神经外科麻醉对体感诱发电位的影响

目的探讨神经外科手术麻醉对体感诱发电位（SEP）的影响,以期为麻醉和手术处理提供依据。方法随机抽取我科17例全麻手术病人,分成颅内疾病手术组（A组）与脊柱、脊髓疾病手术组（B组）,于术前、麻醉（诱导完成）、术始、术中、术毕和术后6个时程连续监测SEP的潜伏期、波幅及波形并记录。结果麻醉后SEP潜伏期延长5.96%,波幅下降24.00%,未出现波形消失的情况。结论麻醉抑制SEP,表现为潜伏期延长和波幅下降,但未出现波形消失的情况。     

Serum cholesterol and risk of cancer in a cohort of 39,000 men and women

Serum cholesterol concentration was studied for its prediction of cancer in 39,268 men and women aged 15-99 years and initially free from cancer. During a median follow-up of 10 years 1381 cancer cases were diagnosed. Serum cholesterol level was inversely associated with cancer incidence among non-smokers. Age-adjusted relative risks of cancer in quintiles of serum cholesterol were in male non-smokers 1.0, 0.81, 0.73, 0.69, and 0.46 and in female non-smokers 1.0, 0.75, 0.84, 0.78, and 0.70. The associations were not found to be confounded by serum vitamins A or E, serum selenium or several other factors. The association between serum cholesterol level and risk of cancer varied from strongly negative to slightly positive according to subpopulation and site of cancer. The strongest negative associations were found to appear during the first years of follow-up, especially for rapidly developing cancers. Thus the increased occurrence of cancer at low cholesterol levels seems mainly to be due to preclinical cancer.     

Weight and mortality in Finnish men

Mortality rates of 22,995 Finnish men aged 25 and over followed up for a median of 12 years were analyzed in relation to body mass index (BMI) at the initial examination. All-cause mortality followed a "U"-shaped distribution, being greatest for the thinnest and fattest men at all ages, or about 1.5-fold for those with BMI less than 19.0 kg/m2 and BMI greater than or equal to 34.0 kg/m2, as compared with men of normal weight (BMI 22.0-24.9 kg/m2). Mortality from cardiovascular diseases (CVD) increased with increasing BMI beyond the normal range. This depended mostly on the association of BMI with the biological risk factors of CVD. Mortality rates from CVD were also elevated among thin men under age 55, which could not be explained by the effect of the biological variables. Mortality rates from non-cardiovascular diseases, including cancers were inversely related to BMI among men of all ages. The high overall mortality of thin men was partly but not entirely attributable to smoking, low social class and antecedent disease. We conclude that both thinness and overweight are detrimental to longevity, but through differing mechanisms and disease patterns.     

High-efficiency gene transfer to primary T lymphocytes by recombinant adenovirus vectors

Recombinant, replication-deficient adenoviruses are efficient vectors for gene transfer to a wide range of cell types, with the exception of T lymphocytes. Here, we show that primary T lymphocytes from peripheral blood, cord blood, and the Jurkat T cell line are efficiently transduced by recombinant adenovirus. Nearly 100% infection efficiency of primary T cells is obtained with high multiplicity of infection (MOI) (5000) of recombinant adenovirus coding for lacZ. Similar infection efficiency by adenovirus-mediated gene transfer was obtained at lower MOI (3000) by activating primary T cells with PHA and PMA. Addition of cationic liposomes together with RAdlacZ markedly enhanced the infection efficiency at lower MOI (1000) resulting in over 90% infection efficiency. Primary T cells express low levels of coxsackievirus and adenovirus receptor (CAR), a cell surface receptor for adenovirus fiber attachment, as well as _vβ₃ and _vβ₅ integrins, cellular receptors for adenovirus internalization. This suggests that adenovirus entry to T cells at high MOI is mediated by other mechanisms. In conclusion, these results demonstrate that genes can be efficiently transferred to primary lymphocytes by adenovirus vectors at high MOI or in combination with cationic liposomes.     

Maternal Vitamin C and Iron Intake during Pregnancy and the Risk of Islet Autoimmunity and Type 1 Diabetes in Children: A Birth Cohort Study

Our aim was to study the associations between maternal vitamin C and iron intake during pregnancy and the offspring’s risk of developing islet autoimmunity and type 1 diabetes. The study was a part of the Finnish Type 1 Diabetes Prediction and Prevention (DIPP) prospective birth cohort including children genetically at risk of type 1 diabetes born between 1997–2004. The diets of 4879 mothers in late pregnancy were assessed with a validated food frequency questionnaire. The outcomes were islet autoimmunity and type 1 diabetes. Cox proportional hazards regression analysis adjusted for energy, family history of diabetes, human leukocyte antigen (HLA) genotype and sex was used for statistical analyses. Total intake of vitamin C or iron from food and supplements was not associated with the risk of islet autoimmunity (vitamin C: HR 0.91: 95% CI (0.80, 1.03), iron: 0.98 (0.87, 1.10)) or type 1 diabetes (vitamin C: 1.01 (0.87, 1.17), iron: 0.92 (0.78, 1.08)), neither was the use of vitamin C or iron supplements associated with the outcomes. In conclusion, no association was found between maternal vitamin C or iron intake during pregnancy and the risk of islet autoimmunity or type 1 diabetes in the offspring.     

