^125I放射微粒微创植入治疗前列腺癌

目的观察^125I放射微粒植入对前列腺癌的治疗效果。方法对26例临床确诊为前列腺癌患者经皮穿刺在癌组织植入^125I放射微粒，每例平均36粒，术后复查肛诊、B超、影像学及血生化指标。结果患者植入治疗经过顺利，2例少量出血，留置导尿后愈合，3个月后经肛诊、直肠B超示结节缩小，前列腺特异性抗原（PSA）降低，多普勒超声显示结节内动脉收缩期最大血流速度（VS）、阻力指数（RI）及动脉搏动指数（PI）均明显下降。结论^125I放射微粒植入对前列腺癌的治疗安全性好、效果可靠。     

Phenotypic variants of the smooth-muscle cells in an atheromatous plaque of the human aorta

The authors investigated the expression of cytoskeletal proteins and the ultrastructure of cells in normal intima and atheromatous plaque of human aorta. It has been established, using double immunofluorescent method and a set of antibodies that intimal smooth muscle cells /SMC/ of normal aorta express myosin, vimentin, alpha-actin and actin but not desmin. In seven out of 28 atherosclerotic plaques the cells contained desmin and all other SMC cytoskeletal proteins were found. These cells had the ultrastructural features of SMC, i.e. well-developed endoplasmic reticulum and Golgi apparatus. Besides, some cells in 13 atherosclerotic plaques proved to be myosin-, alpha-actin- and desmin-negative. The cells were stained with monoclonal antibodies specific to SMC but not with macrophage-specific antibody. Ultrastructurally, the cytoplasm of the cells was filled with rough endoplasmic reticulum and a developed Golgi complex, but a certain portion of the cells retained basal lamina and myofilament bundles. The peculiarities of cytoskeletal protein in expression and ultrastructure of cells in human aortic atherosclerotic plaques may be explained by a phenotypic modulation of vascular SMC.     

Stereological analysis of the nonspecific endocytotic uptake of lipoproteins by aortic endothelium in the initial stages of experimental atherosclerosis in rabbits

Stereological analysis of vesicular transport of low density lipoproteins was performed by electronograms of the aorta endothelium from 42 rabbits in the course of experimental hypercholesterolemia. It was shown that nonspecific endocytosis was activated 1,6 times as compared to control and in some areas of endothelium up to 5-6 times at early stages of experimental hypercholesterolemia.     

MILITANCY TRAUMA : MAXILLOFACIAL INJURY,ANAESTHESIA AND CRITICAL CARE

Eighty four out of 2151 militancy trauma patients sustained severe maxillofacial injury from Jan 1990 to March 1993. The resuscitation, stabilisation and intensive care of these patients was based on management priorities of primary resuscitation, care of airway, management of haemodynamics, oxygenation and monitoring. Anaesthesia was administered in a situation when the airway was likely to be compromised and the patients were critically sick. Initial ventilation and oxygenation was the most difficult and could be achieved with satisfactory seal around the face mask by applying water-soaked guaze pieces around the mouth and nose to “fill-in” the defects. Tracheal intubation could be accomplished with intravenous sedation by an experienced anaesthesiologist. Dental occlusion and wiring necessiated the placement of nasotracheal tube for 48-72 hours after surgery.KEY WORDS: Trauma, Maxillofacial injury, Trauma anesthesia, Anaesthesia and critical care     

Diagnostic and Prognostic Value of Low Density Lipoprotein-Containing Circulating Immune Complexes in Atherosclerosis

