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Steven H.S. Lin

Researcher at University of California, Irvine

Publications -  9
Citations -  997

Steven H.S. Lin is an academic researcher from University of California, Irvine. The author has contributed to research in topics: Neuropeptide & Prolactin-releasing hormone. The author has an hindex of 9, co-authored 9 publications receiving 940 citations.

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Neuropeptide S: A Neuropeptide Promoting Arousal and Anxiolytic-like Effects

TL;DR: It is reported that a neuropeptide, NPS, potently modulates wakefulness and could also regulate anxiety, and it is shown that the LC region encompasses distinct nuclei expressing different arousal-promoting neurotransmitters.
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Novel neurotransmitters as natural ligands of orphan G-protein-coupled receptors

TL;DR: The "orphan" G-protein-coupled receptors (GPCRs) are cloned GPCRs that bind unknown ligands that act as transmitter molecules and have already enriched the understanding of various brain functions.
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Relative contribution of acromioclavicular joint capsule and coracoclavicular ligaments to acromioclavicular stability

TL;DR: The AC joint capsule is a robust anatomical structure that contributes significantly to the AC joint stability, especially in the AP plane, and repair of theAC joint capsule, in addition to the customarily repaired CC ligaments, appears to have a beneficial effect.
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Orphan G protein-coupled receptors: targets for new therapeutic interventions.

TL;DR: The search for the natural primary messengers of orphan GPCRs are reviewed and two recently deorphanized GPCR systems, the melanin‐concentrating hormone (MCH) and prolactin‐releasing peptide (PrRP) systems are focused on to illustrate the strategies applied to solve their function and to exemplify the therapeutic potentials that such systems hold.
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Differential expression of the thyrostimulin subunits, glycoprotein α2 and β5 in the rat pituitary

TL;DR: The cloned rat GPA2 and GPB5, reconstituted the heterodimers in vitro, and confirmed that rat thyrostimulin activates TSHR with an affinity similar to that of TSH confirmed the system as being functionally different to the TSH system.