烹调油烟致大小鼠肺癌的实验研究

[目的]了解烹调油烟（cooking oil fumes，COF）的动物致癌性。[方法]采用动式染毒法给Balb／c小鼠（雌雄各半）吸入COF浓度为9．09、20．65、38．85mg／m^3，染毒1次／1～2d，30min／次，共150次，计8个月；SD大鼠（雌雄各半）吸入COF浓度为6、88、15．06、35．33mg／m^3，染毒1次／2d，30min／次，共191次，计12．5个月。分别制备COF慢性中毒动物模型；两实验均设空白对照组，吸入与实验组相同温度的清洁空气。[结果]COF诱发Balb／c小鼠实验组肺癌总发生率为18、95％（29／153），低、中、高浓度组肺癌发生率分别为15．09％、20、00％和22．00％，与对照组差异均有显著性。但低、中、高三组间差异无显著性（P〉0．05）；COF诱发SD大鼠肺癌总发生率为9、10％（9／99），低、中、高浓度组肺癌发生率分别为6．45％、8．57％、12．12％，高浓度组肺癌发生率高于对照组（P〈0．05）。各性别组间肺癌发生率的差别无显著性（P〉0．05）。[结论]COF可以诱导Balb／c小鼠和SD大鼠肺癌，诱发的肺癌主要为肺腺癌（小鼠28／29，大鼠7／9），余为小细胞肺癌。     

Human osteoblasts' proliferative responses to strain and 17beta-estradiol are mediated by the estrogen receptor and the receptor for insulin-like growth factor I.

The mechanism by which mechanical strain and estrogen stimulate bone cell proliferation was investigated using monolayer cultures of human osteoblastic TE85 cells and female human primary (first-passage) osteoblasts (fHOBs). Both cell types showed small but statistically significant dose-dependent increases in [3H]thymidine incorporation in response to 17beta-estradiol and to a single 10-minute period of uniaxial cyclic strain (1 Hz). In both cell types, the peak response to 17beta-estradiol occurred at 10(-8) - 10(-7) M and the peak response to strain occurred at 3500 microstrain ((mu)epsilon). Both strain-related and 17beta-estradiol-related increases in [3H]thymidine incorporation were abolished by the estrogen receptor (ER) modulator ICI 182,780 (10-8 M). Tamoxifen (10(-9) - 10(-8) M) increased [3H]thymidine incorporation in both cell types but had no effect on their response to strain. In TE85 cells, tamoxifen reduced the increase in [3H]thymidine incorporation associated with 17beta-estradiol to that of tamoxifen alone but had no such effect in fHOBs. In TE85 cells, strain increased medium concentrations of insulin-like growth factor (IGF) II but not IGF-I, whereas 17beta-estradiol increased medium concentrations of IGF-I but not IGF-II. Neutralizing monoclonal antibody (MNAb) to IGF-I (3 microg/ml) blocked the effects of 17beta-estradiol and exogenous truncated IGF-I (tIGF-I; 50 ng/ml) but not those of strain or tIGF-II (50 ng/ml). Neutralizing antibody to IGF-II (3 microg/ml) blocked the effects of strain and tIGF-II but not those of 17beta-estradiol or tIGF-I. MAb aIR-3 (100 ng/ml) to the IGF-I receptor blocked the effects on [3H]thymidine incorporation of strain, tIGF-II, 17beta-estradiol, and tIGF-I. HOBs and TE85 cells, act similarly to rat primary osteoblasts and ROS 17/2.8 cells in their dose-related proliferative responses to strain and 17beta-estradiol, both of which can be blocked by the ER modulator ICI 182,780. In TE85 cells (as in rat primaries and ROS 17/2.8 cells), the response to 17beta-estradiol is mediated by IGF-I, and the response to strain is mediated by IGF-II. Human cells differ from rat cells in that tamoxifen does not block their response to strain and reduces the response to 17beta-estradiol in TE85s but not primaries. In both human cell types (unlike rat cells) the effects of strain and IGF-II as well as estradiol and IGF-I can be blocked at the IGF-I receptor.     

