bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sucking rates of the white‐backed planthopper Sogatella furcifera (Horv.) (Homoptera, Delphacidae) and yield loss of rice
Authors: Zhu Z.‐R. , Cheng J. 
Published: March 2003

AbstractThe sap‐sucking rates of the white‐backed planthopper (WBPH) Sogatella furcifera (Horv.) (Homoptera, Delphacidae) were examined under a series of experimental conditions in the laboratory. The sucking rate increased with the age of the planthopper. The relative sucking rate of nymphs at the 1st, 2nd, 3rd, 4th, and 5th instars and macropterous male adult was 0.19, 0.27, 0.37, 0.49, 0.59, 0.69, and 1 of that of macropterous female adult (set as standard insect [SI]), respectively. The SI sucked at a maximum rate from rice plants at tillering stage. In indica rice varieties, the SI had higher sucking rate than in japonica varieties. The effect of temperature on sucking rate could be described by an exponential quadratic equation. A power equation (W = 0.0001S1.8107) could be used to transfer the relative sucking rate in area (S, mm2) of honeydew excreted by WBPH into absolute dry mass weight (W, mg). The relationship between injury to rice by WBPH in cage and yield loss assessment showed that yield loss was mainly caused by decreased filling percentage of kernels and kernel weights rather than the number of panicles and spikelets per panicle. Finally, experimental results were integrated to a formula that links percentage of yield loss and sucking equivalence of WBPH.
Partial agonistic activity of labetalol, the arylethanolamine, on β3‐adrenoceptors in the guinea‐pig gastric fundus
Authors: Horinouchi T. , Asai S. , Fukushima M. , Koike K. 
Published: March 2003

Summary 1 The agonistic and antagonistic effects of labetalol, the α1‐ and β‐adrenoceptor antagonist, were studied on β3‐adrenoceptors in the guinea‐pig gastric fundus. 2 Labetalol caused a concentration‐dependent relaxation with a pD2 value of 5.58 ± 0.09 and an intrinsic activity of 0.64 ± 0.06, which was not affected by pretreatment with both the selective β1‐adrenoceptor antagonist, (±)‐atenolol (100 μM), and the selective β2‐adrenoceptor antagonist, (±)‐butoxamine (100 μM). 3 However, the non‐selective β1‐, β2‐ and β3‐adrenoceptor antagonist, (±)‐bupranolol (3–30 μM), shifted the concentration–response curve of labetalol to the right (pA2 value=5.97 ± 0.08). 4 In the presence of (±)‐atenolol (100 μM) and (±)‐butoxamine (100 μM), relaxations to catecholamines [(−)‐isoprenaline, (−)‐noradrenaline and (−)‐adrenaline], to the selective β3‐adrenoceptor agonist, BRL37344, and to the non‐conventional partial β3‐adrenoceptor agonist, (±)‐CGP12177A, were weakly antagonized by labetalol (10 μM). 5 These results indicate that labetalol, the arylethanolamine, acts as a partial agonist on β3‐adrenoceptors in the guinea‐pig gastric fundus.
Endothelium‐dependent relaxation in isolated renal arteries of diabetic rabbits
Authors: Yousif M. H. M. , Cherian A. , Oriowo M. A. 
Published: March 2003

