Opiatergic mechanisms of the cardiotropic effect of acute cooling

Changes in myocardial contractility after an acute cold exposure following intracerebroventricular administration of opiate receptor agonists were studied in rat hearts isolated after Langendorff. Cold exposures were carried out individually for each animal in chambers at −10°C for 4 h. Thirty min before being exposed to cold the animals were administered in a brain ventricle 10 μl of μ- or δ-opiate receptor agonists (DAGO or DADLE, respectively). Isolation and perfusion of the hearts were performed directly after the cold exposure was over. The mechanism of reduction of myocardial contractility and coronary flow induced by an acute cold exposure is believed to include stimulation of μ-opiate receptors as one of its main components, and the effect of intracerebral hypertension on hemodynamic parameters is partially mediated through activation of δ-opiate receptors. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, N ^o 12, pp. 582–584, December, 1994 Presented by R. S. Karpov, Member of the Russian Academy of Medical Sciences     

虚拟咬合运动初步仿真模拟的研究与实现

我们试验了利用VR技术进行虚拟咬合仿真制作的全部过程。首先,采用光学三维测量仪对上下颌石膏模型进行数字化,通过预处理获取有效的三角网格曲面模型;其次,对咬合运动模型进行合理的简化,分解为一系列的平移运动和旋转运动;通过动态刷新完成开闭口运动、侧移运动的计算机运动仿真,可视化地观察咬合运动;然后利用模型碰撞检测算法动态地计算咬合接触位,并详细地分析了咬合接触时的咬合点位置分布和咬合剖切面上的咬合点接触关系;最后讨论了目前虚拟咬合仿真存在的问题和今后研究的方向。     

军团菌MOMPS基因的克隆并在原核系统中表达

以军团菌DNA为模板，PCR扩增获得军团菌主要外膜蛋白基因（Major outer membrane protein gene，ompS），与原核表达质粒pUC18定向重组，构建重组质粒，转化大肠杆菌BL21，并用限制性酶酶切分析、聚合酶链式反应、核酸序列分析、十二烷基磺酸钠-聚丙烯酰胺凝胶电泳、Western印迹进行鉴定。实验结果表明我们扩增出了军团菌914bp的ompS基因，成功构建了重组质粒pLPompS，并在原核系统中得到了表达。     

Expression pattern of growth/differentiation factor 3 in human and murine cerebral cortex, hippocampus as well as cerebellum

Growth/differentiation factor 3 is a member of GDF/BMP subfamily of the TGF-beta superfamily, which has been reported to be implicated in testis carcinoma and deposition of adipose tissue. Interestingly, present work indicated that GDF3/Gdf3 genes were expressed in cerebral cortex, hippocampus as well as in cerebellum, as revealed by RT-PCR, in situ hybridization and immunostaining. Results of RT-PCR in 10 human tissues and 12 rat tissues indicated that GDF3/Gdf3 genes were abundantly transcribed in both human and murine brain, including cerebral cortex, hippocampus and cerebellum. In situ hybridization and immunohistochemistry results revealed that in cerebral cortex, GDF3 was evenly distributed. In hippocampus, it was expressed in most of the neurons in CA2 and DG region, especially only in a restricted number of neurons in the regions of CA1 and CA3 and in Purkinje cells in cerebellum. Present data suggested that GDF3 might play important roles in the central nervous system (CNS), especially in cerebral cortex, hippocampus and cerebellum, and it shed new light on further research of GDF3 in the central nervous system.     

A type III secretion system is required for Aeromonas hydrophila AH-1 pathogenesis

Aeromonas hydrophila is a gram-negative opportunistic pathogen in fish and humans. Many bacterial pathogens of animals and plants have been shown to inject anti-host virulence determinants into the hosts via a type III secretion system (TTSS). Degenerate primers based on lcrD family genes that are present in every known TTSS allowed us to locate the TTSS gene cluster in A. hydrophila AH-1. A series of genome walking steps helped in the identification of 25 open reading frames that encode proteins homologous to those in TTSSs in other bacteria. PCR-based analysis showed the presence of lcrD homologs (ascV) in all of the 33 strains of A. hydrophila isolated from various sources. Insertional inactivation of two of the TTSS genes (aopB and aopD) led to decreased cytotoxicity in carp epithelial cells, increased phagocytosis, and reduced virulence in blue gourami. These results show that a TTSS is required for A. hydrophila pathogenesis. This is the first report of sequencing and characterization of TTSS gene clusters from A. hydrophila. The TTSS identified here may help in developing suitable vaccines as well as in further understanding of the pathogenesis of A. hydrophila.     

