78 research outputs found
Projection neurons in lamina III of the rat spinal cord are selectively innervated by local dynorphin-containing excitatory neurons
Large projection neurons in lamina III of the rat spinal cord that express the neurokinin 1 receptor are densely innervated by peptidergic primary afferent nociceptors and more sparsely by low-threshold myelinated afferents. However, we know little about their input from other glutamatergic neurons. Here we show that these cells receive numerous contacts from nonprimary boutons that express the vesicular glutamate transporter 2 (VGLUT2), and form asymmetrical synapses on their dendrites and cell bodies. These synapses are significantly smaller than those formed by peptidergic afferents, but provide a substantial proportion of the glutamatergic synapses that the cells receive (over a third of those in laminae I–II and half of those in deeper laminae). Surprisingly, although the dynorphin precursor preprodynorphin (PPD) was only present in 4–7% of VGLUT2 boutons in laminae I–IV, it was found in 58% of the VGLUT2 boutons that contacted these cells. This indicates a highly selective targeting of the lamina III projection cells by glutamatergic neurons that express PPD, and these are likely to correspond to local neurons (interneurons and possibly projection cells). Since many PPD-expressing dorsal horn neurons respond to noxious stimulation, this suggests that the lamina III projection cells receive powerful monosynaptic and polysynaptic nociceptive input. Excitatory interneurons in the dorsal horn have been shown to possess IA currents, which limit their excitability and can underlie a form of activity-dependent intrinsic plasticity. It is therefore likely that polysynaptic inputs to the lamina III projection neurons are recruited during the development of chronic pain states
Correlation between Tp-Te Interval and Myocardial Blush Grade Value in Anterior ST Elevation Myocardial Infarction Patient
Background: Clinical manifestations of coronary herat disease (CHD) may be an ST-Elevation Myocardial Infarction (STEMI). In STEMI condition, there is a metabolic disorder and ion exchange disturbance which causes dispersion of transmural repolarization, as well as micro coronary circulation disturbance involving mechanism of microvascular dysfunction. The Tp-Te interval is an electrocardiogram paramener that could be described as the transmural dispersion of repolarization. Assessment of Myocardial Blush Grade (MBG) is a coronary angiography densitometry method that can be used to assess microvascular dysfunction. This study aims to examine the correlation between Tp-Te interval and MBG in anterior STEMI.Methods: The research desgin is cross sectional. Data were taken consecutive from August to November 2017. The Tp-Te interval assessment was performed on the basis of an electrocardiogram record from the subjects. The MBG value assessment was performed using a Quantitative Blush Evaluator (QuBE) computer program based on coronary angiography. The Tp-Te interval is divided into 2 groups: Tp-Te interval > 94 ms and Tp-Te interval ≤ 94 ms. The MBG values are divided into 3 groups: MBG QuBE 1, MBG QuBE 2 and MBG QuBE 3. The assessment of Tp-Te interval and MBG value was performed by observer in intra-observer which were acknowledged based on Kappa and blindness conformity test results against patient clinical data. Pearson correlation test was used to analyze the correlation between Tp-Te interval and MBG value, while logistic regression test was used for multivariate test.Results: Of the total 32 study subjects, there were 23 subjects with Tp-Te interval >94 ms and 9 subjects with Tp-Te interval ≤94 ms. There was a negative correlationwith moderate strength between the Tp-Te interval and the MBG value in the anterior STEMI patients (r =-0.501, p =0.004). There was a prevalence ratio of 4.304 between Tp-Te interval >94 milliseconds against MBG QuBE 1 (95%CI: 1.264-14.658, p <0.001). Multivariate tests showed Tp-Te intervals consistently as independent risk factors for MBG values in subjects with anterior STEMI.Conclusion: There is a negative correlation with moderate strength between the Tp-Te interval and the MBG value in the anterior STEMI patients
Tumor necrosis factor-α-induced production of plasminogen activator inhibitor 1 and its regulation by pioglitazone and cerivastatin in a nonmalignant human hepatocyte cell line
