bluuebunny/crossref_metadata_2025_split huggingface dataset:
ROLE OF INTEGRINS IN ENTEROCYTE MIGRATION
Authors: Basson Marc D 
Published: August 2007

1. Enterocyte motility depends critically on cell–matrix interactions. Although still incompletely understood, these appear critically dependent upon integrin‐mediated cell adhesion.2. In addition to providing a mechanism for cell adhesion and traction, the integrins are likely to serve as true receptors for the matrix across which cell motility occurs, initiating signals by both mechanical and chemical means that alter cell phenotype and proliferation as well as cell motility.3. Sound rationale now exists to postulate that soluble growth factors within the extracellular milieu regulate intestinal mucosal healing not only directly but also indirectly by modulating integrin expression and organization.Presented at the Experimental Biology Symposium on the Role of Integrins in Acute Renal Failure, New Orleans, Louisiana, USA, 1997.
ABOLITION OF DRUG‐INDUCED EARLY AFTERDEPOLARIZATIONS BY POTASSIUM CHANNEL ACTIVATORS IN GUINEA‐PIG PURKINJE FIBRES
Authors: Brosch SF , Studenik C , Heistracher P 
Published: August 2007

1. Drug‐induced early afterdepolarizations (EAD) are considered to be the underlying mechanism of the polymorphic ventricular dysrhythmia Torsades de pointes. Sotalol and disopyramide are well known to generate EAD. Therefore, it was of interest to study the effects of potassium channel activators, such as nicorandil, pinacidil and lemakalim, on those drug‐induced EAD in spontaneously beating guinea‐pig Purkinje fibres using the intracellular microelectrode technique.2. Early afterdepolarizations induced by sotalol at concentrations of 80 and 160 μmol/L could be completely abolished by nicorandil at concentrations between 50 and 500 μmol/L. The extracellular K+ concentration was 2.7 mmol/L.3. Disopyramide‐induced EAD at concentrations of 10, 20 and 30 μmol/L in a Tyrode’s solution containing 1.35 mmol/L K+ and these EAD were abolished by pinacidil (30 and 100 μmol/L) and lemakalim (10 and 30 μmol/L).4. Early afterdepolarizations could be regenerated by superfusion of Purkinje fibres with K+ channel activator‐free Tyrode’s solution containing either sotalol or disopyramide.5. Our results demonstrate that drug‐induced EAD can be abolished by K+ channel activators and, therefore, may provide anti‐arrhythmic effects in heart diseases.
CHRONIC CALCITONIN ADMINISTRATION AND RENAL CALCIUM TRANSPORT IN THE RAT
Authors: Carney Shane L , Thompson Lisa 
Published: August 2007

1. While calcitonin (CT) has now been clearly demonstrated to be a renal Ca2+‐conserving hormone and may share similar transport mechanisms with parathyroid hormone (PTH), the effect of prolonged CT exposure on renal Ca2+ transport has not been evaluated.2. Consequently, a submaximal and maximal Ca2+‐conserving concentration of human CT was infused into groups of anaesthetized acutely thyroparathyroidectomized rats that had been treated with twice daily subcutaneous human (h) CT at a low or high dose or vehicle for 12 days.3. The maximal hCT infusion (10 μg bolus and per hour) produced a marked inhibitory effect on renal Ca2+ excretion in vehicle‐treated rats, with the fractional excretion rate of Ca2+ being reduced from 4.49±0.31 to 1.39±0.23% (P<0.001). However, in rats pretreated with high concentrations of hormone (0.25 μg hCT) twice daily for 12 days, marked Ca2+ conservation was measured (fractional excretion 1.09±0.18%), which was not altered by the additional intravenous administration of maximal hCT.4. Renal Mg2+ transport was similarly altered by hCT administration, without any evidence that prolonged CT inhibited renal Mg2+ transport. The increase in glomerular filtration rate caused by hCT also appeared to persist with repeated hormone administration. The fractional excretion of Na+ and PO4 was significantly increased by high‐ but not low‐dose hCT treatment and was not altered by the addition of a maximal hormone dose at day 12.5. The present study failed to demonstrate any down‐ regulation of the response to prolonged hCT administration when renal Ca2+ and Mg2+ transport was measured. If renal escape does occur with CT, as has been suggested but not proven with PTH, other mechanisms, such as hormone production or release, may be responsible.
5‐HYDROXYTRYPTAMINE‐INDUCED CONTRACTION OF THE MARMOSET AORTA IS MEDIATED BY A 5‐HT1‐LIKE RECEPTOR
Authors: Frewin SM Dyer, IS de la Lande, DB , Head RJ 
Published: August 2007