Weight and mortality in Finnish women

Mortality in relation to body mass index (BMI) was studied in 17,159 healthy Finnish women aged 25-79 followed up for a median of 12 years. Mortality from all cases was related to BMI only in non-smokers aged 25-64, among whom the mortality pattern was "U"-shaped, with a minimum in the second quintile of BMI (the reference range), and about 1.5 times higher in quintiles I and V. Most of the excess risk of mortality among overweight women was due to cardiovascular diseases. During the first 7 years of follow-up, and high risk (relative risk (RR) = 1.7, 95% confidence interval (CI) = 1.0-2.9 for quintile V compared to quintile II) depended on the association of BMI with the initial blood pressure level, but in the later years, the relative risk of cardiovascular death, ranging from 1.6 (95% CI = 1.0-2.5) for women in quintile III up to 2.6 (95% Ci = 1.7-4.0) for those in quintile V, was largely independent of the baseline levels of the main biological risk factors. The excess mortality among thin women under the age of 65 was mainly due to non-cardiovascular diseases (RR = 1.7, 95% CI = 1.2-2.3 for quintile I compared to quintile II) and was not attributable to antecedent disease, smoking or the biological risk factors studied. Among women aged 65 and over, overall mortality varied little with BMI, but thinness seemed to predict deaths from cancers (RR = 1.6, 95% CI = 0.9-3.0).(ABSTRACT TRUNCATED AT 250 WORDS)     

Auditory cortex evoked magnetic fields and lateralization of speech processing

Potential use of different auditory evoked brain responses for determining cerebral lateralization of speech function was evaluated. Cortical magnetic fields elicited by plosive syllables or complex non-speech sounds analogous to them were recorded with 122-channel magnetometer. We estimated parameters of magnetic P1, N1 and P2 responses to both stimuli in the two hemispheres and found no hemispheric asymmetry for any of the responses. No correlation between the right-ear advantage, determined with dichotic listening test, and any of asymmetry indexes, calculated for the speech-elicited responses, was observed. These results suggest that P1, N1 and P2 responses to speech signals do not indicate lateralization of speech function in the brain. The results are discussed in relation to previous studies suggesting that the mismatch negativity (MMN) seems to be the only early auditory cortex response sensitive to the lateralization of speech function.     

Immunohistochemical expression of DNA repair proteins in familial breast cancer differentiate BRCA2-associated tumors.

PURPOSE: Morphologic and immunohistochemical studies of familial breast cancers have identified specific characteristics associated with BRCA1 mutation-associated tumors when compared with BRCA2 and non-BRCA1/2 tumors, but have not identified differences between BRCA2 and non-BRCA1/2 tumors. Because BRCA1 and BRCA2 genes participate in the DNA repair pathway, we have performed an immunohistochemical study with markers related to this pathway to establish the profile of the three groups. MATERIALS AND METHODS: We have studied two tissue microarrays that include 103 familial and 104 sporadic breast tumors, with a panel of DNA repair markers including ATM, CHEK2, RAD51, RAD50, XRCC3, and proliferating cell nuclear antigen. RESULTS: We found more frequent expression of CHEK2 in BRCA1 and BRCA2 tumors than in non-BRCA1/2 and sporadic tumors. We found absence of nuclear expression and presence of cytoplasmic expression of RAD51 in BRCA2 tumors that differentiate them from other familial tumors. We validated these results with a new series of patient cases. The final study with 253 familial patient cases (74 BRCA1, 71 BRCA2, 108 non-BRCA1/2), and 288 sporadic patient cases, has allowed us to confirm our preliminary results. Because BRCA2 tumors present a specific immunohistochemical profile for RAD51 and CHEK2 markers that is different from non-BRCA1/2 tumors, we have built a multivariate model with these markers that distinguish both tumors with an estimated probability of at least 76%. CONCLUSION: Our results suggest that BRCA2 tumors demonstrate more cytoplasmic and less nuclear RAD51 staining, and increased CHEK2 staining. This pattern may distinguish BRCA2 from familial non-BRCA1/2 tumors.     

Use of wild-type p53 to achieve complete treatment sensitization of tumor cells expressing endogenous mutant p53

It is known that transfer of the wild-type p53 gene into p53-negative cells from transgenic mice increases their sensitivity to drug and radiation-induced apoptosis. However, unlike many human tumors, these transgenic cells do not express mutant p53, and it is not known from these earlier studies whether wild-type p53 dominates the effects of mutant p53 with respect to drug and radiation sensitivity. We addressed this question in glioblastoma, a disease characterized by an unusually high level of intrinsic resistance to therapy and poor prognosis: mean survival time from diagnosis is only about 1 yr. We introduced the gene for wild-type p53 into human T98G glioblastoma cells, which express endogenous mutant p53 but not wild-type p53. Stable transfectants that co-expressed mutant and wild-type p53 had enhanced sensitivity to cisplatin and gamma radiation, compared with parental cells, control vector-transduced cells, and transduced cells that had lost expression of wild-type p53. Transient wild-type p53 expression after high-efficiency gene transfer by a p53 adenovirus also sensitized the cells to cisplatin and correlated with the induction of apoptosis. The sensitization effect was also observed in p53 adenovirus-infected H23 small cell lung carcinoma cells, which express endogenous mutant p53. Therefore, wild-type p53 gene transfer has dominant effects over mutant p53 in sensitizing tumor cells to therapy, which supports the potential of p53 gene therapy to enhance the efficacy of traditional therapy. © 1995 Wiley- Liss, Inc.