Electrophysiologic investigation of thallium poisoning

Electrophysiologic findings in thallium intoxication are usually untimely, limited in extent, and often uninformative. This report documents serial conduction and electromyographic findings in a case of thallium poisoning, beginning 10 days after symptom onset and ending 24 months later. Initially, the plantar nerves in the foot demonstrated profound axonal loss while the sural and peroneal nerves were essentially normal. The latter two nerves subsequently underwent axonal loss. Two years were required for the sural and peroneal nerves to display recovery. At 24 months, the plantar nerves continue to remain absent. A primarily distal axonopathy, significantly worse in the lower than upper extremities and requiring more than 2 years for recovery, now documents what was previously speculated: the electrophysiologic course of thallium intoxication. Additionally, this case emphasizes the need to examine the plantar nerves of the foot to avoid missing distal axonopathies during the early course of the disease process. The clinical course and pathophysiology of thallium poisoning are also reviewed.     

Digit distribution of proper digital nerve action potential.

Antidromic sensory nerve action potential testing is well characterized and commonly used to assess the sensory component of the upper limb median and ulnar nerves. The final terminal segments of these nerves are the proper digital nerves. Ring recording electrodes are commonly used to detect the proper digital nerves' antidromic responses. Attempts to record the separate contributions of individual digital nerves along the lateral aspects of each finger, using small surface electrodes, is shown to be unreliable for determining the integrity of a single terminal digital branch. We found between 50% to 77% of the stimulated terminal branch's response amplitude when recorded at electrodes positioned over the nonstimulated branch located 180 degrees from the activated terminal branch. Detecting a single terminal nerve response was achieved by using the fourth digit and the second digit with one of the second digit's branches neurophysiologically blocked by local anesthetic. The volume-conducted response from the opposite side of the finger resulted in this relatively large recorded response, which remains within the range of reference values precluding the simple use of antidromic techniques to assess injury to a single proper digital nerve. Techniques are proposed to avoid such pitfalls and to assess most accurately the desired response.     

高效液相色谱法测定炎痛净乳膏中双氯芬酸钠和苯佐卡因的含量

目的：测定炎痛净乳膏中双氯芬酸钠和苯佐卡因的含量。方法：高效液想象以谱法，甲醇为提取溶剂，地西泮为内标，No-va-PakC18色谱柱，甲醇-水-冰醋酸（80：20：0.5)为流动相，检测波长为283nm。结果：双氯芬酸钠和苯佐卡因在5μg/ml-40μg/ml范围内，其浓度与峰面积均呈良好的线性关系（r=0.9999)，平均回收率分别为101.0%,RSD=1.21%,99.8%,RSD=0.62%。结论：本法专属性强，操作简便，结果准确。     

H-2-restricted cytotoxic effectors generated in vitro by the addition of trinitrophenyl-conjugated soluble proteins

Murine spleen cells from normal donors were cultured in vitro with trinitrobenzene sulfonate (TNBS)-conjugated soluble proteins, i.e., bovine gamma globulin (TNP-BGG) or bovine serum albumin (TNP-BSA). Addition of 100 μg of any of these TNP-proteins to the spleen cell cultures led to the generation of cytotoxic T-cell effectors which were H-2-restricted and TNP- specific. The lytic potential of such effectors was comparable to that generated by sensitization with TNBS-modified syngeneic cells, and was restricted to haplotypes shared at the K or K plus I-A, or the D regions of the H-2 complex. Greater effecter cell activity was generated by addition of TNP-BGG against TNBS-modified targets which shared K plus I-A than against modified targets which shared the D region with the responding cells, which suggests that the same immune response genes are involved when the response is generated by the addition of TNP-conjugated soluble proteins or of TNBS- modified cells. H-2-restricted, TNP-specific effecter cells were generated by culturing mouse spleen cells with syngeneic cells which had been preincubated with TNP- BGG or TNP-BSA for 1.5 h. The addition of unconjugated soluble proteins to the cultures did not result in cytotoxic effectors detectable on H-2-matched targets, whether the targets were prepared by modification with TNBS, or by incubation with either the unconjugated or TNP-conjugated proteins. Depletion of phagocytic cells in the tumor preparation by Sephadex G-10 column fractionation before incubation with TNP-BSA had no effect on their lysis by the relevant effector cells. Immunofluorescent staining of tumor target cells with anti-TNP antibodies indicated that TNP could be detected on the tumor cells within 10 rain of incubation with TNP-BSA. The cytotoxic response generated by addition of the TNP-proteins to spleen cell cultures was found to be T-cell dependent at the effector phase, as shown by the sensitivity of the lytic phase to absorbed RAMB and complement. Furthermore, the response did not appear to be attributable to antibody-dependent cellular cytotoxicity. Three mechanisms were considered which could account for the generation of H-2-restricted, TNP-specific, cytotoxic T-cell effectors by the addition of soluble TNP-proteins. These include covalent linkage of activated TNP groups from the soluble proteins to cell surface components, macrophage processing of the soluble conjugates and presentation to the responding lymphocytes in association with H-2-coded self structures, or hydrophobic interaction of the TNP-proteins to cell surfaces. Results obtained from sodium dodecyl sulfate gel patterns indicating that cell-bound TNP was still linked to BSA, and the observation that phagocytic-depleted cells could interact with the soluble TNP-proteins and function as H-2-restricted targets, appear not to favor the first two proposed mechanisms.     

