Introduction Phototherapy, the therapeutic application of light in the treatment of diseases has evolved over thousands of years from its origins in Asia. The earliest understanding that photonic energy in visible light could be harnessed through the presence of a photoreactive substance to promote a biological effect in an oxygenated tissue is attributed to the work of Professor von Tappeiner on xanthene derivatives, first published in 1900 (1). This work led to the realization that the destructive skin lesions observed in porphyrias could be attributable to a photodynamic effect.
Evidence suggests that γ‐aminobutyric acid (GABA) and its receptors are present in the peripheral nervous system. We have now investigated the effect of GABA and related substances on non‐adrenergic, non‐cholinergic (NANC) neurally‐evoked bronchoconstriction in the anaesthetised guinea‐pig. Bilateral vagal stimulation (5 V, 5 ms, 3 or 5 Hz) for 30 s, after propranolol (1 mg kg −1 i.v.) and atropine (1 mg kg −1 i.v.) evoked a NANC bronchoconstrictor response manifest as a mean tracheal pressure rise of 21.9 ± 1.04 cmH 2 O ( n = 70). The bronchoconstrictor response was reproducible for any given animal. GABA (10 μg‐10 mg kg −1 i.v.) did not alter basal tracheal pressure but reduced the NANC bronchoconstrictor response to vagal stimulation in a dose‐dependent manner (ED 50 = 186 μg kg −1 with a maximal inhibition of 74 ± 3.4% at 10 mg kg −1 ). Neither the opioid antagonist naloxone (1 mg kg −1 i.v.) nor the α‐adrenoceptor antagonist phentolamine (2.5 mg kg −1 i.v.) had any significant effect on the inhibitory response produced by GABA (500 μg kg −1 ). GABA‐induced inhibition was not antagonised by the GABA A ‐antagonist bicuculline (2 mg kg −1 i.v.). The GABA B ‐agonist baclofen (10 μg‐3 mg kg −1 i.v.) caused a dose‐dependent inhibition of the NANC response (ED 50 = 100 μg kg −1 with a maximal inhibition of 35.5 ± 2.8% at 3 mg kg −1 ). The GABA A ‐agonist, 4,5,6,7‐tetrahydroisoxazolo[5,4‐C] pyridin‐3‐ol (THIP), also inhibited the NANC bronchoconstrictor response. However, the dose of THIP required for this effect was high (3 mg kg −1 ) and the effect (< 10% inhibition) was small. Substance P (SP; 5 μg kg −1 or 25 μg kg −1 ), produced a bronchoconstrictor response equivalent to that produced by NANC vagal stimulation. This response was significantly increased by injection of GABA. Baclofen had no significant effect on responses evoked by exogenous SP. We conclude that GABA inhibits the release of transmitter from NANC nerves via an action at GABA B receptors and that GABA might play a role in the regulation of neurogenic responses in the airways.
Aluminum alloys are being increasingly used in a wide range of construction applications owing to their sound mechanical properties, lightness in weight, strong corrosion resistance, ability to be formed into complex and efficient cross-sectional shapes, and natural aesthetics. Aluminum alloys are characterized by a rounded stress–strain response, with no sharply defined yield point. Such behavior can be accurately represented using Ramberg–Osgood-type equations. In the present study, use of a two-stage Ramberg–Osgood model to describe the full-range stress–strain behavior of aluminum alloys is proposed and, following careful analysis of a comprehensive database of aluminum alloy coupon test data assembled from the literature, standardized values or predictive expressions for the required input parameters are derived. The experimental database includes over 700 engineering stress–strain curves obtained from 56 sources and covers five common aluminum alloy grades: 5052-H36, 6061-T6, 6063-T5, 6082-T6, and 7A04-T6. The developed model is shown to be more accurate in predicting the full-range stress–strain response of aluminum alloys than existing expressions, and is suitable for use in the analytical modeling, numerical simulation, and advanced design of aluminum alloy structures.
◆ The autonomic nervous system of the gut, or the enteric nervous system (ENS), acts to a large degree independently of the rest of the autonomic nervous system.
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