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IntroductionUnderstanding patterns and processes of microbial biogeography in soils is important for monitoring ecological responses to human activities, particularly in ecologically vulnerable areas such as the Qinghai-Xizang Plateau. Highland barley is the staple food of local people and has mainly been cultivated along the Yarlung Zangbo River valley in Xizang.MethodsHere we investigated soil bacterial communities from 33 sampling sites of highland barley farmland in this region and compared them to those from wild ecosystems including alpine tundra, meadow, forest, and swamp. Additionally, the effects of environmental factors on bacterial communities, as well as the relative importance of stochastic and deterministic processes in shaping the beta diversity of soil bacterial communities in alpine ecosystems were assessed.ResultsIn contrast to soils of wild ecosystems, these farmland samples harbored a highly homogeneous bacterial community without significant correlations with geographic, elevation, and edaphic distances. Discriminant bacterial taxa identified for farmland samples belong to Acidobacteria, with Acidobacteria Gp4 as the dominant clade. Although Acidobacteria were the most abundant members in all ecosystems, characterized bacterial taxa of meadow and forest were members of other phyla such as Proteobacteria and Verrucomicrobia. pH and organic matter were major edaphic attributes shaping these observed patterns across ecosystems. Null model analyses revealed that the deterministic assembly was dominant in bacterial communities in highland barley farmland and tundra soils, whereas stochastic assembly also contributed a large fraction to the assembly of bacterial communities in forest, meadow and swamp soils.DiscussionThese findings provide an insight into the consequences of human activities and agricultural intensification on taxonomic homogenization of soil bacterial communities in the Qinghai-Xizang Plateau.

Objective: To observe the effect of vitaminD3 on airway inflammation and osteopontin (OPN) expression on cough variant asthma (CVA) models. Methods: SD rats were randomly divided into blank group, model group and treatment group, each group with 10 rats. The CVA model was induced by intraperitoneal injection combined with aerosolized ovalbumin (OVA), the treatment group was given 100 mg / ml of vitaminD3 30 minutes before challenge by administered orally. Airway hyperreaction were measured by airway resistance after inhalation of acetylcholine (Ach). Wright-Gimsa staining was used to observe the inflammatory cells in bronchoalveolar lavage fluid (BALF). HE and PAS were used to observe the morphological changes of lung tissue. OPN expression was detected by immunohistochemistry. Results: 1) Airway hyperreaction: airway resistance after inhalation Ach in model group and treatment group were significantly higher than that in blank group (P <0.01), airway resistance in treatment group were lower than that in model group (P <0.01); 2) Classification of inflammatory cells: The percentage of macrophages, lymphocytes, neutrophils, and eosinophils in the BALF of the model group and the treatment group were increased compared with the blank group (P <0.01),furthermore, the number of treatment group were lower than the model group(P <0.05); 3) Morphological changes of lung tissue: a large amount of inflammatory cells and goblet cell proliferation were observed in the lung tissue of the model group, and these changes were slight in treatment group compared with model group; OPN expression in lung tissue: The expression of OPN in model and treatment group were increased compared with blank group (P <0.05), and the treatment group was lower than that of model group (P <0.05). The OPN content was positively correlated with the percentage of inflammatory cells in BALF (P < 0.05). Conclusions: Vitamin D3 can reduce airway hyperreaction and airway inflammation in CVA rats. The mechanism may be related to the intervention of OPN expression in lung tissue. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of low-frequency rTMS combined with fasudil on neurological function in patients with acute cerebral infarction and its mechanism. Method:120 patients with acute cerebral infarction admitted from January 2016 to January 2019 were randomly divided into four groups: control group (n = 30), fasudil group (n = 30), rTMS group (n = 30), fasudil + rTMS group (n = 30). The changes of NIHSS score, ADL score, serum GAP- 43, serum RhoA and serum ROCK-II were observed and recorded before and after treatment. Results: The ADL scores and serum GAP-43 levels of the four groups after treatment were higher than those before treatment (P < 0.05); the NIHSS scores, serum RhoA and serum ROCK-II levels of the four groups after treatment were lower than those before treatment (P < 0.05); After treatment, ADL score and serum GAP-43 level in fasudil+rTMS group were higher than those in other three groups (P < 0.05); After treatment, NIHSS score, serum RhoA and serum ROCK-II levels in fasudil+rTMS group were lower than those in other three groups (P < 0.05). After treatment, NIHSS score was positively correlated with RhoA and ROCK-II content, negatively correlated with GAP-43 content and ADL score. Conclusions: Low-frequency rTMS combined with fasudil in the treatment of acute cerebral infarction can significantly improve neurological deficits, improve daily living ability, promote axonal remodeling and regeneration. It may be one of its mechanisms by increasing the expression of GAP-43 in serum and reducing the expression levels of RhoA and ROCK-II in serum. It has high clinical value. [ABSTRACT FROM AUTHOR]

