Asbestos disease risk communication conducted by the New Jersey department of health

Since October 1985, the New Jersey Department of Health (NJDOH) has required hospitals to report all patients with a discharge diagnosis of asbestosis. As follow-up to a needs assessment survey of these patients, the NJDOH developed an educational packet including an information bulletin titled “Asbestos Disease: Medical and Legal Facts for Employees” and a pre-stamped postcard evaluation survey. The packet was sent to 1,418 patients reported by hospitals; 433 patients returned the evaluation questionnaire. The survey assessed attitudinal responses (were the materials helpful and easy to understand?) and behavioral responses (did the respondent plan on discussing the materials with a doctor or lawyer?) to the information in the packet. Of the postcard respondents, 85% found the materials helpful, and approximately half indicated that they would discuss the materials with a doctor or lawyer. Of the 33% who were proxy respondents, half appeared not to have understood that the materials had relevance to them as family members. Modifications to the protocol for the asbestos disease educational packet were made based on the evaluation data. Limitations of the evaluation survey and the value of process evaluations in risk communication projects are discussed. © 1993 Wiley-Liss, Inc.     

内皮超极化因子的研究进展

内皮超极化因子（EDHF）是由内皮释放的NO和PGI_2以外的另一种舒张因子,它通过使平滑肌细胞膜超极化而舒张血管,是内皮依赖性血管松驰的第3种重要机制。EDHF可能是花生四烯酸的细胞色素P450代谢产物EET-s,乙酰胆碱、缓激肽等激动剂作用于内皮细胞,使细胞内游离钙浓度升高,合成和（或）释放EDHF,作用于平滑肌细胞膜,激活钙依赖性钾通道,使细胞膜超极化,抑制电压依赖性钙通道的开放,引起血管松弛。在大血管中NO-cGMP松弛机制可能占主导地位,并且抑制EDHF生成;而在阻力小血管,EDHF则可能是引起血管松弛的主要因素。     

Similarities between the relaxations induced by vasoactive intestinal peptide and by stimulation of the non-adrenergic non-cholinergic neurons in the rat stomach

Summary The characteristics of the non-adrenergic, noncholinergic inhibitory response of the rat stomach fundus to transmural nerve stimulation were compared with the relaxation induced by vasoactive intestinal polypeptide (VIP). Treatment with -chymotrypsin (5 U/ml) or VIP antiserum (1:200) significantly reduced the relaxation induced by transmural nerve stimulation at 30 Hz, indicating that the possible transmitter in the non-adrenergic, non-cholinergic nerves is a peptide and may be VIP or a closely related peptide. VIP was able to relax, fully and dose-dependently, the stomach fundus that had previously been constricted by treatment with 10^–6 M serotonin, and the IC₅₀ value for VIP was 2.4 × 10^–9 M. VIP elevated levels of cyclic AMP in a dose-dependent manner and the EC₅₀ value was 2.8 × 10^–9 M in the presence of 10^–6 M atropine and 10^–6 M guanethidine. The stomach fundus was relaxed by transmural nerve stimulation (30 Hz, 50 mA) and transmural nerve stimulation also caused production of cyclic AMP in the rat stomach in the presence of atropine and guanethidine. The basal level of cyclic AMP in the stomach was 8.7 ± 0.26 pmole/mg protein. When transmural nerve stimulation was applied for 5 min, the contraction of the stomach, induced by 10^–6 M serotonin, was inhibited by 54% in the presence of atropine and guanethidine and the level of cyclic AMP was increased to 13.0 ± 0.73 pmol/mg protein. Apamin inhibited the transmural nerve stimulation-induced relaxation and shifted the dose-response curve for VIP to the right. These results suggest that one of the putative neurotransmitter from non-adrenergic, non-cholinergic nerves in the rat stomach is VIP and that VIP-induced relaxation may be mediated by the production of cyclic AMP and by the opening of apamin-sensitive K⁺-channels.Send offprint requests to K. Kamata at the above address     

Differential potentiation by calcium antagonists of neuromuscular blockade induced by pancuronium and succinylcholine in cats in vivo

Summary The effects of several calcium antagonists (verapamil, nicardipine and two diltiazem isomers, d-cis and l-cis diltiazem) alone and associated to non-depolarizing (pancuronium) and depolarizing (succinylcholine) neuromuscular blockers, were evaluated on sciatic nerve-tibialis anterior muscle preparations from cats in vivo. The calcium antagonists used (at 0.1 and 0.5mg/kg iv) did not modify the height of muscular twitches elicited indirectly. However, these agents potentiated in a dose-dependent way the neuromuscular blockade induced by iv pancuronium (2–40g/kg) and succinylcholine (6–200g/kg). The order of potency in increasing the effects of pancuronium was nicardipine d-cis diltiazem verapamil, whereas the order of potency in enhancing succinylcholine effects was d-cis diltiazem verapamil nicardipine. The effects of diltiazem were stereoselective, thus the potentiation induced by d-cis diltiazem was significantly greater in all cases than that induced by l-cis diltiazem, which suggests that calcium channel blockade plays a role in these interactions. However, other mechanisms such as calcium antagonists-induced nicotinic receptor desensitization may also be involved.     

