检测幽门螺旋杆菌感染的几种方法的比较

目的 :评价几种诊断幽门螺杆菌 (Hp)感染的检测方法 .方法 :对 386例患者行胃镜钳取胃窦粘膜 ,分别经改良Giemsa染色、快速尿素酶 (RUT)试验、14 C 尿素呼气试验 (14 C UBT)检查及HpIgG血清学检查 ,与细菌培养结果对照 ,用 χ2检验进行对比评价 .结果 :RUT ,14 C UBT和改良Giemsa染色的敏感性、特异性较高 ,与细胞培养的符合率相近 ,其中14 C UBT和改良Giemsa染色联合检测的符合率更相近 (99.7% ) ;HpIgG血清学检查的敏感度虽和其余检测方法无差别 ,但其特异度较低 ,尤其是复诊组的特异度 ,与其他检测方法有显著差异 (P <0 .0 1) ,而且与初诊组相比也有差异 (χ2 =35 .18,P <0 .0 1) .结论 :HpIgG血清学检查可用于Hp感染的筛查 ,而不能作为疗效判断的指标 ,14 C UBT和改良Giemsa染色联合检测是较可靠的Hp检测方法     

Accelerated 3D echo-planar spectroscopic imaging at 4 Tesla using modified blipped phase-encoding.

Whole-brain echo-planar spectroscopic imaging (EPSI) often substantially lengthens MRI/MRSI (magnetic resonance spectroscopic imaging) protocols. To halve acquisition time, application of a blipped phase-encoding (PE) gradient during the EPSI readout (RO) was previously suggested by PE of the even RO echoes in k-space at an interstitial location along k(PE), separated from the odd RO echoes, effectively reducing the number of PEs by a factor of 2. However, the approach is very susceptible to phase inconsistencies between even and odd RO echoes in the presence of B(0) inhomogeneities and gradient imbalance, leading to ghosting in the PE direction. In this work, the blipped PE gradient is placed in between pairs of even/odd RO gradient lobes to avoid these problems. This approach is demonstrated in a phantom and in normal human brain in vivo at 4T. While the proposed method allows substantial reduction in metabolite ghosting, it may be limited by the presence of a relatively large spurious signal at the Nyquist frequency.     

氯沙坦通过下调单核细胞趋化蛋白1受体表达抑制单核细胞活化

目的探讨血管紧张素Ⅱ对单核细胞趋化蛋白1受体CCR2表达的影响及氯沙坦的干预作用。方法人单核细胞株与血管紧张素Ⅱ(10-7mol/L)孵育,加或不加氯沙坦(10-7、10-6和10-5mol/L),检测上清液中单核细胞趋化蛋白1水平、单核和内皮细胞粘附情况以及CCR2mRNA的表达。结果与对照组比较,血管紧张素Ⅱ明显增加单核细胞培养上清液中单核细胞趋化蛋白1水平(26.46±3.58ng/L比10.56±2.34ng/L,P<0.01),增加单核内皮细胞间粘附(596±27比268±16,P<0.01)。血管紧张素Ⅱ刺激细胞后明显上调CCR2mRNA表达,氯沙坦能显著抑制血管紧张素Ⅱ的作用,降低单核细胞趋化蛋白1的水平,减少单核内皮细胞间粘附,下调CCR2 mRNA表达。结论氯沙坦通过下调单核细胞趋化蛋白1受体CCR2基因表达抑制单核细胞活化。     

儿童幽门螺杆菌感染的诊断和治疗

幽门螺杆菌（H．pylori）感染主要发生在儿童期，儿童期许多消化系统疾病，如慢性胃炎、消化性溃疡等与H．pylori感染密切相关，并可能与成年后胃癌的发生相关。H．pylori感染还可导致儿童缺铁性贫血。H．pylori感染主要经“口-口”或“粪-口”以及“胃-口”途径从人到人传播，社会经济因素对H．pylori感染的影响是主要的。胃镜活检胃黏膜细菌学检查是诊断H．pylori现症感染的“金标准”，粪抗原的测定和^13C-尿素呼气试验可用于诊断和评价疗效。质子泵抑制剂（PPI）加两种抗生素的三联疗法是目前最佳治疗方案，抗生素耐药的不断增加给治疗带来了困难．儿童H．pylori感染对大环内酯类药物的耐药高于成人。     

