bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diversity and Seasonal Changes of Uncultured
Planctomycetales
in River Biofilms
Authors: Brümmer I. H. M. , Felske A. D. M. , Wagner-Döbler I. 
Published: September 2004

ABSTRACT

Cell counts of planctomycetes showed that there were high levels of these organisms in the summer and low levels in the winter in biofilms grown in situ in two polluted rivers, the Elbe River and the Spittelwasser River. In this study 16S rRNA-based methods were used to investigate if these changes were correlated with changes in the species composition. Planctomycete-specific clone libraries of the 16S rRNA genes found in both rivers showed that there were seven clusters, which were distantly related to the genera
Pirellula
,
Planctomyces
, and
Gemmata
. The majority of the sequences from the Spittelwasser River were affiliated with a cluster related to
Pirellula
, while the majority of the clones from the Elbe River fell into three clusters related to
Planctomyces
and one deeply branching cluster related to
Pirellula
. Some clusters also contained sequences derived from freshwater environments worldwide, and the similarities to our biofilm clones were as high as 99.8%, indicating the presence of globally distributed freshwater clusters of planctomycetes that have not been cultivated yet. Community fingerprints of planctomycete 16S rRNA genes were generated by temperature gradient gel electrophoresis from Elbe River biofilm samples collected monthly for 1 year. Sixteen bands were identified, and for the most part these bands represented organisms related to the genus
Planctomyces.
The fingerprints showed that there was strong seasonality of most bands and that there were clear differences in the summer and the winter. Thus, seasonal changes in the abundance of
Planctomycetales
in river biofilms were coupled to shifts in the community composition.
Platelet activation induces metalloproteinase-dependent GP VI cleavage to down-regulate platelet reactivity to collagen
Authors: Stephens Gillian , Yan Yibing , Jandrot-Perrus Martine , Villeval Jean-Luc , Clemetson Kenneth J. , Phillips David R. 
Published: September 2004

AbstractGlycoprotein (GP) VI, the primary collagen receptor on platelets, has been shown to have variable expression, possibly as a consequence of immune modulation. The present study was designed to determine the mechanism by which GP VI clearance occurs. We found that direct activation of GP VI both by a GP VI–specific antibody and by GP VI ligands (collagen and convulxin) reduced binding of biotinylated convulxin to the stimulated platelets. Analysis of immunoblots of platelets and supernatants showed that the stimulated platelets contained less GP VI, while the soluble fraction contained a 57-kDa cleavage product. Stimulation of platelets with PAR-1 agonists (TRAP peptide and thrombin) also caused GP VI cleavage, although the amount of GP VI loss was less than that observed with direct GP VI ligands. The metalloproteinase (MMP) inhibitors GM6001 and TAPI prevented both the clearance of GP VI from the platelet surface and the appearance of the soluble cleavage product. Induction of GP VI cleavage caused specific down-regulation of collagen-induced platelet aggregation, providing a mechanism for the modulation of platelet responsiveness to this important platelet agonist.
Long acting β2agonists for stable chronic obstructive pulmonary disease with poor reversibility: a systematic review of randomised controlled trials
Authors: Husereau Don , Shukla Vijay , Boucher Michel , Mensinkai Shaila , Dales Robert 
Published: September 2004

Abstract
Background
The long acting β2-agonists, salmeterol and formoterol, have been recommended, by some, as first line treatment of stable chronic obstructive pulmonary disease (COPD). We reviewed evidence of efficacy and safety when compared with placebo or anticholinergic agents in patients with poorly reversible COPD.

Methods
After searching MEDLINE, EMBASE, HealthSTAR, BIOSIS Previews, PASCAL, ToxFile, SciSearch, the Cochrane Library, and PubMed, as well as Web sites, selected journals, reference lists, and contacting drug manufacturers, two reviewers independently screened reports of randomised controlled trials of parallel or crossover design lasting four weeks or longer and including patients with a forced expiratory volume in one second (FEV1) ≤ 75% of predicted, a ratio of FEV1 to forced vital capacity (FVC) ≤ 88% of predicted, and < 15% improvement from baseline FEV1 after a dose of a β2 agonist. We included trials comparing salmeterol or formoterol with placebo or with ipratropium bromide and reporting one of these outcomes: lung function; exercise capacity; quality of life scores; dyspnea; exacerbations; rescue inhaler use; incidence of tachycardia, hypokalemia, or dry mouth. Two reviewers assessed the quality of included reports using the Jadad scale and allocation concealment, and abstracted data.

Results
Twelve trials satisfied our inclusion criteria; eight were high quality (Jadad score >2) and four were low quality (≤ 2). The adequacy of allocation concealment was unclear in all of them. We did not perform a meta-analysis due to differences in trial design and how outcomes were reported.
Two trials comparing salmeterol with ipratropium did not detect differences; one trial comparing formoterol and ipratropium described greater improvement with formoterol in morning PEFR (15.3 versus 7.1 l/min, p = 0.040).
Of twelve trials comparing long acting β2 agonists with placebo, six reported no improvement in exercise capacity, eleven reported improvements in FEV1 lung function (one reported no improvement), six reported less rescue inhaler usage (one reported no difference) and five reported improved dyspnea scores (two reported no improvement). Differences in quality of life were detected in one salmeterol trial ; however, two salmeterol, and one formoterol trial reported no differences. Adverse effects of interest were not reported.

