Search

The supplementation level of barley was limited because of high contents of fiber in monogastric animals. Barley contained high soluble fiber, thus it could prevent to diarrhea of weaning pigs. Moreover, as the barley break down by enzymes, free sugars come out from the barley, which could be used as an energy source in weaning pigs and replace milk by-products in weaning pig’s diet. Therefore, present study was conducted to investigate the influence of barley to replace milk by-product in weaning pig’s diet on growth performance, blood profile, nutrient digestibility, diarrhea incidence, and economic analysis in weaning pigs. A total of 112 crossbred ([York-shire × Landrace] × Duroc, weaned at 28 days of age) piglets were allotted to 4 treatments in a randomized complete block (RCB) design. Each treatment has 7 replications with 4 pigs per pen. Pigs were fed each treatment diet which containing different levels of barley (0%, 10%, 20%, and 30%) at the expense of whey powder and lactose. Three phase feeding programs were used for 6 weeks of growth trial (phase 1: 0–2 weeks; phase 2: 3–4 weeks; phase 3: 5–6 weeks). During 0–2 week, body weight (BW), average daily gain (ADG) and G:F ratio were decreased as barley level increased in the diet (linear response, p < 0.01). In blood profile, blood urea nitrogen was decreased as the barley level increased in the diet (linear, p < 0.01). However, no significant differences were observed in blood glucose level. In nutrient digestibility, crude fat digestibility was linearly increased as barley increased (linear, p < 0.01). The incidence of diarrhea was improved as increasing barley contents in all phases (linear, p < 0.01). These results demonstrated that supplementation of barley to replace milk by-product influenced negatively on growth performance during 0–2 week. However, the incidence of diarrhea and later growth performance from 3 week postweaning were improved as dietary barley level increased.

Objective This experiment was conducted to evaluate the optimal space allowance on growth performance, blood profile and pork quality of growing-finishing pigs. Methods A total of ninety crossbred pigs [(Yorkshire×Landrace)×Duroc, 30.25±1.13 kg] were allocated into three treatments (0.96: four pigs/pen, 0.96 m2/pig; 0.80: five pigs/pen, 0.80 m2/pig; 0.69: six pigs/pen, 0.69 m2/pig) in a randomized complete block design. Pigs were housed in balanced sex and had free access to feed in all phases for 14 weeks (growing phase I, growing phase II, finishing phase I, and finishing phase II). Results There was no statistical difference in growing phase, but a linear decrease was observed on average daily gain (ADG, p

IntroductionPrimary blast affects the kidneys due to direct shock wave damage and the production of proinflammatory cytokines without effective treatment. CD28 has been reported to be involved in regulating T cell activation and secretion of inflammatory cytokines. The aim of this study was to investigate the influence of primary blast on the kidney and the effect of CD28 in mice.MethodsA mouse model of primary blast-induced kidney injury was established using a custom-made explosive device. The severity of kidney injury was investigated by H&E staining. ELISA was applied to study serum inflammation factors’ expression. Western blot assays were used to analyse the primary blast-induced inflammatory factors’ expression in the kidney. Immunofluorescence analysis was used to examine the PI3K/Akt signalling pathway.ResultsHistological examination demonstrated that compared with the primary blast group, CD28 deficiency caused a significant decrease in the severity of the primary blast-induced renal injury. Moreover, ELISA and western blotting revealed that CD28 deficiency significantly reduced the levels of interleukin (IL)-1β, IL-4 and IL-6, and increased the IL-10 level (pConclusionsCD28 deficiency had protective effects on primary blast-induced kidney injury via the PI3K/Akt signalling pathway. These findings improve the knowledge on primary blast injury and provide theoretical basis for primary blast injury treatment.

Using hexagonal ordered straight-pore SBA-15 silica as hard template, mesoporous cobalt oxide (Co3O4) nanowires SBA-15 materials are synthesized by a nanoreplication route, and X-ray diffraction (XRD), high-resolution transmission electron microscopy (HRTEM), field-emission scanning electron microscopy (FESEM), and N2 physisorption isotherms are used to characterize the microstructure of columnar SBA-15 particles, Co3O4-doped SBA-15 (Co3O4/SBA-15) and Co3O4 nanowires array. The results indicate that Co3O4 exist in the mesochannels of SBA-15 to form Co3O4/SBA-15 nanocomposites and Co3O4 nanowires present mesostructure. Furthermore, the magnetic properties of Co3O4 nanowires array are measured and discussed by vibrating sample magnetometer (VSM) and surperconducting quantum interference device (SQUID), and the prepared Co3O4 nanowires array present superparamagnetism. Owing to surface effect of the uncompensated spins at the surface of Co3O4 nanowires, it presents a weak ferromagnetic behavior at low temperature.

