Doctor Channels MacGyver to Help Asthmatic Toddler Aboard Transatlantic Flight – ABC News

Doctor Channels MacGyver to Help Asthmatic Toddler Aboard Transatlantic Flight
ABC News
A New York doctor became a hero in the skies recently when he turned into a medical MacGyver by creating a device that helped an asthmatic toddler struggling to breathe during a transatlantic flight. Dr. Khurshid Guru, director of Robotic Surgery at

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Parents Should Suck Kid’s Pacifiers To Prevent Asthma, Rashes – Study – CHANNELS


CHANNELS

Parents Should Suck Kid's Pacifiers To Prevent Asthma, Rashes – Study
CHANNELS
Toddlers are less likely to have asthma and itchy rashes if their parents “cleaned” their pacifiers by sucking on them when the kids were infants, a small new study suggests. The findings don't prove that technique protects kids against asthma, eczema
Sucking Your Child's Pacifier Clean May Have BenefitsNew York Times (blog)
Bathing Binky in Spit May Curb Baby's Allergy Risk – MedPage TodayMedPage Today
Parents' Saliva On Pacifiers Could Ward Off Baby's Allergies – for KUHFKUHF-FM
dailyRx
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Molecular expression and functional role of canonical transient receptor potential channels in airway smooth muscle cells.

Molecular expression and functional role of canonical transient receptor potential channels in airway smooth muscle cells.

Adv Exp Med Biol. 2011;704:731-47

Authors: Wang YX, Zheng YM

Multiple canonical or classic transient receptor potential (TRPC) molecules are expressed in animal and human airway smooth muscle cells (SMCs). TRPC3, but not TRPC1, is a major molecular component of native non-selective cation channels (NSCCs) to contribute to the resting [Ca(2+)](i) and muscarinic increase in [Ca(2+)](i) in freshly isolated airway SMCs. TRPC3-encoded NSCCs are significantly increased in expression and activity in airway SMCs from ovalbumin-sensitized/challenged “asthmatic” mice, whereas TRPC1-encoded channel activity, but not its expression, is largely augmented. The upregulated TRPC3- and TRPC1-encoded NSCC activity both mediate “asthmatic” membrane depolarization in airway SMCs. Supportively, tumor necrosis factor-? (TNF?), an important asthma mediator, increases TRPC3 expression, and TRPC3 gene silencing inhibits TNF?-mediated augmentation of acetylcholine-evoked increase in [Ca(2+)](i) in passaged airway SMCs. In contrast, TRPC6 gene silencing has no effect on 1-oleoyl-2-acetyl-sn-glycerol (OAG)-evoked increase in [Ca(2+)](i) in primary isolated cells. These findings provide compelling information indicating that TRPC3-encoded NSCCs are important for physiological and pathological cellular responses in airway SMCs. However, continual studies are necessary to further determine whether, which, and how TRPC-encoded channels are involved in cellular responses in normal and diseased (e.g., asthmatic) airway SMCs.

PMID: 21290324 [PubMed – in process]

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