1. 5‐Hydroxytryptamine (5‐HT) exerts both contractile and relaxant effects in the marmoset isolated aorta, actions that are unaffected by the 5‐HT2 antagonist ketanserin. The aim of the present study was to define the receptors mediating the contractile activity of 5‐HT in the marmoset aorta.2. Contractile responses were elicited in aortic rings that were either: (i) precontracted submaximally with the thromboxane A2 agonist U44069 in order to amplify the responses; or (ii) exposed to Nω‐nitro‐L‐arginine (100 μmol/L) plus LY 53857 (0.1 μmol/L; a 5‐HT2 receptor antagonist shown previously to inhibit relaxation). The effect of 5‐HT on adenosine 3′,5′‐cyclic monophosphate (cAMP) formation was also investigated.3. The effects of agonists and antagonists comprised: (i) agonist potencies in the order 5‐carboxamidotryptamine > 5‐HT > sumatriptan > 8‐hydroxy‐2‐(di‐n‐propylamino)tetralin; (ii) inhibition of contractile action of 5‐HT by the 5‐HT1D antagonist GR 127935; (iii) a contractile response to methysergide; (iv) a lack of effect of tropisetron, an antagonist of 5‐HT3 and 5‐HT4 receptors; and (v) inhibition of forskolin‐stimulated cAMP formation by 5‐HT (in the presence of LY 53857), indicative of negative coupling to adenylate cyclase.4. The above effects fulfil the criteria for a 5‐HT1‐like receptor. In view of the previous finding that this contractile response is insensitive to ketanserin, it is concluded that the contractile effects of 5‐HT in the marmoset aorta are mediated exclusively by a 5‐HT1‐like receptor.
DEXAMETHASONE‐INDUCED CHANGES IN ENDOMETRIAL GROWTH AND INDUCIBLE NITRIC OXIDE SYNTHASE DURING DECIDUALIZATION IN RATS
Authors: Spencer Fitzgerald , Chi Limen , Zhu Ming‐Xia 
Published: August 2007

1. The present study investigated the time‐dependent inhibitory responses of endometrial growth and inducible nitric oxide synthase (iNOS) to dexamethasone during deciduoma development that was surgically induced on day 4 of pseudopregnancy (PG).2. Groups of rats (n = 6) were subcutaneously injected with dexamethasone (1.5 mg/rat per day) for 3 days (PG days 1–3, 4–6, 7–9, 10–12 and 12–15). Rats in each group were killed on the last injection day.3. Dexamethasone produced comparable temporal inhibitory changes in endometrial growth (wet weight, protein and DNA concentrations; P<0.0001) and in iNOS activity (130 kDa protein band), which peaked after PG days 4–6 and 7–9 pretreatments.4. Endometrial matrix metalloproteinases (72 and 92 kDa) activity profiles displayed maximal reductions (36 and 53%, respectively) following PG days 4–6 pretreatment. Serum progesterone levels were equally (P<0.0001) but asynchronously inhibited by dexamethasone on PG days 9 and 12.5. Dexamethasone inhibition of endometrial growth and in situ iNOS was most pronounced during decidual development (PG days 4–9). Minor reductions in these endometrial parameters occurred before deciduoma induction (PG days 1–3) and during deciduoma regression (PG days 10–15).6. These results indicate that, in the endometrium, the iNOS/ endogenous nitric oxide system may be linked to the biochemical and metabolic mechanisms responsible for the developmental responsiveness of the deciduoma to dexamethasone exposure. These time‐dependent changes in endometrial growth and iNOS apparently were not mediated by progesterone.
ANGIOTENSIN II RECEPTORS IN CARDIAC LEFT VENTRICLES OF DAHL RATS
Authors: Sumida Yoichi , Umemura Satoshi , Kobayashi Shun‐ichi , Kihara Minoru , Tamura Kouichi , Ishigami Tomoaki , Ochiai Hisao , Chiba Eiko , Nyui Nobuo , Ishii Masao 
Published: August 2007