In this paper, the steering stability and control strategy of forklift are put forward. Drive based on yawing moment distribution of rotary torque coordination control method, through analyzing the linear two degree of freedom model of forklift truck, forklift yawing angular velocity and mass center side-slip Angle of expectations, as the control target parameters system, using fuzzy controller output driving forklift steering the yawing moment, to drive rotary torque distribution, make the forklift truck to drive horizontal pendulum angular velocity and side-slip Angle tracking reference model very well. In this paper, the lateral stability control system were designed, the joint simulation in MATLAB/Simulink, the simulation results show that under the different partial load, the control system can effectively to control side forklift lateral stability, enhanced the forklift driving safety, for the side forklift steering stability study provides a theoretical basis.

SiC/ZTM (zirconia-toughened mullite) nanocomposites were prepared by hot pressing mixtures of mullite gel, 2Y-TZP, and SiC nanopowders. The intimate mixing of Al2O3 and SiO2 components in the starting powder prevented intermediate ZrSiO4 phase formation during sintering. Addition of nano-sized SiC significantly retarded the matrix grain growth, making the microstructure much finer and more uniform. Transmission electron microscopy and high-resolution transmission electron microscopy revealed that many SiC nanoparticles were found in mullite and ZrO2 grains, and low-energy grain boundaries and mullite–liquid interfaces parallel to the {110} planes of rodlike mullite grains were formed. It is deduced that the formation of rodlike mullite grains is the result of the preferential development of these low-energy grain boundaries and mullite–liquid interfaces. The mechanical properties of the SiC/ZTM nanocomposite showed significant improvement over those of ZTM, and further enhancement in the mechanical properties was achieved by combinative strengthening with nano- and micro-sized SiC.

Virtually all of the biological actions of angiotensin II (ANG II) have been thought to be mediated by the type 1 (AT1) angiotensin receptor and the function of the type 2 (AT2) receptor is unknown. We now describe a novel physiological action of ANG II to release nitric oxide (NO) mediated by the AT2 receptor in both the kidney and gastrointestinal tract. We present an integrated model for a counter-regulatory protective action of the AT2 receptor mediated by nitric oxide. In the kidney, ANG II at the AT2 receptor stimulates a vasodilator cascade of bradykinin (BK), NO and cyclic GMP which is tonically activated only during conditions of increased ANG II, such as sodium depletion. In the absence of the AT2 receptor, pressor and antinatriuretic hypersensitivity to ANG II is associated with BK and NO deficiency. In angiotensin-dependent hypertension, the hypotensive effect at AT1 receptor blockade is due at least in part to AT2 receptor stimulation and consequent increased activity of the vasodilator cascade. In the gastrointestinal tract, physiological quantities of ANG II stimulate the AT2 receptor releasing NO and cGMP leading to increased sodium and water absorption. In conclusion, NO is an important physiological mediator of ANG II at the AT2 receptor.

DTPA-Octreotide(Pentetreotide), a somatostatin analogue which can bind specifically and with high affinity to somatostatin receptor in vitro and vivo, labeled with99mTc by tin reduction in acetate buffer, has been characterized by Reverse-phase High performance Liquid Chromatography. The effect of different solvents, mobile phase pH, linear gradient and the injected volume on the separation efficiency was evaluated. The results show that the separation efficiency is best using μBondapak-C18 (300×3.9 mm2), linear gradient of 40% to 80% methanol (1.0 ml/min) in 0.05M acetate buffer (pH 5.5) over a 30 min period and maintaining for another 10 min. The labeled product is a mixture which mainly consists of five components (a, b, c, d, e) successfully proved by HPLC. Paper chromatography is also evaluated in this paper. It may be used to determine the radiochemical purity of the labeling product, but is not a good choice for the verification each components.

The preparation of a cold kit was introduced in the paper, and the effective quantities of the components (Vc, HEDP and SnCl2·2H2O) in the kit were determined. At the sametime, the effects of labelling kit on the reaction time, reaction temperature and animal distribution were studied in detail. The initial animal experiment showed the high uptake in the skeletal tissue, the clearance in the blood was quick.