Recently, it has been shown that increased level of LDL-containing circulating immune complexes (LDL-CIC) possess high diagnostic significance in clinically manifested atherosclerosis, but little is known about its diagnostic and prognostic significance in early atherosclerosis. Two-years prospective study was performed in 98 asymptomatic men aged 40–74. The rate of atherosclerosis progression was estimated by high-resolution B-mode ultrasonography as the increase in intima-media thickness (IMT) of common carotid arteries. The patients with elevated baseline levels of LDL-CIC were characterized by significantly higher levels of total and LDL cholesterol as well as significantly increased mean IMT of common carotid arteries. Among all baseline lipid parameters, only LDL-CIC and LDL cholesterol were contingent with the extent of early carotid atherosclerosis (p?=?0.042 and p?=?0.049, respectively) and had the highest levels of relative risk and odds ratio. During the follow up, significant IMT increase was registered in 53.1 % (n?=?52) patients, IMT significant reduction was observed in 21.4 % (n?=?21) patients. The increased levels of LDL-CIC, total serum cholesterol and LDL cholesterol had similar prognostic significance with the respect of atherosclerosis progression. The normal level of LDL-CIC (below than 16.0 μg/ml) was the only lipid parameter that predicted the absence of carotid atherosclerosis progression for two following years at prognostic value of 78.3 %. The results of the study allow assuming that LDL-CIC level may be employed not only as a marker of early atherosclerosis, but also has a sufficient prognostic value for clinical implications.     

显微镜辅助下颈前路椎间盘切除植骨融合术治疗多节段脊髓型颈椎病

目的探讨显微镜辅助下颈前路椎间盘切除植骨融合术(anterior cervical discectomy with fusion,ACDF)治疗多节段脊髓型颈椎病的疗效。方法回顾性分析2011年1月~2012年8月本院行颈前路手术治疗的60例脊髓型颈椎病患者的临床资料,根据手术方式分为常规ACDF组(A组,30例)和显微镜辅助ACDF组(B组,30例)。比较2组的手术时间、术中出血量、住院天数及并发症,以日本骨科学会(Japanese Orthopaedic Association,JOA)评分(17分法)及其改善率评价术后神经功能改善情况。结果 A组手术时间为(132.5±8.9)min,B组为(137.0±9.1)min,差异无统计学意义(P0.05)。A组术中出血量为(113.6±8.0)m L,B组为(93.7±5.3)m L,差异有统计学意义(P0.01)。A组住院(7.37±1.73)d,B组(6.63±1.13)d,差异无统计学意义(P0.05)。A组术前JOA评分为6.60±1.21,术后12个月为13.83±0.91,改善率为(69.72±7.66)%;B组术前JOA评分为6.87±1.46,术后12个月为14.23±1.17,改善率为(72.51±11.26)%。A组和B组改善率差异有统计学意义(P0.05)。结论显微镜辅助ACDF和常规ACDF是治疗多节段脊髓型颈椎病有效的方法,但显微镜辅助ACDF可减少术中出血量,是治疗多节段脊髓型颈椎病优先选择的手术方案。     

Vascular smooth muscle cell in atherosclerosis

Vascular smooth muscle cells (VSMCs) exhibit phenotypic and functional plasticity in order to respond to vascular injury. In case of the vessel damage, VSMCs are able to switch from the quiescent ‘contractile’ phenotype to the ‘proinflammatory’ phenotype. This change is accompanied by decrease in expression of smooth muscle (SM)‐specific markers responsible for SM contraction and production of proinflammatory mediators that modulate induction of proliferation and chemotaxis. Indeed, activated VSMCs could efficiently proliferate and migrate contributing to the vascular wall repair. However, in chronic inflammation that occurs in atherosclerosis, arterial VSMCs become aberrantly regulated and this leads to increased VSMC dedifferentiation and extracellular matrix formation in plaque areas. Proatherosclerotic switch in VSMC phenotype is a complex and multistep mechanism that may be induced by a variety of proinflammatory stimuli and hemodynamic alterations. Disturbances in hemodynamic forces could initiate the proinflammatory switch in VSMC phenotype even in pre‐clinical stages of atherosclerosis. Proinflammatory signals play a crucial role in further dedifferentiation of VSMCs in affected vessels and propagation of pathological vascular remodelling.