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Biomedical subjects

H J Yan

Publications and source records attributed to H J Yan.

At least 19 recordsLinked to original sources
PubMed2006

Dietary functional ingredients: performance of animals and quality and storage stability of irradiated raw turkey breast.

The objective of this study was to evaluate the effect of dietary functional ingredients vitamin E (VE), Se, and conjugated linoleic acid (CLA), alone or in combination, on the quality of irradiated turkey breast meat. A total of 480 male turkeys (11-wk-old, raised on a cornsoybean basal diet) were randomly allotted to 32 pens and fed 1 of 8 experimental diets (4 pens/treatment) supplemented with none (control), 200 IU/kg of VE (VE), 0.3 ppm Se (Se), 2.5% CLA (CLA), 200 IU/kg of VE + 0.3 ppm Se (VE + Se), 200 IU/kg of VE + 2.5% CLA (VE + CLA), 2.5% CLA + 0.3 ppm Se (CLA + Se), 200 IU/kg of VE + 0.3 ppm Se + 2.5% CLA (VE + Se + CLA) for 4 wk. At 15 wk of age, all birds were slaughtered, and breast muscles of 8 birds from each pen were separated, pooled, and ground. Patties were prepared using the ground meat, aerobically packaged, and irradiated at 0 or 1.5 kGy absorbed dose. Lipid oxidation, color, and volatiles of the patties were measured after 0, 7, and 12 d of storage at 4 degrees C. The content of VE and Se and fatty acid composition of lipids were also determined. Dietary supplementation of VE and CLA increased their concentrations in turkey breast. Dietary CLA decreased monounsaturated and non-CLA polyunsaturated fatty acids content in meat. Irradiation increased (P < 0.05) Hunter color redness value of turkey breast and accelerated lipid oxidation, regardless of dietary treatments. However, dietary VE, Se, and CLA, alone and in combinations, decreased (P < 0.05) lipid oxidation in meat caused by both irradiation and storage. It was concluded that dietary supplementation of VE, Se, and CLA, alone and in combination, improved the storage stability of irradiated turkey breast meat.

Animal Feed↗
PubMed2006

Effects of dietary functional ingredients and packaging methods on sensory characteristics and consumer acceptance of irradiated turkey breast meat.

Raw and cooked breast patties from turkeys fed 8 different diets [control; 200 IU/kg of vitamin E (VE); 0.3 mg/kg of Se; 2.5% conjugated linoleic acids (CLA); 200 IU/kg of VE + 0.3 mg/kg of Se; 200 IU/kg of VE + 2.5% CLA; 0.3 mg/kg of Se + 2.5% CLA; and 200 IU/kg of VE + 0.3 mg/kg of Se + 2.5% CLA] were treated with 2 irradiation doses (0 and 1.5 kGy) and 2 packaging methods (vacuum and aerobic). Raw and cooked samples from 32 treatments were tested by 8 trained sensory panelists for turkey aroma and irradiation off-aroma. Based on the sensory scores, the 3 dietary treatments producing the most and the least off-aroma were selected and used for a consumer acceptance study. Sensory results of raw meat showed that turkey aroma was intense in aerobically packaged meat, whereas irradiation off-aroma was intense with vacuum packaging. Raw meats from dietary treatments containing CLA (CLA, VE + CLA, Se + CLA, VE + Se + CLA) had greater turkey aroma scores, whereas those containing VE (VE and VE + Se) had lower scores than the control. Dietary treatments containing VE (VE, VE + Se, VE + Se + CLA) significantly lowered (P < 0.05) irradiation off-aroma in raw turkey breast meat, whereas CLA increased it, especially when the meats were packaged aerobically. In cooked meat, however, irradiation and packaging had no effect on turkey meat aroma and irradiation off-aroma. Cooked meat from turkeys supplemented with VE (VE and VE + Se) had less (P < 0.05) irradiation off-odor than other dietary treatments. Dietary CLA increased the irradiation off-aroma in cooked meat, which could not be reduced, even when VE and Se were combined in the diet. Irradiation off-aroma of raw meat was not pleasant for most consumers, and dietary supplementation of VE and VE + Se improved consumer acceptance of irradiated raw meat. For cooked meat samples, consumers preferred both color and flavor of irradiated meat to nonirradiated meat.

Animals↗
PubMed2001

Intracerebral infusion of a second-generation ciliary neurotrophic factor reduces neuronal loss in rat striatum following experimental intracerebral hemorrhage.