Abstract The present study determines whether the in vivo injection of TGFβ1 and CTGF mediated by AAV2 to transfect nucleus pulposus cells in degenerative lumbar discs can reverse the biological effects of rhesus lumbar disc degeneration. A total of 42 lumbar discs obtained from six rhesus monkeys were classified into three groups: experimental group, control group, and blank group. Degenerative lumbar discs were respectively injected with double gene‐transfected human nucleus pulposus cells using minimally invasive techniques. Immumohistochemical staining, RT‐PCR, and western blot were performed to observe the biological effects of double gene‐transfected human nucleus pulposus cells in degenerative lumbar discs on rhesus lumbar disc degeneration. At 4, 8, and 12 weeks after the transplantation of nucleus pulposus cells, the expression levels of TGF‐ß1, CTGF, proteoglycan mRNA, and type‐II collagen were detected by RT‐PCR. The values of immumohistochemical staining and RT‐PCR in the experimental group increased at 8 weeks, decreased with time at 12 weeks, and remained greater than the values in the control group, and the differences were statistically significant (P

Phosphate-solubilizing fungi (PSF) play an important role in increasing the bioavailability of phosphorus in soils for plants. Thirteen fungal strains, one collected from air and 12 from soil, were screened and described here in detail. These fungal strains were tested for their ability to solubilize tricalcium phosphate (TCP) on both solid and liquid Pikovskaya (PVK) media in vitro. The airborne fungal strain KUMCC 18-0196 (Aspergillus hydei sp. nov.) showed the most significant phosphate solubilizing activity on a solid PVK medium with the solubilization index (SI) (2.58 ± 0.04 cm) and the highest solubilized phosphates (1523.33 ± 47.87 μg/mL) on a liquid PVK medium. To the best of our knowledge, A. hydei sp. nov. is the first phosphate-solubilizing fungus reported from air. We also provide the identification especially for Aspergillus, Penicillium and Talaromyces, generally reported as PSF. It is important to not only screen for PSF but also identify species properly so that researchers have a clearer taxonomic picture for identifying potential taxa for future plant growth-promoting applications. Herein, A. hydei (section Nigri), Gongronella hydei, Penicillium soli (section Lanata-Divaricata) and Talaromyces yunnanensis (section Talaromyces) are fully described and introduced as new to science. These four new species are identified based on both morphological characteristics and multigene phylogenetic analyses, including the genealogical concordance phylogenetic species recognition method where necessary. Penicillium austrosinense is considered to be a synonym of P. guaibinense.

