Autosomal dominant neovascular inflammatory vitreoretinopathy

Twenty-eight of 61 members of a six-generation family are affected by an autosomal dominant eye disease which has not been described previously. Affected patients are asymptomatic in early adulthood, but have vitreous cells and the selective loss of the b-wave on the electroretinogram. Later, peripheral retinal scarring and pigmentation, peripheral arteriolar closure, and neovascularization of the peripheral retina at the ora serrata or occasionally neovascularization of the optic disc develop. Cystoid macular edema, vitreous hemorrhage, tractional retinal detachment, and neovascular glaucoma can cause profound visual loss. Vitrectomy reduces traction on the retina and allows for retinal reattachment. The role of argon laser photocoagulation or cryopexy in reducing the neovascular complications remains uncertain.     

Increase in the activities of plasma pseudocholinesterase dependent on the blood glucose level and its relation to the hypersensitivity to acetylcholine in striated muscles of KK-CAy mice with diabetes

Acetylcholinesterase activity and pseudocholinesterase activity were examined in plasma and in striated muscles (whole heart and diaphragm muscles) of diabetic KK-CAy mice. Both activities of acetylcholinesterase in heart muscle and pseudocholinesterase in plasma were significantly increased in diabetic KK-CAy mice compared to pre-diabetic KK-CAy mice. Both acetylcholinesterase and pseudocholinesterase activities in skeletal muscle were not changed by the diabetic state. The increases in activity of plasma pseudocholinesterase was significantly correlated to the increase in blood glucose level in alloxan-, streptozotocin (STZ)-diabetic ddY mice and diabetic KK-CAy mice. The increase was not correlated to the body weight in non-diabetic female-KK-CAy mice. Furthermore, the activity of heart acetylcholinesterase was significantly correlated with the activity of plasma pseudocholinesterase (r = 0.79, P less than 0.01). The activities of acetylcholinesterases in heart muscles from STZ- and alloxan-diabetic ddY mice also tended to increase. The hypersensitivity of the pulse rate to a low dose (1 mg/kg) of acetylcholine was correlated to the activity of plasma pseudocholinesterase (r = -0.51, P less than 0.05). These results demonstrate that the activities of plasma pseudocholinesterase were increased by the diabetic state being associated with the increasing alteration of cardiac sensitivity to acetylcholine in the whole body.     

Replantation of the distal part of the leg

We successfully replanted five amputated legs in five patients and followed the patients for two years or more (average, six years and three months). Although some patients found it impossible to squat and to run because of joint contractures, muscle weakness, or deformities of the foot, all patients could perform other activities without difficulty. None had important pain or any intolerance to cold, and all were satisfied with the results of the replantation.     

Glued Carbon Fiber Electrodes for Diaphragm Pacing

Carbon fibers with fibrin glue were used as electrodes for diaphragm pacing. The electrodes were applied to three mongrel dogs and the effectiveness was tested. The carbon leads were glued to phrenic nerves by means of the fibrinogen and thrombin bilaterally. The tidal volumes and threshold current level for stimulation were measured at various time up to 9 weeks after implantation. Effective contraction of diaphragm were observed for 9 weeks. By using this electrode, the exfoliation of the nerve is not necessary, the nerve can be maintained in an intact state, and the risk of the implanting operation can be minimized.     

大鼠心肌缺血再灌注时心肌细胞凋亡caspase-3活性变化规律及药物对其影响

目的　探讨大鼠心肌缺血再灌注 (Ischemiareperfusion ,IR)不同时相的心肌细胞凋亡、caspase 3活性变化规律及caspase 3抑制剂Ac DEVD CHO的影响。方法　Wistar大鼠 12 2只 ,设立IR组 ,IR +Ac DEVD CHO组和假手术对照组并分设缺血 3 0min后再灌注 1、3、6、12、2 4h 5个时相点 ;以缺口末端标记法 (TUNEL)标记凋亡细胞 ,用荧光分析法检测caspase 3活性 ,行TTC染色测定心肌梗死范围。结果　心肌细胞凋亡与caspase 3活性随心肌再灌注不同时相而变化 ,心肌细胞凋亡指数 (Apoptosisindex ,AI)与caspase 3活性于再灌注 12h最高 [AI :( 3 4 83± 9 3 5 ) % ;caspase 3活性 :( 1 3 4±0 2 ) ] ,其后基本维持在平台状态 ;心肌梗死范围随IR时间逐渐增加 ,至 2 4h仍未见下降趋势 ,三者间呈显著正相关 (P <0 0 5 )。IR +Ac DEVD CHO组上述指标虽也明显增高 ,但比IR组明显减小 (P <0 0 5 )。结论　Caspase 3激活及心肌细胞凋亡参与了心肌缺血再灌注损伤过程 ,Ac DEVD CHO减轻心肌缺血再灌注损伤可能部分与其抑制心肌细胞凋亡有关。     