脑出血大鼠脑组织膜型基质金属蛋白酶、基质金属蛋白酶2和基质金属蛋白酶9表达及益气活血中药的干预效应

目的:观察益气活血中药对脑出血大鼠脑组织中膜型基质金属蛋白酶、基质金属蛋白酶2和基质金属蛋白酶9表达量的影响,从脑出血损伤区微血管系统重建的角度,探讨益气活血中药治疗脑出血的作用机制。方法:实验于2006-03/10在中南大学湘雅医院中西医结合研究所实验室完成。实验材料:补阳还五汤全方(黄芪,当归,赤芍,红花,川芎,地龙,桃仁按20∶3∶3∶3∶2∶3∶3的比例);补阳还五汤益气成分(黄芪按上述比例);补阳还五汤活血成分(当归,赤芍,地龙,川芎,桃仁,红花按3∶3∶3∶2∶3∶3的比例)。用蒸馏水两次水煎,分别浓缩为1.54,0.81和0.73g/mL。实验分组:155只SD大鼠随机分为正常对照组、假手术组、模型组、益气活血组、益气组、活血组。正常对照组5只大鼠,其余每组30只,再随机分为术后灌胃2,4,7,14,21,28d6个观察时间点,各个时间点5只大鼠。实验干预:造模:采用立体定位技术将胶原酶Ⅶ注入大鼠大脑右苍白球制成脑出血大鼠模型。假手术组大鼠仅注入2μL生理盐水,其余手术过程相同。给药:正常对照组:普通饲养,自由饮水;假手术组和模型组术后予蒸馏水灌胃2次/d,2mL/次;益气活血组、益气组、活血组分别给予补阳还五汤全方、补阳还五汤益气成分、补阳还五汤活血成分30.80,16.20,14.60g/(kg·d)(按体表面积计算为临床70kg成人剂量的3倍)灌胃,2次/d,2mL/次。各组大鼠分别于灌胃2,4,7,14,21,28d麻醉下取脑,制备切片;正常组动物于28d处死。实验评估:免疫组织化学染色方法检测各组灌胃不同时间脑组织基质金属蛋白酶2、基质金属蛋白酶9和膜型基质金属蛋白酶的阳性微血管数。结果:155只大鼠均进入结果分析。①正常组、假手术组皮质偶见膜型基质金属蛋白酶、基质金属蛋白酶2和基质金属蛋白酶9表达。②模型组膜型基质金属蛋白酶、基质金属蛋白酶2呈双峰表达,4d为最高峰,至14～21d再有小高峰出现。③益气活血组给药4d时,膜型基质金属蛋白酶、基质金属蛋白酶2为表达低谷,低于模型组(P<0.01)、益气组和活血组(P<0.05);在中后期,益气活血组膜型基质金属蛋白酶表达高峰为7～14d,较模型组提前出现,21d后与模型组比,各治疗组膜型基质金属蛋白酶已表达极少(P<0.01);益气活血组基质金属蛋白酶2在7d后一直呈高水平维持,高于其他各组(P<0.05),28d后开始逐渐下降。④模型组基质金属蛋白酶9在造模后4d达最高峰(P<0.01),两周后几乎无表达。益气活血组基质金属蛋白酶9高峰推迟至7d出现(P<0.05),之后逐渐下降。结论:益气活血中药可通过调节脑出血后膜型基质金属蛋白酶、基质金属蛋白酶2和基质金属蛋白酶9表达,改善出血后脑组织的微环境,有利于微血管系统重建,促进组织修复。     

超声微泡造影影像学及治疗作用的研究进展

包裹型气体微泡已经发展为临床应用的超声造影剂.微泡造影剂不仅已广泛用于血池和组织灌注显像,其治疗作用也日渐突显,例如溶栓和作为药物或基因的载体.造影剂微泡的平均直径小于红细胞直径,因而能够自由运行于微循环.微泡能将生物活性物质(例如药物或基因)结合在其内或其外膜表面,并将此物质转运于体内特定组织,例如将抗肿瘤药物转运并结合于特定肿瘤组织.靶向性微泡能将肽段等特定性配体结合于其微泡表面,这种特定性配体可特异性地与血管壁表达的受体相结合,微泡因而在靶组织区域积聚[1].     

The premotor potential

A small waveform precedes the compound muscle action potential evoked from the thenar eminence with median nerve stimulation with high amplifier gains. This potential is believed to emanate from fibers destined to innervate the volar aspect of the first digit. It has been suggested recently that the source of the premotor potential is the palmar cutaneous branch of the median nerve. In this study, the palmar cutaneous branch of the median nerve was blocked at the wrist. A localized zone of anesthesia was observed over the proximal midpalm, not the thenar eminence, and the premotor response remained unchanged as did a midpalmar potential. The median nerve was then blocked at the base of the thenar eminence; only then did the premotor potential disappear. The palmar cutaneous branch of the median nerve innervates only a small portion of the medial aspect of the thenar eminence and does not produce the thenar premotor potential. Additionally, because of the close proximity of the main median nerve to its palmar cutaneous branch, volume conduction of stimuli and responses precludes an electrophysiologic technique which exclusively localizes the palmar cutaneous branch of the median nerve.