健胃愈疡颗粒对消化性溃疡大鼠胃黏膜PS2和PAF表达的影响

目的研究健胃愈疡颗粒对溃疡的影响，并探讨其机制。方法以Okabe改良法复制大鼠实验性胃溃疡，观察其对溃疡指数和胃黏膜血流的影响，并用RT—PCR观察乳癌相关肽PS2和血小板活化因子（PAF）表达的变化。结果健胃愈疡颗粒能提高PS2mRNA和下调PAFmRNA的表达，明显降低溃疡指数，促进溃疡愈合。结论健胃愈疡颗粒可通过提高PS2mRNA和下调PAFmRNA的表达，通过影响胃黏膜疏水性，加强黏液凝胶层稳定性，从而防止溃疡的产生和复发，这可能是其促进溃疡愈合的机制之一。     

秋水仙素诱导的神经元突起溃变对Aβ分泌的影响

目的研究秋水仙素诱导的体外培养新生小鼠大脑皮层神经元突起溃变对β-淀粉样蛋白(amyloid beta-protein,Aβ)分泌的影响,并初步探讨其可能的机制。方法体外无血清培养新生小鼠大脑皮层神经元,采用NSE免疫细胞化学染色法进行神经元鉴定,选择培养4d的神经元进行实验;通过细胞形态学观察和四唑盐(MTT)比色实验,筛选和确定秋水仙素(colchicine)合适的造模浓度;用ELISA法检测秋水仙素组和溶媒对照组Aβ在不同时间点的分泌量;用RT-PCR测定β淀粉样前体蛋白(APP)、早老素1(PS1)和β位点APP内切酶(BACE)基因的表达。结果细胞形态学观察结果表明,终浓度为0.5mg·L-1的秋水仙素作用4h后,神经元突起明显缩短而胞体形态无变化,同时MTT比色实验测得其吸光度与对照组比差异无显著性,胞体活性没有受到明显影响。ELISA法实验结果表明,神经元突起溃变后,Aβ分泌量在4、8h时升高,与溶媒对照组相比差异有显著性。RT-PCR法表明,APP、PS1和BACE mRNA在4、8h时的表达量较溶媒对照组增加,差异有显著性。结论秋水仙素诱导的神经元突起溃变可增加Aβ分泌,其可能与增加APP,PS1和BACE基因表达有关。     

白芍总甙对大白鼠睡眠节律的影响

白芍总甙(TGP)每日ig 50mg·kg~(-1),连续7d可延长正常大鼠慢波睡眠(SWS)的持续时间.并能使咖啡因(12.5 mg·kg~(-1),ip)诱导的失眠大鼠睡眠各参数恢复到接近正常水平。TGP 50mg·kg~(-1)×3d)还可明显延长游泳大鼠(水温25±1℃.游泳时间30min)SWS和异相睡眠的总时间。上述实验结果提示TGP可改善不同功能状态下的大鼠睡眠。     

Dendritic arborization and axon trajectory of neurons in the hypothalamic arcuate nucleus of the rat--updated

Neurons in the hypothalamic arcuate nucleus (arcuate neurons) were traced on Golgi-impregnated sections. Dendrites of arcuate neurons showed characteristic orientation patterns. Dendrites along the lateral side follow the convex border of the nucleus by running parallel to the tanycyte processes. Neurons located in the ventrolateral portion of the nucleus have dendrites running parallel to the basal surface of the hypothalamus. Fine, beaded axons of arcuate neurons project mostly ventrally, and less frequently dorsally and dorsolaterally. Ventrally projecting axons converge towards the tuberoinfundibular sulcus which emerges into the ventral portion of the arcuate nucleus from below.     

Evaluation of postoperative exocrine pancreatic function using chymotrypsin labile peptide

The assessment of exocrine pancreatic function by the oral administration of a chymotrypsin labile peptide N-benzoyl-L-tyrosyl-p-aminobenzoic acid (BT-PABA) has proved to be an easy and reliable test of exocrine pancreatic function. It has the additional advantage that it can be used to study exocrine pancreatic function in all operative cases, even after gastrointestinal reconstruction. The recovery of p-aminobenzoic acid (PABA) correlates significantly with parameters of the PZ/CCK secretin (PS) test. Following Billroth II gastrectomy, the recovery of PABA decreased to 39.8±3.2% to weeks after and to 45.4±4.5% one to two months after operation, significantly lower than the 80.6±3.4% in normal subjects. In cases of cancer of the head of the pancreas, the exocrine function was 44.0±3.7%, and decreased to 17.5±3.0% after total pancreatectomy. Thus, BT-PABA enables a pertinent evaluation of pancreatic function in postoperative patients with various types of gastrointestinal reconstruction and also in cases when the PS test cannot be feasibly used.     

Measurement of the severity of natural smooth surface (interproximal) caries lesions with polarization sensitive optical coherence tomography

BACKGROUND AND OBJECTIVES: Previous studies have demonstrated that polarization sensitive optical coherence tomography (PS-OCT) can be used to image early dental caries. The purpose of this study was to compare the measured reflectivity of natural caries lesions found on smooth surfaces (interproximal lesions) with the mineral loss measured using digital microradiography (DM) in order to determine if PS-OCT can be used as a non-destructive method to measure the severity of dental decay and resolve the internal structure of caries lesions. MATERIALS AND METHODS: A PS-OCT system operating at 1,310 nm was used to acquire polarization resolved images of natural white spot lesions and pigmented lesions on the smooth surfaces of extracted teeth. The integrated reflectivity from lesion areas was compared to polarized light microscopic images (PLM) and to the integrated mineral loss from the same lesion area measured using high resolution DM. RESULTS: The frequently complex internal structure of caries lesions could be resolved with PS-OCT. Such structural information is potentially useful for determining whether or not the lesion is active and progressing or whether it has become arrested and remineralized and does not require intervention. There was a strong correlation between the integrated mineral loss of the caries lesions measured using DM and the integrated reflectivity in the perpendicular polarization axis of the PS-OCT system. CONCLUSIONS: The integrated reflectivity in the perpendicular polarization channel can be used to represent the severity of demineralization in natural early caries lesions. Therefore, PS-OCT has considerable potential as a non-destructive clinical probe of early caries lesions to assess their severity, monitor their progression over-time and potentially assess lesion activity.     