Neuronal and glial cell death in the striatum of a rat model of collagenase-induced intracerebral hemorrhage begins at 1 day and continues for at least 3 weeks. We hypothesized that administration of a neurotrophic agent would reduce neuronal loss in this experimental model. Because it has been shown to protect striatal neurons against excitotoxic injury, a second-generation ciliary neurotrophic factor (CNTF) (AXOKINE) was administered by continuous intracerebral infusion (2 microg/day) beginning 28 h after hemorrhage and continuing for 2 weeks. Magnetic resonance imaging showed that the hematoma size was comparable in control and treated rats prior to treatment. Counts of medium-sized striatal neurons within 320 microm of the hematoma 8 weeks after the hemorrhage revealed a slight but statistically significant benefit with a 42.5% loss in treated rats compared to 51.7% loss in controls. The results suggest that AXOKINE might be protective of striatal neurons in the vicinity of a hemorrhagic lesion.

Animals↗
PubMed2001

Adenosine A2A receptor activation reduces proinflammatory events and decreases cell death following intracerebral hemorrhage.

The ubiquitous neuromodulator adenosine inhibits the production of several proinflammatory cytokines through activation of specific cell-surface adenosine receptors. We demonstrated recently that antisense oligonucleotides to tumor necrosis factor-alpha (TNF-alpha) are neuroprotective in a rat model of intracerebral hemorrhage. Therefore, we hypothesized that activation of adenosine receptors would provide protection against intracerebral hemorrhage-induced TNF-alpha production and inflammatory events. In vitro experiments showed that adenosine A1, A2A, and A3 receptor subtypes were present on U937 cells, and activation of these subtypes inhibited TNF-alpha production with a rank order of A2A > > A1 > A3. Prolonged treatment of U937 cells with the A2A receptor agonist 2-p-(carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine hydrochloride (CGS 21680) desensitized adenosine A2A, A1, and A3 receptors. CGS 21680 administration directly into the striatum immediately prior to the induction of intracerebral hemorrhage inhibited TNF-alpha mRNA and, 24 hours following induction, reduced parenchymal neutrophil infiltration (p < 0.001) and TUNEL-positive cells (p < 0.002) within and bordering the hematoma. These results suggest that pharmacological strategies targeting A2A receptors may provide effective inhibition of acute neurotoxic proinflammatory events that occur following intracerebral hemorrhage.

Adenosine↗
PubMed2001

Effect of FK-506 on inflammation and behavioral outcome following intracerebral hemorrhage in rat.

Beginning 15 min after induction of intracerebral hemorrhage (ICH) by intrastriatal administration of collagenase, rats were treated intramuscularly with FK-506 (3 mg/kg) or with vehicle. Treatment was repeated daily for 7 days. MR imaging 1, 7, and 28 days post-ICH showed that treatment did not affect hematoma size or its subsequent resolution. Two days post-ICH, neutrophil infiltration around the hematoma was decreased in the FK-506-treated rats, as was the number of TUNEL-positive cells at the edge of the hematoma and in the peripheral region. The decreased inflammatory response was accompanied by functional improvement in the treated rats. The neurological deficit induced by the ICH (beam walking ability, postural reflex, spontaneous circling) was significantly decreased from 3 to 21 days post-ICH by treatment with FK-506. Skilled use of the forelimb ipsilateral to the ICH was improved and sensory neglect of the same limb was decreased 8-9 weeks post-ICH in rats treated with FK-506. However, neuronal loss assessed 9 weeks post-ICH was not different in the treated and untreated rats.

