Effect of melatonin in the prevention of post-operative adhesion formation in a rat uterine horn adhesion model

BACKGROUND: Our main aim was to investigate the effects of melatonin (ME), possibly the most powerful free-radical scavenger, on the prevention of i.p. adhesion formation in rat uterine horn. Our secondary aim was to determine whether different methods of administration of ME were beneficial. METHODS: Animals were randomly assigned into seven groups, each consisting of 13 rats. Measured serosal injury was created using a standard technique. While control and two sham groups were not given ME, two of the remaining four groups were given a single dose of 10 mg/kg (2 mg) of ME i.p. immediately after injury and 30 min prior to injury respectively. In the two other groups, ME treatment was continued daily for 5 days. All animals were killed 2 weeks after surgery and adhesions were determined and scored by a examiner blinded to the test. RESULTS: The extent, severity and total scores of adhesion were found to be significantly reduced in all of the ME treatment groups when compared with control and sham groups. There were no statistically significant differences between the treatment groups. CONCLUSIONS: This study showed that even single dose ME therapy was effective in the prevention of post- operative i.p. adhesion formation.     

Inhibition of chemokines prevents intraperitoneal adhesions in mice

BACKGROUND: The present study evaluates the efficacy of a broad-spectrumchemokine inhibitor, NR58-3.14.3, in the prevention of adhesionformation after i.p. surgery in mice. METHODS: A total of 110eight week old female Balb/c mice underwent laparotomy. Fortyanimals were randomly assigned to receive daily i.p. injectionsof either vehicle (control) or NR58-3.14.3. Time-course of adhesionformation was assessed. A titration of NR58-3.14.3 was conductedfor i.p. and s.c. administrations. The effectiveness of a singleintra-operative dose of NR58-3.14.3 was evaluated. Number, extent,location and type of adhesions were recorded. Immunohistochemistryof adhesions was done with leukocyte common antigen, CD45. RESULTS:Adhesion scores peaked on post-operative days 6–8. Onboth days 6 and 8, there were smaller adhesion size and lowercumulative adhesion scores in NR58-3.14.3-treated group. Moreover,on day 8, there were significantly fewer adhesions in NR58-3.14.3-treatedgroup compared to controls. The least effective dose for i.p.administration of NR58-3.14.3 was 0.45 mg/animal. Subcutaneousand single intra-operative i.p. administrations were also effectivein the prevention of i.p. adhesions. Although NR58-3.14.3 decreasedthe number of CD45⁺ inflammatory cells in the adhesions by 22.5%compared to control group, this was not significant. CONCLUSIONS:Our results show that this broad-spectrum chemokine inhibitorprevents post-operative adhesions in mice and may have a potentialclinical use.     

Noninvasive Measurement of Acceleration at the Knee Joint in Patients with Rheumatoid Arthritis and Spondyloarthropathy of the Knee

Spondyloarthropathy represents a group of joint diseases with a tendency to reactive new bone formation. Spondyloarthropathy includes Reiter's syndrome, ankylosing spondylitis, and the arthropathy of inflammatory diseases (ulcerative colitis and Crohn's disease). Usually, an extensive investigation is required to distinguish spondyloarthropathy of the knee joint from rheumatoid arthritis. Recently, Reddy et al. (Ann. Biomed. Eng. 23:78–84, 1995) have developed the accelerometry technique to characterize various types of arthritis. The question remains if noninvasive acceleration measurements can be used to distinguish between spondyloarthropathy and rheumatoid arthritis. An ultraminiature accelerometer was placed on the patella, and the subject was asked to rhythmically rotate the knee from 90 flexion to full extension. Results have shown that the mean power of acceleration signal in the range of 100–500 Hz is significantly different (p < 0.05) for spondyloarthropathy patients when compared to rheumatoid arthritis patients. The noninvasive accelerometry technique represents a potential tool for characterization of spondyloarthropathy patients. © 2001 Biomedical Engineering Society. PAC01: 8719St, 8719Xx, 0630Gv     

螺旋血泵的CFD分析

溶血和血栓是目前国内心室辅助装置不能应用于临床的主要原因。血泵的不良血液动力学特性是导致溶血和血栓的主要因数。计算流体力学（CFD）方法目前被广泛应用于血泵设计,它可以准确有效地反映血泵内部流场状态、血泵压力流量曲线以及血泵内部流场剪切力分布状态等。本研究采用CFD方法对自制螺旋血泵的泵腔、出入流口进行流场分析,内部流场采用三维彩图显示。结果显示CFD分析结果很好的与体外实验结果吻合。血泵血液动力学特性,以及内部血流状态采用CFD方法分析,可以有效地分析血泵血液相溶性方面的问题。     