1. Dahl Iwai salt‐sensitive (DS) rats have been reported as becoming hypertensive with left ventricular hypertrophy (LVH) and heart failure when on a high‐salt diet. Their circulating renin–angiotensin system (RAS) has been reported to be suppressed. To evaluate the role of angiotensin II (AngII) type 1 and type 2 receptors (AT1 and AT2, respectively) in LVH, we compared cardiac AT1 and AT2 receptors in 10‐week‐old DS rats and Dahl Iwai salt‐resistant (DR) rats.2. Seven pairs of 6‐week‐old male DS and DR rats were fed either a low‐ or high‐salt diet (0.3 or 8% NaCl, respectively) for 4 weeks. Left ventricular AngII receptors were measured by radioligand binding assays using [125I]‐[Sar1,Ile8]‐AngII in plasma membrane fractions from these four groups. The AT1 and AT2 receptors were distinguished using their specific antagonists CV 11974 and PD 123319, respectively.3. The high‐salt diet increased blood pressure and the left ventricle:bodyweight ratio in DS rats. However, neither Bmax for AT1 and AT2 receptors nor Kd for [125I]‐[Sar1,Ile8]‐AngII differed between the groups. These results are different from those of other reports of pressure‐overload LVH, such as spontaneously hypertensive rats or renovascular hypertension rats, in which AT1 and AT2 receptors were reported to be up‐regulated.
COSEGREGATION OF THE Tnfα LOCUS WITH CARDIOVASCULAR PHENOTYPES IN THE F2 GENERATION OF A NEW ZEALAND GENETICALLY HYPERTENSIVE AND BROWN NORWAY CROSS
Authors: Harris Eugenie L , Grigor Murray R , Thompson Caryn M 
Published: August 2007

1. The association of the Tnfα locus with several cardiovascular phenotypes and body mass has been studied in the F2 generation of a reciprocal cross between rats of the New Zealand genetically hypertensive (GH) and the normotensive Brown Norway (BN) strains. In the total F2 population the GH allele of Tnfα cosegregated with increased intra‐arterial blood pressure (BP) in a recessive manner. A similar but weaker effect was observed for tail BP.2. An association between genotype and body mass in females with GH grandfathers was also detected.3. An association between genotype and pulse rate was observed for females.4. This work supports other evidence pointing to an association of a gene (or genes) on rat chromosome 20 with hypertension.
EPITHELIAL CELL SHEDDING IN ACUTE RENAL INJURY
Authors: Racusen Lorraine C 
Published: August 2007

1. To address the postulate that sublethally injured tubular cells may be shed from renal epithelium while still viable, studies were undertaken in vivo in human ‘acute tubular necrosis’ and in rabbit models of renal tubular injury.2. Substantial numbers of viable tubular cells were voided in the urine. When placed in culture, these cells gave rise to monolayers, confirming viability. The majority of intact cells demonstrated markers of proximal tubule.3. In vitro studies of human renal proximal tubular cells exposed to hypoxia/anoxia showed rounding and retraction associated with disruption of actin microfilaments. Phalloidin stabilized the filaments and prevented the changes in cell shape indicative of altered adherence.Presented at the Experimental Biology Symposium on the Role of Integrins in Acute Renal Failure, New Orleans, Louisiana, USA, 1997.
POISONING AND EPIDEMIOLOGY: ‘TOXICOEPIDEMIOLOGY’
Authors: Buckley Nicholas A 
Published: August 2007

