A study on various symptoms of chronic hepatitis treated with radix astragali and its regulative effect to levels of serum hormone

Sixty-seven cases of chronic hepatitis were treated with Radix Astragali. After treatment (2-month course), the clinical improvement rate in 38 cases of the Stagnation of the Liver-Qi and Deficiency of the Spleen type was 92.1%, and in 26 cases of the Deficiency of Liver Yin and Kidney Yin type was 88.5%, more effective than in the control group (P<0.05). The regulative effect to the levels of serum hormone was observed in the patients of the Stagnation of the Liver-Qi and Deficiency of the Spleen type treated with this medicine. The results showed that the levels of serum triiodothyronine, estradiol (female) and testosterone (male) were increased after treatment (1.40±1.38 ng/dl, 129.30±1.23 pg/ml and 496.24±1.47 ng/dl). Pre-treatment levels were 1.22±1.49 ng/dl, 104.60±1.45 pg/ml and 398. 17±1.55 ng/dl respectively (P<0.05); however, the level of serum prolactin (2.75±4.46 ng/ml) was lower after treatment than before treatment (3.20±3.82 ng/ml,P<0.05). No obvious changes were observed in the levels of serum follicle stimulating hormone, luteinizing hormone, thyroid stimulating hormone, thyroxine, triiodothyronine uptake ratio and cortisol after treatment.     

Contributions of ion conductances to the onset responses of octopus cells in the ventral cochlear nucleus: simulation results

The onset response pattern displayed by octopus cells has been attributed to intrinsic membrane properties, low membrane impedance, and/or synaptic inputs. Although the importance of a low membrane impedance generally is acknowledged as an essential component, views differ on the role that ion channels play in producing the onset response. In this study, we use a computer model to investigate the contributions of ion channels to the responses of octopus cells. Simulations using current ramps indicate that, during the "ramp-up" stage, the membrane depolarizes, activating a low-threshold K(+) channel, K(LT), which increases membrane conductance and dynamically increases the current required to evoke an action potential. As a result, the model is sensitive to the rate that membrane potential changes when initiating an action potential. Results obtained when experimentally recorded spike trains of auditory-nerve fibers served as model inputs (simulating acoustic stimulation) demonstrate that a model with K(LT) conductance as the dominant conductance produces realistic onset response patterns. Systematically replacing the K(LT) conductance by a h-type conductance (which corresponds to a hyperpolarization-activated inward rectifier current, I(h)) or by a leakage conductance reduces the model's sensitivity to rate of change in membrane potential, and the model's response to "acoustic stimulation" becomes more chopper-like. Increasing the h-type conductance while maintaining a large K(LT) conductance causes an increase in threshold to both current steps and acoustic stimulation but does not significantly affect the model's sensitivity to rate of change in membrane potential and the onset response pattern under acoustic stimulation. These findings support the idea that K(LT), which is activated during depolarization, is the primary membrane conductance determining the response properties of octopus cells, and its dynamic role cannot be provided by a static membrane conductance. On the other hand, I(h), which is activated during hyperpolarization, does not play a large role in the basic onset response pattern but may regulate response threshold through its contribution to the membrane conductance.     

Polysaccharide-protein surface modification of titanium via a layer-by-layer technique: characterization and cell behaviour aspects

To improve the surface biocompatibility of titanium films, a layer-by-layer (LBL) self-assembly technique, based on the polyelectrolyte-mediated electrostatic adsorption of chitosan (Chi) and gelatin (Gel), was used leading to the formation of multilayers on the titanium thin film surfaces. The film growth was initialized by deposition of one layer of positively charged poly(ethylene imine) (PEI). Then the thin film was formed by the alternate deposition of negatively charged Gel and positively charged Chi utilizing electrostatic interactions. The LBL film growth was monitored by several techniques. The chemical composition, surface topography as well as wettability were investigated by using X-ray photoelectron spectroscopy (XPS), atomic force microscopy (AFM), confocal laser scanning microscopy (CLSM) and water contact angle measurement, respectively. Quantitative XPS analysis showed the alternative change of C/N ratio after four sequential cycles coating of Ti/PEI/Gel/Chi/Gel, which indicated the discrete layer structure of coatings. Uncoated titanium (control sample) displayed a smooth surface morphology (root mean square (RMS) roughness was around 2.5 nm). A full coverage of coating with Gel/Chi layers was achieved on the titanium surface only after the deposition layers of PEI/(Gel/Chi)2. The PEI/Gel/(Chi/Gel)3 layer displayed a rough surface morphology with a tree-like structure (RMS roughness is around 82 nm). These results showed that titanium films could be modified with Chi/Gel which may affect the biocompatibility of the modified titanium films. To confirm this hypothesis, cell proliferation and cell viability of osteoblasts on LBL-modified titanium films as well as control samples were investigated in vitro. The proliferation of osteoblasts on modified titanium films was found to be greater than that on control (p<0.05) after 1 and 7 days culture, respectively. Cell viability measurement showed that the Chi/Gel-modified films have higher cell viability (p<0.05) than the control. These data suggest that Chi/Gel were successfully employed to surface engineer titanium via LBL technique, and enhanced its cell biocompatibility. The approach presented here may be exploited for fabrication of titanium-based implant surfaces.     