Desensitization of acetylcholine induced inositol 1,4,5-trisphosphate formation in neuroblastoma SH-SY5Y cells following repetitive acetylcholine stimulations

In this study, the desensitization of acetylcholine-induced inositol 1,4,5-trisphosphate [I(1,4,5)P₃] formation, upon short-time prestimulations, was investigated in cultures of human neuroblastoma SH-SY5Y cells. Four repeated stimulations for 10 seconds with 10 μM acetylcholine were necessary to induce a desensitization of the I(1,4,5)P₃ formation. The desensitization was observed 4 hours after the initiation of repetitive stimulations. The same effect was obtained by a single prestimulation with 1 mM acetylcholine. Preincubation of the cells with phorbol 12-myristate 13-acetate (PMA) markedly down-regulated the acetylcholine-induced I(1,4,5)P₃ formation. However, the protein kinase C (PKC) inhibitors H7 and staurosporine did not influence the desensitization induced by four repeated stimulations with 20 μM acetylcholine. These results indicate that the signal transduction can be desensitized following repeated stimulations with sub-maximal concentrations of receptor agonist and although activation of PKC can induce the same down-regulation, PKC is most likely not involved in the desensitization induced by repetitive acetylcholine-stimulations.     

Parabrachial neuron discharge in the cat is altered during the carbachol-induced REM sleep-like state (DCarb)

Pontine parabrachial neurons have been suggested to play a regulatory role in both respiratory and sleep cycle control. Encouraged by the finding that microinjections of the cholinergic agonist carbachol into the medial pontine reticular formation (mPRF) of the cat produced respiratory changes paralleling those observed during rapid eye movement (REM) sleep (Neurosci. Lett., 102 (1989) 211–216), this study tested the hypothesis that cholinergic mechanisms in the mPRF can also cause state-dependent changes in the discharge of parabrachial neurons. This paper describes extracellular recordings of parabrachial neurons during REM sleep and during the carbachol-induced REM sleep-like state (DCarb). Cells which were activated (REM-on) or inactivated (REM-off) during REM maintained these same state-dependent firing patterns during the DCarb state. These results support the hypothesis that cholinergic mechanisms in the mPRF can cause state-dependent changes in the discharge of parabrachial neurons.     

A quantitative study of the brainstem cholinergic projections to the ventral part of the oral pontine reticular nucleus (REM sleep induction site) in the cat

The ventral part of the cat oral pontine reticular nucleus (vRPO) is the site in which microinjections of small dose and volume of cholinergic agonists produce long-lasting rapid eye movement sleep with short latency. The present study determined the precise location and proportions of the cholinergic brainstem neuronal population that projects to the vRPO using a double-labeling method that combines the neuronal tracer horseradish peroxidase–wheat germ agglutinin with choline acetyltransferase immunocytochemistry in cats. Our results show that 88.9% of the double-labeled neurons in the brainstem were located, noticeably bilaterally, in the cholinergic structures of the pontine tegmentum. These neurons occupied not only the pedunculopontine and laterodorsal tegmental nuclei, which have been described to project to other pontine tegmentum structures, but also the locus ceruleus complex principally the locus ceruleus and peri-, and the parabrachial nuclei. Most double-labeled neurons were found in the pedunculopontine tegmental nucleus and locus ceruleus complex and, much less abundantly, in the laterodorsal tegmental nucleus and the parabrachial nuclei. The proportions of these neurons among all choline acetyltransferase positive neurons within each structure were highest in the locus ceruleus complex, followed in descending order by the pedunculopontine and laterodorsal tegmental nuclei and then, the parabrachial nuclei. The remaining 11.1% of double-labeled neurons were found bilaterally in other cholinergic brainstem structures: around the oculomotor, facial and masticatory nuclei, the caudal pontine tegmentum and the praepositus hypoglossi nucleus. The disperse origins of the cholinergic neurons projecting to the vRPO, in addition to the abundant noncholinergic afferents to this nucleus may indicate that cholinergic stimulation is not the only or even the most decisive event in the generation of REM sleep.     

