Deletion of AcMNPV AC16 and AC17 results in delayed viral gene expression in budded virus infected cells but not transfected cells

This study investigated the combined function of the Autographa californica multiple nucleopolyhedrovirus overlapping genes ac16 (BV/ODV-E26, DA26) and ac17. Ac17 is a late gene and the promoter is within the ac16 open reading frame. A double ac16-ac17 knockout virus was generated to assess the function of each gene independently or together. Loss of ac17 did not affect viral DNA synthesis but budded virus (BV) production was reduced. Deletion of both ac16-ac17 resulted in reduced viral DNA synthesis and a further reduction in BV production. In BV infected Sf9 cells, viral gene expression was delayed up to 12 h in the absence of both AC16 and AC17 but not if either gene was present. Cells infected by transfecting viral DNA, by-passing the BV particle, exhibited no delay in gene expression from the double knockout virus. AC16 and AC17 are therefore required for rapid viral gene expression in cells infected by BV.     

间接失活术对儿童牙科畏惧症的预防作用

目的观察间接失活术对儿童牙科畏惧症的预防作用。方法186例患儿采用间接失活术,两个对照组分别186例患儿采用常规无痛法,疗效对比。结果引起牙科畏惧症者为3.22%,对照组分别为51.61%和58.06%,卡方检验,均P〈0.01。结论间接失活术对由医源性因素引起的儿童牙科畏惧症有一定的预防作用,值得临床加以推广。     

Modulation of dendritic release of dopamine by metabotropic glutamate receptors in rat substantia nigra

A superfusion system was used to study the effects of metabotropic glutamate receptor (mGluR) ligands upon the release of [(3)H]dopamine ([(3)H]DA) previously taken up by rat substantia nigra (SN) slices. trans-(+/-)-1-Amino-(1S,3R)-cyclopentane dicarboxylic acid (trans-ACPD; 100 and 600 microM), a group I and II mGluR agonist, evoked the release of [(3)H]DA from nigral slices. This last effect was reduced significantly by (2S,3S,4S)-2-methyl-2-(carboxycyclopropyl)-glycine (MCCG; 300 microM), an antagonist of group II mGluR, or by the addition of tetrodotoxin (D-APV; 1 microM) to the superfusion medium. D-(-)-2-Amino-5-phosphono-valeric acid (100 microM), an N-methyl-D-aspartate receptor antagonist, or the presence of Mg(2+) (1.2mM) in the superfusion medium did not modify trans-ACPD-induced [(3)H]DA release. In addition, a group II mGluR agonist such as (2S,1'R,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)-glycine (DCG-IV; 100 microM) significantly induced the release of [(3)H]DA from nigral slices, whereas a group I mGluR agonist such as (RS)-3,5-dihydroxyphenylglycine (DHPG; 50 and 100 microM) did not modify the release of the [(3)H]-amine. Further experiments showed that the NMDA (100 microM)-evoked release of [(3)H]DA was decreased significantly by prior exposure of SN slices to trans-ACPD. Finally, partial denervation of the DA nigro-striatal pathway with 6-hydroxydopamine (6-OH-DA) increased trans-ACPD-induced release of [(3)H]DA, whereas it decreased trans-ACPD inhibitory effects on NMDA-evoked release of [(3)H]DA from nigral slices. The present results suggest that the dendritic release of DA in the SN is regulated by mGluR activation. Such nigral mGluR activation may produce opposite effects upon basal and NMDA-evoked release of DA in the SN. In addition, such mGluR-induced effects in the SN are modified in response to partial denervation of the DA nigro-striatal pathway.     

牙科焦虑症患者治疗中医患关系的研究

牙科焦虑症(dental anxiety;DA),又称牙科恐惧症(dental fear;DF)是牙科患者在口腔治疗中的一种心理障碍.近年来DA在国内外逐渐成流行趋势,严重影响着国内外口腔患者的身心健康和生活质量.本文就DA治疗中的医患关系作一探讨.     

Sulpiride increases and dopamine decreases intracranial temperature in rats when injected in the lateral hypothalamus: an animal model for the neuroleptic malignant syndrome?

Sulpiride in the perifornical lateral hypothalamus (pfLH) (4, 8 and 16 μg/ 0.5 μl) increased intracranial temperature (Tic). The hyperthermia started immediately after the injection, peaked 30 min later and lasted for more than 90 min. Sulpiride (12 μg) accelerated recovery from hypothermia in anesthetized animals. Forty-five min after sulpiride Tic raised 1.17±0.06°C. After a control injection the raise was only 0.5±0.13°C. Locally applied dopamine (DA) (5, 10 and 20 μg) 5 min before sulpiride (12 μg) attenuated sulpiride hyperthermia. The largest DA dose reduced Tic (−1.21°C) when administered alone. These findings suggest the existence of D2 receptors in the LH involved in thermoregulation. Chances are that D2 receptors in the human LH could be responsible for the neuroleptic malignant syndrome (NMS), and that sulpiride injections in the rat LH could be used as a model for the study of the pathogenesis of this syndrome.     