Animals↗
PubMed2001

Antisense oligodeoxynucleotide inhibition of tumor necrosis factor-alpha expression is neuroprotective after intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Tumor necrosis factor-alpha (TNF-alpha) expression is increased in brain after cerebral ischemia, although little is known about its abundance and role in intracerebral hemorrhage (ICH). A TNF-alpha-specific antisense oligodeoxynucleotide (ORF4-PE) was used to study the extent to which TNF-alpha expression influenced neurobehavioral outcomes and brain damage in a collagenase-induced ICH model in rat. METHODS: Male Sprague-Dawley rats were anesthetized, and ICH was induced by intrastriatal administration of heparin and collagenase. Immediately before or 3 hours after ICH induction, ORF4-PE was administered directly into the site of ICH. TNF-alpha mRNA and protein levels were measured by reverse transcriptase-polymerase chain reaction and immunoblot analyses. Cell death was measured by terminal deoxynucleotidyl transferase-mediated uridine 5'triphosphate-biotin nick end labeling (TUNEL). Neurobehavioral deficits were measured for 4 weeks after ICH. RESULTS: ICH induction (n=6) elevated TNF-alpha mRNA and protein levels (P:<0.01) at 24 hours after the onset of injury compared with sham controls (n=6). Immunohistochemical labeling indicated that ICH was accompanied by elevated expression of TNF-alpha in neutrophils, macrophages, and microglia. Administration of ORF4-PE (2.0 nmol) directly into striatal parenchyma, 15 minutes before (n=4) or 3 hours after (n=6) ICH, decreased levels of TNF-alpha mRNA (P:<0.001) and protein (P:<0. 01) in the brain tissue surrounding the hematoma compared with animals treated with saline alone (n=6). Mean+/-SEM striatal cell death (cells per high-powered field) was also reduced in animals receiving ORF4-PE (34.1+/-5.0) compared with the saline-treated ICH group (80.3+/-7.50) (P:<0.001). ORF4-PE treatment improved neurobehavioral deficits observed at 24 hours (P:<0.001) after induction of ICH (n=6) compared with the untreated ICH group (n=6). This improvement was maintained at 28 days after hemorrhage induction (P:<0.001). CONCLUSIONS: These results indicate a pathogenic role for TNF-alpha during ICH and demonstrate that reducing TNF-alpha expression using antisense oligodeoxynucleotides is neuroprotective.

Animals↗
PubMed1999

Effect of fucoidan treatment on collagenase-induced intracerebral hemorrhage in rats.

Inflammatory cells are postulated to mediate some of the brain damage following ischemic stroke. Intracerebral hemorrhage is associated with more inflammation than ischemic stroke. We tested the sulfated polysaccharide fucoidan, which has been reported to reduce inflammatory brain damage, in a rat model of intracerebral hemorrhage induced by injection of bacterial collagenase into the caudate nucleus. Rats were treated with seven day intravenous infusion of fucoidan (30 micrograms h-1) or vehicle. The hematoma was assessed in vivo by magnetic resonance imaging. Motor behavior, passive avoidance, and skilled forelimb function were tested repeatedly for six weeks. Fucoidan-treated rats exhibited evidence of impaired blood clotting and hemodilution, had larger hematomas, and tended to have less inflammation in the vicinity of the hematoma after three days. They showed significantly more rapid improvement of motor function in the first week following hemorrhage and better memory retention in the passive avoidance test. Acute white matter edema and eventual neuronal loss in the striatum adjacent to the hematoma did not differ between the two groups. Investigation of more specific anti-inflammatory agents and hemodiluting agents are warranted in intracerebral hemorrhage.

Animals↗
PubMed1999

Serial magnetic resonance imaging of rat brain after induction of renal hypertension.

BACKGROUND AND PURPOSE: Hypertension is a major risk factor for ischemic and hemorrhagic stroke and may also cause more chronic and subtle brain injury. Progressive brain changes in a rat model of renal hypertension have been assessed to better understand the pathogenesis of hypertensive brain damage. METHODS: Young adult rats were made hypertensive by partial occlusion of both renal arteries. MR images of brain were obtained weekly, and histopathological outcome was assessed. A separate group of rats was used to measure brain specific gravity and Evans blue dye content as an indicator of extravasation. RESULTS: Rats developed maximal mean systolic blood pressures of 173 to >300 mm Hg, reaching a plateau in 6 to 8 weeks. Rats whose mean systolic pressure never exceeded 210 mm Hg never had brain lesions, while rats whose mean systolic pressure exceeded 276 mm Hg consistently developed brain lesions. Brain T2 values increased with increasing blood pressure. Lesions seen on MRI corresponded to those seen histologically. MRI also demonstrated transient brain expansion, probably due to diffusely increased water content, and rarely demonstrated focal cortical edema, which had no histological correlate. These transient phenomena, as well as hemorrhagic and ischemic infarcts, occurred mainly during the phase of climbing blood pressure and early stages of stable hypertension. CONCLUSIONS: Serial MRI reveals aspects of hypertensive brain disease that cannot be studied by histological examination alone. The observed phenomena are likely related to loss of autoregulation and/or blood-brain barrier integrity. Breach of blood vessel integrity is less likely once the vessels become accustomed to high pressures.

Animals↗
PubMed1998

Protective effects of free radical inhibitors in intracerebral hemorrhage in rat.

