bluuebunny/crossref_metadata_2025_split huggingface dataset:
PLASMA CONCENTRATION OF BRAIN NATRIURETIC PEPTIDE IS RELATED TO DIASTOLIC FUNCTION IN HYPERTENSION
Authors: Cheung Bernard MY 
Published: June 2007

SUMMARY1. The plasma brain natriuretic peptide (BNP) concentration is elevated in patients with essential hypertension and normal systolic function. This may be related to left ventricular hypertrophy or diastolic dysfunction, both of which commonly occur in hypertension.2. Echocardiography was performed on 32 patients with newly diagnosed untreated mild‐to‐moderate hypertension (19 men, 13 women; mean±SD age 51±15 years; diastolic blood pressure 99±12mmHg; systolic blood pressur. 153.2±18.0 mmHg; plasma creatinine 86±15 μmol/L; creatinine clearance 92.2±20.5 mL/min; left ventricular mass index 116±28 g/m2; left ventricular ejection fraction 66±9%). A 15 mL peripheral venous blood sample was obtained at the time of echocardiography for radioimmunoassay of BNP.3. Sixteen patients had abnormal Doppler transmitral flow (E/A rati. < 1) and a higher median plasma BNP concentration compared with those patients with E/A ≥1 (12.9 vs 5.9 pmol/L, respectively; P = 0.006). The plasma BNP level correlated significantly with E/A ratio (r = ‐0.50; P = 0.035). Multivariate analysis showed that the E/A ratio is related to plasma BNP, independent of age and blood pressure.4. Our results suggest that the plasma BNP level is influenced by diastolic dysfunction. Further studies are needed to determine whether assay of plasma BNP helps to identify patients with diastolic dysfunction.
ROLE OF LIPOPROTEIN‐X IN FOAM CELL FORMATION AND RAT MESANGIAL CELL PROLIFERATION
Authors: Lynn Edward G. , O Karmin 
Published: June 2007

SUMMARY1. In the present study, the effect of reconstituted lipoprotein‐X (rLp‐X) on lipid accumulation and foam cell formation in rat peritoneal macrophages was evaluated. Furthermore, the combined effect of rLp‐X and macrophages on mesangial cell proliferation was examined.2. Incubation of macrophages with rLp‐X (177 and 387nmol unesterified cholesterol (FC)/mL) resulted in an increase of cellular cholestero. (162%) and cholesteryl esters (223 to 245%) relative to control.3. Oil Red O staining of macrophages treated with rLp‐X revealed the presence of foa. cells.4. In conclusion, rLp‐X had no effect on the proliferation of mesangial cells incubated in macrophage‐conditione. medium.
ENDOTHELIAL DYSFUNCTION EXACERBATES THE IMPAIRMENT OF RELAXATION BY LYSOPHOSPHATIDYLCHOLINE IN PORCINE CORONARY ARTERY
Authors: Leung Susan WS , Teoh Hwee , Quan Adrian , Man Ricky YK 
Published: June 2007

SUMMARY1. Current evidence suggests that lysophosphatidylcholine (LPC), a component found in oxidized low‐density lipoprotein (Ox‐LDL), inhibits endothelium‐dependent relaxation (EDR) mediated by endothelium‐derived relaxing factor (EDRF) and endothelium‐derived hyperpolarizing factor (EDHF). An objective of the present study was to characterize the roles of the different elements of EDR in LPC‐induced impairment within the porcine coronary artery. Concomitantly, we sought to determine whether impairment of one component of EDR would increase the sensitivity of the endothelium to LPC.2. Bradykini. (0.1 nmol/L‐0.3 μmol/L) relaxed U46619 (30 nmol/L)‐precontracted porcine coronary artery rings in a concentration‐dependent manner. A reduction in the bradykinin‐elicited response was observed in NG‐nitro‐L‐arginine methyl ester (L‐NAME; 300 μmol/L)‐ and ouabain (50 μmol/L)‐treated rings. Pretreatment with LPC (20 μmol/L), which on its own had no effect on normal endothelial relaxation, resulted in further inhibition of EDRF‐ and EDHF‐induced relaxations.3. Our results demonstrate that EDRF and EDHF are the primary mediators of EDR in the porcine coronary artery. Our data also show that while a low concentration of LPC (20 μmol/L) does not impair EDR, it can evoke vascular dysfunction following blockade of either the effects of EDRF or EDHF. Therefore, these data suggest that the partially damaged vascular endothelium could be more sensitive to threshold levels of this atherogenic phospholipid.
EPIDEMIOLOGY OF CARDIOVASCULAR RISK FACTORS IN HONG KONG
Authors: Janus ED ,   for the Hong Kong Cardiovascular Risk Factor Prevalence Study Group
Published: June 2007