The Drosophila Mutant tetanic Interacts with a Gene Complex Including the Structural Locus of K+ Channels and Shows Altered Dephosphorylation and Learning

The tetanic (tta; X.-52.6) mutation has been isolated on the basis of its sensitivity to extradoses of the normal Shaker gene complex (ShC) where the K+ channel la is encoded. The mutant shows up to threefold elevation of the membrane bound protein phosphatase type 1 (PP1) activity in body extracts, probably due to reduced levels of the PP1 specific inhibitor 2 (I-2). By contrast, PP1 activity in the head is only half of the normal value. In addition, tta fails to perform normally in a negative reinforcement olfactory paradigm. The functional relationships between phosphorylation, K+ currents, phosphatase activity and modulation of synaptic activity during learning and memory are discussed in the light of their possible genetic links.     

Synthetic peptides corresponding to the sequence of noxiustoxin indicate that the active site of this K+ channel blocker is located on its amino-terminal portion

Summary A nonapeptide Thr-Ile-Ile-Asn-Val-Lys-Cys-Thr-Ser (NTX_1–9) and a decapeptide Met-Asn-Gly-Lys-Cys-Lys-Cys-Tyr-Asn-Asn (NTX_30–39) corresponding to the N-terminal and C-terminal sequences respectively of Noxiustoxin (NTX) were synthesized by the solid phase method of Merrifield (1963). The first synthetic peptide (NTX_1–9) was shown to be toxic to mice independently of the route of administration: intraperitoneally, subcutaneously or intraventricularly (100–200 g/20 g mouse weight). The second (NTX_30–39) was not toxic even at higher dose (400 g/20 g mouse). When the effects of the peptide NTX_1–9 and of the authentic toxin (Noxiustoxin) were studied on the liberation of [³H] 4-aminobutyric acid (³H-GABA) from mouse synaptosomes, both gave essentially the same results, except that peptide NTX_1–9 was needed at higher concentration. Synthetic peptide NTX_30–39 had no effect in the same preparation at even higher doses. The GABA release produced by toxic peptide NTX_1–9 was not affected by tetrodotoxin but was completely abolished by the presence of the K⁺ ionophore valinomycin, mimicking the effect of native NTX in the same system (Sitges et al., 1986). These results indicate that the toxic active site of Noxiustoxin is possibly located in or near the N-terminal amino acid portion of the molecule.Abbreviations used BOC amino acids ter-butyloxycarbonyl-amino acids - BOC amino acid-PAM-resin ter-butyloxycarbonyl-aminoacyl-4-(oxymethyl)-phenacetamidomethyl-resin - GABA 4 aminobutyric acid - HPLC high performance liquid chromatography - MSA mouse serum albumin - NTX Noxiustoxin - NTX _(numbers) synthetic peptides with amino acid sequences of NTX at position start (first number) to position end (second number) of the sequence according to Fig. 1 - TTX tetrodotoxin Supported in part by the Mexican Council of Science and Technology (CONACyT), grants PVT/QF/NAL/84/2182, PVT/AI/NAL/85/3029 to L.D.P.; PCSACNA 022640 to A.B. A patent request claiming rights on the use of synthetic NTX and related peptides was presented in Washington, DC (U.S.A.), Serial number 07/132,169, filing date December 14, 1987.     

