Revascularized fibula for tibia replacement in adamantinoma

Adamantinoma of long bones is one of the rarest of malignant bone tumors; it is commonly located in the middle or lower third of the diaphysis of the tibia. A case with multiple occurrences affecting both the tibia and fibula is presented. En bloc resection with wide operative margins was performed, and a large tibial defect of 23 cm was effectively bridged by a revascularized free fibular flap. At 13 months follow-up, there was no sign of local recurrence or metastasis, and the patient was mobile.     

Lugol液染色对食管早期癌和癌前病变的诊断价值

目的 探讨Lugol液染色对食管早期癌和癌前病变的诊断价值。方法 对45例食管黏膜可疑病变经内镜以2％Lugol液喷洒染色，观察黏膜染色情况，并取活检送病理组织学检查。结果 45例食管病变染色后，39例呈浅染色或不染色，其中食管癌8例（食管早期癌5例，进展期癌3例），Barrett食管5例，轻至中度不典型增生1l例。本组Lugol液染色对食管早期癌和癌前病变的检出率达46．7％。结论 内镜下应用Lugol液染色结合活检有助于食管早期癌和癌前病变的诊断，且操作简便，具有重要的临床价值。     

彩色多普勒超声在Graves''''病诊断中的作用

目的:探讨彩色多普勒超声在Graves’病(又称弥漫性甲状腺肿)诊断中的作用。方法:用能量多普勒超声观察40例Graves’病患者及40例正常对照组双侧甲状腺组织的血液供应及分布情况;用脉冲多普勒测量颈总动脉的收缩期峰值流速(VPS),甲状腺上动脉的收缩期峰值流速(VPS)及阻力指数(RI),测量甲状腺上动脉的内径。结果:Graves’病组甲状腺实质内的血供极为丰富,血流分级以Ⅲ级为主,呈“火海征”,Graves’病组与正常对照组相比有显著性差异,P<0.005。Graves’病组颈总动脉的收缩期峰值流速为(162.1±31.5)cm/s,正常对照组颈总动脉的收缩期峰值流速为(98.2±20.9)cm/s,Graves’病组甲状腺上动脉的收缩期峰值流速(108.7±35.6)cm/s,正常对照组甲状腺上动脉的收缩期峰值流速(42.1±15.1)cm/s,以上各参数Graves’病组甲状腺上动脉的阻力指数为0.55±0.11,正常对照组甲状腺上动脉的阻力指数为0.73±0.19。Graves’病组与正常对照组相比有显著性差异P<0.01。Graves’病组甲状腺上动脉的内径为3.34±1.16mm,正常对照组甲状腺上动脉的内径为1.62±1.24mm。Graves’病组与正常对照组相比有显著性差异P<0.01。结论:彩色多普勒超声在Graves’病诊断中有重要的作用。     

A prospective, randomized clinical trial comparing two hyperbaric treatment protocols for carbon monoxide poisoning.

INTRODUCTION: The optimal hyperbaric oxygen (HBO2) treatment protocol for acute carbon monoxide (CO) poisoning is unknown. This is indicated by one study that found 18 different protocols to treat CO poisoning by North American multiplace hyperbaric facilities. A pilot study was conducted to evaluate the feasibility of randomizing patients to different protocols and to determine whether any large differences in clinical outcome were present between the two most common protocols. METHODS: Adult patients with accidental CO poisoning resulting in transient loss of consciousness, presentation to the emergency department within 12 hours, primary language English, high school education, and residence within 100 miles of the hyperbaric facility were recruited. Enrolled patients were randomized to one HBO2 treatment at 2.4 atmospheres absolute (atm abs) pressure with 90 minutes of 100% oxygen breathing vs. treatment by the US Air Force CO protocol (3.0 atm abs maximum pressure). A neurocognitive screening test was performed immediately after hyperbaric treatment and repeated 14-21 days later. RESULTS: From 1995 to 2002, 30 patients age 21 to 88 years were randomized, 18 to treatment at 2.4 atm abs and 12 to 3.0 atm abs. Average carboxyhemoglobin level for the population was 24.8 +/- 8.8% (mean +/- SD). Delay to hyperbaric treatment averaged 313 +/- 129 minutes. Neither variable was different between treatment groups. Six patients had abnormal neurocognitive testing immediately following hyperbaric treatment, 4 in the 2.4 atm abs group (22%) and 2 in the 3.0 atm abs group (17%) (P=0.71). One patient in each group demonstrated abnormality on delayed testing (p=0.75). One in each group did not return for follow-up. CONCLUSIONS: It is feasible to randomize CO-poisoned patients to different hyperbaric treatment protocols. Determination of differences in efficacy between treatment protocols will require a large multicenter trial with the use of detailed neurocognitive testing.     

丹参对持续癫痫幼鼠脑损伤保护作用的实验研究

目的 探讨丹参对持续癫痫发作诱发幼鼠脑神经元损伤是否具有保护作用。方法 皮下及腹腔注射贝美格针诱发健康幼龄鼠癫痫持续状态发作。光镜下观察神经元病变情况；电镜观察海马神经元超微结构的改变。结果 持续癫痴组幼鼠脑组织光镜下可见明显的神经元病变。电镜下可见海马区神经元的超微结构病变。丹参治疗组神经元病变均轻于持续癫痴组；而正常对照组未见类似病变。结论 丹参在组织、细胞和亚细胞水平对持续癫病幼鼠脑神经元损伤具有一定的保护作用，为临床有效防治小儿惊厥性脑损伤提供了可靠的实验依据。     

166Ho-DOTMP radiation-absorbed dose estimation for skeletal targeted radiotherapy.