Summary 1 In this study, we have investigated the vasodilator response to acetylcholine under diabetes conditions in isolated renal arteries of rabbits. We have also examined the contribution of endothelium‐derived nitric oxide (EDNO) and endothelium‐derived hyperpolarizing factor (EDHF) to the endothelium‐dependent relaxation caused by acetylcholine in the renal arteries of alloxan‐induced diabetic rabbits. 2 Acetylcholine (10−10−10−4 m) produced cumulative concentration–response curve in the renal arteries of both control and diabetic rabbits. The EC50 values and maximal responses to acetylcholine were not significantly different relative to diabetic conditions. In order to isolate the EDHF component of acetylcholine‐induced vasodilator response, l‐nitro‐methyl arginine ester (l‐NAME, 10−4 m) and indomethacin (10−6 m) were added to the Krebs' solution throughout the experiment. Under these conditions, acetylcholine induced vasodilatation in the isolated renal arteries from both control and diabetic rabbits. The vasodilator response to acetylcholine was not affected under diabetic conditions. 3 Sodium nitroprusside (SNP)‐induced relaxation was increased in the diabetic rabbits compared with the control animals. 4 Tetrabutyl ammonium (TBA, 0.5 mm) produced a significant reduction in acetylcholine‐induced vasodilatation in both preparations from control and diabetic animals, consistent with involvement of K+ channels in mediating this response. Glibenclamide (1 μm) attenuated acetylcholine‐induced vasodilatation in preparations from control animals only, while iberiotoxin (0.05 μm) significantly reduced the vasodilator response to acetylcholine in preparations from both control and diabetic animals. 5 The role of EDNO in mediating acetylcholine‐induced vasodilatation was examined. The vascular preparations were incubated with 20 mm K+‐Krebs' solution to inhibit the EDHF contribution to acetylcholine‐induced vasodilatation. Under this condition, acetylcholine induced a vasodilator response in both preparations from control and diabetic rats. Pretreatment with l‐NAME (10−4 m) attenuated acetylcholine‐induced vasodilatation in both preparations, indicating an nitric oxide‐mediated vasodilator response. 6 Our results indicated that acetylcholine‐induced vasodilatation in the isolated renal arteries of alloxan‐induced diabetic rabbits was not affected under diabetic conditions. Acetylcholine‐induced vasodilatation is mediated by two vasodilator components; namely, EDHF and EDNO. The contribution of EDHF and EDNO to acetylcholine‐induced vasodilatation was not affected under diabetic conditions and there was no indication of endothelial dysfunction associated with diabetes. EDHF component was found to act mainly through high conductance Ca2+‐activated K+ channels under normal and diabetic conditions, while the adenosine triphosphate‐dependent K+ channels were involved in mediating acetylcholine vasodilator response in the control preparations only.
Inhibitory effects of cortical steroids and adrenocorticotropic hormone on catecholamine secretion in guinea‐pig perfused adrenal glands
Authors: Yonekubo K. , Ohta T. , Nakazato Y. , Ito S. 
Published: March 2003

Summary 1 We investigated the effects of exogenously applied steroids and endogenously released cortisol on catecholamine (CA) secretion induced by cholinergic agonists in perfused guinea‐pig adrenal glands. 2 Acetylcholine (ACh) and electrical stimulation induced CA secretion, which was reversibly inhibited by cortisol. Adrenocorticotropic hormone (ACTH) increased the concentration of cortisol in the perfusion effluent and partly inhibited the secretory response to ACh. 3 Cortisol or aldosterone dose‐dependently inhibited secretory responses to nicotine and muscarine. These inhibitory effects were not antagonized by mifepristone and spironolactone, respective cortisol and aldosterone receptor blockers. 4 Dexamethasone, cortisone, corticosterone, 11‐deoxycortisol, 11‐deoxycorticosterone, prednisolone and cholesterol inhibited nicotine‐evoked CA secretion. The secretory response to muscarine was inhibited by these compounds except for dexamethasone and prednisolone. 5 Dexamethasone, cortisol and aldosterone had no effect on CA secretion induced by high KCl. 6 These results suggest that steroids affect nicotinic and muscarinic ACh receptor‐mediated responses through distinct mechanisms, and that cortisol released from the adrenal cortex inhibits CA secretion from the adrenal medulla.
The effects of hypochlorite‐induced oxidative stress on presynaptic M2‐receptors at sympathetic nerve endings in the rat tail artery
Authors: Sand C. , Peters S. L. M. , Mathy M.‐J. , Pfaffendorf M. , Van Zwieten P. A. 
Published: March 2003

