大肠癌免疫组化表达与临床病理的关系

目的:探讨大肠癌CEA、P53、nm23、Ki-67、MRP免疫组化表达特点和相互关系,及其与临床病理的关系．方法:回顾性分析2003-01／2006-07我院收治的73例大肠癌患者的临床病理及随访资料,并对其石蜡标本采用免疫组化SP染色法检测CEA、P53、nm23、Ki-67、MRP,分析其免疫组化特点及其与临床病理之间的关系．结果:CEA、P53、nm23、Ki-67、MRP在大肠癌中的阳性表达率依次为82．2％、68．5％、75.3％、84．9％和64．4％．CEA、MRP与大肠癌患者的各因素无统计学差异．P53、Ki-67和nm23与肿瘤的Dukes分期和淋巴结转移有关, P53、Ki-67在Dukes C、D期的阳性表达率(依次为82．8％和100％1明显高于Dukes A、B期者(59．1％和75．0％)(P<0．05),而nm23在Dukes C、D期的阳性表达率(58．6％)明显低于Dukes A、B期者(86．4％)(P<0．05)．CEA与nm23的表达呈明显的负相关(r=-0．296,P=0．011),而P53和Ki-67表达之间呈现明显的正相关(r= 0．308,P=0．008),其他各指标间的表达无相关性．nm23、P53和Ki-67与预后因素关系明显,nm23在生存期≥3 a患者的阳性表达率(92．9%)高于生存期<3 a者(71．2％)(P<0．05),而P53和Ki-67在生存期≥3 a患者的阳性表达率(依次为42．9％和64.3％)明显低于生存期<3 a者(74．6％和89．8％)(P<0．05)．结论:P53、Ki-67和nm23的表达与大肠癌的侵袭转移和预后密切相关．CEA可能是大肠癌的侵袭转移的促进因素．MRP所引起的耐药机制是一个相对独立的机制．CEA、P53、nm23、Ki-67可作为判断大肠癌恶性程度、侵袭转移以及预后的指标．     

A KINETIC STUDY OF SULINDAC IN THE ELDERLY

To study the disposition of the anti-inflammatory drug sulindac, its active sulphide metabolite, and the inactive sulphone metabolite, sulindac (200 mg twice daily) was given to eight elderly subjects for at least 14 consecutive days. The drug was then ceased for 72 hours, and suitable samples were collected to study its elimination. The mean steady-state concentration for sulindac was 5.0 μg/ml, for sulindac sulphide was 6.5 μg/ml, and for sulindac sulphone was 13.2 μg/ml. These are approximately twice the reported steady-state levels for the respective redox forms in healthy young adults. The mean half-lives of sulindac, sulindac sulphide, and sulindac sulphone were 18.3 hours, 22.3 hours, and 54.6 hours, respectively. One patient who had mildly abnormal liver function tests developed more severe abnormalities whilst receiving sulindac. These returned towards normal after cessation of treatment. This patient had the highest steadystate plasma concentration of sulindac sulphone. It is concluded that care should be taken with the use of sulindac in the elderly, and control of patients' symptoms should be attempted with lower doses of the drug before the standard dose of 200 mg twice daily is administered.     

Congenital middle-ear deafness: CT study

Computed tomography (CT) was used to study 25 patients with congenital conductive hearing loss and normal external auditory canals. Deformities were subdivided according to ossicular, fenestral, and cholesteatomatous origin. Isolated ossicular deformities were found in 14 patients (five bilateral), cholesteatoma in eight, oval-window nondevelopment (with ossicular deformity) in one, and normal studies in two (congenital stapes fixation at the level of the annular ligament). Ossicular deformities may be subdivided into incudostapedial disconnections into incudostapedial disconnections (most common), malleoincudal fixations, and stapes fixations. Most are due to developmental anomaly of the first or second branchial arch. The stapes has a dual origin (second arch and otic capsule). A cholesteatoma is defined as congenital only if there is no history of otitis and the tympanic membrane is intact. In this series, six were in the middle ear proper, and two were within the attic beyond otoscopic view. Their CT appearance, with one exception, was essentially identical to that of acquired lesions.     

