bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acute Confusional States in Patients Undergoing Hip Surgery
Authors: Duppils Gill Sörensen , Wikblad Karin 
Published: April 2003

<i>Background:</i> There is general agreement that acute confusional state (ACS) is common among elderly patients admitted to hospital, although exact figures are difficult to obtain. The objective of the current study was to investigate the onset of ACS during hospital stay and to isolate possible predisposing, facilitating and precipitating factors associated with the onset of ACS. <i>Methods:</i> Non-confused patients, ≥65 years of age, undergoing orthopedic hip surgery, were consecutively included in the study (n = 225). Of these, 149 patients were operated on because of acute hip fracture and 76 underwent elective hip-replacement surgery. ACS was diagnosed by the DSM-IV criteria for delirium. Structured observations of ACS onset were performed every 2nd to every 4th hour during the patients’ entire hospital stay. A protocol was used to document the observations on sleep, activities, well being and behavior. The Mini-Mental State Examination was used to measure cognitive functioning. <i>Results:</i> Of 225 patients 20% were diagnosed with ACS. The incidence of ACS was 24.3% in the group of hip-fractured patients and 11.7% in the hip-replacement surgery patients. The onset of ACS was postoperative (mean 24 ± 21 h after surgery) in all but 8 patients. The duration of ACS among recovered patients was generally less than 48 h (mean 42 ± 43 h). Predisposing factors were older age, cognitive impairment and pre-existing cerebrovascular or other brain diseases. Facilitating factors related to ACS were associated with communication and social isolation, e.g. impaired hearing and sight, reticence and passivity. One precipitating factor, besides surgery, may be the use of psychopharmacological drugs. <i>Conclusion:</i> The incidence of ACS was 20% among hip surgery patients. Older age and social isolation were factors associated with ACS. Increased attention and interaction with older patients could be of value in avoiding ACS during hospitalization.
Effects of Endurance Training on Selected Parameters of Immune Function in Elderly Women
Authors: Fahlman M. , Boardley D. , Flynn M.G. , Braun W.A. , Lambert C.P. , Bouillon L.E. 
Published: April 2003

<i>Background:</i> Immune function decreases with age, rendering the elderly more susceptible to infection and tumor development. In addition, intense exercise has been shown to decrease immune function in some populations. Few studies have examined the effects of exercise on immune function in the elderly and, to our knowledge, no studies have examined the effects of exercise on a population of active, but nonexercising elderly. <i>Objective:</i> The purpose of this study was to examine the effects of a 10-week endurance training program on selected parameters of immune function in active elderly women. <i>Methods:</i> A total of 29 healthy, active women, aged 70–87, were randomly assigned to either an exercise (76 ± 5 years, n = 15) or control (77 ± 6 years, n = 14) group. The exercise group walked 3 days/week at 70% heart rate reserve (HRR). The duration on day 1 was 20 min and it was increased by 5 min each day until subjects were walking for 50 min (week 3). It remained at 50 min for the duration of the study, while controls maintained normal activity. Blood samples were obtained from both groups at rest, and from the exercise group after 20 min of walking at 70% HRR and after 2 h of recovery. Blood samples were collected prior to endurance training and again after 10 weeks of endurance training. <i>Results:</i> There was a significant decrease in 1-mile walk times as well as heart rate at completion of the walk in the exercise group. Natural cell-mediated cytotoxicity (NCMC) was significantly higher post-exercise, compared to pre-exercise both before and after training. After training it remained significantly elevated 2 h post-exercise. The resting NCMC was significantly decreased in controls at week 10 but not in the exercise group. <i>Conclusion:</i> Ten weeks of endurance training resulted in a significant decrease in both the 1-mile walk time and the post-walk heart rate in the exercisers but not the controls, without resulting in either an acute or chronic suppression of immune function. Further, endurance training may lead to an attenuation of the decrease in cellular immune measures which occurs during the winter, since the control group experienced a decrease in NCMC and the exercisers did not.
The Effect of Anti-Platelet Aggregation to Prevent Pressure Ulcer Development: A Retrospective Study of 132 Elderly Patients
Authors: Matsuyama Narihisa , Takano Kikuo , Miura Akinori , Yamamoto Takatsugu , Mashiko Takaomi , Ohotani Hideki 
Published: April 2003