1. There is little hypothesis‐testing clinical research performed in toxicology. Randomized clinical trials are rare and most observational studies are performed on highly selected patients and are subject to marked bias. Thus, for many poisonings, our approach has been based almost entirely on deduction from known pharmacological/toxicological effects, generalizations from drugs within the same therapeutic class, animal data and case reports. This is also far from satisfactory, as many toxicological mechanisms are poorly understood and not related to the therapeutic class.2. Although we need much better data to address the clinical and public health aspects of poisoning, there are many practical and ethical reasons why randomized clinical trials are difficult in this field. However, the scope for observational research, in particular population‐based clinical epidemiology, is almost unlimited. The collection of data on human poisoning is facilitated because most non‐fatal overdoses are admitted to hospital and by legal requirements to report to the coroner deaths that are due to poisoning. In the present article I argue that ‘toxicoepidemiology’, meaning the application of epidemiological methods to the problem of acute poisoning, is the best means we have of addressing deficiencies in our knowledge of poisoning.3. Examples are given of a variety of observational research strategies, ranging from audit to meta‐analysis, that may be applied to clinical toxicology. From coronial and clinical data obtained from reasonably well‐defined populations, it has been possible to identify a number of previously unrecognized differences in the severity and spectrum of toxicity between and within drug classes. Also, the demographic risk factors for poisoning and the reproducibility, validity and optimal use of diagnostic and therapeutic interventions can be assessed.4. The major limitations to the range of associations and interventions that may be studied are the need to achieve adequate power to study uncommon outcomes or poisonings and the ability to replicate findings at other centres using similar methodology. The expansion of data collection to other centres has the potential largely to overcome these obstacles.
ENHANCED SENSITIVITY OF MEDULLARY DEPRESSOR NEURONS TO N‐METHYL‐D‐ASPARTATE–GLYCINE SITE ANTAGONISTS IN THE SPONTANEOUSLY HYPERTENSIVE RAT
Authors: Kapoor Ranjna , Kapoor Vimal 
Published: August 2007

1. The effects of the specific N‐methyl‐D‐aspartate (NMDA)–glycine site antagonist 5‐fluoro indole‐2‐carboxylic acid (FICA) and NMDA, microinjected into the vasodepressor caudal ventrolateral medulla, were compared in spontaneously hypertensive rats (SHR) and in Wistar‐Kyoto (WKY) rats.2. 5‐Fluoro indole‐2‐carboxylic acid elicited a significant pressor response (+20.0±4.9 mmHg) in SHR, but no change was found in the basal blood pressure of WKY rats.3. The depressor response due to NMDA microinjection was significantly larger in SHR (–48.0±4 mmHg) than in WKY rats (–23.0±1.9 mmHg).4. Pre‐injection of FICA attenuated the depressor effects of NMDA significantly, this blockade being significantly more pronounced in SHR (37.0±2.7 mmHg) than in WKY rats (12.0± 1.2 mmHg).5. The enhanced responses to FICA may reflect the lower levels of the endogenous NMDA–glycine antagonist kynurenic acid in SHR compared with WKY rats.
ABSENCE OF DETECTABLE REGRESSION OF HUMAN HYPERTENSIVE LEFT VENTRICULAR HYPERTROPHY FOLLOWING DRUG TREATMENT FOR 1 YEAR
Authors: Laufer Eljas , Reid Christopher , Qi X Ling , Jennings Garry L 
Published: August 2007