A polymerized liposome (PLS) was prepared using a synthesized phosphatidylethanolamine with a diacetylene moiety that showed a reversibly precipitable property on addition and removal of salt. To prepare a soluble-insoluble immobilized enzyme, chymotrypsin was covalently immobilized on the outer surface of the PLS. The carbodiimide method was employed for the enzyme immobilization. Coupling was rapid and nearly complete at a weight ratio of enzyme to the PLS of0.12. The immobilized enzyme showed favorable activity yields for both low- and high-mol-wt substrates, i.e., 90 +/- 9% for N-benzoyl-L-tyrosine ethyl ester and 59 +/- 5% for casein up to an enzyme coupling density of 0.38 g/g-PLS. The immobilized enzyme was reusable and more stable at high temperature and long-term incubation than the native enzyme.

Utilisation d'un procedure relativement nouvelle incluant le developpement et la propagation controlee d'une cloque pour l'etude de l'influence du pretraitement de la surface sur l'adherence d'une laque sur l'aluminium. Discussion et explication des faibles performances obtenues par un polissage mecanique de la surface et des nettes ameliorations enregistrees lors du depot par conversion de chromate.

Previous studies indicated that the anticancer agent adriamycin (ADR) could induce activation of cytotoxic T lymphocytes (CTL) and natural killer cells. In this study, we investigated the effect of ADR on the susceptibility of human renal cell carcinoma (RCC) cells to lysis by peripheral blood lymphocytes (PBL) and tumor infiltrating lymphocytes (TIL). Treatment of human RCC cell line ACHN and freshly derived RCC cells with ADR at 1 microg/ml or more for 3 h significantly enhanced their susceptibility to lysis by PBL (P

Myosin light chain kinase (MLCK) plays a pivotal role in regulation of cellular functions, the evidence often relying on the effects of extracelluarly administered drugs such as ML-9. Here we report that this compound exerts non-specific inhibitory actions on the TRPC6 channel, a transient receptor potential (TRP) protein.Macroscopic and single channel currents were recorded from transfected HEK293 cells by patch-clamp techniques.Cationic currents elicited by carbachol (CCh; 100 microM) in HEK293 cells overexpressing murine TRPC6 (I(TRPC6)) were dose-dependently inhibited by externally applied ML-9 (IC(50)=7.8 microM). This inhibition was voltage-dependent and occurred as fast as external Na(+) removal. Another MLCK inhibitor, wortmannin (3 microM), and MLCK inhibitory peptides MLCK-IP(11-19) (10 microM) and -IP(480-501) (1 microM) showed little effects on I(TRPC6) density and the inhibitory efficacy of ML-9. The extent of the inhibition also unchanged with co-expression of wild-type or a dominant negative mutant of MLCK. Inhibitory effects of ML-9 on I(TRPC6) remained unaffected whether TRPC6 was activated constitutively or by a diacylglycerol analogue OAG (100 microM). Similar rapid inhibition was also observed with a ML-9 relative, ML-7. Intracellular perfusion of ML-9 via patch pipette, dose-dependently suppressed I(TRPC6). In inside-out patch configuration, bath application of ML-9 (and ML-7) rapidly diminished approximately 35pS single TRPC6 channel activities. Contrarily, currents due to TRPC7 expression were rapidly enhanced by externally applied ML-9 and ML-7, which was not prevented by MLCK inhibitory peptides.These results strongly suggest that ML compounds inhibit TRPC6 channels via a mechanism independent of inhibition of MLCK activity.