<i>Background:</i> As the number of bedridden elderly patients increases, prevention of pressure ulcers is becoming a more important issue. However, an approach to this problem using medication has not been considered sufficiently in the clinical context. <i>Objective:</i> To test the hypothesis that anti-platelet aggregation therapy administered to the elderly patients may be helpful in preventing pressure ulcer formation, the medical records of 132 bedridden elderly patients were analyzed. In addition, the propensity of platelets to aggregate was also measured in some of the bedridden patients. <i>Methods:</i> Patients were divided into two groups, with pressure ulcers (group P, 52 patients) and without (group N, 80 patients). Subsequently, six factors defining the clinical characteristics age and gender, underlying disease, cause of being bedridden, level of consciousness, mobility and activity as defined on the Braden scale, and frequency of anti-platelet aggregation medication were investigated in groups P and N. In addition, physical findings (three factors): body mass index, blood pressure (BP), and heart rate were investigated in both groups. Furthermore, laboratory data (seven factors): total protein (TP), albumin, total cholesterol, hemoglobin (Hb), hematocrit (Hct), platelets, and platelet aggregation were compared between two groups. <i>Results:</i> There were no significant differences in clinical characteristics between the two groups with the exception of the frequency of anti-platelet aggregation medication (23.1% of group P vs. 40.0% of group N, χ<sup>2</sup> = 4.06, p < 0.05). There was also no significant difference in physical findings except a difference between systolic and diastolic BP (48.4 mm Hg in group P vs. 57.1 mm Hg in group N, p < 0.01). Values of TP, albumin, Hb, and Hct in both groups were lower than the normal range, but there was no significant difference between the two groups. The platelet count was significantly greater in group P than in group N after lying supine (p < 0.03), and platelet aggregation in group P was significantly higher compared with group N (p < 0.03). <i>Conclusions:</i> Although our hypothesis must be tested by a randomized prospective trial, these results indicate that increased platelet aggregation is possibly associated with the development of pressure ulcers; therefore anti-platelet aggregation therapy may prevent their occurrence in bedridden elderly patients.
Plazebokontrollierte DHEA-Substitution beim älteren Mann
Authors: Reiter Werner J. , Pycha A. 
Published: April 2003

Wir haben eine plazebokontrollierte prospektive Untersuchung über die Dihydroepiandrosteron-(DHEA-)Substitution bei älteren Männern mit erektiler Dysfunktion durchgeführt. Fünfzig Männer wurden in zwei Gruppen zu je 25 Patienten randomisiert und mit 50 mg DHEA oder einem Plazebo therapiert. Der Erfolg der Substitution wurde mit dem Internationalen Index für Erektile Funktion, einem international validierten Fragebogen, evaluiert. Es konnte eine deutliche Verbesserung der erektilen Dysfunktion nach DHEA-Substitution nachgewiesen werden. Unsere Daten zeigen die Ergebnisse einer kleinen Pilotstudie, die aber aufgrund der positiven Ergebnisse als Grundlage für zukünftige Studien dienen könnte.
Cleavage of Human IgE Mediated by <i>Schistosoma mansoni</i>
Authors: Pleass Richard J. , Kusel John R. , Woof Jenny M. 
Published: April 2003