Elevated Levels of Matrix Metalloproteinase 9 and Tissue Inhibitor of Metalloproteinase 1 during the Acute Phase of Kawasaki Disease

Kawasaki disease (KD) is an acute, self-limiting, multisystem vasculitis of unknown etiology affecting infants and young children. Unless treated promptly with high-dose intravenous gamma globulin and aspirin, patients frequently develop coronary aneurysms. Previously, matrix metalloproteinase 9 (MMP-9), which is secreted complexed to tissue inhibitor of metalloproteinase 1 (TIMP-1), has been implicated in abdominal aortic aneurysm formation. Since the clinical and pathological features of KD include inflammation and weakening of blood vessels, we analyzed acute- and convalescent-phase paired plasma or serum samples from 31 KD patients, 7 patients who did not completely meet the criteria for KD, and 26 non-KD controls (9 febrile and 17 afebrile patients) for pro-MMP-9 (92 kDa) enzyme activity by gelatin zymography and for active MMP-9 (83 kDa), pro-MMP-9, and TIMP-1 protein levels by enzyme-linked immunosorbent assay. Statistical analysis was performed by using Student t tests, linear regression, and the Wilcoxon rank-sum test. Markedly elevated pro-MMP-9 enzymatic activity, pro-MMP-9 protein levels, and TIMP-1 protein levels were found during the acute phase of illness in patients with clinically established KD and in patients who were suspected of having KD but did not meet all of the criteria. There was no significant difference in active MMP-9 levels. Furthermore, pro-MMP-9 and TIMP-1 protein levels were significantly elevated among KD patients, compared to those of febrile and afebrile non-KD controls. The significantly elevated pro-MMP-9 enzyme and protein levels during the acute phase of KD may reflect vascular remodeling or an inflammatory response to a microbial agent, suggesting a pathophysiological role for MMP-9 in coronary aneurysm formation.     

Ras homolog gene family H (RhoH) deficiency induces psoriasis-like chronic dermatitis by promoting TH17 cell polarization

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Use of immunoblotting to detect Aspergillus fumigatus antigen in sera and urines of rats with experimental invasive aspergillosis.

Immunoblotting was used to detect Aspergillus fumigatus antigen in sera and urines of immunosuppressed rats experimentally infected with A. fumigatus. Organisms were administered by both intravenous and intratracheal injections. Intravenously infected rats developed disseminated aspergillosis, but intratracheally infected rats developed pulmonary disease only. Fungal cultures of blood and urine samples from infected rats were negative. In the urines of intravenously infected rats, antigen was detected 24 to 48 h after infection; in the urines of intratracheally infected animals, antigen was detected on days 4 to 5 after infection. Antigen in serum was detected later than antigen in urine was. Following sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting of serum and urine samples, the most strongly reacting antigenic materials were found in the 88-, 40-, 27-, and 20-kilodalton regions. These dominant antigens appeared to be the same as those of control antigens prepared from A. fumigatus grown in vitro. Rabbit antiserum to Aspergillus filtrate antigen was found to be more immunoreactive than antiserum to mycelial or conidial antigen. No mycelium-specific antigens were detected.     

Fos oncoprotein expression in the rat forebrain following muscimol-induced absence seizures

Fos oncoprotein expression is a marker of neuronal activation following seizures. Here, using this method we examined the anatomical locations of muscimol-induced absence seizures in the rat forebrain. Six hours after a systemic injection of muscimol a massive Fos immunoreactivity appeared in the olfactory system, retrosplenial cortex and paraventricular thalamic nucleus, whereas other cortical areas contained low level of Fos expression. These results provide the first functional morphological evidence suggesting that these forebrain structures with Fos expression may play an important role in the pathophysiology of muscimol-induced absence seizures.     

Regulation of 5-hydroxytryptamine-induced calcium mobilization by cAMP-elevating agents in cultured canine tracheal smooth muscle cells

The effects of increases in cellular adenosine 3′5′-cyclic monophosphate (cAMP) on 5-hydroxytryptamine-(5-HT-) induced generation of inositol phosphates (IPs) and increases in intracellular Ca²⁺ ([Ca²⁺]_i) were investigated using canine cultured tracheal smooth muscle cells (TSMCs). Cholera toxin and forskolin induced concentration- and time-dependent cAMP formation with half-maximal effects (−logEC₅₀) produced at concentrations of 7.0 ± 0.5 and 4.9 ± 0.4  respectively. Pretreatment of TSMCs with either forskolin or dibutyryl cAMP inhibited 5-HT-stimulated responses. Even after treatment for 24h, these agents still inhibited the 5-HT-induced Ca²⁺ mobilization. The inhibitory effects of these agents produced both depression of the maximal response and a shift to the right of the concentration response curves of 5-HT. The water-soluble forskolin analogue L-858051 [7-deacetyl-7β-(γ-N-methylpiperazino)-butyryl forskolin] significantly inhibited the 5-HT-stimulated accumulation of IPs. In contrast, the addition of 1,9-dideoxy forskolin, an inactive forskolin analogue, had little effect on this response. Moreover, SQ-22536 [9-(tetrahydro-2-furanyl)-9-H-purin-6-amine], an inhibitor of adenylate cyclase, and both H-89 [N-(2-aminoethyl)-5-isoquinolinesulphonamide] and HA-1004[N-(2-guanidinoethyl)-5-isoquinolinesulphonamide], inhibitors of cAMP-dependent protein kinase (PKA), attenuated the ability of forskolin to inhibit the 5-HT-stimulated accumulation of IPs. These results suggest that activation of cAMP/PKA was involved in these inhibitory effects of forskolin. The AlF₄ ⁻-induced accumulation of IPs was inhibited by forskolin, suggesting that G protein(s) are directly activated by AlF₄ ⁻- and uncoupled from phospholipase C by forskolin treatment. These results suggest that activation of cAMP/PKA might inhibit the 5-HT-stimulated phosphoinositide breakdown and consequently reduce the [Ca²⁺]_i increase or inhibit both responses independently. Received: 14 March 1996/Accepted: 10 April 1996