The influence of haloperidol and aminooxyacetic acid on etonitazene, alcohol, diazepam and barbital consumption

Four groups of rats were given free choice between water and solutions of either 3 micrograms/ml etonitazene, 5% ethanol (v/v), 0.1 mg/ml diazepam or 3 mg/ml barbital for 10-14 days. With the exception of barbital, some rats spontaneously preferred the drug solutions to water. This preference was reduced by addition of 7 micrograms/ml haolperidol. In a forced drug fluid consumption procedure, the daily administration of 15 mg/kg i.p. of the gamma-aminobutyric acid (GABA)-transaminase blocker aminooxyacetic acid (AOAA) led to a reduction of ethanol and diazepam intake, but not of etonitazene and barbital. It is suggested that the diminished consumption of ethanol and diazepam as caused by GABA-T-inhibition may also be mediated by dopamine which seems to act indirectly, via benzodiazepine receptors and GABA neurons.     

Electrical axis and voltage criteria on left ventricular hypertrophy.

The voltage criteria of left ventricular hypertrophy were studied in 229 hypertensive patients undergoing treatment and 62 patients who were not treated. The limb-lead voltage criterion (R Lead aVL greater than or equal 11 mm.) was found more frequently in patients with radiographic evidence of cardiomegaly than other voltage criteria. This may have been due to a more negative axis in patients with cardiomegaly than in patients without cardiomegaly. It is possible that dilatation of the left ventricle to the left and posteriorly accentuates limb-lead criteria at the expense of V-lead criteria. Left anterior hemiblock occured in less than 10 per cent of the hypertensive patients. In 10 out of 16 patients with left anterior hemiblock, the hemiblock disappeared after treatment of the hypertension for 4 years whereas all five hemiblocks in untreated hypertensives persisted. Development of left anterior hemiblock subsequently occurred in only one patient with treatment and one without treatment over a 4-year period.     

Effects of priming stimulation of catecholamine containing nuclei in rat brain on runway performance

Rats were implanted with bipolar fine wire stimulating electrodes in the region of the pontine nucleus locus coerulus (LC) and the pars compacta of the substantia nigra (SN). The reinforcing properties of stimulation of each electrode were determined. Subsequently, rats were run in a two alley runway and the effects of priming stimulation on performance in acquisition, discrimination and reversals were measured. It was found that LC priming caused an increased latency to exit from start box. Also, LC priming reduced running time in the rewarded alley in a reversal task whereas SN priming affected both performance in the rewarded and non-rewarded alley.     

The 4-O-methyl metabolites of catecholamines. Homo-iso-vanillin acid in rat urine and brain; urinary iso-vanyl compounds after intraperitoneal administration of dopamine and of dopamine precursors and derivatives

Homo-iso-vanillic acid (3-hydroxy, 4-methoxyphenylacetic acid, iso-HVA was detected in rat urine and brain, with a molar ratio of iso-HVA to HVA of 0·07 in urine and about 0·35 in brain. The free urinary iso-vanyl and vanyl phenolcarboxylic acids were studied after intraperitoneal loads with the following compounds: l-dopa, $\text{l}\text{-3-O-}\text{methyldopa}\text{,}\text{l}\text{-4-O-}\text{methyldopa}$, dopamine, 3-O-methyldopamine, 4-O-methyldopamine and 3,4-dihydroxyphenylacetic acid. The results suggest the following conclusions. (1) The molar ratio iso-HVA/HVA is not constant. After dopa as well as dopamine loads it rises with the increase of the dose of precursor administered, showing that, in vivo, the 4-O-methylation process depends, to some extent, on the substrate concentration. (2) In contrast with the other catechols (dopamine and 3,4-dihydroxyphenylacetic acid), l-dopa itself does not seem to be para-O-methylated. It is therefore unlikely that 4-O-methyldopa would be a metabolite of l-dopa in vivo. (3) Distinct urinary metabolites from $\text{l}\text{-3-O-}\text{methyldopa}$ (vanylmandelic and vanillic acids) on one hand and from l-4-O-methyldopa (unknown iso-vanyl phenolcarboxylic acid) on the other, support evidence that some of the metabolic transformations of the side-chain of the O-methyl-catecholamines are different according to whether the methyl group is bound on the meta or on the para position. (4) The high level of cerebral iso-HVA might be due to either a lower iso-HVA than HVA transport outside the brain, or to the existence, in addition to the dopamine source, of a second cerebral metabolic pathway for the production of iso-HVA.