共查询到20条相似文献,搜索用时 31 毫秒
1.
Parildar-Karpuzoğlu H Doğru-Abbasoğlu S Balkan J Aykaç-Toker G Uysal M 《Amino acids》2007,32(1):115-119
Summary. We aimed to investigate the effect of decreased taurine levels on endogenous and induced lipid peroxide levels in liver, brain,
heart and erythrocytes as well as prooxidant and antioxidant balance in the liver of rats administered β-alanine (3%, w/v)
in drinking water for 1 month to decrease taurine levels of tissues. This treatment caused significant decreases in taurine
levels of liver (86%), brain (36%) and heart (15%). We found that endogenous and ascorbic acid-, NADPH- and cumene hydroperoxide-induced
malondialdehyde (MDA) levels did not change in the liver, brain and heart homogenates following β-alanine treatment. Also,
H2O2-induced MDA levels remained unchanged in erythrocytes. In addition, we did not observe any changes in levels of MDA, diene
conjugates, glutathione, α-tocopherol, ascorbic acid and the activities of superoxide dismutase, glutathione peroxidase and
glutathione transferase in the liver. According to this, buffering or sequestering capacity of tissues to exogenous stimuli
was not influenced by reduced taurine levels in tissues of rats. 相似文献
2.
Summary. Mice were supplemented with β-alanine (3%) in drinking water for one week. β-Alanine intake reduced hepatic taurine levels,
but elevated cysteine levels significantly. Hepatotoxicity of CCl4 in mice fed with β-alanine was decreased as determined by changes in serum enzyme activities. Hepatic glutathione and taurine
concentrations after CCl4 challenge were increased markedly by β-alanine intake. The enhanced availability of cysteine for synthesis of glutathione
and/or taurine appears to account for the hepatoprotective effects of β-alanine against CCl4-induced liver injury. 相似文献
3.
Summary Male Wistar-Kyoto rats were given either tap water (control) or 3%-alanine (taurine-depleted) for three weeks. To prepare for the kidney function studies, the animals were then implanted with femoral vessels and bladder catheters. Two days after surgery, each rat was given an intravenous infusion of saline at the rate of 50l/min and urine samples were collected at specific time intervals. An isotonic saline solution (0.9% NaCl) was infused for determination of baseline parameters and was followed by the infusion of a hypotonic saline solution (0.45% NaCl). Two days later, the infusion protocol was repeated in the same animals; however, a hypertonic saline solution (1.8% NaCl) was substituted for the hypotonic saline solution. Renal excretion of fluid and sodium increased in the control, but not taurine-depleted, rats during the hypotonic saline infusion. Interestingly, diuretic and natriuretic responses were similar between the groups during hypertonic saline infusion. The results suggest that taurine-depletion in rats affects renal excretory responses to a hypotonic, but not a hypertonic, saline solution. 相似文献
4.
Stout JR Cramer JT Zoeller RF Torok D Costa P Hoffman JR Harris RC O'Kroy J 《Amino acids》2007,32(3):381-386
Summary. This study examined the effects of 28 days of β-alanine supplementation on the physical working capacity at fatigue threshold
(PWCFT), ventilatory threshold (VT), maximal oxygen consumption (
O2-MAX), and time-to-exhaustion (TTE) in women. Twenty-two women (age ± SD 27.4 ± 6.1 yrs) participated and were randomly assigned
to either the β-alanine (CarnoSyn™) or Placebo (PL) group. Before (pre) and after (post) the supplementation period, participants
performed a continuous, incremental cycle ergometry test to exhaustion to determine the PWCFT, VT,
O2-MAX, and TTE. There was a 13.9, 12.6 and 2.5% increase (p < 0.05) in VT, PWCFT, and TTE, respectively, for the β-alanine group, with no changes in the PL (p > 0.05). There were no changes for
O2-MAX (p > 0.05) in either group. Results of this study indicate that β-alanine supplementation delays the onset of neuromuscular
fatigue (PWCFT) and the ventilatory threshold (VT) at submaximal workloads, and increase in TTE during maximal cycle ergometry performance.
However, β-alanine supplementation did not affect maximal aerobic power (
O2-MAX). In conclusion, β-alanine supplementation appears to improve submaximal cycle ergometry performance and TTE in young women,
perhaps as a result of an increased buffering capacity due to elevated muscle carnosine concentrations. 相似文献
5.
