Abstract: A method for stimulating the synthesis of nasal nitric oxide and nasal and lung surfactants to inhibit the docking and adhesion of viruses to cellular receptors, including ACE2, to reduce viral replication, duration, spread and severity of infections, and also to inhibit lung fibrosis, increase the synthesis of serotonin to reduce coughing and mouth breathing, reduce the cytokine storm produced by LI-6 caused by viruses such as COVID-19 and flu in patients susceptible to these infections, including patients with hypoxemia, asthma, chronic obstructive pulmonary disease, cystic fibrosis, diabetics, interstitial lung disease, pulmonary fibrosis, allergic rhinitis, sinusitis, smokers, sleep apnea and lung cancer, which includes: contacting mammalian cells with a therapeutically effective amount of a composition, said composition including the following constituents: sodium pyruvate; a phosphate; a salt of calcium; and a salt of magnesium.

Abstract: Methods for the treatment of patients with both Chronic Obstructive Pulmonary Disease (COPD) and pulmonary fibrosis, and of patients with idiopathic pulmonary fibrosis without COPD, by stimulating the synthesis of human and animal patient lung and sinus surfactants to increase lung functions, inhibiting fibrosis and reducing coughing and nasal erythema, include the following steps: A) analyzing and diagnosing a patient with a lung ailment selected from the group consisting of i) both COPD and pulmonary fibrosis; and ii) idiopathic pulmonary fibrosis without COPD; and, B) treating the patient to raise the patient's lung functions including FEV1/FVC ratio by contacting mammalian cells with a [therapeutically effective amount of a treatment] composition that includes: a) a pyruvate salt; b) a phosphate; c) a salt of calcium; and d) a salt of magnesium, in an aqueous carrier, containing no more than 2.2 grams of said pyruvate salt per liter.

Abstract: The present invention has shown that not all salts of pyruvic acid enhance lung functions or enhance the synthesis of lung surfactants and that certain salts of pyruvic acid with the correct concentrations of calcium, phosphate and magnesium, are synergistic in their ability to enhance the synthesis of lung surfactants that will enhance lung alveoli functions, while decreasing coughing and lung tightness, and increasing oxygen saturation values to prevent hypoxemia. This patent demonstrates that the sodium pyruvate formula with calcium, phosphate and magnesium was superior over standard sodium pyruvate formula in saline alone in the removal of mucus, reduction of lung or sinus infections, and in reducing drug side effects and congestion.

Abstract: The present invention provides novel methods for treating a pulmonary disease state in mammals by up or down regulating indigenous in vivo levels of an inflammatory agent in mammalian cells comprising contacting the mammalian cells with a therapeutically effective amount of an inflammatory regulator, wherein the inflammatory agent is selected from the group consisting of cytokines, transforming growth factor-?, elastase, and white blood cells, and wherein the inflammatory regulator is selected from the group consisting of pyruvates and pyruvate precursors.

Abstract: The present invention pertains to a method for treating a pulmonary disease state in mammals by altering indigenous in vivo levels of nitric oxide in mammalian cells. The method comprises contacting the mammalian cells with a therapeutically effective amount of a nitric oxide mediator selected from the group consisting of pyruvates, pyruvate precursors, &agr;-keto acids having four or more carbon atoms, precursors of &agr;-keto acids having four or more carbon atoms, and the salts thereof. The method may further comprise contacting the mammalian cells with a therapeutic agent and a nitric oxide source selected from the group consisting of nitric oxide, nitric oxide precursors, and nitric oxide stimulators.

Abstract: The present invention is directed to a method for treating bronchial constriction in mammals. The method comprises contacting mammalian lung with a compound selected from the group consisting of pyruvate and pyruvate precursors. The compound is present in a therapeutically effective amount to produce bronchial dilation. The present invention is also directed to a method for treating airway disease in mammals. The method comprises contacting mammalian lung with a compound selected from the group consisting of pyruvate and pyruvate precursors. The compound is present in an amount from about 0.0001 millimoles to about 0.005 millimoles. The present invention is further directed to a method for treating airway disease in mammals. The method comprises contacting the mammalian lung with a compound selected from the group consisting of pyruvate and pyruvate precursors. The compound is present in a therapeutically effective amount to prevent bronchial spasm.

Abstract: A method for treating the disease state in mammals caused by mammalian cells involved in the inflammatory response is disclosed. Mammalian cells participating in the inflammatory response are contacted with an inflammatory response mediator which reduces the undesired inflammatory response and is an antioxidant. The inflammatory response mediator may further provide a cellular energy source and be a building block in the cellular synthesis of other cellular components. Compositions for reducing and treating undesired inflammatory response are also disclosed.

Abstract: A method for treating the disease state in mammals caused by mammalian cells involved in the inflammatory response is disclosed. Mammalian cells participating in the inflammatory response are contacted with an inflammatory response mediator which reduces the undesired inflammatory response and is an antioxidant. The inflammatory response mediator may further provide a cellular energy source and be a building block in the cellular synthesis of other cellular components. Composition, for reducing and treating undesired inflammatory response are also disclosed.

Abstract: A method for treating emphysema and other disease states in mammals caused by mammalian cells involved in the inflammatory response is disclosed. Mammalian cells participating in the inflammatory response are contacted with an inflammatory response mediator which reduces the undesired inflammatory response and is an antioxidant. The inflammatory response mediator may further provide a cellular energy source and be a building block in the cellular synthesis of other cellular components. Compositions for reducing and treating undesired inflammatory response are also disclosed.

Abstract: A method for treating the disease state in mammals caused by mammalian cells involved in the inflammatory response is disclosed. Mammalian cells participating in the inflammatory response are contacted with an inflammatory response mediator which reduces the undesired inflammatory response and is an antioxidant. The inflammatory response mediator may further provide a cellular energy source and be a building block in the cellular synthesis of other cellular components. Compositions for reducing and treating undesired inflammatory response are also disclosed.