Trans-synaptically induced bursts in regular spiking non-pyramidal cells in deep layers of the cat motor cortex

In deep layers of the cat motor cortex, we have investigated the properties of neurons displaying trans-synaptically induced bursts. In in vivo experiments, extracellularly recorded burst neurons were separated into two subtypes based on their dependence on stimulation sites, the medullary pyramid or the ventrolateral (VL) thalamic nucleus, from which bursts of 10-20 spikes were triggered. The spike amplitude attenuation and frequency adaptation during a burst were more prominent in pyramid-dependent burst neurons than in VL-dependent burst neurons. Intracellular recordings in in vivo experiments revealed that pyramid-dependent bursts emerged from a long-lasting depolarization, while each spike during a VL-dependent burst was narrow in half-width and was followed by a fast AHP, similar to fast spiking neurons. In in vitro slice experiments, intracellular recordings were obtained from neurons that displayed a burst of attenuated spikes emerging from a long-lasting depolarization, and were also obtained from fast spiking neurons. They were morphologically recovered to be multipolar cells with sparsely spiny dendrites and local axonal networks, suggesting that they are inhibitory interneurons. The multipolar neurons displaying bursts of attenuated spikes may mediate the recurrent inhibition of pyramidal tract cells.     

Axonal cytoskeleton changes in experimental optic neuritis

Axonal loss and degeneration in multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE) have been suggested by brain imaging, pathological and axonal transport studies. Further elucidation of the processes and mechanisms of axonal degeneration in demyelinating diseases is therefore of potential importance in order to alleviate the permanent disabilities of MS patients. However, detailed studies in this area are impeded by the small number of reliable models in which the onset and location of demyelination can be well-controlled. In this study, microinjection of polyclonal rabbit anti-galactocerebroside (anti-Gal C) antibody and guinea pig complement was used to induce local demyelination in the rat optic nerve. We found that treatment with appropriate volumes of the antibody and complement could induce local demyelination with minimal pressure- or trauma-induced damage. Local changes in neurofilaments (NFs) and microtubules (MTs) were examined with both immunohistochemistry (IHC) and electron microscopy (EM). On day 1 after microinjection, we observed moderate NF and MT disassembly in the local demyelinated area, although in most cases, no apparent inflammatory cell infiltration was seen. The NF and MT changes became more apparent on days 3, 5, 7 after microinjection, along with gradually increased inflammatory cell infiltration. These results suggested that acute demyelination itself may induce local cytoskeleton changes in the demyelinated axons, and that the ensuing local inflammation may further enhance the axonal damage. When the lesions were stained with specific antibodies for T lymphocytes, macrophages, and astrocytes, we found that most of the cells were macrophages, suggesting that macrophages may play a greater role in inflammation-related axonal degeneration and axonal loss. These results were confirmed and further characterized on the ultrastructural level.     

D-amphetamine-induced depletion of energy and dopamine in the rat striatum is attenuated by nicotinamide pretreatment

The present study examined the effects of nicotinamide on the D-amphetamine (AMPH)-induced dopamine (DA) depletion and energy metabolism change in the rat striatum. In chronic studies, co-administration of AMPH with desipramine, a drug that retards the metabolism of AMPH, (10 mg/kg, intraperitoneal [i.p.], respectively) caused a significant decrease of striatal DA content measured 7 days later. Pretreatment with nicotinamide (500 mg/kg, i.p.), the precursor molecule for the electron carrier molecule nicotinamide adenine dinucleotide (NAD), attenuated this effect of AMPH, whereas itself exerted no long-term effect on striatal DA content. In acute studies, a decrease in striatal adenosine triphospate/adenosine diphosphate (ATP/ADP) ratio was found 3 h after co-injection of AMPH and desipramine. However, nicotinamide pretreatment blocked the reduced striatal ATP/ADP ratio and resulted in a striking increase in striatal NAD content in AMPH-treated rats. Furthermore, nicotinamide was noted to increase striatal ATP/ADP ratio and NAD content in saline-treated rats. These findings suggest that nicotinamide protects against AMPH-induced DAergic neurotoxicity in the striatum of rats via energy supplement.     