Cardiovascular effects of endothelin 1 in pithed spontaneously hypertensive rats: evaluation of its mechanism(s) of action

Summary The present experiments were carried out to investigate the cardiovascular effects of endothelin 1 (ET) in pithed spontaneously hypertensive (SH) rats and to evaluate its mechanism of action. The results show that ET (0.1 – 3 nmol/kg i.v.) is a powerful vasoconstrictor agent in the pithed rat. However, at a dose of 3 nmol/kg i.v. all the pithed animals died following a gradual decrease in mean arterial blood pressure and pulse pressure and changes in the form of the electrocardiogram (ECG). The predominant feature of the change in the ECG was a progressive decrease in the amplitude of the T wave resulting in a depression of the curve representing repolarization. Investigations in isolated perfused SH rat hearts showed that ET powerfully reduces coronary flow concentration-dependently (IC₅₀ 2.1 ±0.3 nM) an effect associated with sinus bradycardia and a decrease in coronary pressure amplitude. No overt ECG changes were seen. Control experiments with mechanical flow restriction suggest that bradycardia is a consequence of reduced coronary flow and that the ECG changes observed in vivo can be explained on the basis of coronary insufficiency and resulting myocardial hypoxia. Vasoconstrictor responses to angiotensin II (0.4 g/kg i.v.), phenylephrine (8 g/kg i.v.) and ET (0.5 nmol/kg i.v.) were antagonised by around 70% by isradipine (0.03 mg/kg i.a.). The results suggest that endothelin-induced vasoconstriction may involve receptor operated channel activation and opening of voltage sensitive Ca²⁺ channels.Send offprint requests to A. K. Mir at the above address     

Inhibitory effect of amiloride and gadolinium on fine afferent nerves in the rat knee: evidence of mechanogated ion channels in joints

Synovial joints are complex sensory organs which provide continuous feedback regarding position sense and degree of limb movement. The transduction mechanisms which convert mechanical forces acting on the joint into an electrochemical signal which can then be transmitted to the central nervous system are not well understood. The present investigation examined the effect of the mechanogated ion channel blockers amiloride and gadolinium on knee joint mechanosensitivity. In deeply anaesthetised rats (sodium thiopental: 100–120 mg/kg, i.p.), single unit extracellular recordings were made from knee joint group III (Aδ) and group IV (C) primary afferents in response to mechanical rotation of the joint. Afferent firing rate was measured before and after topical application of either amiloride (0.1 mM, 1 mM) or gadolinium (250 μM) onto the receptive field of the sensory unit and recording was continued every 10 min up to a total of 50 min. With normal rotation of the knee, joint mechanosensitivity was significantly reduced by both amiloride (P<0.0001; n=10–21) and gadolinium (P=0.001; n=12) and this effect was sustained throughout the recording period. This investigation provides the first in vivo electrophysiological evidence that joint mechanotransduction involves the activation of amiloride and gadolinium-sensitive mechanogated ion channels. Future studies to determine the mechanogated ion channel subtypes present in joints and the modulation of their gating properties during inflammation may yield novel approaches for the control of arthritis pain. Funding: JJMcD is funded by the Alberta Heritage Foundation for Medical Research, the Canadian Institutes for Health Research, and the Arthritis Society of Canada.     

经络综合导引治疗仪的研制

经络综合导引治疗仪是根据祖国医学的经络学说和养气功理论，应用呼气启动导引，视觉模型提示和穴位电刺激的多因素共同作用，导引气血沿经络运行。主要用于强化瘫痪肢体的康复。该治疗仪以单片微机为程控中心，通过硬件设计和软件开发，实现了呼气触发，视觉提示和位电刺激同步发，１６和电极依次选通和数字化幅度调节等多种功能。     

Effect of papaverine on tone and contractions of the depolarized smooth muscle of the guinea pig taenia coli

Experiments were carried out on isolated strips of guinea pig taenia coli. The smooth muscle was depolarized in a solution with high potassium concentration (120 mM KCl). The effect of papaverine (in concentrations of 10^–5 to 3.10^–5 g/ml) on the tone and off-response to a prolonged and strong hyperpolarizing current was investigated on the denervated muscle. Papaverine was found: 1) to abolish contractile responses to application of histamine, bradykinin, and acetylcholine; 2) to reduce the tone of the depolarized muscle and abolish the effect of an increase in the Ca⁺⁺ concentration in the external medium on muscle tone; 3) to have no effect on the amplitude and velocity of the ascending phase of the off-response; 4) to accelerate the descending phase of the off-response. The following hypotheses are put forward to explain the result: 1) in the cell membrane there are chemically excitable calcium channels which are blocked by papaverine; 2) in the membrane there are calcium leakage channels responsible for the maintenance of tone and blocked by papaverine; 3) papaverine has negligible effect on electrically excitable calcium channels.A. V. Vishnevskii Institute of Surgery, Academy of Medical Sciences of the USSR, Moscow. Bio-Inorganic Chemicals BIKhS Research Institute, Kupavna, Moscow Region. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Fedorov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 85, No. 2, pp. 177–180, February, 1978.