Vasoconstrictor response of large cerebral arteries of cats to endothelin, an endothelium-derived vasoactive peptide

Endothelin, a 21-amino acid peptide produced by vascular endothelial cells, caused a sustained constriction of isolated large cerebral arteries of cats in a dose-dependent manner. The increased tone of the tissue did not return to the resting level after repeated washings. No vasodilator response was evoked by endothelin in the presence of an active tone. The contractile response of cerebral arteries was not inhibited by rubbing of the endothelium, cold storage denervation or indomethacin. In contrast, nicardipine or diltiazem antagonized the endothelin-induced contraction non-competitively. No contraction was evoked by endothelin in a Ca2+-free solution while the addition of Ca2+ ions in the presence of endothelin in a Ca2+-free solution caused a sustained contraction. Ca2+-induced contraction in the Ca2+-free solution containing endothelin was also inhibited by nicardipine. Therefore, endothelin causes a direct contraction of the smooth muscles of cat cerebral arteries, probably by activating the influx of Ca2+ ions through L-type Ca2+ channels of smooth muscles.     

A large AVM extensively involving the parietal region and posterior fossa

A 47-year-old male was concerned with a large AVM involved extensively in the parietal region and the posterior fossa. Radiological examinations showed multiple radiolucencies in the parietal and occipital bone and torturous vascular nets (nidus) in those bones on the angiograms. Nidus was found also in the dura mater in the posterior fossa. Therefore, this case seemed to be an extremely rare case of calvarial AVM in the parietal region with the mixed calvarial dural AVM in the posterior fossa. His symptoms were bruit, transient hemiparesis and Gerstmann's syndrome in addition to the symptoms due to raised intracranial pressure. Favorable results of therapies could be attained by extensive exfoliation of dura mater from the cranial bone and incision of proximal dura mater in the sinus.     

Amlodipine-induced reduction of oxidative stress in the brain is associated with sympatho-inhibitory effects in stroke-prone spontaneously hypertensive rats.

Amlodipine is a dihydropyridine calcium channel blocker that is widely used for the treatment of hypertensive patients and has an antioxidant effect on vessels in vitro. The aim of the present study was to examine whether treatment with amlodipine reduced oxidative stress in the brains of stroke-prone spontaneously hypertensive rats (SHRSP). The animals received amlodipine, nicardipine or hydralazine for 30 days in their drinking water. Levels of thiobarbituric acid-reactive substances (TBARS) in the brain (cortex, cerebellum, hypothalamus, and brainstem) were measured before and after each treatment. Systolic blood pressure decreased to similar levels in the amlodipine-, nicardipine-, and hydralazine-treated groups. Urinary norepinephrine excretion was significantly reduced in SHRSP after treatment with amlodipine, but not with nicardipine or hydralazine. Levels of TBARS in the cortex, cerebellum, hypothalamus, and brainstem were significantly higher in SHRSP than in Wistar-Kyoto rats (WKY), and were reduced in amlodipine-treated, but not in nicardipine- or hydralazine-treated, SHRSP. Electron spin resonance spectroscopy revealed increased levels of reactive oxygen species in the brains of SHRSP, which were reduced by treatment with amlodipine. Intracisternal infusion of amlodipine also reduced systolic blood pressure, urinary norepinephrine excretion, and the levels of TBARS in the brain. These results suggested that oxidative stress in the brain was enhanced in SHRSP compared with WKY rats. In addition, antihypertensive treatment with amlodipine reduced oxidative stress in all areas of the brain examined and decreased blood pressure without a reflex increase in sympathetic nerve activity in SHRSP.