<i>Background:</i> IgE-mediated mechanisms are important in protection against helminth parasites. However, schistosomes are long-lived in mammalian hosts, presumably as a result of immune evasion strategies. We sought evidence for one such strategy, namely specific cleavage of host IgE. <i>Methods:</i> Human IgE, IgA and IgG were incubated with extracts from cercarial and schistosomular stages of <i>Schistosoma mansoni</i> or with schistosomular culture supernatants. The resulting products were analysed by Western blotting with Ig-specific antibodies. Numerous protease inhibitors were assessed for ability to inhibit the observed cleavage of IgE by the extracts. Partial purification of the IgE-proteolytic activity from cercarial extract was achieved by gel filtration. To test IgE function, we compared the abilities of untreated and schistosomular-treated IgE to mediate rosette formation through interaction with Fcε receptors. <i>Results:</i> Cercarial and schistosomular extracts were found to cleave human, mouse and rat IgE but not human IgA1, IgA2 or IgG1. Schistosomular culture supernatants displayed similar proteolytic activity towards IgE. Immunoblotting suggested that cleavage occurred close to the Cε2/Cε3 domain interface of the IgE heavy chain. PMSF and elastatinal inhibited cleavage, suggesting that the protease involved is an elastase-like serine protease, particularly since porcine pancreatic elastase also cleaved IgE to give similar-sized products. Further, the chloromethyl ketone derivatized peptide MeO-Suc-Ala-Ala-Pro-Leu- CMK, known to specifically inhibit the schistosome elastase, prevented IgE cleavage. Cleavage of human IgE rendered the antibody molecule unable to interact with U937 cells expressing FcεRII. <i>Conclusions:</i> An elastase-like protease in <i>S. mansoni</i> is able to render IgE non-functional.
A Sensitive Monoclonal Antibody Sandwich ELISA for the Measurement of the Major Olive Pollen Allergen Ole e 1
Authors: van Ree Ronald , Aalbers Marja , Kea Olga , Marco de la Calle Francisco M. , Sempere Ortells José M. , Villalba Mayte , Rodriguez Rosalia , Aalberse Rob C. 
Published: April 2003

<i>Background: </i>Olive pollen is a major cause of inhalant allergy in countries around the Mediterranean sea. The major allergen of olive pollen is Ole e 1. Measurement of the major allergen content of allergen products for diagnosis and therapy is becoming an essential element of standardization protocols. This study aimed at the development of a monoclonal antibody (mAb) sandwich ELISA for Ole e 1. <i>Methods: </i>Balb/c mice immunized with Ole e 1 were used for the production of mAbs. Screening of mice and hybridomas was performed in a RIA with radiolabeled purified Ole e 1. Purified mAbs were used as catching and/or (biotinylated) detecting antibodies in sandwich ELISA. <i>Results: </i>Four mAbs (IgG1κ) directed to nonoverlapping epitopes on Ole e 1 were obtained: 1A12, 5C1, 10A12 and 3H8. Both 1A12 and 10A12 were successfully used for affinity purification of Ole e 1 from olive pollen extract. Two sandwich ELISAs were developed, with 1A12 and 10A12 as catching, and 5C1 and 3H8 as detecting antibodies, respectively. Both catching and detecting antibodies were used in similar concentrations, ranging from 60 to 100 ng/well. For both ELISAs, the sensitivity was approximately 1 ng/ml of Ole e 1. The measuring range was from 1 to 25 ng/ml. No significant differences were observed, when the performance of both ELISAs in standardization of olive pollen extracts was compared. <i>Conclusions: </i>Two sensitive sandwich ELISAs for the major olive pollen allergen Ole e 1 were developed. They will prove to be useful tools in allergen standardization protocols.
Hexamethylene Diisocyanate Causes Contraction of Canine Tracheal Smooth Muscles through Activation of Muscarinic Receptors
Authors: Tomari Shinya , Shimoda Terufumi , Kawano Tetsuya , Mitsuta Kazuko , Obase Yasuishi , Matsuse Hiroto , Fukushima Chizu , Kohno Shigeru 
Published: April 2003