中药赤芍对球囊损伤术后血管重构的干预研究

目的 观察中药赤芍防止球囊损伤术后血管重构作用。方法 新西兰白兔随机分为对照组、单纯高脂组、赤芍高剂量组、低剂量组。高脂喂养6周建立动脉粥样硬化模型,行颈动脉球囊损伤术,8周时取材作病理形态学检查。结果(1)与高脂组比较,赤芍高、低剂量组增生内膜面积、中层面积,内膜、中膜、外膜PCNA阳性着色均显著减少(P<0.05或P<0.01)。(2)各组内皮增生成分主要为平滑肌细胞;巨噬细胞阳性着色主要分布在外膜,与高脂组比较,赤芍高、低剂量组阳性着色较少。(3)高脂组动脉损伤侧外膜Ⅰ型胶原增多,赤芍组Ⅰ型胶原增加较少。结论 赤芍对高脂喂养兔颈动脉球囊损伤术后血管重构有显著防止作用。     

Ultrastructure of the neuroglial fatty metamorphosis (virchow) in the perinatal period

Summary The ultrastructure of neuroglial fatty metamorphosis (GFM) has been investigated in the telencephalic white matter of 12 premature and mature infants (gestational age 22–40 weeks; survival 0–96 days). GFM was found in all cases apart from a 22-week-old fetus, and involves predominantly astrocytic cells (68.8%), then glioblasts (43.5%), but only 7.4% of oligodendrocytes. GFM, therefore, seems to be independent of the myelination process and indicates the vulnerability of the immature neuroglial population in the metabolic and circulatory disorders of the perinatal period. Since GFM is found in almost all children dying within the early postnatal period, this subtle alteration reflects a special form of minimal brain damage. The relationship between GFM, astrocytic hypertrophy and periventricular leucomalacia and their role in the telencephalic leucoencephalopathy are discussed.

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Zusammenfassung Die Gliazellverfettung im unreifen Großhirn-Marklager wurde bei 12 Kindern ultrastrukturell untersucht (Gestationsalter 22–40 Wochen; Überlebenszeit 0–96 Tage). Die fettige Metamorphose der Neuroglia (Virchow) fand sich in allen Fällen, ausgenommen den 22 Wochen alten Feten, und betrifft vorwiegend junge Astrozyten (68,8%), ferner zu 43,5% unreife Vorstufen, jedoch nur zu 7.4% die (z.Z. der Geburt erst in Erscheinung tretende) Oligodendroglia. Die Fett-Metamorphose der unreifen Glia stellt einen sensiblen Indikator für metabolisch-zirkulatorische Störungen der Perinatalperiode dar und erfolgt unabhängig von dem Prozeß der Markscheidenbildung. Zusammen mit einer oft auffälligen Astroglia-Proliferation ist die intracytoplasmatische Akkumulation nicht membrangebundener Lipide Ausdruck einer temporären Differenzierungsstörung der unreifen Neuroglia. Die resultierende Reifungsdissoziation mit Unterdrückung der oligodendrozytären Zellinie führt zur retardierten Markscheidenbildung und dem Bild der telencephalen Leucoencephalopathie.

     

The role of COX-2 in angiogenesis and rheumatoid arthritis

Recent evidence suggests that cyclooxygenase (COX)-2 is a mediator of angiogenesis, and COX-2 activity is known to be upregulated in the rheumatoid arthritis (RA) synovium. We examined whether mediation of angiogenesis by COX-2 was occuring in cells of the RA synovium and in microvascular endothelial cells (ECs) that are similar to those found in the RA synovium. We demonstrate that rofecoxib, a selective COX-2 inhibitor, acts directly on human dermal microvascular ECs (HMVECs) to inhibit their chemotactic and tube forming ability. Likewise, pretreatment of HMVECs with rofecoxib significantly inhibited their ability to form tubes induced by conditioned media (CM) of activated RA synovial fibroblasts. When RA synovial fibroblasts were pretreated with rofecoxib for 16 h and then stimulated with interleukin (IL)-1beta, their CM induced significantly less HMVEC tube formation when compared with CM from vehicle-treated RA synovial fibroblasts. ELISAs performed on activated RA fibroblast CM for known proangiogenic factors demonstrated a significant reduction in bFGF, in addition to the expected decrease in PGE(2). Our studies suggest that COX-2-induced angiogenic activity is an active mechanism within diseased synovium and may provide an additional rationale for the use of COX-2 inhibitors in RA.