A single-blind, placebo-controlled trial of a simple acupuncture treatment in the cessation of smoking.
BACKGROUND: Tobacco smoking is a major cause of preventable disease and premature death. Physicians should play an active role in the control of smoking by encouraging cessation and helping the smoker to choose the most suitable aid to cessation. AIM: To evaluate a simple, ear acupuncture treatment for the cessation of smoking. METHOD: Randomized, single-blind, placebo-controlled trial of 78 currently smoking volunteers from the general public. Volunteers attended an acupuncture clinic in a general practice setting and were given a single treatment of electroacupuncture using two needles at either an active or a placebo site plus self-retained ear seeds for two weeks. The major outcome measure was biochemically validated total cessation of smoking at six months. RESULTS: A total of 12.5% of the active treatment group compared with 0% of the placebo group ceased smoking at six months (P = 0.055, 95% confidence interval -0.033 to 0.323). CONCLUSION: This simple ear electroacupuncture treatment was significantly more effective in helping volunteers to quit smoking than placebo treatment. (+info)
Townes-Brocks syndrome (TBS) is an autosomal dominant disorder with multiple malformations and variable expression. Major findings include external ear anomalies, hearing loss, preaxial polydactyly and triphalangeal thumbs, imperforate anus, and renal malformations. Most patients with Townes-Brocks syndrome have normal intelligence, although mental retardation has been noted in a few. (+info)
Precontraction with elevated concentrations of extracellular potassium enables both 5-HT1B and 5-HT2A "silent" receptors in rabbit ear artery.
The present study was conducted to determine the effect of a small (<10%) K+-induced precontraction on the response to vasoconstrictors in the rabbit aorta and ear artery rings. In both tissues, 15 mM K+ shifted the methoxamine concentration response curve (CRC) approximately 2.4-fold to the left. There was no change in the sensitivity of the control and amplified CRCs to the alpha1 adrenoceptor antagonist prazosin (100 nM). In the aorta, the CRC for serotonin was shifted 4.5-fold to the left in the presence of 15 mM K+, and both the control and amplified CRCs were antagonized equally by the 5-HT2A antagonist ketanserin (10 nM). In contrast, 16 and 20 mM K+ caused up to an approximately 60-fold leftward shift of the serotonin CRC in the rabbit ear artery. This effect of 16 mM K+ was not altered by mechanical removal of the endothelium or by in vitro denervation using 6-hydroxydopamine. The K+-amplified CRC was insensitive to 100 nM prazosin at serotonin concentrations below 3 microM, but was significantly antagonized by 10 nM ketanserin, suggesting that 5-HT2A receptors are involved in the K+-amplified response. The 5-HT1B-selective antagonist, GR 127935, did not affect control responses to serotonin, but significantly blocked the K+-amplified response. Furthermore, the combination of ketanserin and GR 127935 produced a significantly greater blockade of the amplified response than either antagonist alone, supporting the conclusion that both 5-HT2A and 5-HT1B receptors mediate the K+-amplified response to serotonin in the rabbit ear artery. (+info)
Clinical characteristics of CHARGE syndrome.
CHARGE syndrome, first described by Pagon, was named for its six major clinical features. They are: coloboma of the eye, heart defects, atresia of the choanae, retarded growth and development including CNS anomalies, genital hypoplasia and/or urinary tract anomalies, and ear anomalies and/or hearing loss. We experienced three cases of CHARGE syndrome who displayed ocular coloboma, heart defects, retarded growth and development, and external ear anomalies, and we also review the previously reported literature concerning CHARGE syndrome. (+info)
Experimental infusion phlebitis: tolerance pH of peripheral vein.
This study aims to determine the pH that peripheral veins can tolerate. Intravenous nutrient solutions with different pHs (from 4.52 to 6.71) were infused into rabbit ear veins, and the veins were examined histopathologically. After 6-hr infusion at 10 mL/kg/hr, a commercial 2.72% amino acid/7.5% glucose solution with electrolytes (AG) caused obvious phlebitic changes, such as loss of venous endothelial cells, inflammatory cell infiltration, and perivascular edema, in all 6 rabbits because of its low pH (4.52) and high titratable acidity (22 mEq/L). The phlebitis was reduced when the solution was neutralized with NaOH to pH 5.93, and was almost eliminated when the pH was neutralized to 6.49. After 8-hr infusion at 15 mL/kg/hr, AG-adjusted pH to 6.30 caused slight phlebitic changes, but AG-adjusted pH to 6.71 scarcely caused any change. Furthermore, 24-hr infusion of the pH 6.49 solution caused no histopathological changes in 3 rabbits. These results suggest that the tolerance pH for the peripheral vein is about 6.5, and that an infusion solution does not cause phlebitis due to acidity if the pH is not lower than the tolerance pH. (+info)
A study of NPY-mediated contractions of the porcine isolated ear artery.