Hyperfibrinogenemia is an independent risk factor for atherosclerotic renal artery stenosis

It is important to identify patients at risk for atherosclerotic renal artery stenosis because renal artery stenosis is a progressive disease and a potentially correctable problem. To determine the risk factors for atherosclerotic renal artery stenosis, we performed renal arteriography at the time of cardiac catheterization in 270 patients (M:F, 193:77, mean age: 59 years) with clinical ischemic heart disease. Before the procedure, demographic data, medical history, physical findings and laboratory data were obtained. The degree of coronary artery stenosis and renal artery stenosis was quantified with automatic edge detection technique. Significant renal artery stenosis, defined as a narrowing of the diameter by more than 50%, was identified in 28 (10%) patients. Three patients (1%) had bilateral disease. Significant coronary artery disease, defined as a narrowing of the diameter by more than 50%, was present in 231 patients (85%). By univariate logistic regression analysis, older age (68 +/- 8 vs. 58 +/- 10 years), the presence of hypertension (61% vs. 38%), the extent of coronary artery disease, a high fibrinogen level (391 +/- 93 mg/dl vs. 335 +/- 109 mg/dl), a low albumin level (3.9 +/- 0.4 g/dl vs. 4.1 +/- 0.4 g/dl), and a low hemoglobin level (12.5 +/- 1.6 g/dl vs. 13.5 +/- 1.6 g/dl) were associated with the presence of renal artery stenosis (p < 0.05). Serum lipids, lipoprotein(a), creatinine, sex, smoking, or diabetes were not associated. By multivariate logistic regression analysis, older age (OR: 2.43 analyzed by 10 years increment, p = 0.0001), the presence of hypertension (OR: 2.68, p = 0.039) and a higher fibrinogen level (OR: 1.63 analyzed by 100 mg/dl increment, p = 0. 038) were significant risk factors of renal artery stenosis. Fibrinogen level was negatively correlated with albumin level (r = -0.18, p = 0.004). These results suggest that hyperfibrinogenemia as well as old age and hypertension are independent risk factors for atherosclerotic renal artery stenosis. Copyright Copyright 1999 S. Karger AG, Basel     

5-氟尿嘧啶在胰十二指肠切除术患者血液和胰液中的动态分布

探讨５－氟尿嘧啶能否通过胰十二指肠切除术后的残留胰腺组织进入胰液中,并达有效的治疗浓度,为胰腺为临床合理化疗提供理论依据。方法通过观察胰十二指肠切除术患者胰快速推注５－氟尿嘧啶后血液和胰液中药物动态分布及相关性,术后静脉一次性快速推注５－氟尿嘧啶１．０ｇ／ｍ＾２,在给药前后按设计时间点分别采集静脉血和胰液,采用高效液相色谱法测定血浆和胰液５－氟尿嘧啶药物浓度,应用ＰＣＮＯＮＬＩＮ程序程序计算共动态     

磁共振尿路造影在上尿路梗阻诊断中的

目的 评估磁共振尿路造影技术在诊断上尿路梗阻性疾患中的价值。方法 采用磁共振尿中造影术（ＭＲＵ）诊断上尿路梗阻患者３５例。结果 所有病例均清晰显示梗阻部位及尿路积水情况。结论 ＭＲＵ是一种无创性、无需造影剂的诊断上尿路梗阻的方法。     

5-氟尿嘧啶加奥曲肽对乳腺癌细胞凋亡的影响

目的 探讨５－氟尿嘧啶（５－ＦＵ）加奥曲肽（善得定）对乳腺癌细胞凋亡的影响。方法取手术切除的１６例乳腺癌标本,制备癌单细胞悬液。每例癌细胞均分成４组：５－ＦＵ组（加入５－ＦＵ１０μｇ／ｍｌ）、善得定组（加入善得定０．１μｇ／ｍｌ）、５－ＦＵ加善得定组（加入５－ＦＵ１０μｇ／ｍｌ、善和定０１μｇ／ｍｌ）及对照组（不加任何药物）。用ＤＮＡ断端标记法（ＴＤＴ法）检测乳腺癌细胞癌细胞凋亡率。结果 １６例标     

结肠、直肠癌术前区域动脉灌注化疗的临床病理观察

目的 探讨结直肠癌术前区域动脉灌注化疗对临床病理特征的影响及其可行性。方法 对３０例结、直肠癌患者以Ｓｅｌｄｉｎｇｅｒ方法插管、行选择性区域动脉并行灌注化疗。结果 所有病例病理检查均发现沿血管周围的癌细胞发生核固缩、碎裂,胞浆凝固、坏死、细胞间质水肿、纤维增生、炎细胞浸因和出现内膜增生、血管炎及血栓形成。结论订前选择性区域动脉灌注化疗要明显发迹结直肠癌患者的组织学形态,并使患者临床症状改善,对结直