心血管疾病并发焦虑抑郁症状2050例心理干预治疗分析

目的:了解心血管疾病并发焦虑抑郁症状的情况并探讨心理干预等对焦虑抑郁症状的影响。方法:对住院的2050例心血管疾病并发焦虑抑郁症状的患者进行回顾性分析。结果:心血管疾病患者中并发有焦虑抑郁症状者占56%;其常表现为类似心绞痛、左心衰竭症状,可并发有心律失常;高血压病并发有焦虑抑郁患者对血压升高的耐受性差,动态血压检查以非勺型改变者居多;单纯使用心血管药物治疗效果欠佳,心理干预,焦虑抑郁症状严重者结合抗焦虑抑郁药物疗效显著。结论:心血管疾病患者常并发焦虑抑郁症状,心理干预治疗等可有效改善患者的症状。     

Studies on Toxicity of Nitroquine-Dapsone Compound and Therapeutic Effects of Folic or Folinic Acid on Toxicated Animals

The toxic effects of nitroquine-dapsone compound(NQD)in mice and dogs were studied.The therapeutic index of NQDin mice is 1911,the greatest among the 6 antimalarials tested.Thetoxic effects of NQD(50 mg/kg/day for 3 days per os)and nitro-quine in dogs were manifested by injuries on the adrenal cortexand intestinal epithelium.When folic acid(4 mg/kg/day for 4 days)or calcium leucovorinum(0.3 mg/kg/day for 4 days)were usedconcomitantly with NQD,the death rate and the incidence of dia-rrhea in the toxicated dogs were greatly reduced,the injury on theintestinal epithelium was much milder,and the goblet cells weremuch more numerous than those without treatment.The results suggestthat folic acid and calcium leucovorinum can protect the undifferen-tiated cells in the intestinal crypts from being injured by NQD.     

Delta hepatitis virus infection in China

To assess the prevalence, epidemiological features and prognostic implications of hepatitis D (Delta) in Sichuan Province, The People's Republic of China, 649 sera (515 from HBsAg positive patients and 134 from HBsAg negative subjects) were tested by radioimmunoassay (RIA) for antibody to the hepatitis D virus (anti-HD). Forty-seven sera (7.2%) showed some degree of reactivity. Serial dilutions of these sera indicated that prozoning was not responsible for the equivocal results. Thirty-four of the 47 sera were submitted under code to a second laboratory for independent analysis. According to those results anti-HD antibodies were detected in four of these sera. The overall prevalence of anti-HD in the HBsAg positive patients therefore was 0.8% (4/515). On the basis of clinical, biochemical and histological data 427 HBsAg positive sera were further divided into acute Type B hepatitis, chronic Type B hepatitis, healthy carrier state and hepatocellular carcinoma (HCC) subgroups. Two of 65 (3.1%) anti-HD positive sera belonged to the acute Type B hepatitis group; one of 104 (0.9%), the chronic Type B hepatitis group and one of 246 (0.4%), the healthy carrier group. No antibody was detected in sera from 12 HBsAg positive HCC patients. All HBsAg negative patients were negative for anti-HD antibody. The results of this study indicate that despite a high prevalence of hepatitis B virus infection, positive serology for delta virus is uncommon in Sichuan Province, The People's Republic of China.     