Enhanced contractions of the porcine isolated ear artery by the alpha2-adrenoceptor agonist UK14304 are uncovered by pharmacological manipulation. As both neuropeptide Y (NPY) receptors and alpha2-adrenoceptors are negatively-coupled to adenylyl cyclase in this tissue, we determined whether NPY is also able to produce an enhanced contraction in the same tissue, under the same conditions. NPY (0.1 microM) produced a small contraction of porcine isolated ear arteries which was 5.1+/-0.8% of the response to 60 mM KCl (n = 14). An enhanced NPY response was uncovered if the tissue was pre-contracted with 0.1 microM U46619, and relaxed back to baseline with 1-2 microM forskolin before the addition of NPY (49.8+/-5.3%, n = 14). Forskolin (1 microM) stimulated cyclic AMP accumulation in porcine ear artery segments in the presence of 0.1 microM U46619 and 1 mM isobutylmethylxanthine (IBMX), NPY (0.1 microM) inhibited this response by 40%, but had no effect on basal levels of cyclic AMP. An enhanced response to 0.1 microM NPY was also obtained after pre-contraction with 0.1 microM U46619 and relaxation with either SNP (28.9+/-5.7%, n = 14), or dibutyryl cyclic AMP (21.2+/-4.6%, n = 14). This indicates that at least part of the enhanced response to NPY is independent of the agonist's ability to inhibit adenylyl cyclase. In conclusion, an enhanced contraction to NPY in the porcine isolated ear artery can be obtained by prior pharmacological manipulation. The enhanced responses are mediated through adenylyl cyclase-dependent and independent pathways similar to those reported for alpha2-adrenoceptors in this preparation. (+info)
Nickel allergy in mice: enhanced sensitization capacity of nickel at higher oxidation states.
Attempts to induce contact hypersensitivity to nickel in mice using, e.g., Ni(II)Cl2 often failed. Here, we report that sensitization was achieved by injecting Ni(II)Cl2 in combination with either CFA or an irritant, such as SDS and PMA, or IL-12, or by administering nickel at higher oxidation states, i.e., Ni(III) and Ni(IV). Although Ni(II), given alone, was ineffective in T cell priming, it sufficed for eliciting recall responses in vivo and in vitro, suggesting that Ni(II) is able to provide an effective signal 1 for T cell activation, but is unable to provide an adequate signal 2 for priming. Immunization of mice with nickel-binding proteins pretreated with Ni(IV), but not with Ni(II), allowed them to generate nickel-specific CD4+ T cell hybridomas. Ni(II) sufficed for restimulation of T cell hybridomas; in this and other aspects as well, the hybridomas resembled the nickel-specific human T cell clones reported in the literature. Interestingly, restimulation of hybridomas did not require the original Ni(IV)-protein complex used for priming, suggesting either that the nickel ions underwent ligand exchange toward unknown self proteins or peptides or that nickel recognition by the TCR is carrier-independent. In conclusion, we found that Ni(III) and Ni(IV), but not Ni(II) alone, were able to sensitize naive T cells. Since both Ni(III) and Ni(IV) can be generated from Ni(II) by reactive oxygen species, released during inflammation, our findings might explain why in humans nickel contact dermatitis develops much more readily in irritated than in normal skin. (+info)
Leukotriene B4 receptor transgenic mice reveal novel protective roles for lipoxins and aspirin-triggered lipoxins in reperfusion.
Polymorphonuclear neutrophil (PMN) activation is pivotal in acute inflammation and injury from reperfusion. To elucidate components controlling PMNs in vivo, we prepared novel transgenic mice with the human leukotriene (LT) B4 receptor (BLTR) for functional characterization. Overexpression of BLTR in leukocytes dramatically increased PMN trafficking to skin microabscesses and lungs after ischemia-reperfusion, whereas mice deficient in 5-lipoxygenase (5-LO) showed diminished PMN accumulation in reperfused lungs. Hence, both BLTR expression and LT biosynthesis are critical for PMN infiltration in reperfusion-initiated second-organ injury. Also, in BLTR transgenic mice, 5-LO expression and product formation were selectively increased in exudates, demonstrating that receptor overexpression amplifies proinflammatory circuits. Endogenous lipoxin (LX) A4 was produced in ischemic lungs and elevated by reperfusion. Because LXA4 and aspirin-triggered 15-epimeric LXA4 (ATL) selectively regulate leukocyte responses, they were tested in BLTR transgenic mice. Despite excessive PMN recruitment in BLTR transgenic mice, intravenous injection of ATL sharply diminished reperfusion-initiated PMN trafficking to remote organs, and topical application of LX was protective in acute dermal inflammation. These results demonstrate a direct role for BLTR with positive feedback, involving BLTR and 5-LO signaling in controlling PMNs. Moreover, LXA4 and ATL counter BLTR-amplified networks, revealing a novel protective role for LX and ATL in stress responses that has applications in perioperative medicine. (+info)