Gu JW, Manning RD Jr, Young E, Shparago M, Sartin B, Bailey AP. Vascular endothelial growth factor receptor inhibitor enhances dietary salt-induced hypertension in Sprague-Dawley rats. Am J Physiol Regul Integr Comp Physiol 297: R142-Rl48, 2009. First published May 6, 2009; doi: 10.1152/ajpregu.90972.2008.-Clinical evidence links the inhibition of VEGF to hypertension. However, the mechanisms by which VEGF affects the pathogenesis of hypertension remain in question. We determined I) whether administration of VEGF receptor inhibitor SU5416 enhances dietary salt-induced hypertension in Sprague-Dawley (SD) rats, and 2) whether VEGF or SU5416 directly affects proliferation of cultured human renal proximal tubular epithelial cells (HRPTEC) and endothelial nitric oxide synthase (eNOS) expression in cultured human glomerular microvesset endothelial cells (HGMEC). Ten 10-wk-old male SD rats received a high sodium diet (HS; 8%) and the other 10 SD rats received a normal sodium diet (NS; 0.5%) for 4 wks. After 2 wks of the dietary program, five rats were administered with SU5416 at 10 mgkg day ip or DMSO (vehicle) for 14 days in HS and NS groups. Mean arterial pressure was significantly higher in rats treated with SU5416, as opposed to those treated with DMSO and fed with HS for 4 wk (157.6 ± 3.9 vs. 125.9 ± 4.3 mmHg, P < 0.01). Increased proteinuria and albuminuria were associated with marked renal histological abnormalities in HS group with SU5416 administration, compared with those in the vehicle HS group. 3H-thymidine incorporation assay showed that SU5416 blocked the actions of both exogenous and endogenous VEGF on the proliferation of HRPTEC. VEOF (10 ng/ml) significantly increased eNOS protein levels by 29% in cultured HGMEC, but its action was completely abolished by SU5416. These results suggest that VEGF receptor inhibition enhances dietary saltinduced hypertension and kidney injury, possibly by direct damage on renal cells and decreasing NO production by eNOS. [ABSTRACT FROM AUTHOR]

Molecular mechanisms of salt-sensitive (SS) hypertension related to renal inflammation have not been defined. We seek to determine whether a high-salt (HS) diet induces renal activation of NF-κB and upregulation of TNF-α related to the development of hypertension in Dahl SS rats. Six 8-wk-old male Dahl SS rats received a HS diet (4%), and six Dahl SS rats received a low-sodium diet (LS, 0.3%) for 5 wk. In the end, mean arterial pressure was determined in conscious rats by continuous monitoring through a catheter placed in the carotid artery. Mean arterial pressure was significantly higher in the HS than the LS group (177.9 ± 3.7 vs. 109.4 ± 2.9 mmHg, P < 0.001). There was a significant increase in urinary albumin secretion in the HS group compared with the LS group (22.3 ± 2.6 vs. 6.1 ± 0.7 mg/day; P < 0.001). Electrophoretic mobility shift assay demonstrated that the binding activity of NF-κB p65 proteins in the kidneys of DahI SS rats was significantly increased by 53% in the HS group compared with the LS group (P = 0.007). ELISA indicated that renal protein levels of TNF-α, but not IL-6, interferon-γ, and CCL28, were significantly higher in the HS than the LS group (2.3 ± 0.8 vs. 0.7 ± 0.2 pg/mg; P = 0.036). We demonstrated that plasma levels of TNF-α were significantly increased by fivefold in Dahl SS rats on a HS diet compared with a LS diet. Also, we found that increased physiologically relevant sodium concentration (10 mmol/l) directly stimulated NF-κB activation in cultured human renal proximal tubular epithelial cells. These findings support the hypothesis that activation of NF-κB and upregulation of TNF-α are the important renal mechanisms linking proinflammatory response to SS hypertension. [ABSTRACT FROM AUTHOR]

