Abstract: The present disclosure provides a bispecific antibody including a binding domain that binds to CD112R and a binding domain that binds to TIGIT, and the binding domain that binds to CD112R includes: HCDR1, HCDR2 and HCDR3 of the amino acid sequence set forth in SEQ ID NO: 1, and/or LCDR1, LCDR2 and LCDR3 of the amino acid sequence set forth in SEQ ID NO: 2; and the HCDR1, HCDR2, HCDR3, LCDR1, LCDR2 and LCDR3 are defined according to the Kabat, IMGT, Chothia, AbM or Contact numbering system. The present disclosure further provides a polynucleotide encoding the antibody, an expression vector, a host cell and a method for expressing and purifying the antibody, a pharmaceutical composition including the antibody of the present disclosure, and use of the bispecific antibody for treating cancer.

Abstract: A data transmission method includes a vehicle-side device that sends, to a network side device, a first message to obtain vehicle driving-related information. The vehicle-side device receives, from the network side device, a second message including the vehicle driving-related information, where content or a format of the second message is determined by the network side device based on the first message.

Abstract: The motor rotor assembly structure includes a rotating shaft, a plurality of rotor cores formed by a plurality of rotor punches neatly laminated, and rotor pressure plates installed at front and rear ends of the rotor core. The rotor core is provided with a shaft hole for mounting the rotating shaft in the middle in an axial direction. Two rotor pressure plates press the plurality of rotor punches. The rotating shaft is a hollow shaft. The plurality of rotor punches has the same structure. Each of the rotor punches is provided with a plurality of sets of positioning holes. The plurality of rotor punches is positioned and fixed to the rotating shaft through the plurality of sets of positioning holes to realize oblique poles between rotor segments. The motor rotor assembly structure is made by laminating one type of rotor punches.

Abstract: Provided are a method and an apparatus controlling a water flooding failure in a fuel cell dual-stack system. The method includes: acquiring a hydrogen pressure drop reference value of the stack system in each normal working condition to obtain a control value; collecting a current pressure drop at a hydrogen side, and determining whether the current pressure drop at the hydrogen side is higher than the control value corresponding to a current normal working condition; determining a faulted stack according to voltages or currents of the first stack and the second stack if the current pressure drop at the hydrogen side is higher than the control value corresponding to the current normal working condition; reducing an opening degree of a flow regulating valve of the faulted stack, and increasing an opening degree of a flow regulating valve of the other stack.

Abstract: The motor rotor assembly structure includes a rotating shaft, a plurality of rotor cores formed by a plurality of rotor punches neatly laminated, and rotor pressure plates installed at front and rear ends of the rotor core. The rotor core is provided with a shaft hole for mounting the rotating shaft in the middle in an axial direction. Two rotor pressure plates press the plurality of rotor punches. The rotating shaft is a hollow shaft. The plurality of rotor punches has the same structure. Each of the rotor punches is provided with a plurality of sets of positioning holes. The plurality of rotor punches is positioned and fixed to the rotating shaft through the plurality of sets of positioning holes to realize oblique poles between rotor segments. The motor rotor assembly structure is made by laminating one type of rotor punches.

Abstract: Provided are a method and an apparatus controlling a water flooding failure in a fuel cell dual-stack system. The method includes: acquiring a hydrogen pressure drop reference value of the stack system in each normal working condition to obtain a control value; collecting a current pressure drop at a hydrogen side, and determining whether the current pressure drop at the hydrogen side is higher than the control value corresponding to a current normal working condition; determining a faulted stack according to voltages or currents of the first stack and the second stack if the current pressure drop at the hydrogen side is higher than the control value corresponding to the current normal working condition; reducing an opening degree of a flow regulating valve of the faulted stack, and increasing an opening degree of a flow regulating valve of the other stack.

Abstract: A plasma oil-free ignition system in oxygen enriched environment comprises a plasma generator and a burner. The plasma oil-free ignition system comprises a sleeve group coaxially arranged with the burner, and the sleeve group comprises multiple coaxially sleeved sleeves. Annular spaces are formed between adjacent sleeves and between the sleeves and the burner. Oxygen ducts are arranged on the sleeves, and oxygen ducts are arranged on the burner. Plasmas jetted by the plasma generators form a local high temperature zone filled with high temperature plasma and pulverized coal air flow.

Abstract: A plasma oil-free ignition system in oxygen enriched environment comprises a plasma generator and a burner. The plasma oil-free ignition system comprises a sleeve group coaxially arranged with the burner, and the sleeve group comprises multiple coaxially sleeved sleeves. Annular spaces are formed between adjacent sleeves and between the sleeves and the burner. Oxygen ducts are arranged on the sleeves, and oxygen ducts are arranged on the burner. Plasmas jetted by the plasma generators form a local high temperature zone filled with high temperature plasma and pulverized coal air flow.

