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2539 results about "Nicotine" patented technology

This medication can help you quit smoking by replacing the nicotine in cigarettes. The nicotine in tobacco is an important part of cigarette addiction. When you stop smoking, your nicotine levels drop quickly.

Electronic Atomization Cigarette

The present invention relates to an electronic atomization cigarette which only contains nicotine without harmful tar. The electronic atomization cigarette includes a shell and a mouthpiece. The external wall of the shell has an air inlet. An electronic circuit board, a normal pressure cavity, a sensor, a vapor-liquid separator, an atomizer, a liquid-supplying bottle are sequentially provided within the shell, wherein the electronic circuit board comprises an electronic switching circuit and a high frequency generator. A stream passage of the sensor is provided on one side of the sensor, and a negative pressure cavity is provided in the sensor. The atomizer and the liquid-supplying bottle is in contact with each other. An atomization cavity is arranged in the atomizer. A retaining ring for locking the liquid-supplying bottle is provided between one side of the liquid-supplying bottle and the shell, and an aerosol passage is provided on the other side of the liquid-supplying bottle. The air inlet, normal pressure cavity, vapor-liquid separator, atomizer, aerosol passage, gas vent and mouthpiece are sequentially interconnected. The advantages of the present invention include smoking without tar, significantly reducing the cancerogenic risk. Furthermore, users still feel as if they are smoking and experiencing the same excitement, and the cigarette is no need to be lit and is no fire risk.
Owner:FONTEM VENTURES

Composition and methods for treatment of neurological disorders and neurodegenerative diseases

It has been discovered that the stimulation of beta-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta-adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, forskolin, or nicotine ditartrate is inhibited by immunosuppressants or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.
Owner:MASSACHUSETTS INST OF TECH

Compositions and methods for treatment of neurological disorders and neurodegenerative diseases

It has been discovered that the stimulation of beta -adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta -adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta -adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta -adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, forskolin, or nicotine ditartrate is inhibited by immunosuppressants or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.
Owner:MASSACHUSETTS INST OF TECH
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