SUMMARY1. To facilitate the development of appropriate population‐wide coronary heart disease prevention strategies and to monitor their long‐term impact, a comprehensive baseline Hong Kong Cardiovascular Risk Factor Prevalence Study was conducted in 1995–96.2. The data obtained from 2875 men and women aged 25–74 years showed a high prevalence of diabetes mellitus and impaired glucose tolerance, particularly in those aged 65 years and over. Other risk factors, such as hypercholesterolemia and hypertension as well as being overweight, were particularly prominent in older women.
MYOCARDITIS AS SYSTEMIC DISEASE: NEW PERSPECTIVES ON PATHOGENESIS
Authors: Carthy Christopher M. , Yang Decheng , Anderson Daniel R. , Wilson Janet E. , McManus Bruce M. 
Published: June 2007

SUMMARY1. Myocarditis may be an early indicator of or may subsequently lead to dilated cardiomyopathy in humans. This hypothesis has evolved from research on viruses that induce myocarditis, wherein the coxsackie B group viruses (CVB) in the family Picornaviridae are the most common known viral infectants of heart muscle.2. Many competing hypotheses exist as to the pathogenesis of CVB3‐induced myocarditis, including direct virus‐induced myocyte damage and immunopathological disease with autoimmune sequelae. Evidence to support the direct‐damage and viral RNA‐persistence hypothesis is derived from in situ hybridization and gene amplification studies.3. Recent use of terminal deoxynucleotidyl transferase‐mediated nick‐end labelling indicates that this injury in target organs is largely non‐apoptotic in nature. Most apoptotic bodies in cardiac tissue are derived from immune cells.4. Beyond infection of heart muscle, CVB3 can also associate with, infect and persist in cells of immune origin. The CVB3 localizes to follicles in spleens and lymph nodes of the murine host and this particular localization may continue in mice susceptible to more aggressive myocarditis. Whether virus‐immune cell association in these compartments is advantageous (or essential) to the host in the evolution of anti‐viral immune responses or whether it is more advantageous to the virus in immunosuppression of the host is not known.5. We suggest that CVB3 can directly perturb or alter the immune response, thereby delaying viral clearance from vulnerable systemic organs. Both host and viral genetic factors can influence susceptibility, persistance and disease progression.6. Picornaviruses use a unique method for the initiation of translation, involving the internal binding of the ribosome on a sequence element of the 5′ untranslated region, termed an internal ribosome entry sit. (IRES).7. The IRES of CVB3 is located at approximately stem loops G, H and I, spanning nucloetides 530 and 630. Arrest of host translation is also a feature of picornavirus infection. Such regulation of host cell translation machinery no doubt fosters viral replication at the expense of the host cell.8. Differences between cell types in the mechanisms, along with those at other key steps in the viral life cycle and in signalling via kinase pathways, may determine viral tropism and cellular destruction and the physiological outcome of neighbourin. cells.
POSSIBLE MECHANISM FOR THE ANTI‐ATHEROSCLEROTIC ACTION OF THE CALCIUM CHANNEL BLOCKER AE0047 IN CHOLESTEROL‐FED RABBITS
Authors: Hayashi Kazutaka , Imada Teruaki , Yamauchi Takeshi , Kido Hideaki , Shinyama Hiroshi , Matzno Sumio , Nakamura Norifumi , Kagitani Yoshio 
Published: June 2007