Abstract: The present invention includes methods of modulating cellular secretory processes. More specifically the present invention relates to modulating or reducing the release of inflammatory mediators from inflammatory cells by inhibiting the mechanism associated with the release of inflammatory mediators from the vesicles or granules in the inflammatory cells in a subject with a chronic inflammatory disease. In this regard, the present invention discloses an intracellular signaling mechanism that illustrates several novel intracellular targets for pharmacological intervention in disorders involving secretion of inflammatory mediators from vesicles in inflammatory cells. MANS peptide and active fragments thereof are useful in such methods.

Abstract: Methods and compounds for decreasing MARCKS-related inflammation and MARCKS-related mucus hypersecretion or decreasing MARCKS-related inflammation in a subject by the administration of a N-terminal myristoylated protein fragment of the N-terminal region of MARCKS protein or a peptide fragment thereof are disclosed.

Abstract: A dense phase swirl pulverized coal burner comprises a primary air channel, a direct flow secondary air channel and a outermost swirl secondary air channel; and multiple levels of pulverized coal concentration rings are arranged axially at intervals along the oil gun casing in a straight tube section of the primary air channel, so that pulverized coal air flow is distributed thickly outside and thinly inside the primary air nozzle. In the invention, dense phase pulverized coal outside the primary air nozzle passes through guide vanes, forms disturbed flow, is ejected into a furnace and mixes with high temperature backflow flue gas rapidly and sufficiently at an outlet. Meanwhile, dilute pulverized coal air flow at the center is ejected into the furnace by direct flow, ensuring subsequent mixing and combustion of pulverized coal flow.

Abstract: Methods and compounds for increasing or decreasing mucus secretion in subjects, and particularly mucus secretion in the airways, are described. Methods of screening compounds for the ability to increase or decrease mucus secretion are also described.

Abstract: Methods and compounds for decreasing MARCKS-related inflammation and MARCKS-related mucus hypersecretion or decreasing MARCKS-related inflammation in a subject by the administration of a N-terminal myristoylated protein fragment of the N-terminal region of MARCKS protein or a peptide fragment thereof are disclosed.

Abstract: The present invention includes methods of modulating cellular secretory processes. More specifically the present invention relates to modulating or reducing the release of inflammatory mediators from inflammatory cells by inhibiting the mechanism associated with the release of inflammatory mediators from the vesicles or granules in the inflammatory cells. In this regard, the present invention discloses an intracellular signaling mechanism that illustrates several novel intracellular targets for pharmacological intervention in disorders involving secretion of inflammatory mediators from vesicles in inflammatory cells. MANS peptide and active fragments thereof are useful in such methods.

Abstract: Methods and compounds for increasing or decreasing mucus secretion in subjects, and particularly mucus secretion in the airways, are described. Methods of screening compounds for the ability to increase or decrease mucus secretion are also described.

Abstract: Methods and compounds for increasing or decreasing mucus secretion in subjects, and particularly mucus secretion in the airways, are described. Methods of screening compounds for the ability to increase or decrease mucus secretion are also described.

Abstract: The present invention includes methods of modulating cellular secretory processes. More specifically the present invention relates to modulating or reducing the release of inflammatory mediators from inflammatory cells by inhibiting the mechanism associated with the release of inflammatory mediators from the vesicles or granules in the inflammatory cells. In this regard, the present invention discloses an intracellular signaling mechanism that illustrates several novel intracellular targets for pharmacological intervention in disorders involving secretion of inflammatory mediators from vesicles in inflammatory cells. MANS peptide and active fragments thereof are useful in such methods.

Abstract: The present invention includes methods of modulating cellular secretory processes. More specifically the present invention relates to modulating the release of inflammatory mediators. Additionally, the present invention discloses an intracellular signaling mechanism that regulates airway mucin secretion as well as illustrating several novel intracellular targets for pharmacological intervention in disorders involving aberrant secretion of respiratory mucins and/or secretion of inflammatory mediators from membrane-bound vesicles.

Abstract: The present invention includes methods of modulating cellular secretory processes. More specifically the present invention relates to modulating the release of inflammatory mediators. Additionally, the present invention discloses an intracellular signaling mechanism that regulates airway mucin secretion as well as illustrating several novel intracellular targets for pharmacological intervention in disorders involving aberrant secretion of respiratory mucins and/or secretion of inflammatory mediators from membrane-bound vesicles.