Abstract: A frac sand separator system includes a sand separator having an inlet fluidly connected to a well for receiving a fracking return mixture from the well. The sand separator is configured to separate water of the fracking return mixture from particulate matter of the fracking return mixture. The sand separator includes an outlet. The frac sand separator system includes a collection container fluidly connected to the outlet of the sand separator for receiving the particulate matter from the sand separator. At least one outlet valve is fluidly connected between the outlet of the sand separator and the collection container. The frac sand separator system includes a computing device operatively connected to the at least one outlet valve. The computing device includes a processor configured to automatically open the at least one outlet valve such that the particulate matter is released from the sand separator into the collection container.

Abstract: A frac sand separator system includes a sand separator having an inlet fluidly connected to a well for receiving a fracking return mixture from the well. The sand separator is configured to separate water of the fracking return mixture from particulate matter of the fracking return mixture. The sand separator includes an outlet. The frac sand separator system includes a collection container fluidly connected to the outlet of the sand separator for receiving the particulate matter from the sand separator. At least one outlet valve is fluidly connected between the outlet of the sand separator and the collection container. The frac sand separator system includes a computing device operatively connected to the at least one outlet valve. The computing device includes a processor configured to automatically open the at least one outlet valve such that the particulate matter is released from the sand separator into the collection container.

Abstract: A frac sand separator system includes a sand separator having an inlet fluidly connected to a well for receiving a fracking return mixture from the well. The sand separator is configured to separate water of the fracking return mixture from particulate matter of the fracking return mixture. The sand separator includes an outlet. The frac sand separator system includes a collection container fluidly connected to the outlet of the sand separator for receiving the particulate matter from the sand separator. At least one outlet valve is fluidly connected between the outlet of the sand separator and the collection container. The frac sand separator system includes a computing device operatively connected to the at least one outlet valve. The computing device includes a processor configured to automatically open the at least one outlet valve such that the particulate matter is released from the sand separator into the collection container.

Abstract: According to one aspect, a system is adapted to actively control one or more operating parameters associated with: a wellbore extending in a subterranean formation, and/or wellbore fluid flowing out of the wellbore via a wellhead. The system includes one or more sensors; an electronic controller adapted to receive from the one or more sensors measurement data; and a valve through which the wellbore fluid is adapted to flow. The valve is adapted to be in communication with the electronic controller. The active control of the at least one of the one or more operating parameters is adapted to facilitate: maintenance of the integrity of the wellbore, and/or enhancement of oil and/or gas production out of the wellbore. In one embodiment, the wellbore fluid flow is frac flow-back. In another aspect, a system is adapted to monitor vent gas separated from wellbore fluid flowing out a wellhead.

Abstract: According to one aspect, a system is adapted to actively control one or more operating parameters associated with: a wellbore extending in a subterranean formation, and/or wellbore fluid flowing out of the wellbore via a wellhead. The system includes one or more sensors; an electronic controller adapted to receive from the one or more sensors measurement data; and a valve through which the wellbore fluid is adapted to flow. The valve is adapted to be in communication with the electronic controller. The active control of the at least one of the one or more operating parameters is adapted to facilitate: maintenance of the integrity of the wellbore, and/or enhancement of oil and/or gas production out of the wellbore. In one embodiment, the wellbore fluid flow is frac flow-back. In another aspect, a system is adapted to monitor vent gas separated from wellbore fluid flowing out a wellhead.

Abstract: According to one aspect, a system is adapted to actively control one or more operating parameters associated with: a wellbore extending in a subterranean formation, and/or wellbore fluid flowing out of the wellbore via a wellhead. The system includes one or more sensors; an electronic controller adapted to receive from the one or more sensors measurement data; and a valve through which the wellbore fluid is adapted to flow. The valve is adapted to be in communication with the electronic controller. The active control of the at least one of the one or more operating parameters is adapted to facilitate: maintenance of the integrity of the wellbore, and/or enhancement of oil and/or gas production out of the wellbore. In one embodiment, the wellbore fluid flow is frac flow-back. In another aspect, a system is adapted to monitor vent gas separated from wellbore fluid flowing out a wellhead.

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: According to one aspect, a system is adapted to actively control one or more operating parameters associated with: a wellbore extending in a subterranean formation, and/or wellbore fluid flowing out of the wellbore via a wellhead. The system includes one or more sensors; an electronic controller adapted to receive from the one or more sensors measurement data; and a valve through which the wellbore fluid is adapted to flow. The valve is adapted to be in communication with the electronic controller. The active control of the at least one of the one or more operating parameters is adapted to facilitate: maintenance of the integrity of the wellbore, and/or enhancement of oil and/or gas production out of the wellbore. In one embodiment, the wellbore fluid flow is frac flow-back. In another aspect, a system is adapted to monitor vent gas separated from wellbore fluid flowing out a wellhead.

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-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: 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: 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: A starting gate apparatus and method for use in bicycle races is provided. The starting gate includes a main platform, a plurality of gates connected to the main platform and a gate actuation arrangement to drive the gates from a bike stopping position to a bike releasing position. The gate actuation arrangement permits variations in at least one gate actuation parameter including an intermediate stopping position along a gate travel path, the driving force of the gate along the gate travel path, and/or an interval between initiation of an actuation sequence and actuation of the gate of the starting gate. Embodiments of the gate actuation arrangement permit a gate to independently act on an obstruction, provide for reversing, momentarily actuation of the gate during gate actuation or varying the duration or disposition of the interval of the gate actuation sequence.