SUMMARY1. The present study was designed to investigate the anti‐atherosclerotic effect of AE0047, a calcium channel blocker, and to compare it with that of nilvadipine in cholesterol‐fed rabbits. Furthermore, the effects of AE0047 on low‐density lipoprotein (LDL) oxidation were studiedin vitro.2. A 7 week treatment period with AE0047 (3 and 10 mg/kg, p.o.) led to a dose‐dependent reduction in the lipid deposition area by Oil Red‐O staining (surface index) without affecting serum lipid levels. There was no reduction in the surface index following treatment with the same dose of nilvadipine (10 mg/kg).3. In a vehicle‐administered high‐fat diet group of rabbits, levels of total cholesterol (TC) and esterified cholesterol (EC) and calcium content in the aorta were increased approximately two‐ to three‐fold over those of the normal diet group. Increased levels of TC and EC and calcium content were reduced to the same levels as the normal diet group by AE0047 treatment, whereas nilvadipine did not affect TC and EC levels.4. In anin vitrostudy, AE0047 (10 μol/L) inhibited LDL oxidation and the aggregation of apolipoprotein (Apo) B‐100 induced by Cu2+. Furthermore, AE0047 inhibited the degradation of oxidized LDL by macrophages. In contrast, the same dose of nilvadipine (10 μol/L) did not inhibit either LDL oxidation or the aggregation of ApoB‐100.5. In summary, AE0047 inhibited LDL oxidation, resulting in a decrease of its uptake into macrophages and an inhibition of cholesterol esterification. This leads to an anti‐atherosclerotic effect of AE0047. Thus, AE0047 may have therapeutic potential in preventing cardiovascular disease in hypertensive patients.
OCCLUSION OF THE ADRENAL VEIN LEADS TO AN INCREASE IN RENAL VASCULAR RESISTANCE IN THE IPSILATERAL KIDNEY
Authors: Abramczyk Piotr , Ziȩcina Rafal , Lisiecka Aurora , Przybylski Jacek 
Published: June 2007

SUMMARY1. The aim of the present study was to investigate the effect of an acute increase in blood flow through the adrenal‐renal vascular connection (ARVC), due to occlusion of the adrenal vein, on renal blood flow (RBF) and renal vascular resistance (RVR).2. Experiments were performed in Wistar‐Kyoto rats. Animals were divided into four groups. In the first group, the adrenal vein was clamped using a metal clip. In the second group, the tissue between the adrenal gland and the kidney was cut before clamping. In the third and fourth groups, α‐adrenoceptor blockade was induced by intravenous infusion of phentolamine before clamping the adrenal vein. In addition, in the fourth group, tissue between the adrenal gland and the kidney was cut before clamping.3. In the first group, occlusion of the adrenal vein caused an increase in RVR, followed by a decrease in RBF. In the second, third and fourth groups, the same procedure did not change either RBF or RVR.4. We conclude that the augmented inflow of catecholamines to the kidney through the ARVC changes the haemodynamics of the kidney and may contribute to development of arterial hypertension due to occlusion of the adrenal vein.
RECYCLING OF ACETYLCHOLINE FOLLOWING IMPULSE TRANSMISSION IN RAT MUSCLE REVEALED IN THE PRESENCE OF NEOSTIGMINE
Authors: Uramoto I. , Miyamoto K. , Watanabe K. , Totsuka T. 
Published: June 2007