Summary. Muscle carnosine synthesis is limited by the availability of β-alanine. Thirteen male subjects were supplemented with β-alanine
(CarnoSyn™) for 4 wks, 8 of these for 10 wks. A biopsy of the vastus lateralis was obtained from 6 of the 8 at 0, 4 and 10 wks. Subjects undertook a cycle capacity test to determine total work done (TWD)
at 110% (CCT110%) of their maximum power (Wmax). Twelve matched subjects received a placebo. Eleven of these completed the CCT110% at 0 and 4 wks, and 8, 10 wks. Muscle biopsies were obtained from 5 of the 8 and one additional subject. Muscle carnosine
was significantly increased by +58.8% and +80.1% after 4 and 10 wks β-alanine supplementation. Carnosine, initially 1.71 times
higher in type IIa fibres, increased equally in both type I and IIa fibres. No increase was seen in control subjects. Taurine
was unchanged by 10 wks of supplementation. 4 wks β-alanine supplementation resulted in a significant increase in TWD (+13.0%);
with a further +3.2% increase at 10 wks. TWD was unchanged at 4 and 10 wks in the control subjects. The increase in TWD with
supplementation followed the increase in muscle carnosine. 相似文献
6.
Mühling J Burchert D Langefeld TW Matejec R Harbach H Engel J Wolff M Welters ID Fuchs M Menges T Krüll M Hempelmann G 《Amino acids》2007,33(3):511-524
Summary. We examined the effects of DON [glutamine-analogue and inhibitor of glutamine-requiring enzymes], alanyl-glutamine (regarding
its role in neutrophil immunonutrition) and alanyl-glutamine combined with L-NAME, SNAP, DON, β-alanine and DFMO on neutrophil
amino and α-keto acid concentrations or important neutrophil immune functions in order to establish whether an inhibitor of
•NO-synthase [L-NAME], an •NO donor [SNAP], an analogue of taurine and a taurine transport antagonist [β-alanine], an inhibitor
of ornithine-decarboxylase [DFMO] as well as DON could influence any of the alanyl-glutamine-induced effects. In summary,
irrespective of which pharmacological, metabolism-inhibiting or receptor-mediated mechanisms were involved, our results showed
that impairment of granulocytic glutamine uptake, modulation of intracellular glutamine metabolisation and/or de novo synthesis
as well as a blockade of important glutamine-dependent metabolic processes may led to significant modifications of physiological
and immunological functions of the affected cells. 相似文献
7.
Chaswal M Das S Prasad J Katyal A Mishra AK Fahim M 《Physiological research / Academia Scientiarum Bohemoslovaca》2012,61(2):135-144
We studied the effect of losartan on baroreflex sensitivity (BRS) and heart rate variability (HRV) of adult Wistar rats during acute and chronic inhibition of nitric oxide synthesis by N(G)-nitro-L-arginine methyl ester (L-NAME). Chronic L-NAME administration (50 mg/kg per day for 7 days, orally through gavage) increased mean arterial pressure (MAP), heart rate but significantly decreased BRS. In addition, a significant fall of standard deviation of normal RR intervals, total spectral power, high frequency spectral power and a rise of low frequency to high frequency (LF: HF) ratio was seen. Acute L-NAME administration (30 mg/kg, i.v. bolus dose) also raised MAP and impaired HRV but it was associated with augmented BRS for bradycardia reflex. Losartan treatment (10 mg/kg, i.v.) in both acute and chronic L-NAME treated rats, decreased MAP but the difference was not significant. On the other hand, losartan administration normalized depressed BRS for bradycardia reflex and significantly reduced LF to HF ratio in chronic L-NAME treated rats. But this improvement was not observed in acute L-NAME group. These results indicate importance of mechanisms other than renin-angiotensin system in the pressor response of both acute as well as chronic L-NAME. However, autonomic dysregulation especially following chronic L-NAME appears to be partly angiotensin dependent. 相似文献
8.