Abstract  The role of angiostatic factors, including endostatin, in regulating physiological angiogenesis is poorly understood. We used normal adult rats under physiological resting conditions to examine the relationship between tissue endostatin, VEGF, and capillary density (CD) in the heart (high metabolic activity) versus the skeletal muscle (relatively low metabolic activity). The heart (left ventricle, LV) and skeletal muscle (anterior tibialis, AT) were dissected from 12-week-old male Sprague–Dawley rats. Transverse cryosections of LV and AT were stained with FITC-conjugated GS-I-lectin. CD was determined by analysis of randomly acquired digital images of the cryosections using Optimas software. Tissue protein levels of endostatin and VEGF were determined by ELISA assays. Tissue endostatin levels were lower in the LV and higher in the AT (135 ± 39 vs. 663 ± 114 pg/mg) and VEGF levels were higher in the LV and lower in the AT (41 ± 3 vs. 27 ± 4 pg/mg), respectively (n = 7, P < 0.01). CD in LV and AT were 3632 ± 428 and 437 ± 44/mm2, respectively (P < 0.01). We demonstrated that an 8.3-fold greater capillary density is related to a 4.9-fold lower level of tissue endostatin and a 1.5-fold higher level of tissue VEGF in the heart (LV) versus the skeletal muscle (AT) of normal rats under physiological resting conditions. Also, exercise training increased capillary density, decreased tissue endostatin and increased tissue VEGF in the skeletal muscle (AT). These findings suggest that tissue endostatin content correlates inversely with capillary network in the muscle tissues with different metabolic activity, and that tissue endostatin may play a very important role in the metabolic control of angiogenesis under physiological conditions. [ABSTRACT FROM AUTHOR]

X-ray CT plays a great role both in medical fields and in industrial nondestructive tests. In imaging, metal objects absorb X-rays greatly, which introduces streaks on reconstructed images. In this paper, we propose a method for metal artifacts reduction. Firstly, the metal projection region is accurately identified and an interpolation method based on such identification is applied to get the projection data without metal. The image excluding metal is reconstructed from the modified projection data. Secondly, the image without metal is combined with the image of metal to form a complete reconstruction. Numerical simulations and a phantom experiment demonstrate that the metal artifacts can be effectively suppressed using our method and the reconstructed image is more accurate in depicting the details of cross-sections, especially in the immediate neighborhood of the metal object. The proposed method is computationally efficient and can be easily adapted to current commercial CT scanners. [ABSTRACT FROM AUTHOR]

Background: Many in vitro studies have shown that adenosine (Ado) can induce vascular endothelial growth factor (VEGF) mRNA and protein expression and stimulate endothelial proliferation. In the present study, we seek to determine whether Ado can increase circulating levels of VEGF protein in the intact human. Methods: Five outpatients 49.3 ± 6.7 years of age and weighing 88.2 ± 8.5 kg were selected. They were given a 6 min intravenous infusion of Ado (0.14 mg kg-1 min-1) in conjunction with sestamibi myocardial perfusion scans. Mean blood pressure (MBP, calculated from systolic and diastolic values) and heart rate (HR) were determined before Ado infusion and every 2 min for the next 10 min. Plasma VEGF concentrations (ELISA) were determined immediately before Ado infusion and 1 h, 2 h, and 8 h after the infusion. Results: Plasma VEGF concentration averaged 20.3 ± 2.0 pg ml-1 prior to Ado infusion, and increased to 62.7 ± 18.1 pg ml-1 at 1 h post- infusion (p < 0.01). VEGF plasma concentration returned to basal levels 2 h after infusion (23.3 ± 3.4 pg ml-1). MBP averaged 116 ± 7 mmHg and heart rate averaged 70 ± 7 prior to Ado infusion. MBP decreased by a maximum of ∼22% and HR increased by a maximum of ∼17% during the infusion. Conclusion: We conclude from these preliminary findings that intravenous infusion of adenosine can increase plasma levels of VEGF in humans. [ABSTRACT FROM AUTHOR]

