is # imgabs0, wherein R is # imgabs1 # imgabs2 #, and the preparation method comprises the following steps: S1, preparing the compound A; and S2, preparing the nano AIE probe. The nano AIE probe has AIE characteristics, excellent phototoxicity, good cancer cell specificity, low cell dark toxicity and good biocompatibility, can well distinguish cancer cells from normal cells, can be applied to tumor treatment as a photosensitizer, and has a good application prospect.

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 discloses a nucleotide for targeted degradation of newly found reverse shear RNA ts-TIMP2 and application of the nucleotide, and is characterized in that the nucleotide achieves the effect of inhibiting lung cancer by inhibiting ts-TIMP2 mRNA without influencing normal cells, and the sequence of the nucleotide is CAUGCAGUGAUCAGGGCCdTdT and a complementary sequence GGCCCUGAUCACUGCAAUGdTdT thereof. The oligonucleotide disclosed by the invention can degrade ts-TIMP2 in a targeted manner, inhibits A549 cell proliferation under the condition of not influencing normal cell 16HBE, and can improve the anti-tumor effect by being combined with an anti-tumor drug inorganic arsenic for treatment.

The invention discloses a lithium battery monomer internal short circuit fault detection method, system, medium and equipment, and the method comprises the steps: carrying out an over-discharge induced internal short circuit fault circulation experiment for a normal monomer battery, and obtaining different internal short circuit fault monomer samples; establishing an impedance spectrum database of the battery in a normal state and a fault state under a wide-temperature working condition and in a full charge state, and calculating charge transfer internal resistance and SEI internal resistance values in impedance spectrum data through the area of a relaxation time distribution curve; the method comprises the following steps of: establishing a database based on temperature distribution by taking the resistance value change amplitude of the single battery transited from a normal state to a fault state in different temperature states as a threshold value fitting function, and performing impedance spectrum measurement and temperature measurement on the single battery to be measured after each charge-discharge cycle is finished; performing relaxation time distribution quantification to obtain charge transfer internal resistance and SEI internal resistance values; and if the resistance value change amplitudes of the charge transfer internal resistor and the SEI internal resistor both exceed a threshold value, determining that an internal short circuit fault exists in the single battery.

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 embodiment of the invention discloses a communication method and device. The method comprises: a terminal obtaining first information, the first information being used for indicating whether a first cell is a first type of cell, the first type of cell being a cell supporting on-demand request sending of a synchronization signal block SSB and / or a first system information block SIB1; the first cell is a candidate cell for cell selection or cell reselection; the terminal determines whether to execute a first behavior based on the first information, the first behavior comprising at least one of the following: performing cell selection or cell reselection; and adjusting the cell selection or cell reselection priority of the first cell to the lowest priority. According to the embodiment of the invention, in the process of cell selection or cell reselection, the terminal supporting the on-demand synchronization signal block (on demand SSB) characteristic can identify that the first cell is the first type of cell; therefore, selection and / or reselection of the first type of cells as normal cells can be avoided or postponed by means of additional cell selection or reselection or priority reduction.

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.