Summary 1 It was shown recently that stimulation of cardiac muscarinic M2‐receptors revealed an enhanced negative inotropic response in isolated rat left atria after exposure to hypochlorite‐induced oxidative stress. This phenomenon was not observed after stimulation of the cardiac A1‐receptor, which like the M2‐receptor is coupled to Gi‐proteins. Since even the contractile response to M3‐receptor stimulation was not amplified in the rat portal vein, we hypothesized a M2‐receptor specificity of this hypochlorite‐induced enhancement. 2 The present study was performed in order to investigate whether the sympathoinhibitory response to presynaptically located M2‐receptor stimulation would also be modified after exposure to hypochlorite in the rat tail artery. We applied electrical field stimulation (EFS) in order to mimic sympathetic neurotransmission. 3 EFS increased the vascular tone frequency‐dependently (0.3–4 Hz). EFS‐induced vasoconstriction could be attenuated by acetylcholine (30 nm−1 μm) in a concentration‐dependent manner. Hypochlorite (10 and 100 μm) did not affect the sympathoinhibitory effect of acetylcholine (100 nm). 4 In conclusion, in contrast to cardiac M2‐receptors, hypochlorite did not amplify the sympathoinhibitory effects of presynaptic M2‐receptors. The different responsiveness between neuronal and cardiac M2‐receptors to hypochlorite may be explained by the different G‐protein subunits involved in the activation of the underlying signalling cascade.
Evidence that the hypotensive effect of WAY 100635, a 5‐HT1A receptor antagonist, is related to vascular α1‐adrenoceptor blockade in the adult rat
Authors: Villalobos‐Molina R. , López‐Guerrero J. J. , Gallardo‐Ortíz I. A. , Ibarra M. 
Published: March 2003

Summary 1 The effect of WAY100635 (N‐[2‐[4‐(2‐methoxyphenyl)‐1‐piperazinyl]ethyl]‐N‐(2‐pyridinyl) cyclohexanecarboxamide trihydrochloride), a 5‐HT1A receptor antagonist, on cardiovascular function was studied. 2 The i.v. injection of WAY100635 dose‐dependently decreased blood pressure in anaesthetized rats; while in pithed rats WAY100635 (1 mg kg−1) displaced the phenylephrine pressor effect. 3 WAY100635 antagonized phenylephrine‐induced contraction in rabbit and rat aorta (pA2 of 6.88 and 7.93 and Schild slopes of −0.83 and −1.21, respectively); while in rat caudal artery pKB was 7.45 and the Schild slope of −0.56, suggesting a complex interaction in this vessel. 4 The results show that WAY100635 induced hypotension in the anaesthetized rat and suggest that this effect could be partially explained by antagonism of vascular α1‐adrenoceptors.
Muscarinic receptors of the urinary bladder: detrusor, urothelial and prejunctional
Authors: Chess‐Williams R. 
Published: March 2003

Summary 1 The parasympathetic nervous system is responsible for maintaining normal bladder function, contracting the bladder smooth muscle (detrusor) and relaxing the bladder outlet during micturition. 2 Contraction of the bladder involves direct contraction via M3 receptors and an indirect ‘re‐contraction’ via M2‐receptors whereby a reduction in adenylate cyclase activity reverses the relaxation induced by β‐adrenoceptor stimulation. 3 Muscarinic receptors are also located on the epithelial lining of the bladder (urothelium) where they induce the release of a diffusible factor responsible for inhibiting contraction of the underlying detrusor smooth muscle. The factor remains unidentified but is not nitric oxide, a cyclooxygenase product or adenosine triphosphate. 4 Finally, muscarinic receptors are also located prejunctionally in the bladder on cholinergic and adrenergic nerve terminals, where M1‐receptors facilitate transmitter release and M2 or M4‐receptors inhibit transmitter release. 5 In pathological states, changes may occur in these receptor systems resulting in bladder dysfunction. Muscarinic receptor antagonists are the main therapeutic agents available for treatment of the overactive bladder, but whether their therapeutic effect involves actions at all three locations (detrusor, prejunctional, urothelial) has yet to be established.
Characterization of adenosine receptors mediating the vasodilator effects of adenosine receptor agonists in the microvasculature of the hamster cheek pouch in vivo
Authors: Nicholls J. , Hourani S. M. O. , Hall J. M. 
Published: March 2003