Objective:The role of VEGF in vascular remodeling of target organs exposed to chronic hypertension is poorly understood. The authors compared capillary density (CD), capillary-to-fiber ratio (C/F), and VEGF mRNA expression in the hearts (left ventricle [LV]), and skeletal muscles (soleus and anterior tibialis [AT]) of 18-week-old male spontaneously hypertensive rats (SHR) and age-matched male Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats.Methods:CD or C/F in LV, soleus, and AT of SHR, WKY, and SD rats was determined by analysis of randomly acquired digital images of cryosections stained with FITC-conjugated GS-I lectin. VEGF mRNA expressions in the tissues were determined by Northern blot.Results:VEGF mRNA expressions in LV of SHR were 3.84- and 5.05-fold higher, compared to SD and WKY rats, respectively (n=6;p .05). CD in LV of SHR (4975±167) was significantly higher than WKY or SD rats, 4151±169 and 3807±187 mm-2, respectively (p< .05). In LV of SHR, C/F increased (35%) more significantly than CD (increased 20%), compared to WKY rats. CD, or C/F in soleus or AT of SHR was similar to that observed in WKY or SD rats.Conclusions:VEGF expression, CD, and C/F in the heart (LV) of SHR are significantly increased, compared to WKY and SD rats. The data are consistent with the possibility that VEGF may contribute to capillary growth as a compensatory response to hypertension. [ABSTRACT FROM AUTHOR]

Cytokine gene expression profiles in kidney medulla and cortex of obese hypertensive dogs. Background. The molecular mechanisms linking abnormal kidney function and obesity hypertension are poorly understood. This study compared gene expression profiles in the kidney medulla and cortex of obese and lean dogs. Methods. Lean dogs ( N= 4) were fed a standard kennel ration and obese dogs ( N= 4) were fed the standard diet plus 0.5 to 0.9 kg of cooked beef fat per day for 10 weeks. The dogs were instrumented for continuous monitoring of mean arterial pressure (MAP), heart rate, glomerular filtration rate (GFR), and effective renal plasma flow (RPF). The relative mRNA levels of 375 genes in renal cortex and medulla were determined simultaneously using cDNA membrane arrays (R&D Systems). Results. The high fat diet increased body weight by 57% and MAP increased by 24 mm Hg (112 ± 1 mm Hg vs. 88 ± 3 mm Hg) in obese compared to lean dogs. In obese dogs, expression of 11 and 13 genes changed significantly ( N= 4; P < 0.05) in the renal medulla and the cortex, respectively, relative to the lean dogs. Differences in renal gene expression profiles between lean and obese dogs were closely related to functional pathways, including those associated with sympathetic activation, inflammatory response, matrix formation, angiogenesis, endothelial dysfunction, attenuated actions of leptin, and attenuated cell survival. Conclusion. A high fat diet in dogs is associated with marked changes in renal gene expression profiles that provide potential molecular links to pathways associated with altered renal function and structure in obesity hypertension. [ABSTRACT FROM AUTHOR]

Background: Physical inactivity increases the risk of atherosclerosis. However, the molecular mechanisms of this relation are poorly understood. A recent report indicates that endostatin, an endogenous angiostatic factor, inhibits the progression of atherosclerosis, and suggests that reducing intimal and atherosclerotic plaque tissue neovascularization can inhibit the progression atherosclerosis in animal models. We hypothesize that exercise can elevate the circulatory endostatin level. Hence, exercise can protect against one of the mechanisms of atherosclerosis. Results: We examined treadmill exercise tests in healthy volunteers to determine the effect of exercise on plasma levels of endostatin and other angiogenic regulators. Oxygen consumption (VO2) was calculated. Plasma levels of endostatin, vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF) were determined using ELISA. The total peak VO2 (L) in 7 male subjects was 29.5 ± 17.8 over a 4-10 minute interval of exercise. Basal plasma levels of endostatin (immediately before exercise) were 20.3 ± 3.2 pg/ml, the plasma levels increased to 29.3 ± 4.2, 35.2 ± 1.8, and 27.1 ± 2.2 ng/ml, at 0.5, 2, and 6 h, respectively, after exercise. There was a strong linear correlation between increased plasma levels of endostatin (%) and the total peak VO2 (L) related to exercise (R2 = 0.9388; P < 0.01). Concurrently, VEGF levels decreased to 28.3 ± 6.4, 17.6 ± 2.4, and 26.5 ± 12.5 pg/ml, at 0.5, 2, and 6 h, respectively, after exercise. There were no significant changes in plasma bFGF levels in those subjects before and after exercise. Conclusions: The results suggest that circulating endostatin can be significantly increased by exercise in proportion to the peak oxygen consumption under physiological conditions in healthy volunteers. These findings may provide new insights into the molecular links between physical inactivity and the risk of angiogenesis dependent diseases such as atherosclerosis. [ABSTRACT FROM AUTHOR]