Complement activation promotes muscle inflammation during modified muscle use

Modified muscle use can result in muscle inflammation that is triggered by unidentified events. In the present investigation, we tested whether the activation of the complement system is a component of muscle inflammation that results from changes in muscle loading. Modified rat hindlimb muscle loading was achieved by removing weight-bearing from the hindlimbs for 10 days followed by reloading through normal ambulation. Experimental animals were injected with the recombinant, soluble complement receptor sCR1 to inhibit complement activation. Assays for complement C4 or factor B in sera showed that sCR1 produced large reductions in the capacity for activation of the complement system through both the classical and alternative pathways. Analysis of complement C4 concentration in serum in untreated animals showed that the classical pathway was activated during the first 2 hours of reloading. Analysis of factor B concentration in untreated animals showed activation of the alternative pathway at 6 hours of reloading. Administration of sCR1 significantly attenuated the invasion of neutrophils (-49%) and ED1(+) macrophages (-52%) that occurred in nontreated animals after 6 hours of reloading. The presence of sCR1 also reduced significantly the degree of edema by 22% as compared to untreated animals. Together, these data show that increased muscle loading activated the complement system which then briefly contributes to the early recruitment of inflammatory cells during modified muscle loading.     

The role of beta-catenin, TGF beta 3, NGF2, FGF2, IGFR2, and BMP4 in the pathogenesis of mesenteric sclerosis and angiopathy in midgut carcinoids

A subset of midgut carcinoids (MCs) result in mesenteric angiopathy (MA) and bowel infarction as a consequence of vascular compression caused by extensive mesenteric sclerosis (MS). The goal of this study was to determine whether the level of expression of several fibrosing-related growth factors was related to the finding of MA and/or MS in MCs. Eighteen cases of MC, 6 with both extensive MS and MA (group I), 5 with extensive MS only (group II), and 7 with ordinary MS only (group III), were analyzed for immunoexpression of beta-catenin, transforming growth factor-beta 2 (TGF beta 2), nerve growth factor 2 (NGF2), fibroblast growth factor 2 (FGF2), insulin growth factor receptor (IGFR), and bone morphogenic protein 4 (BMP4) in formalin-fixed, paraffin-embedded sections. Standard immunohistochemical technique was used following antigen retrieval. Immunostaining was scored semiquantitively as the product of the percentage and intensity (0 to 2+) of the immunostaining, giving a possible range of 0 to 200. One-way analysis of variance and Mann-Whitney nonparametric analyses were used for statistical analysis. The mean scores of immunoreactivity of each factor in groups I, II, and III were as follows: 135, 174, and 147 for beta-catenin (cytoplasmic reactivity only); 106, 112, and 92 for TGF beta 3; 1.67, 32, and 36 for NGF-2; 2.5, 48, and 55 for FGF-2; 19, 112, and 66 for IGFR2; 140, 45, and 52 for BMP4. There were significant differences in NGF-2 immunoreactivity between groups I and III (P = 0.0023) and in BMP4 immunoreactivity between groups I and II (P = 0.017) and groups I and III (P = 0.022). All MCs expressed high levels of membranous beta-catenin, moderate levels of TGF beta 3 and IGFR2, and low levels of FGF-2, with no significant differences seen among the groups. MCs with prominent MS and MA (group I) expressed significantly higher BMP4 than those in groups II and III, suggesting a potential role of BMP4 in the pathogenesis of MA. The level of NGF-2 expression was significantly lower in group I than in group III, possibly indicating abnormal angiogenesis in the formation of angiopathy.     

血管内皮生长因子和E26转录因子在乳腺癌中的表达及意义

目的 试图揭示血管内皮生长因子（VEGF）和E26转录因子（E26 transformation-specificl,ETS-1)在乳腺癌组织中的表达规律,探讨其在血管生成和肿瘤浸润转移中的作用机制。方法 应用原位杂交和免疫组织化学链霉素抗生物系－过氧化物酶复合物法（SP）法,检测48例乳腺癌组织中VEGF和ETS－1的mRNA和蛋白的表达。结果 乳腺癌细胞高表达VEGF mRNA和蛋白,阳性率分别为75％（36／48）,70．8％（34／48）,而血管内皮细胞几乎不表达;ETS－1既表达在乳腺癌细胞,也表达在血管内皮细胞。癌细胞中mRNA和蛋白表达阳性率分别为85．4％（41／48）,79．2％（38／48）;VEGF和ETS－1高表达组的血管密度明显高于低表达组（均P＜0．01）;VEGF和ETS－1的表达与组织学分级和淋巴结转移密切相关,并且高表达组的微血管密度明显高于低表达组（P＜0．01）。结论 VEGF和ETS－1可促进乳腺癌血管形成,同时也促进肿瘤的浸润和转移;检测VEGF和ETS－1的表达可做为乳腺癌恶性度,浸润转移等生物学行为的参考指标。     