Hp相关胃炎患者血清表皮生长因子（ECG）和β2—微球蛋白（β2—MG）水平研究

目的探索EGF和β2-MG在CSG -CAG -GC演变模式中的变化规律 ,探讨Hp对EGF和β2-MG有无影响。方法应用尿素酶试验法、血清学试验法和组织学诊断法 ,进行Hp检查 ,应用放射免疫法检测血清EGF及β2-MG水平。结果(一)EGF水平(μg/L) :(1)按CSG -CAG -GC逐渐升高 ,依次为0.3229±0.225 ,0.8823±0.2549,1.3999±0.8935,GC组高于CSG组 (P<0.01) ,也高于CAG组 (P<0.05) ,CAG组高于CSG组 (P<0.01)。(2)CSG患者Hp(+)组 (0.2404±0.1103)低于Hp( -)组 (0 .4492±0.2931) (P<0.01) ;CAG患者Hp(+)组 (0 .8119±0.279)低于Hp(- )组(1.0056±0.1704) ,GC患者Hp(+)组 (1.159±0 .9229)低于Hp(- )组(1 .4963±0 .9127) ,均无统计学差异 (P>0.05)。(二 ) β2-MG水平 (mg/l) :(1)按CSG -CAG -GC顺序增高 ,依次为 :1.659±0.4321 ,1 .9661±1 .0802,2.3431±0 .5951 ,GC组高于CSG组 (P<0.01),CAG组高于CSG组 ,GC组高于CAG组 ,均无统计学意义 (P>0.05)。(2)同一胃病Hp( +)组与Hp( -)组比较血清β2-MG水平均无明显差异 (P>0.05)。结论按CSG -CAG -GC ,EGF水平逐渐升高 ,β2-MG有此种趋势。Hp有降低EGF的作用 ,Hp对β2-MG水平无明显影响     

幽门弯曲菌感染快速诊断试剂盒的研制及临床应用

介绍两种幽门弯曲菌(CP)感染快速诊断试剂盒的制备,用其检测244例胃粘膜标本,同时与细菌培养及组织学检查结果比较。试剂盒1号、3号对诊断CP感染的敏感性分别为97％和91％,均无假阳性。CP数量、试剂盒中尿素浓度与试剂盒的反应时间呈负相关。用试剂盒3号检测在10min之内即可出结果。具有敏感性强,特异性高及简便、快速的优点,尤其适于在内镜室内使用。     

CHARACTERISTICS OF MEMBRANE TRANSPORT PROCESSES OF MACULA DENSA CELLS

1. Macula densa (MD) cells are located within the thick ascending limb (TAL) and have their apical surface in contact with tubular fluid and their basilar region in contact with the glomerulus. These cells sense changes in luminal fluid sodium chloride concentration ([NaCl]) and transmit signals resulting in changes in vascular resistance (tubuloglomerular feedback) and renin release. 2. Current efforts have focused on understanding the cellular transport mechanisms of MD cells. Progress in this area has benefited from the use of the isolated perfused TAL-glomerular preparation, which permits direct access to MD cells. 3. Using microelectrodes to measure basolateral membrane potential (V_BL) of MD cells, it was found that VBL was very sensitive to changes in luminal fluid [NaCl]. As [NaCl] was elevated from 20 to 150mmol/L, V_BL was found to depolarize by over 30 mV. 4. Basolateral membrane potential measurements were also used to identify an apical Na⁺: 2CI^?: K⁺ cotransport pathway in MD cells that is the major pathway for NaCl entry into these cells. 5. Other work identified a basolateral chloride channel that is presumed to be responsible for changes in V_BL during alterations in luminal [NaCl]. This channel, which is the predominant conductance across the basolateral membrane, may be regulated by intracellular Ca²⁺ and cAMP. 6. An apical Na⁺: H⁺ exchanger in MD cells was detected by measuring changes in intracellular pH using the fluorescent probe 2′,7′-bis-(2-carboxyethyl)-5(and-6) carboxyfluorescein. 7. Using patch-clamp techniques, a high density of pH- and Ca²⁺-sensitive K⁺ channels was observed at the apical membrane of MD cells. 8. Other studies found that, at the normal physiological conditions prevailing at the end of the TAL (luminal [NaCl] of 20–60 mmol/L), reabsorption mediated by MD cells is very sensitive to changes in luminal [NaCl].     