Summary 1 The aim of this study was to characterize the adenosine receptor mediating vasodilation in the microvasculature of the hamster cheek pouch in vivo. A range of adenosine agonists was used including N6‐cyclopentyladenosine (CPA) (A1 agonist), 5′‐N‐ethylcarboxamidoadenosine (NECA) (non‐selective), 2‐chloroadenosine (2CADO) (non‐selective), 2‐p‐(2‐carboxyethyl)‐phenethylamino‐5′‐N‐ethylcarboxamidoadenosine (CGS 21680) (A2A agonist), N6‐(3‐iodobenzyl)‐adenosine‐5′‐N‐methyluronamide (IBMECA) (A3 agonist) and adenosine, as well as the adenosine antagonists 8‐sulphophenyltheophylline (8‐SPT) (A1/A2 antagonist), 1,3‐dipropyl‐8‐cyclopentylxanthine (DPCPX) (A1 antagonist) and 4‐(2‐[7‐amino‐2‐(2‐furyl)[1,2,4]‐triazolo[2,3‐a][1,3,5]triazin‐5‐ylamino]ethyl)phenol (ZM 241385) (A2A antagonist). 2 All the adenosine analogues used induced vasodilation at concentrations between 10 nm and 1 μm, and the potency order was NECA > CGS 21680 > 2CADO > CPA=IBMECA >> adenosine, indicating an action at A2A receptors. 8‐SPT (50 μm) antagonized vasodilator responses to NECA with an apparent pKB of 5.4, consistent with an action at A1 or A2 receptors and confirming that A3 receptors are not involved in this response. 3 DPCPX (10 nm) had no effect on vasodilation evoked by NECA, suggesting that this response was not mediated via A1 receptors, while ZM 241385 (10 nm) antagonized dilator responses to NECA with an apparent pKB of 8.9 consistent with an action via A2A receptors. 4 Overall these results suggest that adenosine A2A receptors mediate vasodilation in the hamster cheek pouch in vivo.
Control of non‐adrenergic non‐cholinergic reflex motor responses in circular muscle of guinea‐pig small intestine by Met‐enkephalin
Authors: Ivancheva Chr. , Radomirov R. 
Published: March 2003

Summary 1 A triple organ bath method allowing the synchronous recording of the motor activity of the circular muscle layer belonging to the oral and anal segments of guinea‐pig small intestine adjacent to an electrically stimulated middle segment was developed to study the ascending and descending reflex motor responses. 2 Electrical field stimulation (0.8 ms, 40 V, 5 Hz, 10 s) applied to the middle part of the segments elicited tetrodotoxin (1 μm)‐sensitive ascending and descending contractile responses of the nonstimulated parts, oral and anal, respectively. The ascending contraction was more pronounced as compared with the descending contraction. 3 In the presence of phentolamine (5 μm), propranolol (5 μm) and atropine (3 μm) a significant decrease in the amplitude of the ascending contraction was seen and a descending relaxation, instead of a contraction was observed. 4 Met‐enkephalin applied at a single concentration (0.1 μm) or cumulatively (0.001–1 μm) inhibited both non‐adrenergic non‐cholinergic (NANC) descending relaxation and ascending contraction with similar efficacy but different potency, IC50 being 5.9 ± 0.3 and 39.0 ± 4 nm, respectively. Naloxone (0.5 μm) prevented the effects of Met‐enkephalin. 5 L‐NNA (0.5 mm), an inhibitor of nitric oxide synthesis, increased the ascending contraction and strongly reduced but not abolished the descending relaxation. l‐Arginine (0.5 mm) restored the motor responses to the initial level in l‐NNA‐pretreated preparations, d‐Arginine (0.5 nm) had no effects. 6 Met‐enkephalin (0.1 μm) depressed the l‐NNA‐dependent increase of the ascending contraction and failed to change the l‐NNA‐resistant part of the descending relaxation. 7 Met‐enkephalin did not alter spontaneous NANC mechanical activity. SNP (1 or 10 μm), an exogenous donor of nitric oxide, caused a concentration‐dependent relaxation. The effects of SNP persisted in Met‐enkephalin (0.1 μm)‐pretreated preparations. 8 NANC reflex ascending contraction and descending relaxation were synchronously induced by a local nerve stimulation indicating a functional coactivation of NANC orally projected excitatory and anally directed inhibitory pathways. Acting prejunctionally, Met‐enkephalin provided a negative controlling mechanism inhibiting both ascending and descending, mainly nitric oxide mediated, reflex responses. A higher sensitivity of the descending relaxation to Met‐enkephalin was observed suggesting an essential role of opioid(s) in reducing the efficacy of descending motor activity.
Mitochondrial dysfunction leads to telomere attrition and genomic instability
Authors: Liu Lin , Trimarchi James R. , Smith Peter J. S. , Keefe David L. 
Published: March 2003