A carotid infusion of angiotensin (AII) (10 ng/kg/min) has been found to increase significantly higher mean arterial pressure (MAP) and produces significantly lower bradycardia than AII intravenous infusions at the same dose and rate. Besides, i.v. administration of AII elicits greater impairment on baroreflex sensitivity than carotid infusion of AII does. On the other hand, vasopressin vascular receptor blockade did not modify the baroreflex sensitivity either in the carotid or in the i.v. infusions of AII, and plasma AVP measurements did not change significantly in any group. It clearly indicates that neither AVP nor baroreflex impairment plays any role on the pressor action of AII intracarotid infusions at a low dose. The present results further suggest that baroreflex impairment in rats may unlikely be located in the region irrigated by the carotid artery. 相似文献
9.
Summary. N-alkyl-β-alanine oligomers (β-peptoids) with α-chiral side chains [(R)- or (S)-1-(phenylethyl)amino groups] were synthesized and analyzed by CD spectroscopy. These chiral β-peptoid homomers exhibited
chain-length-dependent and solvent-dependent ellipticity, strongly indicating the presence of a secondary structure in solution.
The CD behaviour was only slightly temperature-dependent upon heating, as also previously observed for stable α-peptoid helices
containing the same type of side chains. Thus, the data presented here comprise the first evidence for a chain length-dependent
secondary folding of compounds with this novel peptidomimetic backbone design. In addition, applicability of a novel hyphenated
technique, HPLC-SPE-NMR/MS, for analysis of crude SPPS reaction products was demonstrated.
Authors’ address: Dr. C. A. Olsen, Department of Medicinal Chemistry, Faculty of Pharmaceutical Sciences, University of Copenhagen,
Universitetsparken 2, DK-2100 Copenhagen, Denmark; Present address: The Scripps Research Institute 相似文献
10.
Intracerebroventricular (i.c.v.) choline (50–150 g) increased blood pressure and decreased heart rate in spinal cord transected, hypotensive rats. Choline administered intraperitoneally (60 mg/kg), also, increased blood pressure, but to a lesser extent. The pressor response to i.c.v. choline was associated with an increase in plasma vasopressin. Mecamylamine pretreatment (50 g; i.c.v.) blocked the pressor, bradycardic and vasopressin responses to choline (150 g). Atropine pretreatment (10 g; i.c.v.) abolished the bradycardia but failed to alter pressor and vasopressin responses. Hemicholinium-3 [HC-3 (20 g; i.c.v.)] pretreatment attenuated both bradycardia and pressor responses to choline. The vasopressin V1 receptor antagonist, (-mercapto-, -cyclopenta-methylenepropionyl1, O-Me-Tyr2, Arg8)-vasopressin (10 g/kg) administered intravenously 5 min after choline abolished the pressor response and attenuated the bradycardia-induced by choline. These data show that choline restores hypotension effectively by activating central nicotinic receptors via presynaptic mechanisms, in spinal shock. Choline-induced bradycardia is mediated by central nicotinic and muscarinic receptors. Increase in plasma vasopressin is involved in cardiovascular effects of choline. 相似文献
11.
The newly described endogenous peptide, endothelin, was administered to five chronically instrumented conditioned dogs. Endothelin produced significant and simultaneous increases in both heart rate (HR) and mean arterial pressure (MAP) in conscious dogs. Endothelin also produced significant increases in MAP in anesthetized animals. Ganglionic suppression induced by hexamethonium (10 mg/kg) and atropine (0.1 mg/kg) blocked HR responses and markedly inhibited the pressor responses to endothelin in conscious animals. These results suggest that endothelin in part acts to elevate blood pressure and heart rate through modification of autonomic nervous system tone. When endothelin and angiotensin II were administered in mole equivalent doses, angiotensin II produced a pressor response of greater magnitude than did endothelin in conscious animals. 相似文献
12.
The effects of naloxone and morphine on mean arterial blood pressure (MBP) and heart rate (HR) responses to angiotensin II (AII) were studied in conscious cynomolgus monkeys. Graded doses of AII (0.3, 1 and 3 micrograms/min for 8-10 min) were infused i.v. 20 min apart, preceded by an i.v. injection of either naloxone (1, 3 or 10 mg/kg), morphine (0.3, 1 or 3 mg/kg) or saline. Pretreatment with naloxone (10 mg/kg) attenuated the pressor response to AII (0.3 or 1 microgram/min) by 25-50% but did not alter similar pressor responses to phenylephrine. Pretreatment with morphine had little or no effect on MBP or HR responses to AII. 相似文献
13.
