Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.

Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.

Abstract: An instant messaging message processing method is disclosed and includes: receiving, by a server, an instant messaging message, user account information of a destination user terminal, and user account information of a source user terminal from the source user terminal; determining, by the server, a risk level of the instant messaging message according to a preset rule and the user account information of the source user terminal; and if the risk level of the instant messaging message reaches a first risk level, transmitting, by the server when, the instant messaging message and preset pre-warning information to the destination user terminal according to the user account information of the destination user terminal, wherein the pre-warning information comprises security prompt information which is used for prompting a user of the destination user terminal to notice a security risk of the instant messaging message. An instant messaging message processing device is also disclosed.

Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.

Abstract: A method and an apparatus for processing data are provided. The method includes: receiving, through a network, a data processing request sent by a first device, where the first device is connected to the network via a wireless access point; obtaining a distance value between the first device and the wireless access point in a case that the wireless access point is a credit access point for the first device; calculating, based on the distance value between the first device and the wireless access point, a credit value associated with the first device in a case that the distance value exceeds a preset distance threshold; and accepting the data processing request in a case that the credit value is greater than or equal to a credit threshold.

Abstract: An identity verifying method, an account acquiring method, a mobile terminal, and a storage medium are disclosed, and the account acquiring method includes: receiving, by a first mobile terminal, a user operation of accepting identity verification on the first mobile terminal, playing voice information which is stored in the first mobile terminal and has a correspondence relationship with a user account of a user of the first mobile terminal, and meanwhile collecting voice data of the played voice information using voice receiving means; sending, by the first mobile terminal, verification information comprising the user account and the voice data to a server to allow the server to determine whether the user passes the identity verification according to the verification information; and receiving, by the first mobile terminal, an identity verification result returned by the server. Thus, the voice information is used for identity verification.

Abstract: An instant messaging message processing method is disclosed and includes: receiving, by a server, an instant messaging message, user account information of a destination user terminal, and user account information of a source user terminal from the source user terminal; determining, by the server, a risk level of the instant messaging message according to a preset rule and the user account information of the source user terminal; and if the risk level of the instant messaging message reaches a first risk level, transmitting, by the server when, the instant messaging message and preset pre-warning information to the destination user terminal according to the user account information of the destination user terminal, wherein the pre-warning information comprises security prompt information which is used for prompting a user of the destination user terminal to notice a security risk of the instant messaging message. An instant messaging message processing device is also disclosed.

Abstract: An identity verifying method, an account acquiring method, a mobile terminal, and a storage medium are disclosed, and the account acquiring method includes: receiving, by a first mobile terminal, a user operation of accepting identity verification on the first mobile terminal, playing voice information which is stored in the first mobile terminal and has a correspondence relationship with a user account of a user of the first mobile terminal, and meanwhile collecting voice data of the played voice information using voice receiving means; sending, by the first mobile terminal, verification information comprising the user account and the voice data to a server to allow the server to determine whether the user passes the identity verification according to the verification information; and receiving, by the first mobile terminal, an identity verification result returned by the server. Thus, the voice information is used for identity verification.

Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.

Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-I or angiotensin II.

Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.

Abstract: This invention relates generally to compositions and methods which utilization nuclear receptors for regulating adipogenesis in cells. Specifically, the invention is directed to compositions which regulate transcription factor PPAR?, and enhance or inhibit the transcription of genes responsible for directing cell differentiation towards a pathway of adipogenesis. More specifically, disclosed herein is a novel polypeptide coactivator of PPAR?, and fragments thereof, which possess coactivator or corepressor activity. Also related are nucleotide sequences which express these polypeptides. Also disclosed is an interfering RNA that may be used to inhibit adipogenesis.

Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.

Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.

Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.

Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.

Abstract: This invention relates generally to compositions and methods which utilization nuclear receptors for regulating adipogenesis in cells. Specifically, the invention is directed to compositions which regulate transcription factor PPAR?, and enhance or inhibit the transcription of genes responsible for directing cell differentiation towards a pathway of adipogenesis. More specifically, disclosed herein is a novel polypeptide coactivator of PPAR?, and fragments thereof, which possess coactivator or corepressor activity. Also related are nucleotide sequences which express these polypeptides. Also disclosed is an interfering RNA that may be used to inhibit adipogenesis.

Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.

Abstract: This invention relates generally to compositions and methods which utilization nuclear receptors for regulating adipogenesis in cells. Specifically, the invention is directed to compositions which regulate transcription factor PPAR?. and enhance or inhibit the transcription of genes responsible for directing cell differentiation towards a pathway of adipogenesis. More specifically, disclosed herein is a novel polypeptide coactivator of PPAR?, and fragments thereof, which possess coactivator or corepressor activity. Also related are nucleotide sequences which express these polypeptides. Also disclosed is an interfering RNA that may be used to inhibit adipogenesis.

Abstract: We found that FIZZ1/RELM? is inducible by hypoxia in lung. The hypoxia-upregulated expression of FIZZ1/RELM? was located in the pulmonary vasculature, bronchial epithelial cells, and type II pneumocytes. Recombinant FIZZ1/RELM? protein stimulates rat pulmonary microvascular smooth muscle cell (RPSM) proliferation dose-dependently. Therefore, we renamed this gene as hypoxia-induced mitogenic factor (HIMF). HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 inhibits HIMF-activated Akt phosphorylation. It also inhibits HIMF-stimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. HIMF also has angiogenic and vasoconstrictive activity. Notably, HIMF increases pulmonary arterial pressure and vascular resistance more potently than either endothelin-1 or angiotensin II.