Iron compounds formed in the degradation of a hematoma can accelerate the formation of free radicals in adjacent ischemic or hypoperfused tissue. The purpose of this study was to examine the efficacy of compounds that quench free radicals in improving the outcome in rats with experimental intracerebral hemorrhage. Intracerebral hemorrhage was induced in rats by injection of bacterial collagenase and heparin into the caudate nucleus. Rats were treated with alpha-tocopherol plus ascorbic acid starting before hemorrhage, or with dimethylthiourea or alpha-phenyl-N-tert-butyl nitrone starting 2 h after hemorrhage, with treatment continued for 10 days after induction of hemorrhage. Outcome was assessed by behavioral analyses, magnetic resonance imaging, and histopathology. A trend towards behavioral improvement was found for rats treated with alpha-tocopherol/ascorbic acid, while behavior was significantly improved following intracerebral hemorrhage in rats treated with dimethylthiourea or alpha-phenyl-N-tert-butyl nitrone. These results suggest that free radicals may play a role in the development of brain injury following intracerebral hemorrhage, and that compounds that interrupt the free radical cascade may improve outcome. However, treatment did not significantly affect edema, resolution of the hematoma, or neuronal injury in tissue adjacent to the hemorrhage.

Animals↗
PubMed1998

Calcified chronic subdural hematoma: case report.

Calcified or ossified chronic subdural hematoma is a rare entity that usually presents as a space-occupying lesion over the cerebral convexity. We report a case of calcified and ossified chronic subdural hematoma in an unusual location that has not been previously reported. A 24-year-old man with a history of tonic-clonic convulsions since 7 months of age was admitted because of increasing frequency and duration of seizures. Computed tomography and magnetic resonance imaging demonstrated a fusiform extra-axial lesion just above the tentorium and adjacent to the cerebral falx. A calcified and ossified chronic subdural hematoma was noted and was almost completely removed by craniotomy. Better seizure control was achieved by removal of the calcified chronic subdural hematoma. Calcified subdural hematoma, calcified epidural hematoma, calcified empyema, meningioma, calcified arachnoid cyst, and calcified convexity of the dura mater with acute epidural hematoma should be considered for the differential diagnosis of an extra-axial calcified lesion.

Adult↗
PubMed1997

Active oxidants mediate IFN-alpha-induced microvascular alterations in rat mesentery.

The present study was designed to investigate the influences of IFN-alpha on the microcirculatory hemodynamics. The mesenteric microcirculation of male Wistar rats was observed through an intravital fluorescence microscopic system. The leukocyte behavior, RBC velocity, and albumin leakage were monitored simultaneously before and after a continuous infusion of IFN-alpha. In other rats, the oxidant-sensitive fluorescence probe dihydrorhodamine-123 (DHR) fluorescence was observed in the same set up. Administration of IFN-alpha increased the number of adherent and emigrated leukocytes and decreased the RBC velocity in mesenteric venules. Oxidative stress indicated by DHR fluorescence was exacerbated in microvessels of IFN-alpha-treated rats. Following the leukocyte recruitment and oxidative stress, an exaggerated albumin leakage was observed. Thrombus formation in venules and hemorrhage along venules were frequently observed in rats treated with IFN-alpha. N,N'-dimethylthiourea, a scavenger of hydrogen peroxide and a hydroxyl radical, largely prevented these microvascular responses. Pretreatment of rats with mAb directed against either CD18 or ICAM-1 also attenuated the IFN-alpha-induced microvascular alterations. It is concluded, therefore, that a high concentration of IFN-alpha stimulates CD18/ICAM-1-dependent adhesive interactions with endothelial cells and oxidant production of leukocytes, which leads to microcirculatory derangements characterized by decreased barrier function and reduced anticoagulant activity of venular endothelial cells.

Animals↗
PubMed1997

RAPD analysis of natural populations of Acanthopanax brachypus.

Random Amplified Polymorphic DNA (RAPD) analysis is a new technology of molecular marking which has proved very powerful in detecting genetic diversity at the level of population. The genomic DNAs used in our experiment were extracted from fresh leaves taken from 59 individuals sampled from three natural populations in Yan An, Shanxi Province. Through more than 2,000 PCRs, deep-going RAPD analysis was carried out on DNA samples from 49 individuals. The percentage of polymorphic RAPD loci found in these three populations were respectively 27.2%, 18.6% and 5.4%; the average genetic distances within population, 0.055, 0.036 and 0.008; the average genetic distances between populations (I-II), (I-III) and (II-III), 0.105, 0.096 and 0.060. The genetic diversity of A. brachypus within and between populations was found, for the first time, to be rather poor, thus revealing innate factors as the cause contributing to its endangered status. In addition, our work also provides basic materials for elucidating the underlying cause of its endangerment and for its protection biology.