Investigates whether moderate levels of ethanol can stimulate vascular endothelial growth factor (VEGF) expression and induce angiogenesis. Effect of ethanol on cell proliferation; VEGF messenger RNA expression in chick embryo; Metabolic response to ethanol in cultured coronary artery vascular smooth muscle cells.

Tests the hypothesis that the inhibition of adenosine kinase induces expression of vascular endothelial growth factor (VEGF) mRNA and protein in myocardial myoblasts. Cell proliferation; Influence of exposure to hypoxia on the induction of VEGF protein expression; Increase in the interstitial concentration of adenosine during hypoxic conditions.

Investigates whether adenosine upregulates vascular endothelial growth factor (VEGF) expression in cultured myocardial vascular smooth muscle cells. VEGF protein expression in normoxia; Dose-related effect of adenosine on VEGF protein expression in myocardial vascular smooth muscle cells.

Endophytic bacteria associated with medicinal plants possess unique strategies that enhance growth and suvival of host plants, many of which are mediated by distinctive secondary metabolites. These bacteria and their secondary metabolites are important subjects for both basic and applied research aimed at sustainable agriculture. In the present study, 114 endophytic strains isolated from the wild ethnomedicinal plant Glycyrrhiza uralensis (licorice) were screened for their in vitro antimicrobial activities against common fungal pathogens of tomato (Fusarium oxysporum f. sp., Fulvia fulva, Alternaria solani), cotton (Fusarium oxysporum f. sp. Vesinfectum, Verticillium dahliae), pomegranite (Ceratocystis fimbriata), Cymbidinium (Colletotrichum gloeosporioides), and Tsao-ko (Pestalotiopsis microspora and Fusarium graminearum) and the common bacteria Staphylococcus aureus, Bacillus cereus, Salmonella enteritidis, and Escherichia coli. Several Bacillus strains, particularly Bacillus atrophaeus and Bacillus mojavensis, had a broad spectrum of antifungal and antibacterial activity. A total of 16 strains, selected based on broad antimicrobial activity, were shown to contain at least one putative secondary metabolite-encoding gene (i.e., polyketide synthase or non-ribosomal peptide synthetase) and/or one lytic enzyme (i.e., protease, cellulase, lipase, chitinase), which may be important mediators of antagonistic activity against pathogens. Five strains, representing Bacillus atrophaeus and Bacillus mojavensis, were selected for plant growth chamber experiments based on strong in vitro antifungal activities. All five strains significantly reduced disease severity in Arabidopsis thaliana plants challenged with V. dahlia infection. Gas-chromatography/mass-spectrometry analysis of cell-free extracts of Bacillus atrophaeus strain XEGI50 showed that at least 13 compounds were produced only during co-cultivation with V. dahlia, including putative compounds known to have antimicrobial activity, such as 1,2-benzenedicarboxylic acid, bis (2-methylpropyl) ester; 9,12-octadecadienoic acid (Z,Z)-, methyl ester; 9-octadecenoic acid, methyl ester, (E)-; and decanedioic acid, bis(2-ethylhexyl) ester. To our knowledge, this study is the first to report that bacteria isolated from G. uralensis have biocontrol abilities. Our findings provide new insights into the antimicrobial activities of natural endophytes, particularly B. atrophaeus, and suggest this species may a promising candidate as a biocontrol agent to confer resistance to Verticillium wilt disease and other phytopathogens in cotton and other crops.