1. The present study was designed to compare and contrast the effects of 1 year’s treatment with angiotensin‐converting enzyme inhibition (captopril 25–100 mg daily) and beta‐blockade (atenolol 50–100 mg daily) on hypertensive cardiac structure and function as well as the other established cardiovascular risk factors of high blood pressure (BP), lipid profile and blood glucose.2. This was a prospective randomized open drug trial with blinded end‐point echocardiographic and cardiac Doppler assessment in 37 subjects who had primary essential hypertension and left ventricular hypertrophy of captopril (n = 20) versus atenolol (n = 17), adding hydrochlorothiazide if BP was not controlled by 1 month. Multiple time point measurements throughout the 1 year treatment period of the study were made of BP, echocardiographic parameters of cardiac structure and function, as well as lipid profile and blood glucose.3. There were no significant between‐group differences for captopril or atenolol with regard to BP (at baseline (mean ± SD) 154.0/101.1 ± 13.3/5.1 and 152.5/101.8 ± 10.0/5.8 mmHg, respectively) which was normalized by 1 month (138.7/85.6 ± 18.8/11.7 and 135.4/88.5 ± 16.9/9.5 mmHg, respectively) in both treatment groups (both P < 0.01 vs baseline). Also, there were no between‐group or within‐group differences for any of the measures of left ventricular hypertrophy or systolic function throughout the 12 month treatment period; however, captopril alone significantly increased left ventricular early diastolic filling (P < 0.05 vs baseline) at most of the measured time points. Furthermore, there were no significant between‐ or within‐group differences with regard to metabolic (lipids and glucose) profile over the 1 year treatment period of the present study.4. Markers of cardiovascular risk, including BP, echocardiographic measures of left ventricular hypertrophy, lipid profile and blood glucose were not significantly different between therapies. Despite good BP control by 1 month, neither drug regimen regressed left ventricular hypertrophy. However, captopril significantly increased left ventricular early diastolic filling after 3 months of treatment.
EFFECT OF EXPERIMENTAL DIABETES MELLITUS ON GENTAMICIN‐INDUCED ACUTE RENAL FUNCTIONAL CHANGES IN THE ANAESTHETIZED RAT
Authors: Garland K Hamilton, EJ Eaton, HO , Old S 
Published: August 2007

1. Rats with streptozotocin (STZ) diabetes are protected from gentamicin (GEN) nephrotoxicity. Because the chronic renal damage from GEN is preceded by acute renal functional changes (notably hypercalciuria), the present study aims to determine whether diabetes may also protect against the acute effects of the drug. If there is a link between the rapid physiological actions of GEN and its subsequent nephrotoxicity, the former may also be affected by the diabetic condition.2. Standard renal clearance techniques were performed on anaesthetized rats that had been injected with STZ or vehicle 2 weeks previously. All animals were infused with 0.9% NaCl for 5 h and then either GEN (0.28 mg/kg per min) or 0.9% NaCl alone for 2 h.3. Baseline fractional calcium excretion (FECa) of diabetic rats was three‐fold that of control animals (6.6±0.2 vs 2.2±0.2%, respectively; P<0.01, MANOVA). Following GEN infusion, a comparable increase in FECa occurred in control and diabetic rats (5.3±0.6 vs 5.3±0.8%, respectively; NS).4. Streptozotocin diabetes, therefore, does not alter the acute hypercalciuric response to GEN. This may suggest that the acute effects of GEN on renal calcium handling do not contribute to the subsequent nephrotoxicity. However, the higher baseline FECa seen in diabetic rats may afford protection against the renal injury caused by gentamicin.
RATES OF GROWTH, RESPIRATION AND PHOTOSYNTHESIS OF UNICELLULAR ALGAE AS RELATED TO CELL SIZE—A REVIEW1,2
Authors: Banse Karl 
Published: August 2007

SUMMARYThe decline of growth rate with increasing species size of unicellular algae grown under uniform conditions is quantified by applying to published data the equation, growth, (cell · time)−1= a (cell carbon)b where a and b are coefficients. The degree of size‐dependence might be highest under optimal conditions of growth where b is 0.75. Respiration rate is shown to decline with size in the same manner. It is postulated that gross photosynthesis and processes underlying growth are similarly size‐dependent. Growth, efficiency (net over gross photosynthesis) cannot be shown to be size‐dependent. Cell size, expressed as carbon, is proposed as a scaling factor in comparative algal physiology.
POLYMORPHISM OF THE DIATOM PINNULARIA BREBISSONII IN CULTURE AND A FIELD COLLECTION1,2
Authors: Hostetter H. P. , Rutherford Kenneth D. 
Published: August 2007