<i>Background:</i> Asthma caused by occupational exposure to hexamethylene diisocyanate (HDI) is well known; however, the exact pathogenic mechanisms remain unclear. <i>Methods:</i> Experiments were performed using a standard canine tracheal smooth muscle (CTSM) strip preparation in an isolated bath to determine the effect of HDI on tracheal smooth muscle contraction. HDI concentration-response curves were constructed and the effects of different receptor antagonists on HDI-induced smooth muscle contraction were determined. To determine whether HDI and acetylcholine (ACh) bind to a common muscarinic receptor, ACh concentration-response curves in the absence or presence of HDI and concentration-response curves for HDI and ACh in the presence or absence of atropine were plotted. <i>Results:</i> HDI caused contraction of CTSM, with a threshold concentration of 10<sup>–7</sup> <i>M</i>. The EC<sub>50</sub> (HDI concentration that produced 50% of the maximal response) was 6.2 ± 0.7 × 10<sup>–7</sup> <i>M</i> and the maximal contractile response (174 ± 55 g/g of tissue) occurred at a concentration of 5.0 ± 0.8 × 10<sup>–6</sup> <i>M</i>. Atropine, a muscarinic blocker, significantly inhibited HDI-induced contractile responses. HDI shifted the ACh concentration-response curve to the right. The mean pA<sub>2</sub> for atropine against ACh (8.93 ± 0.27) was not significantly different from that against HDI (8.03 ± 0.12). <i>Conclusions:</i> Our results indicated that HDI causes contraction of CTSM through the activation of muscarinic receptors. Direct stimulation of muscarinic receptors by HDI may play an important role in HDI-induced asthma.
Calcium-Dependent Phospholipase A<sub>2</sub> Mediates the Production of Endothelium-Derived Hyperpolarizing Factor in Perfused Rat Mesenteric Prearteriolar Bed
Authors: Adeagbo Ayotunde S.O. , Henzel Mary K. 
Published: April 2003

The isolated, perfused rat mesenteric bed releases a cytochrome P450-linked metabolite of arachidonic acid (AA) as endothelium-derived hyperpolarizing factor (EDHF) in response to acetylcholine and histamine. This study assessed the relative contribution of two AA-generating pathways, phospholipase A<sub>2</sub> (PLA<sub>2</sub>) and diacylglycerol (DAG) lipase, to EDHF-mediated dilation of the rat mesenteric bed. We tested the hypothesis that PLA<sub>2</sub>-mediated release of AA is essential for the production of EDHF. Mesenteric beds were perfused with physiological salt solution (PSS) containing indomethacin and nitro-<i>L</i>-arginine methyl ester to block cyclooxygenase and nitric oxide synthase, respectively, and constricted with cirazoline (an α<sub>1</sub>-adrenoceptor agonist). Bolus applications of acetylcholine and histamine caused dose-dependent dilation of the constricted beds. The 85-kDa PLA<sub>2</sub> inhibitor, arachidonyl trifluoromethyl ketone (AACOCF<sub>3</sub>), at 3 µ<i>M</i>, profoundly blunted decreases in perfusion pressure initiated by 1 nmol acetylcholine (94.3 ± 1.7%) and by 100 nmol histamine (88.5 ± 3.3%) to 9.6 ± 7.5 and 8.6 ± 6.0%, respectively. AACOCF<sub>3</sub> also blocked cirazoline-stimulated release of 6-keto-PG<sub>1α</sub>, but did not alter the vasodilation initiated by sodium nitroprusside (a nitric oxide donor), cromakalim (a K<sup>+</sup> channel activator), or by Na<sup>+</sup>/K<sup>+</sup>-ATPase activation, as measured by KCl vasodilation in preconstricted beds perfused with K<sup>+</sup>-free PSS. The 14-kDa PLA<sub>2</sub> inhibitor, oleyloxyethyl phosphorylcholine, also blocked EDHF vasodilation and also significantly inhibited K<sup>+</sup> channel activity. Neither the Ca<sup>2+</sup>-independent PLA<sub>2</sub> inhibitor, HELSS [E-6-(bromomethylene)-tetrahydro-3-(1-naphthalenyl)-2H-pyran-2-one], nor DAG lipase inhibitor, RHC-80267 [1,6-bis-(cyclohexyloximino-carbonylamino)-hexane] altered EDHF-mediated vasodilation. However, RHC-80267 blocked cirazoline-stimulated release of 6-keto-PGF<sub>1α</sub>. We conclude that Ca<sup>2+</sup>-dependent PLA<sub>2</sub>, rather than DAG lipase, generates the AA for the production of EDHF in the perfused rat mesenteric bed.
Effects of Chemical Sympathectomy on Angiotensin II-Induced Neointimal Growth in the Balloon-Injured Rat Carotid Artery
Authors: Bruijns Richard H.J. , van Kleef Ellen M. , Smits Jos F.M. , De Mey Jo G.R. , Daemen Mat J.A.P. 
Published: April 2003