金沢大学大学院医学系研究科環境社会医学Plasminogen activator inhibitor 1 (PAI-1) is an important mediator of atherosclerosis and liver fibrosis in insulin resistance. Circulating levels of PAI-1 are elevated in obese individuals, and PAI-1 messenger RNA is significantly higher in the livers of obese type 2 diabetic individuals than in nonobese type 2 diabetic individuals. To address the mechanism underlying the up-regulation of hepatic PAI-1 in obesity, we tested the effects of tumor necrosis factor α (TNF-α), an important link between obesity and insulin resistance, on PAI-1 production in the nonmalignant human hepatocyte cell line, THLE-5b. Incubation of THLE-5b cells with TNF-α stimulated PAI-1 production via protein kinase C-, mitogen-activated protein kinase-, protein tyrosine kinase-, and nuclear factor-κB-dependent pathways. A thiazolidinedione, pioglitazone, reduced TNF-α-induced PAI-1 production by 32%, via protein kinase C- and nuclear factor-κB-dependent pathways. The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor cerivastatin inhibited TNF-α-induced PAI-1 production by 59%, which was reversed by coincubation with mevalonic acid. In conclusion, obesity and TNF-α up-regulation of PAI-1 expression in human hepatocytes may contribute to the impairment of the fibrinolytic system, leading to the development of atherosclerosis and liver fibrosis in insulin-resistant individuals. A thiazolidinedione and a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor may thus be candidate drugs to inhibit obesity-associated hepatic PAI-1 production. © 200
ヨコハマカイコウジ ノ ニホンオオドオリ ノ ケイカン ニ タイスル 3Dモデリング ニ ヨル コウサツ
神奈川県横浜市の日本大通りは,横浜港開港時の都市計画や居留地の景観としての観点から,注目されるべき街路である。本研究では,当時の日本大通りを3DCGにて再現することにより,横浜居留地の特徴や街路整備を視覚的に表現することを目的とした。再現に際しては,日本大通りが所在する関内地区の概要や,日本大通りの整備概要等を調査し,調査内容に基づいて建築物や電柱,ガス灯,街路樹帯等の3Dモデリングを行った。その結果,当時の日本大通りにおける詳細の把握が可能となり,実際の距離感や,建物のスケール,また整備前後の印象の変化等を主観的に感じることが可能となった。これにより,1866年の大火災をきっかけに行われた整備が,日本大通りの景観等に対して及ぼした影響を把握することができたといえる。A street of "Nihon-Odori" at Yokohama-city has been receiving more attention from the view point of city planning soon after the opening of Yokohama port and landscape for a colony of foreign people. The Nihon-Odori, begun about 150 years ago, was recreated by using 3DCG, and features of the colony and the street improvement were expressed visually in this paper. In order to recreate the Nihon- Odori, the overview of Kan-nai region and the street improvement were researched, and 3D modeling for building, electric pole, gas lamp, street tree and so on was carried out. As a result, the details of landscape for the Nihon-Odori could be grasped visually, and the change of impression due to the street improvement could be confirmed
Dynorphin is expressed primarily by GABAergic neurons that contain galanin in the rat dorsal horn
Background
The opioid peptide dynorphin is expressed by certain neurons in the superficial dorsal horn of the spinal cord, but little is known about the types of cell that contain dynorphin. In this study, we have used an antibody against the dynorphin precursor preprodynorphin (PPD), to reveal the cell bodies and axons of dynorphin-expressing neurons in the rat spinal cord. The main aims were to estimate the proportion of neurons in each of laminae I-III that express dynorphin and to determine whether they are excitatory or inhibitory neurons.
Results
PPD-immunoreactive cells were concentrated in lamina I and the outer part of lamina II (IIo), where they constituted 17% and 8%, respectively, of all neurons. Around half of those in lamina I and 80% of those in lamina II were GABA-immunoreactive. We have previously identified four non-overlapping neurochemical populations of inhibitory interneurons in this region, defined by the presence of neuropeptide Y, galanin, parvalbumin and neuronal nitric oxide synthase. PPD co-localised extensively with galanin in both cell bodies and axons, but rarely or not at all with the other three markers. PPD was present in around 4% of GABAergic boutons (identified by the presence of the vesicular GABA transporter) in laminae I-II.
Conclusions
These results show that most dynorphin-expressing cells in the superficial dorsal horn are inhibitory interneurons, and that they largely correspond to the population that is defined by the presence of galanin. We estimate that dynorphin is present in ~32% of inhibitory interneurons in lamina I and 11% of those in lamina II. Since the proportion of GABAergic boutons that contain PPD in these laminae was considerably lower than this, our findings suggest that these neurons may generate relatively small axonal arborisations
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