SummaryMitochondrial dysfunction and oxidative stress have been implicated in cellular senescence, apoptosis, aging and aging‐associated pathologies. Telomere shortening and genomic instability have also been associated with replicative senescence, aging and cancer. Here we show that mitochondrial dysfunction leads to telomere attrition, telomere loss, and chromosome fusion and breakage, accompanied by apoptosis. An antioxidant prevented telomere loss and genomic instability in cells with dysfunctional mitochondria, suggesting that reactive oxygen species are mediators linking mitochondrial dysfunction and genomic instability. Further, nuclear transfer protected genomes from telomere dysfunction and promoted cell survival by reconstitution with functional mitochondria. This work links mitochondrial dysfunction and genomic instability and may provide new therapeutic strategies to combat certain mitochondrial and aging‐associated pathologies.
Spatio‐temporal analysis of gene expression during aging in Drosophila melanogaster
Authors: Seroude Laurent , Brummel Ted , Kapahi Pankaj , Benzer Seymour 
Published: March 2003

SummaryThe relationship between gene expression and the regulation of longevity is poorly understood. Previous studies focusing on microarray or tissue‐specific changes in gene expression as a function of age have provided evidence that gene expression is a dynamic process which is regulated, even late in an organism's lifespan. Using the enhancer‐trap technique, a systematic analysis of the spatio‐temporal regulation of gene expression in tissues of adult Drosophila is presented. As many as 80% of enhancer traps analysed displayed (some form of) transcriptional change with age. In some cases the rate of change in expression was found to correlate with changes in longevity under various conditions, suggesting that they may be indicators of ‘physiological age’ and therefore valuable markers for dissecting the aging process. Molecular analysis of enhancer traps that showed increased activity with age was performed to identify candidate genes that may be important in the regulation of longevity; we identified changes in reporters associated with immunity, microtubule organization and muscle function.
The role of chondrocyte senescence in osteoarthritis
Authors: Price Jo S. , Waters Jasmine G. , Darrah Clare , Pennington Caroline , Edwards Dylan R. , Donell Simon T. , Clark Ian M. 
Published: March 2003