The use of psoralens combined with exposure to ultraviolet A radiation is a major form of treatment for psoriasis and a number of other common skin diseases. Although psoralen plus ultraviolet A treatment is highly effective, careful follow-up cohort studies have shown that it greatly increases risk for the development of cutaneous squamous cell carcinoma and melanoma. Strategies to reduce the risk of cancer development in psoralen plus ultraviolet A-treated populations are highly desirable. In prior studies, we demonstrated that green tea and constituent polyphenols protect against ultraviolet B-induced carcinogenesis and reduce the growth rate of established tumors in skin. In this study, we show that pre- and post-treatment with standardized green tea extract in psoralen plus ultraviolet A treatment populations abrogates the psoralen plus ultraviolet A-induced photochemical damage to skin. Intact mouse and human skin and reconstituted human skin were employed to assess the effect of both topical and oral administration of standardized green tea extract against psoralen plus ultraviolet A-induced photodamage. Oral administration of standardized green tea extract prior to and during multiple psoralen plus ultraviolet A treatments reduced hyperplasia and hyperkeratosis in murine skin. Standardized green tea extract treatment also inhibited accumulation of c-fos and p53 protein induction following a single exposure to psoralen plus ultraviolet A. c-fos and p53 positive cells in psoralen plus ultraviolet A-treated skin were found to be increased by 55.4 +/- 13. 6% and 62.3 +/- 10.5%, respectively, compared with saline-treated unexposed control skin. Oral administration of 0.4 or 0.8% standardized green tea extract inhibited c-fos protein accumulation by 18.5% and 46.2% (p0.05), respectively, and p53 protein accumulation by 26.1% and 54.3% (p0.05), respectively. Similarly proliferating cell nuclear antigen staining, a marker of cell proliferation was induced (73.7%) in psoralen plus ultraviolet A-treated skin. Oral administration of 0.4% or 0.8% standardized green tea extract 1 d after psoralen plus ultraviolet A treatment was effective in reducing psoralen plus ultraviolet A-induced inflammatory responses including erythema and edema formation. When standardized green tea extract was applied to EpiDerm, a reconstituted human skin equivalent, psoralen plus ultraviolet A-induced 8-methoxypsoralen-DNA adduct formation and p53 protein accumulation were inhibited. Topical application of 0.2 mg 8-methoxypsoralen per cm2 followed by exposure to ultraviolet A (2.5 J per cm2) resulted in delayed erythema formation in human subjects. Pretreatment of human skin with topical application of 0.2 mg standardized green tea extract per cm2 30 min prior to psoralen plus ultraviolet A treatment resulted in an almost complete abrogation of psoralen plus ultraviolet A-induced erythema. In summary, these data demonstrate that standardized green tea extract protects against psoralen plus ultraviolet A-induced phototoxicity by inhibiting DNA damage and diminishing the inflammatory effects of this modality.

To study the effects of long-term application of dopamine HCl (DA) on the functional changes of dopamine receptor subtypes coupled to adenyl cyclase in rat renal cortex.cAMP levels were measured by radioimmunoassay as an index of dopamine receptor function.Injection of DA (30 mg.kg-1.d-1, i.p. 30 d) reduced the fenoldopam (Fen) (100 mumol.L-1)-induced increments of cAMP production from the control group of +1.26 +/- 0.04 to the DA-treated group of +0.63 +/- 0.22 nmol.min-1/g tissue and the propyl-butyl-dopamine (PBDA) (100 mumol.L-1)-induced decrements of cAMP production in the presence of Sch-23390 (Sch) from the control group of -0.38 +/- 0.18 to the DA-treated group of -0.11 +/- 0.08 nmol.min-1/g tissue with, however, comparable percentile changes for the 2 groups. Sch blocked both Fen- and PBDA-induced increase in cAMP production, while domperidone (Dom) blocked the decreasing effects of PBDA on cAMP accumulation in the presence of Sch.Long-term application of DA produced a marked "down regulation" of both DA1 and DA2 receptors in rat renal cortex with, however, the responsiveness of the remaining receptors unchanged.

In situ hybridization of a biotin-labeled specific dopamine1A (D1A) receptor gene oligonucleotide probe combined with computer-assisted image analyzer was used to directly visualize D1A receptor mRNA and quantify the relative mRNA levels in sections of rat aorta and pulmonary and caudal arteries. Positive D1A receptor mRNA signals were found in rat aorta and pulmonary arteries, while no specific signals could be detected in the caudal artery. D1A receptor mRNA was located mainly within the medial layer of aorta, with intimal distribution in the pulmonary artery. The density of D1A receptor mRNA in different vascular beds demonstrated heterogeneity. D1A receptor mRNA levels in the aorta were much higher than those in the pulmonary artery (p0.01). These results demonstrate the existence of D1A receptor mRNA in both aorta and pulmonary beds, although with different distribution and density. The results further support the heterogeneity of the D1A receptor in different vascular beds.

The effects of anti-peptide antibodies (Ab) against the second extracellular loop of human muscarinic receptor-2 on the cAMP generating system in guinea pig ventricles were studied. These effects were compared with those of the muscarinic receptor agonist carbachol (Carb). It was shown that: (1) both Carb and Ab were able to inhibit the isoproterenol (Iso)-stimulated cAMP production of ventricles in a dose-dependent manner. Carb at 2 microM, 10 microM and 50 microM decreased Iso-stimulated cAMP production by 8.0 +/- 1.1, 15.8 +/- 1.2 and 28.4 +/- 1.7%, respectively; whereas Ab at 50 nM, 100 nM and 400 nM decreased it by 5.8 +/- 0.4, 16.8 +/- 1.4 and 30.6 +/- 2.5%, respectively. (2) Both Carb and Ab could also inhibit the basal cAMP content of ventricles significantly. Carb at 10 microM and Ab at 100 nM decreased it by 46.9 +/- 4.2% and 60.2 +/- 4.6%, respectively. (3) The inhibitory effects of both Ab and Carb on Iso-stimulated cAMP production were significantly prevented by atropine at 1.5 microM. (4) The inhibitory effect of Ab at 100 nM was almost completely abolished by the peptide (700 nM) used as immunogen. These findings suggest that the antibodies exhibit a stimulatory muscarinic activity similar to carbachol in the inhibitory modulation of cAMP production.