A typical amphiphilic star polymer adamantane-[poly(lactic-co-glycolic acid)-bis(2-carboxyethyl) sulfide-poly(ethylene glycol) monomethyl ether)]4 with a specific hydrophilic/redox-sensitive/hydrophobic structure was designed and synthesized through ring opening and esterification reactions. The self-assembled nanomicelles were used as doxorubicin (DOX) delivery vehicles with suitable critical micelle concentrations (5.0 mg/L). After the drug being loaded, drug-loaded micelles showed good drug-loading efficiency (10.39%), encapsulation efficiency (58.1%), and drug release (up to 60%) under simulated biological environment conditions. In addition, the backbone structure of the biodegradable polymer was easily hydrolyzed by the action of biological enzymes. As expected, cell-based studies showed that the designed polymer micelles possessed good biocompatibility (a survival rate of 85% for NH-3T3 cells). Moreover, the drug (DOX) still maintained good anti-cancer effects after being loaded, which caused 40% of MCF-7 cells to survive. These redox-sensitive micelles showed anti-tumor therapeutic potential.

The progression of breast cancer is associated with oxidative stress. However, the effects of pyrrolidine dithiocarbamate (PDTC), known as an antioxidant, on the development of breast cancer are poorly understood. The present study evaluates the effects of PDTC on tumor growth, the expression of vascular endothelial growth factor (VEGF), and angiogenesis of breast cancer in female mice. Eight wk old female mice (C57BL/6J) were given PDTC 50mg/50ml in drinking water for two wks. Each mouse (20 g) usually drinks 2 to 4 ml water per day. Therefore, PDTC was given around 100 to 200 mg/kg/day in mice. The control mice received regular drinking water only. 5x105 E0771 (mouse breast cancer) cells were injected near the pad of the fourth mammary gland of the mice when the experiment started. Tumor size was monitored in two perpendicular dimensions parallel with the surface of the mice using dial calipers. At the end of the experiment, the tumors were isolated for measuring tumor size, intratumoral microvessel (IM) density using CD31 immunohistochemistry staining, and VEGF protein levels using ELISA. PDTC treatment caused a significant decrease in tumor weight over the control (0.64+/-0.22 vs. 1.43+/-0.31 g; n=6; P<0.01), and a significant decrease in IM density (66.1+/-5.3 vs. 84.2+/-9.4 IM#/mmˆ2; P<0.05). There was a significant decrease in tissue protein levels of VEGF (22.6+/-2.1 vs. 32.4+/-2.6 pg/mg; P<0.05) in the breast tumors of mice treated with PDTC, compared to the control group. These results suggest that the antioxidant treatment with PDTC can inhibit the progression of breast cancer through the reduction of VEGF expression and angiogenesis. [ABSTRACT FROM AUTHOR]