SUMMARY1. The recycling process of acetylcholine (ACh) following impulse transmission was studied in terms of muscle potentials evoked by repetitive stimulation in the presence of neostigmine.2. Wistar rats were anaesthetized with urethane and muscle potentials were recorded with concentric electrodes from their exposed medial gastrocnemius muscles before and after the injection of neostigmine.3. All potentials before neostigmine treatment were similar in amplitude. A set of 10 stimuli was given at 0.5 Hz 6–8 min after drug administration. The first potential was as large as that before it. The second potential was greatly depressed. Thereafter, potentials gradually recovered.4. Two sets of 10 stimuli were delivered at a 1 min interval (i.e. with a 40 s rest period between them). The second potential was not depressed so severely in the second set as in the first set. The same procedure was repeated in some rats and the aforementioned phenomenon was noted. When two sets of 10 stimuli were given at an interval of 2 min or more, the second potential was equally depressed in the both sets of stimuli.5. The recycling of ACh following impulse transmission in the junctional region was revealed in terms of muscle potentials in the presence of neostigmine. This process was activated due to repetitive stimulation. Moreover, the activated state seemed to be maintained for a while after the cessation of stimuli. These results suggest the possible existence of a neural mechanism that can exert an influence on the recycling of ACh following impulse transmission beyond a short period of time.
FUNCTIONAL DIVERSITY OF INFILTRATING MACROPHAGES IN INFLAMED HUMAN COLONIC MUCOSA ULCERATIVE COLITIS
Authors: Oshitani Nobuhide , Kitano Atsuo , Kakazu Tomomasa , Hara Junichi , Adachi Kenji , Nakamura Shiro , Matsumoto Takayuki , Kobayashi Kenzo 
Published: June 2007

SUMMARY1. Phenotypical heterogeneity of macrophages infiltrating the colonic mucosa of patients with ulcerative colitis has been shown in many reports. The functional diversity of macrophages in inflamed colonic mucosa remains unclear.2. Intestinal macrophages have been characterized by immunohistochemical staining and their ability to generate free oxygen radicals in inflamed and non‐inflamed mucosa.3. No correlation was found between RFD1 (activated dendritic cells), RFD7 (tissue macrophages) or RFD9 (epithelioid cells, giant cells in association with granuloma) positivity and either CD68 or human histocompatibility complex class II antigen (HLA‐DR) positivity. The proportions of RFD7‐ and RFD9‐positive cells were significantly increased in inflamed colonic mucosa. Nitroblue tetrazolium‐reducing mononuclear cells were CD68 or RFD7 positive but they were rarely positive for HLA‐DR and RFD1.4. These results suggest that nitroblue tetrazolium‐reducing macrophages are (scavenger) macrophages.
HUMAN RESPIRATORY MUSCLES: SENSATIONS, REFLEXES AND FATIGUABILITY
Authors: Gandevia SC , Allen GM , Butler JE , Gorman RB , McKenzie DK 
Published: June 2007

SUMMARY1. Given the importance of the ventilatory ‘pump’ muscles, it would not be surprising if they were endowed with both sensory and motor specializations. The present review focuses on some unexpected properties of the respiratory muscle system in human subjects.2. Although changes in blood gas tension were long held not to influence sensation directly, studies in subjects who are completely paralysed show that increases in arterial CO2 levels elicit strong sensations of respiratory discomfort.3. Stretch reflexes in human limb muscles contain a monosynaptic spinal excitation and a long‐latency excitation. However, inspiratory muscles show an initial inhibition when tested with brief airway occlusions during inspiration. This inhibition does not depend critically on input from pulmonary or upper airway receptors.4. Human inspiratory muscles (including the diaphragm) have been considered to fatigue during inspiratory resistive loading. However, recent studies using phrenic nerve stimulation to test the force produced by the diaphragm show that carbon dioxide retention (hypoventilation) and voluntary cessation of loading occur before the muscles become overtly fatigued.
INCREASED LEVELS OF ENDOTHELIN ETB RECEPTOR mRNA IN HUMAN OMENTAL ARTERIES AFTER ORGAN CULTURE: QUANTIFICATION BY COMPETITIVE REVERSE TRANSCRIPTION‐POLYMERASE CHAIN REACTION
Authors: Möller Sebastian , Adner Mikael , Edvinsson Lars 
Published: June 2007