China↗
PubMed1996

Experimental intracerebral hemorrhage in rats. Magnetic resonance imaging and histopathological correlates.

BACKGROUND AND PURPOSE: Intracerebral hemorrhage is associated with a considerable proportion of strokes and head injuries. The mechanism of brain cell injury associated with hemorrhage may be different from that due to pure ischemia. Therefore, it is essential that models of intracerebral hemorrhage be developed and well characterized. The purpose of this study was to obtain high-field MR images of rat brain at progressive times after induction of intracerebral hemorrhage and to correlate the images with behavior and histological evolution. METHODS: Intracerebral hemorrhage was induced in rats by injection of bacterial collagenase and heparin into the caudate nucleus. Histopathological changes and corresponding MR images were studied from 30 minutes to 3 weeks after injection. Behavioral changes were also followed for 3 weeks. RESULTS: Histological correlation showed that MR is capable of resolving the accumulation and degeneration of the hematoma, a centripetal wave of neutrophils infiltrating from the surrounding tissue beginning at 12 hours, and centripetal invasion of macrophages beginning at 48 hours. Widespread white matter edema was clearly evident on MR images for 1 week after the hemorrhage. Medium-sized striatal neurons were lost in the tissue surrounding the hematoma. Behavioral improvement was rapid during resolution of the edema but incomplete at 3 weeks. CONCLUSIONS: MR images correlate very well with histological changes in this experimental model of intracerebral hemorrhage and can therefore be used to follow changes due to drug treatments in vivo. The intense neutrophilic response to this lesion may contribute to neuronal injury at the periphery of the hematoma.

Animals↗
PubMed1994

In vivo effect of chronic administration of vasoactive intestinal peptide on gut-associated lymphoid tissues in rats.

The in vivo effects of chronic administration of vasoactive intestinal peptides (VIP) on the lymphoid cell traffic and the population and function of cells in intestinal lymph and gut-associated lymphoid tissues were examined in rats. VIP was continuously infused from the superior mesenteric artery in rats at a dose of 10 ng/min/kg body weight for 96 h. Lymphocyte transport through intestinal lymph was significantly reduced by VIP without any changes in lymph flow. When lymphocyte subpopulation was examined in intestinal lymph, T cell subsets were decreased with a dominant reduction in the population of helper T cells. T cell subsets were also decreased in mesenteric lymph nodes, but in this case suppressor/cytotoxic T cell subsets were mainly reduced. Despite of the decrease in lymphocyte transport through intestinal lymph and changes of lymphocyte subpopulation, proliferative response of lymphocytes from intestinal lymph and mesenteric lymph nodes to phytohemagglutinin did not show any significant alteration after administration of VIP. By histochemical study on the lamina propria of the small intestine, the population of pan T cells, especially helper T cells, was demonstrated to be significantly decreased after VIP treatment. There was also a marked decrease in the number of immunoglobulin (Ig) A-containing cells in the lamina propria of the small intestine in VIP-treated rats, while no significant changes were seen in the number of IgG and IgM-containing cells. Our present results showed the possibility that a long-term alteration of serum VIP levels could affect the dynamics of immune effector cells and IgA production in gut-associated lymphoid tissues.

Animals↗
PubMed1991

[Clinical and experimental study of the effect of kang er xin-I on viral myocarditis].

Kang Er Xin-I (KEX-I) is a proved recipe used to treat viral myocarditis. It consists of Lonicera japonica, Ophiopogon japonicus, Astragalus membranaceus mainly and possesses the effect of clearing away heat and toxic materials and supplementing the vital energy and nourishing. The clinical study was carried out with KEX-I according to a random, paired and cross-over design. Coenzyme Q10 was used as a control and left ventricular function was observed. The result showed: after being treated with KEX-I for two weeks, the 26 patients' chief cardiac functional indexes assessed with STI improved markedly, the value of PEP/LVET and ICT/LVCT all decreased and the difference between the two groups was significant. The experimental study showed that KEX-I can inactivate directly the virus of Coxsackie B3, protect the heart cells in mice, prevent attack by Coxsackie B3, promote the growth of internal interferon and increase the NK cell's function to regulate immunity in experimental mice.

Adolescent↗