An electrical admittance based index of thoracic intracellular water during head-up tilt in humans

During 50 degrees head-up tilt (HUT), the number of erythrocytes within the thorax has been shown to be reduced by approximately 25% and this level is retained during a maintained tilt, whilst that in the thigh increases by approximately 70%. To evaluate whether the electrical admittance of intracellular water (ICW) may be used to monitor this redistribution of red cells in humans, we determined the regional difference in the reciprocal value of the impedance at 1.5 and 100 kHz for the thorax (thoraxICW) and for the leg (legICW). In ten subjects all variables remained unchanged during head-down tilt but during HUT, presyncopal symptoms were induced in eight subjects after a mean of 27 (SEM 7) min as mean heart rate dropped from 85 (SEM 4) to 66 (SEM 3) beats x min(-1), mean arterial blood pressure from 80 (SEM 3) to 60 (SEM 5) mmHg, and mean oxygen saturation of venous blood from 76 (SEM 2)% to 73 (SEM 3)% (P < 0.05). The mean haematocrit increased from 50 (SEM 5)% to 52.5 (SEM 3.5)% (P < 0.01) and mean central venous pressure decreased during tilting (from a mean of 1 (SEM 1) to a mean of -1 (SEM 1) mmHg; P < 0.05) and returned to value at rest during the maintained tilt. Mean thoracic impedances increased by 7.0 (SEM 1.0) ohms (1.5 kHz) and 5.4 (SEM 1.2) ohms (100 kHz), and mean leg impedances decreased by 9.3 (SEM 1.2) ohms (1.5 kHz) and 3.1 (SEM 1.0) ohms (100 kHz) (P < 0.01). Mean thoraxICW decreased at 40 degrees HUT and remained reduced by 11 (SEM 2) S x 10(-4) (P < 0.05) until the presyncopal symptoms developed, at which time it was lower by 16 (SEM 2) S x 10(-4) (P < 0.01). Mean legICW increased from 97 (SEM 15) to 99 (SEM 15) S x 10(-4) (P = 0.08) during HUT but decreased during maintained tilt (to 94 (SEM 15) S x 10(-4); P < 0.05). The results suggested that during HUT, the difference in electrical admittance at a high and a low frequency current reflects the reduced number of red cells within the thorax.     

唾液酸化的路易斯寡糖—X抗原在结直肠癌细胞系LoVo,HT29？…

目的 探讨唾液酯化的路易期寡糖－Ｘ（ＳＬｅＸ）抗原的表达与结直肠癌转移潜能的相关性。方法 采用原位分子杂交技术,检测结直肠癌细胞表面ＳＬｅＸ抗原合成酶－－α１,３岩藻糖转移酶（α１,３Ｆｕｃ－Ｔ）在高、低转移民生结直肠癌细胞系ＬｏＶｏ、ＨＴ２９细胞内的ｍＲＮＡ水平的表达,并应用免疫组化ＬＳＡＢ法,流式细胞仪,从定性、定量两个方面直接检测ＳＬｅＸ抗原在ＬｏＶｏ、ＨＴ２９细胞内蛋白水平的表达。结果 高     

Organ distribution of severe acute respiratory syndrome (SARS) associated coronavirus (SARS-CoV) in SARS patients: implications for pathogenesis and virus transmission pathways

We previously identified the major pathological changes in the respiratory and immune systems of patients who died of severe acute respiratory syndrome (SARS) but gained little information on the organ distribution of SARS-associated coronavirus (SARS-CoV). In the present study, we used a murine monoclonal antibody specific for SARS-CoV nucleoprotein, and probes specific for a SARS-CoV RNA polymerase gene fragment, for immunohistochemistry and in situ hybridization, respectively, to detect SARS-CoV systematically in tissues from patients who died of SARS. SARS-CoV was found in lung, trachea/bronchus, stomach, small intestine, distal convoluted renal tubule, sweat gland, parathyroid, pituitary, pancreas, adrenal gland, liver and cerebrum, but was not detected in oesophagus, spleen, lymph node, bone marrow, heart, aorta, cerebellum, thyroid, testis, ovary, uterus or muscle. These results suggest that, in addition to the respiratory system, the gastrointestinal tract and other organs with detectable SARS-CoV may also be targets of SARS-CoV infection. The pathological changes in these organs may be caused directly by the cytopathic effect mediated by local replication of the SARS-CoV; or indirectly as a result of systemic responses to respiratory failure or the harmful immune response induced by viral infection. In addition to viral spread through a respiratory route, SARS-CoV in the intestinal tract, kidney and sweat glands may be excreted via faeces, urine and sweat, thereby leading to virus transmission. This study provides important information for understanding the pathogenesis of SARS-CoV infection and sheds light on possible virus transmission pathways. This data will be useful for designing new strategies for prevention and treatment of SARS.