SUMMARY1. Using competitive reverse transcription‐poly merase chain reaction (RT‐PCR) and in vitro pharmacology, smooth muscle endothelin ETb receptor expression was studied in segments of human omental artery, fresh and after organ culture for 1 and 5 days.2. The competitive RT‐PCR assay used in the present study uses an internal RNA standard bearing a 69 b.p. deletion in order to control all steps of the reaction, including the RT step. Control experiments showed linearity overlive subsequent 1:10 dilutions and a wide range of cycle numbers. The assay was able to quantify subattomolar concentrations in samples under 1 μg total RNA, making it possible to measure mRNA expression even in small tissue biopsies.3. In fresh arteries, ETb mRNA levels were 0.19±0.05 amol/μg total RNA (range 0.03–0.42 amol/μg; n= 8). After organ culture, an increase in ETB mRNA levels by 317 ± 28 and 288 ± 12% was found at days 1 and 5, compared with fresh arteries, respectively.4. In vitro pharmacology showed that endothelin (ET)‐l induced a strong and potent contraction in fresh arteries, whereas the selective ETB receptor agonist IRL1620 failed to induce a significant contraction. The ET‐1‐induced contraction was not altered in potency or Emax after organ culture for 1 and 5 days. In contrast, IRL 1620 induced a clear contraction after 1 day, which increased further in both Emax and potency after 5 days organ culture.5. Our results indicate that a massive new transcription of ETb receptor mRNA is induced by organ culture, resulting in functional contractile ETb receptors on the smooth muscle layer.
EFFECTS OF PROSTAGLANDIN E2 ON RENAL FUNCTION AND LUNG LIQUID DYNAMICS IN FOETAL SHEEP
Authors: Wlodek ME , Hooper SB , Thorburn GD , Tester ML , Harding R. 
Published: June 2007

SUMMARY1. The aim of the present study was to determine the effects of prolonged prostaglandin E2 (PGE2) administration on the function of the foetal kidneys and lungs in order to gain a greater understanding of the role played by PGE2 in the control of foetal fluid balance. By studying the effects of PGE2 at two gestational ages, we have also been able to examine the influence of age.2. We studied the effects of 26 h PGE2 infusion on foetal sheep at a mean (±SEM) of 120.0 ± 0.6 (n= 6) and 139.0 ± 0.8 (n= 4) days of gestation. In both groups, foetal urine production was significantly inhibited throughout the infusion period (P < 0.05). In younger, but not older foetuses, urine production returned to control values within 24 h of ending the infusion (P < 0.05). This PGE2‐induced anti‐diuresis was associated with foetal hypoxaemia and acidaemia, a reduction in free water clearance and an increase in foetal plasma arginine vasopressin concentrations (P < 0.05).3. During PGE2 infusions, foetal breathing movements were inhibited, the effect being greater and more sustained in older foetuses (P < 0.05).4. Infusions of PGE2 led to increased lung liquid production at both ages (P < 0.05); lung liquid volumes were reduced in older foetuses (P < 0.05), but were unchanged in younger foetuses. The reduction in lung liquid volume in older foetuses may have been due to inhibition of foetal breathing.5. We conclude that increased circulating levels of PGE2 have profound effects on foetal renal and lung function which, if sustained, could compromise foetal lung development and perinatal well‐being.
EFFECT AND MECHANISM OF CARDIOPLEGIC ARREST ON THE CORONARY ENDOTHELIUM‐SMOOTH MUSCLE INTERACTION
Authors: He Guo‐Wei 
Published: June 2007