HFE codon 63/282 (H63D/C282Y) dimorphism in German patients with genetic hemochromatosis

Abstract: Genetic hemochromatosis (GH) is closely associated with genes of the major histocompatibility complex (MHC) on chromosome 6. Recently, a candidate gene for GH, with structural similarities to MHC class I genes, designated HLA-H and presently named HFE, has been cloned. The HFE gene is localized telomeric to the MHC and several reports have indicated that the HFE gene is mutated in GH patients. In the present study we have analyzed the relationship of HFE gene variants and disease manifestation in GH patients and family members. Fifty-seven patients with GH, 73 family members and 153 healthy blood donors were studied for the amino acid dimorphism at codon 63 (His63Asp=H63D) and codon 282 (Cys282Tyr= C282Y) of the HFE gene. The codon 63 and 282 dimorphism were defined by PCR amplification of genomic DNA samples and restriction enzyme digestion using RsaI/SnaBI for C282Y and Bcll/Mbo 1 for H63D. Ferritin, transferrin serum levels and total iron-binding capacity were determined prior to therapeutic intervention. The Tyr-282 substitution occurred in 53 (93%) of patients compared with 8 (5.2%) of controls (OR=169, P >0.0001). Fifty-one (90%) patients were Tyr-282 homozygous. In contrast, the Asp-63 substitution was present in 5 (8.8%) of the patients compared with 34 (22%) of controls (OR=0.39, P =NS) with none of the patients being homozygous. In Tyr-282 homozygous GH patients serum ferritin levels, transferrin saturation, liver iron and liver iron index were elevated significantly compared to Tyr-282-negative patients, whereas no difference was observed between Tyr/Cys-282 heterozygous and Tyr-282-negative patients.     

EFFECT OF SOME TRICYCLIC AND NONTRICYCLIC ANTIDEPRESSANTS ON [3H]IMIPRAMINE BINDING AND SEROTONIN UPTAKE IN RAT CEREBRAL CORTEX AFTER PROLONGED TREATMENT

Chronic administration of different antidepressant drugs reduced the number of [3H]imipramine [( 3H]IMI) binding sites in rat cerebral cortex. In the same experimental conditions, fluvoxamine and dothiepin, as well as desmethylimipramine, induced an increase in the maximal velocity of high affinity serotonin (5HT) uptake in cortical slices, whereas citalopram and viloxazine were ineffective in this regard. Our results indicate that even if 5HT uptake and [3H]IMI binding sites are located on the same nerve terminals, they are differently modulated. Increased Vmax of the 5HT uptake process could be due to a rebound phenomenon after withdrawal from drugs that acutely inhibit 5HT uptake. The effect on [3H]IMI sites might be explained through either the agonist properties of the drugs towards these sites or the involvement of mechanisms still unknown.     

Convergence of Genetic, Nutritional and Inflammatory Factors in Gastrointestinal Cancers

Gastrointestinal cancers account for 20% of all cancer incidences worldwide. Colorectal cancer is the second most common cause of all cancer-related mortality and is increasing in Western societies. Infection and inflammation contribute to 15–20% of all malignancies, and are predisposing risk factors for gastrointestinal cancers. Helicobacter pylori infection is commonly associated with gastric cancers, and chronic inflammation increases the risk of colorectal cancer by 1% per year. Micronutrient status and common genetic variations in human populations modify risk for gastrointestinal cancer. Chronic inflammation promotes carcinogenesis by inducing gene mutations, inhibiting apoptosis, and stimulating an-giogenesis and cell proliferation. Inflammation also induces epigenetic alterations that are associated with cancer development. Two key genes in the inflammatory process, cyclooxygenase-2 (COX-2) and nuclear factor-kappa B (NF-kB), provide a mechanistic link between inflammation and cancer and are targets for chemoprevention. Dietary components, and human genetic variation that affects nutrient utilization, can directly modify inflammatory processes and/or suppress genomic alterations that are the molecular antecedents of cancers. The present report focuses on the convergence of genetic, nutritional, and inflammatory factors in the initiation and progression of gastrointestinal cancers, and the emerging dietary strategies for cancer prevention.