To investigate the role of the sympathetic nervous system in angiotensin II (AngII)-stimulated medial and neointimal smooth muscle cell (SMC) replication, we sympathectomized rats with 6-hydroxydopamine (6-OHDA) in which the left carotid artery was injured by a balloon catheter. Balloon injury is associated with a loss of specific [<sup>3</sup>H]-prazosin binding. AngII (250 ng/kg/min), infused 2 weeks after balloon injury of the rat left carotid artery, increased systolic blood pressure by approximately 70 mm Hg. There was no effect of 6-OHDA on this pressor response. AngII increased the cumulative 5-bromo-2′-deoxyuridine (BrdU) labeling fraction (LF) in the uninjured right carotid media and the injured left carotid neointima as compared to controls (5.7 ± 1.6% vs. 0.4 ± 0.1%, p < 0.05; 10.6 ± 0.9% vs. 5.0 ± 0.8%, p < 0.05, respectively). 6-OHDA decreased the AngII-induced increase in LF in the media of the uninjured right carotid artery (AngII/6-OHDA 0.9 ± 0.2% vs. AngII 5.7 ± 1.6%, p < 0.05). 6-OHDA did not decrease the AngII-induced increase in LF in both the injured left carotid media and neointima at 4 weeks after balloon injury. The effects of chemical sympathectomy were comparable with those obtained 12 weeks after balloon injury. Thus, the data show that the sympathetic nervous system mediates the AngII-induced increase in SMC DNA synthesis, but only in the uninjured carotid media. This indicates a differential regulation of AngII-induced SMC replication in injured and uninjured vessels.
Vasodilation Mediated by Angiotensin II Type 2 Receptor Is Impaired in Afferent Arterioles of Young Spontaneously Hypertensive Rats
Authors: Endo Yoshimi , Arima Shuji , Yaoita Hiraku , Tsunoda Kazuo , Omata Ken , Ito Sadayoshi 
Published: April 2003