SUMMARYTwo clones ofPinnularia brebissonii(Kütz.) Rabh. var.brebissoniiwere established and maintained in logarithmic phase of growth. Initial length of the cells was 37 μm. As cell division occurred, the mean length of cells in each population decreased as predicted by the MacDonald‐Pfitzer hypothesis; however, the decrease in mean length was not uniform throughout the growth period. This nonuniformity is probably caused by nonrandom division of cells in the population or by a changing increment of size reduction due to division. The initial increment of size reduction was calculated as 0.7 μm/division. The smallest, cells observed were 8 μm long. As cells decrease in length, cell volume decreases and the proportion of cells with aberrant valve structure increases. More than 90% of the valves were abnormal in a population with mean length of 14 μm. The abnormalities of structure involved the raphe, the central area and the striae.
SEROLOGICAL STUDIES OF MALE AND FEMALE STRAINS OFEUDORINA ELEGANS(CHLOROPHYCEAE)1,2
Authors: Herbst D. S. , Kemp C. L. 
Published: August 2007

SUMMARYMale and female strains ofEudorina elegansEhrenberg were examined by serological methods for flagellar and cellular antigenic differences. No significant differences could be detected between the strains by using agglutination, immobilization and diffusion tests. However, differentiated sperm were neither agglutinated nor immobilized by anti‐vegetative cell sera.
STIMULATION OF GROWTH IN SCENEDESMUS OBLIQUUS (CHLOROPHYCEAE) BY HUMIC ACIDS UNDER IRON LIMITED CONDITIONS1,2
Authors: Giesy John P. 
Published: August 2007

SUMMARYStimulatory affects of humic acids of molecular weight 30,000 or greater on iron‐starved Scenedesmus obliquus (Turp.) Kütz. in association with bacteria were studied by growth and Fe uptake experiments. Humic acids stimulated growth of Fe‐starved cells by decreasing the lag phase and extending the growth phase. Humic acids stimulated increased algal growth in medium containing EDTA as well as in medium containing no EDTA, indicating humic acids are not stimulating algal growth under Fe limiting conditions by creating a soluble Fe pool. Humic acids decreased Fe availability to Fe‐starved S. obliquus. Iron bound to humic acids is unavailable for uptake by Fe‐starved cells indicating growth stimulation is not due to chelation effects alone. Stimulation of growth is not a membrane phenomenon as humic acids show the same stimulatory effect when in contact with cells or separated by dialysis membrane. Humic acids also stimulate growth in the dark, with and without aeration, indicating use as a heterotrophic substrate. A photoheterotrophic mechanism is indicated by increased algal growth caused by illuminating cultures, containing humic acids but excluding CO2.
GROWTH RESPONSES TO SALINITY VARIATION IN FOUR ARCTIC ICE DIATOMS1,2
Authors: Grant W. S. , Horner Rita A. 
Published: August 2007

SUMMARYDuring spring, extensive blooms of microalgae grow on the underside of arctic sea ice. The brownish, algal layer penetrates ca. 2 cm into the bottom surface of the ice and the algae are potentially exposed to very high salinities. Four diatom species, Melosira juergensii Ag., Porosira glacialis (Grun.) Jørg., Navicula transitans var. derasa (Grun.) Cleve, and Coscinodiscus lacustris Grun., isolated from, sea ice samples taken from the Beaufort and Chukchi seas near Barrow, Alaska, were grown at 11 salinities ranging from 5 to 70‰ at 5 C under constant illumination. All of the species grew at 5‰ except N. transitans whose lower growth limit was 15‰. Growth was high over a broad range of salinities, but none of the species grew at salinities above 60‰. These diatom species appear to be well suited to tolerate the salinities in the brine pockets near the bottom of annual arctic sea ice where they are found. High brine‐cell salinity, however, may limit the upward, penetration of ice algae into the bottom of sea ice.
PHOTOSYNTHETIC CAPACITY AND LUXURY UPTAKE OF CARBON DURING PHOSPHATE LIMITATION IN PEDIASTRUM DUPLEX (CHLOROPHYCEAE)1
Authors: Lehman John T. 
Published: August 2007

SUMMARYWhen cells of Pediastrum duplex Meyen experience phosphorus depletion, their capacity for carbon fixation declines, but sizes and carbon contents of the cells increase several‐fold, an apparent instance of “luxury uptake” of carbon. Maximum rates of uptake of phosphate increase during the same period, and are consequently correlated with the enlarged surface area of the cells. Thus the disadvantage of increased cell volume, which may accelerate sinking speed in nature, is offset by the increased capacity of the cells for nutrient uptake.