The localization and density of M2 muscarinic receptors in guinea pig atria and ventricles were studied by immunocytochemical techniques, with anti-peptide antibodies against the second extracellular loop of human muscarinic receptor-2. It was shown that the positive immunoreaction of M2 muscarinic receptor was characterized by brown-yellow granules of variable size and shape, which were located mainly on the cell surface and in the cytoplasm far from nuclei. The positive immunoreactive substances appeared in both atrial and ventricular myocytes, with the density being greater in atria than in ventricles. Pre-incubation with atropine, but not carbachol, significantly reduced the intensity of positive immunoreactivity. This indicates that the binding of antibody to receptor site can be partially blocked by M2 muscarinic receptor antagonist.

The effects of anti-peptide antibodies (Ab) against the second extracellular loop of human muscarinic receptor-2 on cardiac function in rats in vivo were studied. These effects were compared with those of the muscarinic receptor agonist, carbachol (Carb). It was shown that: (1) both Carb and Ab administered intravenously in the same doses of 0.4 nmol, 1.0 nmol, and 2.0 nmol were able to inhibit the maximal rate of rise of ventricular pressure (+dp/dt max) in a dose-dependent manner. (2) The isoproterenol (Iso)-induced increase in HR and +dp/dt max were also markedly inhibited by Carb and Ab. Administration of 1.0 nmol Carb decreased the Iso-stimulated increase of HR from 13.6 +/- 2.0 to 4.9 +/- 0.7% and decreased the increase of +dp/dt max from 27.9 +/- 3.2 to 4.8 +/- 0.6%, respectively; whereas Ab decreased the HR to 6.5 +/- 1.1% and +dp/dt max to 13.5 +/- 1.2%, respectively. (3) Both the inhibitory effects of Carb and Ab could be significantly blocked by atropine (1.4 nmol). These findings suggest that the Ab display a stimulatory muscarinic activity similar to Carb in inhibiting the cardiac function as evidenced by its negative chronotropic and inotropic effects.

By using radioreceptor binding techniques and [3H]SCH23390 as a ligand, a comparative study was performed on the pharmacological properties and the density of dopamine-1 (D1) receptors in different vascular systems. [3H]SCH23390 was specifically bound to membranes from rabbit renal, mesenteric and pulmonary, but not femoral, arteries. The binding was saturable and in a manner consistent with the labeling of D1 receptors. The Kd value and Hill coefficient (nH) were similar in all three arteries with no statistically significant differences (p0.05) among them, indicating a homogenous binding site with a single class of high affinity. In competitive binding tests, the selective D1 antagonist and agonist inhibited the binding much more potently than the D2 antagonist, indicating a pharmacological characteristic of D1 receptors. The Bmax values, however, differed considerably among these arteries, with the value being the largest in the renal artery and smallest in the pulmonary artery. These findings are indicative of the existence of D1 receptor sites with identical properties but diverse density in different vascular beds, which underlies the relative functional importance of the receptors in regulating local blood flow in distinct vessels.

A polymerized liposome (PLS) was prepared using a synthesized phospholipid with a diacetylene moiety in the hydrophobic chain and an amino group in the hydrophilic head. The PLS was used as a novel ligand carrier for affinity precipitation of proteins because it showed a reversibly precipitable property on salt addition and removal. Soybean trypsin inhibitor (STI) was easily immobilized on the PLS by a one-step carbodiimide reaction. The PLS showed no nonspecific adsoprtion of proteins. It had a large ligand coupling capacity, and then a large adsorption capacity for trypsin after STI immobilization. The PLS with immpbilized STI was recycled three times for the purification of trypsin from a crude pancreatic extract. Although the degree of purification was compromised by the impurity of the STI employed, in each run the purification factor reached about 6 and more than 80% of trypsin activity was recovered. The results indicated that the PLS was a potential ligand carrier for affinity precipitation of proteins. © 1995 John Wiley & Sons, Inc.