Rossi NF Maliszewska-Scislo M Chen H 《Canadian journal of physiology and pharmacology》2008,86(6):343-352
Endothelin 1 (ET-1) is increased in heart failure, both in plasma and within the central nervous system. Centrally, ET-1 induces sympathetic hyperactivity and arginine vasopressin (AVP) secretion. Both sympathetic activity and AVP secretion are regulated by the arterial baroreflex, which is typically impaired in heart failure. We hypothesized that central blockade of ETA receptors (ETAR) alters the baroreflex response of heart rate, renal sympathetic nerve activity (RSNA), and plasma AVP levels in a cardiomyopathic model of heart failure. Female Sprague-Dawley rats received weekly intraperitoneal injections of doxorubicin 2.5 mg x kg(-1) (doxorubicin heart failure, doxo-HF) or saline vehicle (control). After 8 weeks, they were instrumented, conditioned to the study environment, and then studied in the awake, non-restrained state. Baseline mean arterial pressure (MAP), RSNA, and plasma osmolality were similar in both groups, but heart rate (p<0.02), left ventricular pressure (p<0.001), and plasma AVP (p<0.01) were higher in the doxo-HF group. ET-1 dose dependently increased MAP, but the rise was significantly attenuated in doxo-HF rats at all doses. Baseline baroreflex control of heart rate and RSNA was similar in both groups. ETAR blockade with 4 nmol BQ123 i.c.v. significantly decreased both the upper plateau (p<0.05) and the range (p<0.05) of the baroreflex response of both heart rate and RSNA in doxo-HF but not in control rats. Despite higher basal plasma levels of AVP, ET-1 evoked a rise in plasma AVP of 13.6+/-3.2 pg x mL(-1) in doxo-HF compared with 0.4+/-0.4 pg x mL(-1) in control rats (p<0.001). To account for the blunted pressor response to ET-1 in the doxo-HF rats, gain of AVP release was calculated as DeltaAVP/DeltaMAP and was also found to be significantly greater in the doxo-HF rats (p<0.001). BQ123 prevented the rise in AVP and restored the gain in doxo-HF rats to that seen in controls. Thus, central ETAR contribute to the sympathoexcitation and AVP responses observed in heart failure due to doxorubicin cardiomyopathy. 相似文献
14.
Resstel LB Tirapelli CR Lanchote VL Uyemura SA de Oliveira AM Corrêa FM 《Life sciences》2006,78(19):2179-2187
Chronic ethanol intake and hypertension are related. In the present work, we investigated the effect of chronic ethanol (20% v/v) intake for 2, 6 and 10 weeks on basal arterial blood pressure, baroreflex and heart rate levels, as well as on the cardiovascular responses to the infusion of vasoactive agents in unanesthetized rats. Mild hypertension was observed after 2 weeks, 6 weeks or 10 weeks of treatment. On the other hand, no changes were observed in heart rate after long-term ethanol intake. Similar baroreflex changes were observed in 2- or 6-week ethanol-treated rats, and affected all parameters of baroreflex sigmoid curves, when compared to the control group. These changes were characterized by an enhanced baroreflex sympathetic component and a reduction in the baroreflex parasympathetic component. No differences in baroreflex parameters were observed in 10-week ethanol-treated animals. The pressor effects of i.v. phenylephrine were enhanced in 2-week ethanol-treated rats; not affected in 6-week treated animals and reduced in 10-week ethanol-treated rats, when compared to respective control and isocaloric groups. The hypotensive response to i.v. sodium nitroprusside (SNP) was enhanced at all different times of treatment, when compared to respective control and isocaloric groups. In conclusion, the present findings showed increased arterial pressure in the early phase of chronic ethanol consumption, which was consequent of rise in both systolic and diastolic pressures. Ethanol intake affected both the sympathetic and the parasympathetic components of the baroreflex. Vascular responsiveness to the pressor agent phenylephrine was initially enhanced and later on decreased during chronic ethanol intake. Vascular responsiveness to the depressor agent SNP was enhanced during chronic ethanol intake. 相似文献
15.