SUMMARY1. During cardiac surgery, the heart is arrested and protected by hyperkalaemic cardioplegia. The coronary endothelium may be damaged by ischaemia‐reperfusion and cardioplegia. Subsequently, this may affect cardiac function immediately after cardiac surgery and cause mortality and morbidity.2. We investigated coronary endothelium‐smooth muscle interaction after exposure to depolarizing (hyperkalaemic; K+ 20 or 50 mmol/L) and hyperpolarizing (the K+ channel opener aprikalim) cardioplegia and organ preservation solution (University of Wisconsin (UW) solution). Endothelium‐dependent relaxation and hyperpolarization of the coronary smooth muscle were studied in the porcine and human large conductance and micro‐coronary arteries. Intracellular free calcium concentration in endothelial cells was also measured.3. The endothelium‐derived hyperpolarizing factor (EDHF)‐mediated relaxation to A23187, bradykinin, and substance Pin arteries contracted by either U46619 (10nmol/L) or K+ (25 mmol/L) was reduced after exposure to either high K+ or UW solution, but was maximally preserved after exposure to aprikalim. The hyperpolarization of the membrane potential in response to the above endothelium‐derived relaxing factor stimuli was also reduced by exposure to depolarizing cardioplegia. Studies in microcoronary arteries are in accordance with findings in large arteries. The intracellular free calcium concentration remained unchanged after exposure to hyperkalaemia.4. We concluded that: (i) during cardiac surgery, the function of coronary circulation may be changed due to exposure to depolarizing cardioplegia or preservation solutions; (ii) the functional change in the coronary circulation is related to the altered interaction between the endothelium and smooth muscle; (iii) depolarizing (hyperkalaemia) cardioplegia or hyperkalaemic organ preservation solutions affect endothelium‐smooth muscle interaction through the EDHF pathway; (iv) EDHF relaxes the porcine large and microcoronary arteries through multiple K+ channels; and (v) that hyperpolarizing vasodilators (K+ channel openers) may protect EDHF‐mediated endothelial function when used as cardioplegia.
ENDOTHELIUM‐SMOOTH MUSCLE INTERACTION IN CARDIAC TRANSPLANTATION
Authors: Skarsgard Peter L. , McManus Bruce M. , van Breemen Casey , Laher Ismail 
Published: June 2007

SUMMARY1. The inducible isoform of nitric oxide synthase (iNOS) is expressed in human and experimental cardiac allografts and is localized to infiltrating macrophages, cardiac myocytes, endothelial cells and smooth muscle cells. A recent clinical report proposes a causal link between myocardial expression of iNOS and ventricular contractile dysfunction, a potentially graft‐ and life‐threatening post‐transplant complication.2. Coronary blood flow is elevated in human graft recipients with biopsy proven cellular rejection, indicating that vasodilation accompanies graft rejection. In Lewis‐to‐F‐344 coronary resistance vessels, which show intimal expression of iNOS, pressure‐induced myogenic tone is significantly inhibited. Selective iNOS inhibition partially reverses the inhibition of myogenic tone, confirming that iNOS produces vasoactive nitric oxide (NO) and may mediate the rejection‐induced vasodilation seen clinically.3. Endothelial dysfunction, identified as loss of endothelium‐dependent dilation, has tremendous prognostic significance in vascular diseases of multiple aetiologies. In transplantation, endothelial dysfunction predicts early cardiac allograft vas‐culopathy and poor clinical outcome. Lewis‐to‐F‐344 coronary vessels develop endothelial dysfunction at 1 week post‐transplantation, but this is preceded by a transient state of endothelial cell hyperfunction, with enhanced endothelial production of NO.4. The normal interaction between endothelial and smooth muscle cells in coronary resistance vessels is critical for the regulation of coronary blood flow and the maintenance of fluid homeostasis. With allospecific expression of iNOS, the inhibition of vascular tone predicts greatly enhanced intravascular pressure in precapillary arterioles and capillaries; this would be expected to cause a net movement of fluid from the intravascular compartment into the myocardial interstitium, resulting in ventricular oedema, non‐compliance and poor contractile performance.
SECOND‐, MINUTE‐ AND HOUR‐METRONOMES OF INTESTINAL PACEMAKERS
Authors: Bywater Robert AR , Spencer Nick J. , Fida Rose , Taylor Grahame S. 
Published: June 2007

SUMMARY1. Movements of the gastrointestinal tract are required for the digestion of food and the expulsion of waste products.2. The present paper will discuss the nature of electrical rhythms underlying some intestinal motility patterns.3. The rhythms are generated by pacemakers with cycle rates appropriate to controlling individual contractions, motor pat‐ternings or switching between different motor programmes.4. Electrical rhythms are discussed with periods of the order of seconds, minutes and hours.5. Particular discussion is centred on rhythms recorded from the small and large intestine of the mouse.