SummaryReplicative senescence occurs when normal somatic cells stop dividing. Senescent cells remain viable, but show alterations in phenotype, e.g. altered expression of matrix metalloproteinases (MMPs); these enzymes are known to be involved in cartilage destruction. It is assumed that cells deplete their replicative potential during aging, and age is a major risk factor for osteoarthritis (OA). Therefore, we hypothesized that chondrocytes in aging or diseased cartilage become senescent with associated phenotypic changes contributing to development or progression of OA.Articular cartilage was obtained from OA patients undergoing arthroplasty, with ‘normal’ cartilage from trauma surgery for hip fracture. Senescent cells were identified using the senescence‐associated β‐galactosidase (SA‐β‐gal) marker. Telomere length was assessed using Southern blot. MMP expression was measured at the mRNA level using Taqman® RT‐PCR.No SA‐β‐gal staining was observed in control cartilage regardless of patient age. In contrast, SA‐β‐gal staining was observed in damaged OA cartilage adjacent to the lesion. Cultured chondrocytes isolated from sites near a lesion contained a greater percentage of SA‐β‐gal positive cells than cultures isolated from distal sites or normal cartilage. Mean telomere length was shorter in cells near the lesion compared to distal sites in the same joint; thus the former population has undergone cell division. The expression of collagenases MMP‐1, ‐8 and ‐13 and tissue inhibitor of metalloproteinases (TIMP)‐1 was altered in OA cartilage, but no difference was detected between lesion and distal sites in the same joint (i.e. no correlation was found between senescent cells and proteinase/inhibitor expression).
Age‐specific metabolic rates and mortality rates in the genusDrosophila
Authors: Promislow Daniel E. L. , Haselkorn Tamara S. 
Published: March 2003

SummaryEarly theories of aging suggested that organisms with relatively high metabolic rates would live shorter lives. Despite widespread tests of this ‘rate of living’ theory of aging, there is little empirical evidence to support the idea. A more fine‐grained approach that examined age‐related changes in metabolic rate over the life span could provide valuable insight into the relationship between metabolic rate and aging. Here we compare age‐related metabolic rate (measured as CO2production per hour) and age‐related mortality rate among five species in the genusDrosophila. We find no evidence that longer‐lived species have lower metabolic rates. In all five species, there is no clear evidence of an age‐related metabolic decline. Metabolic rates are strikingly constant throughout the life course, with the exception of females ofD. hydei, in which metabolic rates show an increase over the first third of the life span and then decline. We argue that some physiological traits may have been shaped by such strong selection over evolutionary time that they are relatively resistant to the decline in the force of selection that occurs within the life time of a single individual. We suggest that comparisons of specific traits that do not show signs of aging with those traits that do decline with age could provide insight into the aging process.
A call to fins! Zebrafish as a gerontological model
Authors: Gerhard Glenn S. , Cheng Keith C. 
Published: March 2003

SummaryAmong the wide variety of model organisms commonly used for studies on aging, such as worms, flies and rodents, a wide research gap exists between the invertebrate and vertebrate model systems. In developmental biology, a similar gap has been filled by the zebrafish (Danio rerio). We propose that the zebrafish is uniquely suited to serve as a bridge model for gerontology. With high fecundity and economical husbandry requirements, large populations of zebrafish may be generated quickly and cheaply, facilitating large‐scale approaches including demographic studies and mutagenesis screens. A variety of mutants identified in such screens have led to modelling of human disease, including cardiac disorders and cancer. While zebrafish longevity is at least 50% longer than in commonly used mouse strains, as an ectothermic fish species, its life span may be readily modulated by caloric intake, ambient temperature and reproductive activity. These features, coupled with a growing abundance of biological resources, including an ongoing genome sequencing project, make the zebrafish a compelling model organism for studies on aging.
The true face of JNK activation in apoptosis
Authors: Lin Anning , Dibling Benjamin 
Published: March 2003

SummaryAge‐associated changes in apoptotic rates have been observed in a number of different tissues. While the implications of these findings remain unclear, a better understanding of how apoptosis is regulated may further our understanding of the aging process. The role of the JNK pathway in apoptosis has been highly controversial with studies suggesting that it plays a pro‐apoptotic, anti‐apoptotic or no role in this process. Here we discuss what is currently known about JNK's role in apoptosis, highlighting recent findings regarding NF‐κB‐mediated inhibition of JNK activation and its impact on TNF‐α induced apoptosis.