Summary. The condensation reactions of sodium trimetaphosphate with single amino acids, namely glycine, L-alanine, β-alanine and γ-aminobutyric
acid or pairs of these amino acids were reinvestigated by electrospray ion-trap mass spectrometry and high performance liquid
chromatography. It was found when mixtures were treated by sodium trimetaphosphate only in the presence of α-amino acid dipeptides
were formed. Without addition of α-amino acids, the β-amino acid or γ-aminobutyric acid could not form peptide either by themselves
or with their mixtures under the same conditions. From the data it is concluded that phosphate might select α-amino acids
to produce the peptides being important precursors for the origin of life.
Authors’ address: Dr. Pengxiang Xu, The Key Laboratory for Chemical Biology of Fujian Province, Department of Chemistry, Xiamen
University, Xiamen 361005, China 相似文献
16.
Summary. The present study was designed to evaluate the relevance of arginine transport in nitric oxide (NO) synthesis in vascular
smooth muscle cells. For this purpose, NO synthesis and arginine transport (system B0,+ and y+) were evaluated in cells treated with IL-1β or angiotensin II (Ang II). In addition, the effects of 5 mM lysine and glutamine, competitive inhibitors of systems y+ and B0,+ respectively, were examined. L-arginine transport was estimated with 3H-labelled arginine and NO was determined with the Griess reagent. These studies were done in control conditions, arginine-starved
cells, and in cells incubated in media containing 10 mM arginine. Our data indicate that induction of NO biosynthesis by IL-1β
depends on external arginine when cells are arginine-depleted for 24 hours. The concentration of arginine producing half maximal
activation of NO synthesis in arginine-depleted cells ([arginine]i < 10 μM) was 41.1 ± 18 μM. By contrast, in normal culture conditions, NO synthesis occurred independently of arginine transport.
Neither 5 mM lysine or glutamine which abolished arginine transport through systems y+ and B0,+, respectively, reduced nitrite release in cells incubated in normal media. This suggests that the relevance of arginine uptake
to NO synthesis depends on the status of intracellular arginine pools. Intracellular arginine concentrations were not affected
by the stimulation of NO production using IL-1β or its inhibition using Ang II, but were markedly reduced by arginine starvation
for 48 h. Aspartate levels were also reduced by arginine-depletion, but were not affected in cells incubated with 10 mM arginine.
By contrast, glutamate levels were reduced in arginine-starved cells and were increased in cells incubated in arginine-supplemented
medium. Ornithine levels were markedly increased by arginine supplementation. Altogether, these findings indicate that NO
synthesis is normally independent of membrane transport. However in arginine-depleted cells, membrane transport is essential
for NO synthesis. It is concluded that arginine transport is required for the long-term maintenance of intracellular arginine
pools.
Received February 7, 1999; Accepted June 21, 1999 相似文献
17.
D L Jones 《Canadian journal of physiology and pharmacology》1988,66(10):1270-1277
These experiments investigated in the awake rat the involvement of noradrenergic projections to the rostral hypothalamus in the drinking and pressor responses elicited by intracerebroventricular (i.c.v.) injections of 25 ng of angiotensin II. Phentolamine mesylate in doses of 2.5-125 micrograms injected into the rostral hypothalamus produced a dose-dependent depression of both the drinking and pressor responses elicited by i.c.v. administration of angiotensin II. A paradoxical increase in heart rate was associated with a decrease in pressor responses with increasing doses of phentolamine. This response was due to tissue injections, since pretreatment by injecting 12.5 micrograms of phentolamine into the ventricle did not block either the cardiovascular or drinking responses to i.c.v. injections of angiotensin II. Yohimbine (0.33-3.3 micrograms), DL-propranolol (25 micrograms), and atenolol (25 micrograms) did not, but prazosin (0.7 microgram) did significantly alter the pressor responses. Although yohimbine also was without effect on drinking, prazosin reduced the drinking responses. These results suggest that alpha 1-adrenergic receptors in the rostral hypothalamus are involved in the control of both the drinking and pressor responses elicited by i.c.v. injections of angiotensin II. In the case of propranolol and atenolol, beta-adrenergic receptors altered only the drinking response in a nonspecific manner by eliciting competing behaviors. Whether they are involved in modifying the drinking response only remains to be demonstrated. 相似文献
18.