Renal vasoconstrictor action of angiotensin II (Ang II) is exaggerated in the spontaneously hypertensive rat (SHR) before development of hypertension. We have recently demonstrated that in the rabbit afferent arteriole (Af-Art) activation of the AT2 receptor causes vasodilation, which modulates the vasoconstrictor action of Ang II mediated by the AT1 receptor. In this study, we tested the hypothesis that vasoconstrictor action of Ang II is exaggerated in SHR Af-Arts due to an impaired function of the AT2 receptor before development of hypertension. Af-Arts were microdissected from the superficial cortex of 4- to 5-week-old SHR or age-matched Wistar Kyoto rats (WKY), and perfused at 60 mm Hg in vitro. Ang II (10<sup>–11</sup> to 10<sup>–8</sup> <i>M</i>) decreased the luminal diameter of Af-Arts of both strains in a dose-dependent manner. However, the constriction was stronger in SHR; at 10<sup>–10</sup> <i>M</i>, the diameter decreased by 34 ± 4% in SHR (n = 6) compared to 18 ± 3% in WKY (n = 6; p < 0.01). Pretreatment with PD123319 (PD), an AT2 receptor antagonist, significantly augmented Ang II-induced constriction in WKY but not SHR Af-Arts; at 10<sup>–10</sup> <i>M</i>, the diameter now decreased by 41 ± 5 and 37 ± 1% in SHR (n = 6) and WKY (n = 6), respectively. Thus, blockade of the AT2 receptor abolished the difference in Ang II action on Af-Arts between strains. Moreover, with the AT1 receptor blockade Ang II caused dose-dependent dilation of preconstricted Af-Arts only in WKY (27 ± 5% at 10<sup>–8</sup> <i>M</i>, n = 5), and the dilation was abolished by simultaneous treatment with PD. In contrast, no such dilation was observed in SHR Af-Arts. These results suggest that activation of the AT2 receptor modulates AT1 receptor vasoconstriction in WKY Af-Arts, while impaired modulatory function of AT2 receptor may play a role in the exaggerated vasoconstrictor action of Ang II on the Af-Art of prehypertensive SHR.
Susceptibility of Staphylococci Isolated from a Burns Unit to Mupirocin and Other Antimicrobial Agents
Authors: Udo E.E. , Mokadas E.M. , Jacob L.E. , Sanyal S.C. , Chugh T.D. 
Published: April 2003

The activity of mupirocin (Bactroban) against coagulase-positive and coagulase-negative staphylococci isolated in a burns unit was tested to ascertain its effectiveness, and to detect any resistant isolates after continuous use of mupirocin for 2.5 years. A total of 395 staphylococci, consisting of 330 <i>Staphylococcus aureus</i> and 65 coagulase-negative staphylococci, were tested for resistance to mupirocin and other antimicrobial agents. The results showed that 94.5% of the isolates were fully susceptible to mupirocin (MIC ≤4 mg/l), and 5.3% expressed low-level resistance (MIC 8–128 mg/l). One <i>Staphylococcus haemolyticus</i> isolate expressed high-level resistance (MIC >1,024 mg/l). It transferred high-level mupirocin resistance to other staphylococci in conjugation experiments, which indicated a capacity to transmit mupirocin resistance between species. The results demonstrated that mupirocin was still highly effective against staphylococci in the burns unit. However, the demonstration that the resistant <i>S. haemolyticus</i> isolate could transfer high-level mupirocin resistance to other staphylococci was of concern. There is a compelling need to test staphylococci from clinical materials for mupirocin resistance. Early detection of resistance can prevent the establishment and spread of the mupirocin-resistant strains in the unit.
Evaluation of Efficacy and Toxicity of Treatment Using Rhenium-186 HEDP in Metastatic Bone Disease
Authors: Ziada Gaber , Faris Lila , Yacoub Shreif , Elgazzar Abdelhamid 
Published: April 2003

<i>Objective:</i> To assess the efficacy and toxicity of rhenium-186 HEDP in treating metastases. <i>Patients:</i> Twenty-six patients with bone pain from metastatic cancer were treated with 35 mCi of <sup>186</sup>Re HEDP administered intravenously in the outpatient clinic. <i>Methods:</i> Patients were followed with pain diaries, records of medication, morbidity, sleep patterns, serial bone scans and a Karnofsky index. Twenty-five patients with complete records were evaluated. Patients were grouped according to the extent of bone metastases as seen in the bone scans. <i>Results:</i> Sixteen patients (64%) showed clinical responses of which 4 became completely pain-free. Pain relief typically began 10–20 days after <sup>186</sup>Re HEDP was administered, while maximum benefit was normally achieved by 6 weeks. Relief of pain was maintained for 4–15 months (mean 6 months). No immediate adverse reactions were observed following the administration of <sup>186</sup>Re HEDP. Only a mild transient fall in platelet levels was noted, which normalized by 6 weeks. <i>Conclusion: </i><sup>186</sup>RE HEDP appears as a safe, convenient and an effective palliative for pain secondary to bone metastases in cancer patients.