Systematically applied chemicals that damage lung tissue

A large, and increasing number of drugs and chemicals have been found which are toxic to lung following systemic administration. These agents damage lung tissue specifically, or in addition to damage to other tissues. Mechanisms explaining the pulmonary damage produced by some lung toxins have been uncovered. These include concentration of the agent within lung, the absence of adequate pulmonary detoxication systems, and bioactivation to a toxic species within specific lung cells or at distant sites followed by transport to the lung. The basic biochemical lesions underlying lung damage, responses of individual lung cells and pulmonary repair processes to the toxic agent, and species and age differences in susceptibility to lung damage have not, however, been well defined for most lung toxins. This review describes the information available on pulmonary biochemical and pathological changes associated with some of these lung-toxic agents. In addition, mechanisms proposed to explain the lung damage are discussed. The agents covered include: paraquat, the thioureas, butylated hydroxytoluene, the trialkylphosphorothioates, various lung-toxic furans and antineoplastic agents, the pyrrolizidine alkaloids, metals and organometallic compounds, amphiphilic agents, hydrocarbons, oleic acid, 3-methylindole, and diabetogenic agents. Detailed reviews on the overall toxicity of many of these agents have been published elsewhere. This review concentrates on their pulmonary toxicity. Information is presented as an overview to illustrate both the extensive literature that is available and the important questions that remain to be answered about systemic chemicals that damage lung tissue.     

Pancreatic enzyme therapy and clinical outcomes in patients with cystic fibrosis

OBJECTIVE: To assess the relationship between pancreatic enzyme therapy (PET) and the clinical outcomes of growth, abdominal pain, constipation, gassiness, and number of stools in cystic fibrosis (CF). STUDY DESIGN: Patients (n = 1215) >4 weeks of age from 33 Cystic Fibrosis Foundation accredited sites who had a sweat chloride >60 mmol/L or two CF-causing mutations were enrolled using a proportionate sampling strategy in a nonblinded study. Patients submitted a stool sample and completed a questionnaire. The study coordinator also completed a questionnaire for each patient. Enzyme dosing and growth, abdominal pain, gassiness, constipation, and number of stools were compared. RESULTS: Of the 1215 enrolled patients, 1131 (93.1%) were prescribed PET. Only 14.9% had pancreatic function assessed before enrolling in this study. Stool elastase-1 analysis identified 1074 (89%) patients as pancreatic insufficient (PI). There was no association between PET and the outcomes: growth, abdominal pain, gassiness, constipation, and number of stools. CONCLUSION: PET dose is not correlated with growth or gastrointestinal symptoms. More sensitive outcome measures of the effectiveness of PET in patients with CF are needed to guide treatment of PI.     

Microinjection of neostigmine into the pontine reticular formation of the mouse: further evaluation of a proposed REM sleep enhancement technique

Microinjections of cholinergic agonists into the pontine reticular formation (PRF) powerfully induce rapid eye movement sleep (REMS) in cats but have comparatively weaker effects in rats. Recently, the cholinomimetic neostigmine has been reported to strongly enhance REMS following microinjection into the PRF of the mouse. That study used behavioral assessments of locomotion in lieu of electrophysiological measures of muscle tone to identify REMS. We sought to confirm that the behavioral state induced in mice by PRF injections of neostigmine meets standard electroencephalogram (EEG) and electromyogram (EMG) criteria for defining REMS. Cortical EEG, nuchal muscle EMG, and PGO waves were recorded from male C57BL/6N mice with chronic indwelling cannulae for the delivery of neostigmine to the PRF. Recordings were made during midday following injections of neostigmine (8.8 mM, 50 nl), 2 h after lights on (LD 12:12). Neostigmine induced a behavioral state characterized by low amplitude, highly desynchronized cortical EEG with little theta, no PGO waves, and a sustained high muscle tone. Behavioral states meeting standard criteria for slow-wave sleep (SWS) and REMS were significantly suppressed compared to baseline recordings, and REMS onset was delayed by 3 h. Consistent with earlier reports, neostigmine did strongly suppress locomotor activity in open field tests and in the home cage. Due to the failure to meet criteria for defining REMS, we conclude that neostigmine microinjection into the PRF of the mouse induces an abnormal waking state rather than REMS.     

Characterization of two novel mutations of the antithrombin gene observed in Japanese thrombophilic patients

We investigated the molecular basis of reduced functional levels of antithrombin (AT) in two individuals suffering from thromboembolic events. In each case direct sequencing of amplified DNA revealed 13,260-13,262 del in one patient and 2511C>A in the other patient, predicting a heterozygous E381del and P16H, respectively. Both patients had no 20210A allele and factor V Leiden mutation. To understand the molecular mechanism responsible for antithrombin deficiency, stable expression experiments were performed using HEK293 cells transfected with the expression vector containing the wild-type or the mutated recombinant cDNA. In these experiments, the media levels of the two mutated antithrombins were the same as that of wild type, but the specific activity of the E381del mutant decreased significantly compared with that of wild type. These results showed that the E381del mutation was responsible for type II deficiency, whereas the other mutation, P16H, did not produce any definite abnormality which could contribute to antithrombin deficiency.