Hemagglutination inhibition of Cromer blood group antibodies with soluble recombinant decay-accelerating factor

BACKGROUND: Cromer blood group antigens are located on decay- accelerating factor (DAF, CD55), which contains four short consensus repeats (SCRs). Cromer system antibodies may be of clinical significance in blood transfusion. STUDY DESIGN AND METHODS: Soluble recombinant DAF (srDAF) constructs, consisting of all four SCRs or of only two SCRs, were expressed in the yeast Pichia pastoris. They are used in hemagglutination-inhibition tests with Cromer system antibodies and with DAF-specific monoclonal antibodies. RESULTS: The srDAF inhibited hemagglutination by all Cromer system alloantibodies in undiluted serum. Antibodies to antigens of other blood group systems were not inhibited by the srDAF. Hemagglutination-inhibition tests with domain-deleted srDAF showed that UMC is on SCR-4 and confirmed that Tca, TcaTcb, and WESb are on SCR-1; Dra is on SCR-3; and Cra is on SCR- 4. CONCLUSIONS: Hemagglutination inhibition with srDAF is useful in the recognition of antibodies that belong to the Cromer blood group system and facilitates pretransfusion testing. This use of domain-deleted srDAF provides an easy method of determining epitope location on DAF and is an aid to more precise identification of Cromer system antibodies.     

Superior mesenteric artery blood flow velocity and estimated volume flow: duplex Doppler US study of preterm and term neonates

To obtain information about intestinal hemodynamics of healthy neonates, the authors assessed velocity and volume of blood flow with duplex Doppler sonography in the superior mesenteric artery (SMA) in 91 stable preterm and term neonates. Blood flow velocity in the SMA and estimated volume blood flow increased linearly with gestational age and increasing body weight. The mean estimated volume blood flow (+/- standard deviation) was 43 mL/kg/min +/- 13 and did not depend on differences in body weight. The authors also assessed blood flow velocity in the SMA and volume blood flow in 18 infants with conditions that may affect blood supply to the bowel. Twelve infants who were small for gestational age appeared to have an abnormally low resistance of the vascular bed of the SMA during the 1st days of life, as compared with stable appropriate-for-gestational-age infants matched for gestational age. Three of six term neonates with cardiovascular abnormalities had left ventricular outflow obstruction and an abnormal blood flow velocity waveform of the SMA, suggesting a decrease in blood supply to the bowel. The results of this study may help in evaluations of intestinal perfusion in infants with abnormal conditions.     

CYSTIC FIBROSIS AND NORMAL FIBROBLASTS HAVE IDENTICAL GLUCOCORTICOID RECEPTOR PROFILES AND INDUCED PROTEIN RESPONSES

The possibility of differences in glucocorticoid sensitivity between normal and cystic fibrosis fibroblasts was studied in cultured cells derived from forearm skin biopsies. Both normal and cystic fibrosis cells bound tritiated dexamethasone with high affinity (K_d 37°C ± 10 nmol/l) to a limited class of sites (concentration ± 50,000/cell); no difference between cystic fibrosis and normal cells was seen in the nuclear transfer of receptor-bound tritiated dexamethasone. After 4 h exposure to dexamethasone and analysis of ³⁵S-methionine labelled proteins by 2-dimensional gel electrophoresis, both normal and cystic fibrosis cells showed increased abundance of protein kappa (molecular weight ～ 41,000; pK_i～6.5) over non-steroid exposed gels. After 16 h exposure, in both cystic fibrosis and normal cells exposed to dexamethasone a decrease in protein omega (mol. wt ～ 42,000; pK_i～ 5.4) was seen compared with control. We interpret these data as evidence against a difference in glucocorticoid receptor or effector mechanisms between cystic fibrosis and normal fibroblasts.