Intracellular chloroplast photorelocation in the moss Physcomitrella patens is mediated by phytochrome as well as by a blue-light receptor 总被引:3,自引:0,他引:3
The light-induced intracellular relocation of chloroplasts was examined in red-light-grown protonemal cells of the moss Physcomitrella patens. When irradiated with polarized red or blue light, chloroplast distribution in the cell depended upon the direction of the
electrical vector (E-vector) in both light qualities. When the E-vector was parallel to the cross-wall (i.e. perpendicular
to the protonemal axis), chloroplasts accumulated along the cross-wall; however, no accumulation along the cross-wall was
observed when the E-vector was perpendicular to it (i.e. parallel to the protonemal axis). When a part of the cell was irradiated
with a microbeam of red or blue light, chloroplasts accumulated at or avoided the illumination point depending on the fluence
rate used. Red light of 0.1–18 W m−2 and blue light of 0.01–85.5 W m−2 induced an accumulation response (low-fluence-rate response; LFR), while an avoidance response (high-fluence-rate response;
HFR) was induced by red light of 60 W m−2 or higher and by blue light of 285 W m−2. The red-light-induced LFR and HFR were nullified by a simultaneous background irradiation of far-red light, whereas the
blue-light-induced LFR and HFR were not affected at all by this treatment. These results show, for the first time, that dichroic
phytochrome, as well as the dichroic blue-light receptor, is involved in the chloroplast relocation movement in these bryophyte
cells. Further, the phytochrome-mediated responses but not the blue-light responses were revealed to be lost when red-light-grown
cells were cultured under white light for 2 d.
Received: 7 September 1999 / Accepted: 15 October 1999 相似文献
19.
Summary. L-Tryptophan (TRP) is the precursor amino acid for the synthesis of serotonin (5-HT). 5-HT is effective both on the food intake
and gastrointestinal system contractility. The aim of this study was to search the effects of systemic TRP treatment on 5-HT
levels of ileum and searching the effect of ileal contractility and oxidant status. Swiss-albino mice were divided into two
groups: 1. Control, 2. TRP-treated (100 mg/kg/24 h, i.p., for 7 days). Body weights were recorded at the beginning and at
the end of experiments. Acetylcholine-induced contractile responses in the isolated ileum were recorded on polygraph. Ileal
tissue malondialdehyde and glutathione levels determined by spectrophotometric and ileal tissue 5-HT levels were measured
by immunohistochemical methods. TRP treatment decreased body weight and increased ileal contractile response. In the TRP-treated
group, ileum malondialdehyde levels increased and glutathione levels decreased. Immunohistochemical detection showed that
ileal 5-HT levels were increased by TRP treatment. There is a relationship between increased oxidative stress and increased
contractility in the ileal tissue of the TRP-treated animals. These effects may be related to increased ileal 5-HT synthesis. 相似文献
20.
Conscious, unrestrained rats were used to determine the hemodynamic (blood pressure and heart rate) responses following intravenous (IV) injection of dynorphin A(1-13) and the possible receptor mechanisms mediating those changes. Male Sprague-Dawley rats (300 g) were given IV bolus injections (via femoral venous catheter) of 6.0 to 600 nmoles/kg of dynorphin A(1-13), 8.0 nmoles/kg of norepinephrine HCl (NE), 14.3 pmoles/kg of angiotensin II or a vehicle control solution. Blood pressure (BP) and heart rate (HR) were monitored via femoral arterial catheter (into abdominal aorta) over 90 sec postpeptide or -amine administration before and 10 min after IV injection of 4.2 mumoles/kg of naloxone HCl (opiate antagonist), yohimbine HCl (alpha 2 receptor antagonist) or prazosin HCl (alpha 1 receptor antagonist). Dynorphin A(1-13) caused a transient but dose-related rise in mean arterial pressure (MAP) whereas mean pulse pressures (MPP) and mean heart rates (MHR) concomitantly fell, from preinjection control values in a dose-dependent fashion. Pretreatment with naloxone blocked the pressor response of only a subsequent injection with 20 nmoles/kg but not 60 nmoles/kg of dynorphin A or NE (8.0 nmoles/kg). Pretreatment with yohimbine suppressed the marked pressor responses of subsequent NE or Dyn A (60 nmoles/kg) administration whereas prazosin antagonized the rise in MAP of only the lower doses of dynorphin as well as NE. The suppression of the pressor responses of dynorphin by opiate or alpha receptor antagonists were not caused by tachyphylaxis for repeated injections of 6.0 or 60 nmoles/kg of dynorphin caused the same rise in MAP.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献