Isoflurane enhances the acute inflammatory response after pulmonary aspiration of acidic solution in rats. However, the mechanisms are poorly understood. Nuclear factor-κ B (NF-κ B) is the transcript factor related to inflammation. In the present study, we determined whether administration of isoflurane increased the lung NF--κ B activation in Sprague-Dawley (SD) rats, compared to the pentobarbital-treated group. Ten wk old male SD rats (Harlan Sprague Dawley) were given isoflurane via a nose cone through oxygen flow using a vaporizer (Surgivet) to sustain at 2 minimum alveolar anesthetic concentration (MAC). The control rats received sodium pentobarbital 50 mg/kg, i.p. The respiratory rate was monitored during anesthesia. The anesthesia conditions were maintained for 2 hrs. At the end of the experiment, plasma and the lung tissue were collected for histological analysis and measurement of NF-κ B, TNFα, and IL-6. The respiratory rate was more significantly slow and deep in the isoflurane group, compared to the pentobarbital group (41±2 vs. 80±7 /min; n=6; P<0.01). Electrophoretic mobility shift assay demonstrated that the binding activity of NF-κ B p65 proteins in the lungs of SD rats were significantly increased by 70% in the isoflurane group, compared to the pentobarbital group (P<0.01). PAS staining demonstrated that there were some inflammations in the lungs of rats treated with isoflurane, compared to the pentobarbital group. ELISA indicated that there were no significant differences in the protein levels of TNFα or IL-6 in plasma and the lung tissues between both groups. These results suggest that isoflurane increases the Lung NF-κ B activation, which may be associated with pulmonary inflammation response. [ABSTRACT FROM AUTHOR]

Epidemiological studies indicate that obesity increases the risk of developing several cancers, including melanoma. Once cancer occurs, obese subjects have poorer prognoses than lean subjects. Obesity increases the expression of several proangiogenic factors required for tumor growth, such as leptin. Leptin can stimulate angiogenesis in the chick chorioallantoic membrane assay. Plasma leptin levels correlate with total body fat and actions of leptin, including stimulation of cell migration and enhancement of angiogenesis, suggest that this hormone may promote tumor growth. However, no studies have directly tested whether obesity stimulates tumor growth via increased secretion of leptin. We injected melanoma cells into lean wild type, obese melanocortin receptor 4 knockout (MC4R(-/-), which have very high leptin levels, and obese leptin deficient (ob/ob) mice. Mean body weights were 29.7 ± 0.3 g, 46.3 ± 1.9 g, and 63.7 ± 0.9 g for lean wild type, MC4R(-/-), and ob/ob mice, respectively. All mice were on the C57BL6/J background. Mice were injected subcutaneously with 1 x 106 B16F10 cells and tumors were harvested and weighed post mortem. Tumors were 2.5 fold larger in obese ob/ob and MC4R(-/-) than lean wild-type mice (5.1 ± 0.9 g and 5.1 ± 0.7 g vs lean 2.1 ± 0.3 g, respectively). These results indicate that obesity enhances melanoma tumor growth by mechanisms that are independent of circulating leptin levels. [ABSTRACT FROM AUTHOR]

Epidemiological studies suggest that alcohol consumption is the leading avoidable risk factor of breast cancer in women. However, the experimental studies are not available for understanding the mechanisms of alcohol-induced breast cancer. The present study evaluates the effects of ethanol (EtOH) intake in physiological relevant doses on tumor growth and angiogenesis of breast cancer in female mice. Six wk old female mice (C57BL/6J) were given 1% EtOH in drinking water for four wks. The control mice received regular drinking water only. In the 2nd wk, 5x105 E0771 (mouse breast cancer) cells were injected near the pad of the fourth mammary gland of the mice. At the end of the experiment, the tumors were isolated for measuring tumor size, intratumoral microvessel (IM) density using CD31 immunohistochemistry staining, and VEGF protein levels using ELISA. EtOH intake caused a 1.96-fold increase in tumor weight over the control (1.39±0.24 vs. 0.71±0.13 g; n=6; P<0.05), and a 1.28-fold increase in IM density (110.7±9.3 vs. 86.8±8.4 1M#/mm2, P<0.05). There was a significant increase in tissue protein levels of VEGF (47.8±2.4 vs. 35.6±2.8 pg/mg; P<0.05) in the tumors of mice treated with EtOH, compared to the control group. The EtOH intake did not cause significant changes in the body weight of mice. These results suggest that the mechanisms of EtOH-induced tumor development of breast cancer are associated with the induction of tumor angiogenesis and VEGF expression. [ABSTRACT FROM AUTHOR]