脊柱复合性损伤的救治风险与早期治疗

目的评估脊柱复合性损伤的特点和救治风险,探讨风险控制与最佳治疗的方法。方法采用AIS、ISS、TRISS及APACHEⅡ等评分方法对273例脊柱复合性损伤患者进行定量评价与救治分类,并依据伤后的损伤分级、参数评定及计量评分等指标进行量化分析和统计处理。结果颈椎合并伤115例,胸椎合并伤141例,胸腰椎合并伤294例,腰骶椎合并伤181例;患者的救治风险和脊椎伤的治疗选择或手术时机与其合并伤的解剖伤势及由此所构成的整体伤情密切相关(P<0.01或<0.05);高风险性伤员往往综合伤势严重,生存概率(Ps)趋低,并发症和死亡率高(P<0.01或<0.05)。结论脊柱脊髓损伤常合并有严重的多发伤,高危伤情不仅可增加其救治风险和脊柱伤的处理难度,且还易于丧失手术最佳时机。分类救治对伤员的风险控制和脊柱伤的专科治疗是有益的。     

Disruption of cellular energy balance by suramin in intact human prostatic carcinoma cells, a likely antiproliferative mechanism.

The antiparasitic drug, suramin, has antiproliferative effects in human carcinoma cells. It has been suggested that this occurs through blockade of growth factor-receptor interactions. Three types of evidence that suramin rapidly inhibits cellular respiration or disrupts cellular energy balance in intact cells of the human prostate carcinoma cell line, DU145, are presented. Beginning at approximately 10(-4) M, suramin rapidly causes dose-dependent inhibition of tetrazolium conversion by mitochondrial dehydrogenases in intact cells, demonstrating an inhibition of respiration. This effect is reversed by exchange with suramin-free media but not by pretreatment with serum, epidermal growth factor, insulin-like growth factor I, acidic and basic fibroblast growth factors, or calcium. Rhodamine 123 (10 micrograms/ml) uptake by mitochondria in intact DU145 cells is inhibited in the presence of 10(-3) M suramin. Treatment with 10(-4)-10(-3) M suramin causes the loss of rhodamine 123 from cells with mitochondria prestained with rhodamine 123, indicating that suramin is acting as an ionophore or respiratory poison. Also shown by electron microscopy are progressive toxic changes in mitochondria of DU145 cells within 1 h after treatment with 10(-4) M suramin. These data indicate that in intact DU145 cells 10(-4) M suramin rapidly disrupts cellular energy balance or respiration as seen by three studies of mitochondrial state. Disruption of energy balance or respiration represents a likely antiproliferative mechanism, as is thought to be a primary mechanism for the action of suramin in parasitic diseases. This proposed mechanism of action for suramin can explain the most prominent observed clinical toxicities of nephrotoxicity, adrenal toxicity, coagulopathy, and demyelinating neuropathy.     

Hepatitis B immunity in adolescents and necessity for boost vaccination: 23 years after nationwide hepatitis B virus vaccination program in Taiwan

The first universal hepatitis B vaccination program for newborns in the world was launched in Taiwan in July 1984. Most studies on the effectiveness of hepatitis B vaccination focused on the seroprevalence of HBs Ag among children under 14 years old. Only few studies focused on the seropositivity of anti-HBs among adolescents aged 15–18 years old. The present study aimed to evaluate the impact of the nationwide hepatitis B vaccination program on the immunity to HBV infection and the necessity of boost among adolescents. In this study including eight annual seroprevalence surveys from 2000 to 2007, 2342 college entrants (1589 15-year-olds in group I and 753 18-year-olds in group II) and 1851 university freshmen (18-year-olds in group III) participated. Subjects identified anti-HBs, HBs Ag and anti-HBc negative were given boost three doses of HBV vaccine. The HBs Ag seroprevalence was 11.6%, 3.5% and 1.0% for participants who were born before 1984, 1984–1986 and after 1986. The anti-HBs-seropositive rates were significantly higher in group II (83.1%) than in group I (53.0%) and group III (53.5%). All 572 participants who were seronegative for anti-HBs, HBs Ag and anti-HBc became anti-HBs-seropositive after catch-up vaccination. It is concluded that the anti-HBs-seropositive rate decreased to 50% in 15 years after vaccination, and boost vaccination was 100% effective. The necessity and age for boost among anti-HBs negative adolescents and the timing of the first immunization should be further evaluated.