166Ho-1,4,7,10-tetraazacyclododecane-1,4,7,10-tetramethylene-phosphonate (DOTMP) is a tetraphosphonate molecule radiolabeled with 166Ho that localizes to bone surfaces. This study evaluated pharmacokinetics and radiation-absorbed dose to all organs from this beta-emitting radiopharmaceutical. METHODS: After two 1.1-GBq administrations of 166Ho-DOTMP, data from whole-body counting using a gamma-camera or uptake probe were assessed for reproducibility of whole-body retention in 12 patients with multiple myeloma. The radiation-absorbed dose to normal organs was estimated using MIRD methodology, applying residence times and S values for 166Ho. Marrow dose was estimated from measured activity retained after 18 h. The activity to deliver a therapeutic dose of 25 Gy to the marrow was determined. Methods based on region-of-interest (ROI) and whole-body clearance were evaluated to estimate kidney activity, because the radiotracer is rapidly excreted in the urine. The dose to the surface of the bladder wall was estimated using a dynamic bladder model. RESULTS: In clinical practice, gamma-camera methods were more reliable than uptake probe-based methods for whole-body counting. The intrapatient variability of dose calculations was less than 10% between the 2 tracer studies. Skeletal uptake of 166Ho-DOTMP varied from 19% to 39% (mean, 28%). The activity of 166Ho prescribed for therapy ranged from 38 to 67 GBq (1,030-1,810 mCi). After high-dose therapy, the estimates of absorbed dose to the kidney varied from 1.6 to 4 Gy using the whole-body clearance-based method and from 8.3 to 17.3 Gy using the ROI-based method. Bladder dose ranged from 10 to 20 Gy, bone surface dose ranged from 39 to 57 Gy, and doses to other organs were less than 2 Gy for all patients. Repetitive administration had no impact on tracer biodistribution, pharmacokinetics, or organ dose. CONCLUSION: Pharmacokinetics analysis validated gamma-camera whole-body counting of 166Ho as an appropriate approach to assess clearance and to estimate radiation-absorbed dose to normal organs except the kidneys. Quantitative gamma-camera imaging is difficult and requires scatter subtraction because of the multiple energy emissions of 166Ho. Kidney dose estimates were approximately 5-fold higher when the ROI-based method was used rather than the clearance-based model, and neither appeared reliable. In future clinical trials with 166Ho-DOTMP, we recommend that dose estimation based on the methods described here be used for all organs except the kidneys. Assumptions for the kidney dose require further evaluation.     

PET imaging of the dopamine transporter with 18F-FECNT: a polar radiometabolite confounds brain radioligand measurements.

18F-2beta-Carbomethoxy-3beta-(4-chlorophenyl)-8-(2-fluoroethyl)nortropane (18F-FECNT), a PET radioligand for the dopamine transporter (DAT), generates a radiometabolite that enters the rat brain. The aims of this study were to characterize this radiometabolite and to determine whether a similar phenomenon occurs in human and nonhuman primate brains by examining the stability of the apparent distribution volume in DAT-rich (striatum) and DAT-poor (cerebellum) regions of the brain. METHODS: Two rats were infused with 18F-FECNT and sacrificed at 60 min. Extracts of brain and plasma were analyzed by high-performance liquid chromatography (HPLC) and liquid chromatography-mass spectrometric (LC-MS) techniques. Two human participants and 3 rhesus monkeys were injected with 18F-FECNT and scanned kinetically, with serial arterial blood analysis. RESULTS: At 60 min after the injection of rats, 18F-FECNT accumulated to levels about 7 times higher in the striatum than in the cortex and cerebellum. The radiometabolite was distributed at equal concentrations in all brain regions. The LC-MS techniques identified N-dealkylated FECNT as a major metabolite in the rat brain, and reverse-phase HPLC detected an equivalent amount of radiometabolite eluting with the void volume. The radiometabolite likely was 18F-fluoroacetaldehyde, the product expected from the N-dealkylation of 18F-FECNT, or its oxidation product, 18F-fluoroacetic acid. The distribution volume in the cerebellum increased up to 1.7-fold in humans between 60 and 300 min after injection and 2.0 +/- 0.1-fold (mean +/- SD; n = 3) in nonhuman primates between 60 and 240 min after injection. CONCLUSION: An 18F-fluoroalkyl metabolite of 18F-FECNT originating in the periphery confounded the measurements of DAT in the rat brain with a reference tissue model. Its uniform distribution across brain regions suggests that it has negligible affinity for DAT (i.e., it is an inactive radiometabolite). Consistent with the rodent data, the apparent distribution volume in the cerebellum of both humans and nonhuman primates showed a continual increase at late times after injection, a result that may be attributed to entry of the radiometabolite into the brain. Thus, reference tissue modeling of 18F-FECNT will be prone to more errors than analysis with a measured arterial input function.