Conclusion
In terms of clinical outcomes and safety, we could not find convincing evidence that salmeterol and formoterol have demonstrated advantages to ipratropium, a less expensive drug, for patients with stable COPD and poor reversibility. Compared to placebo, we found evidence of reduced rescue inhaler usage and improved spirometric outcomes without a significant impact on quality of life or exercise capacity.
Could a simple surgical intervention eliminate HIV infection?
Authors: Tepic Slobodan 
Published: September 2004

Abstract
Background
Human Immunodeficiency Virus (HIV) infection is a dynamic interaction of the pathogen and the host uniquely defined by the preference of the pathogen for a major component of the immune defense of the host. Simple mathematical models of these interactions show that one of the possible outcomes is a chronic infection and much of the modelling work has focused on this state.

Bifurcation
However, the models also predict the existence of a virus-free equilibrium. Which one of the equilibrium states the system selects depends on its parameters. One of these is the net extinction rate of the preferred HIV target, the CD4+ lymphocyte. The theory predicts, somewhat counterintuitively, that above a critical extinction rate, the host could eliminate the virus. The question then is how to increase the extinction rate of lymphocytes over a period of several weeks to several months without affecting other parameters of the system.

Testing the hypothesis
Proposed here is the use of drainage, or filtration, of the thoracic duct lymph, a well-established surgical technique developed as an alternative for drug immunosuppression for organ transplantation. The performance of clinically tested thoracic duct lymphocyte depletion schemes matches theoretically predicted requirements for HIV elimination.
Predictive Factors of Stenosis after Stapled Colorectal Anastomosis: Prospective Analysis of 179 Consecutive Patients
Authors: Bannura Guillermo C. , Cumsille Miguel Angel G. , Barrera Alejandro E. , Contreras Jaime P. , Melo Carlos L. , Soto Daniel C. 
Published: September 2004

AbstractThe incidence, risk factors, and clinical relevance of stenosis of stapled colorectal anastomosis (CRA) were studied prospectively. Anastomotic stricture was defined as the inability of traversing the anastomosis with the rigid proctoscope. The population studied consisted of 179 patients (94 males) with an average age of 59.3 years (range: 20 to 91 years). The main indication for surgery was colorectal cancer in 59% of the cases, followed by diverticular disease in 23%. The first endoscopic control was performed before 4 months in 25% of the patients, between 5 and 10 months in 50%, and during the following 10 months in 25%. Stenosis was verified with the rigid instrument in 21.1% of the cases and with the flexible colonoscope in 4.4%. The barium enema performed in 12 cases confirmed a punctiform stenosis in 5 patients, 4 of whom had been asymptomatic. An endoscopic dilatation was performed on 5 of the 8 symptomatic patients, with one relapse that required an additional dilatation. In the univariate analysis only the lesser 4‐month interval was statistically significant (p = 0.033; odds ratio (OR) = 2.3; confidence interval (CI) 95% = 1.06 to 4.97). Male patients (p = 0.057; OR = 2.08; IC 95% = 0.97–4.44) show a tendency to CRA stricture that does not reach statistically significant levels. In the multivariate analysis, only sex (p = 0.04; OR = 4.11; IC 95% = 1.03 to 5.41) and the time interval (p = 0.012; OR = 2.87; IC 95% = 1.25 to 6.57) appear as independent variables in stenosis risk of a stapled CRA. The incidence of this complication depends on the criteria used for defining it. It is clinically relevant in no more than 5% of the patients. Five out of eight patients in category II were treated successfully with an endoscopic dilatation, while the other three improved spontaneously. Early stenosis, although frequent, is generally asymptomatic and disappears spontaneously. Considering the lack of correlation between the degree of stricture and its symptomatology, it is convenient to combine both the anatomic and the clinical criteria in the selection of candidates for an eventual therapeutic procedure.
Clinicopathologic and Prognostic Characterization of Poorly Differentiated Medullary‐type Gastric Adenocarcinoma
Authors: Otsuji Eigo , Kuriu Yoshiaki , Ichikawa Daisuke , Ochiai Toshiya , Okamoto Kazuma , Hagiwara Akeo , Yamagishi Hisakazu 
Published: September 2004

AbstractPoorly differentiated medullary‐type gastric adenocarcinoma has been reported to differ biologically from poorly differentiated scirrhous adenocarcinoma, and we have characterized the differences in greater detail. Clinicopathologic comparisons were made between the former and latter tumor types as well as well‐differentiated gastric adenocarcinoma. Poorly differentiated medullary cancers were smaller, invaded less deeply, and were less likely to arise from the upper part of the stomach than scirrhous cancers. Poorly differentiated medullary cancers less often gave rise to lymph node and peritoneal metastases than scirrhous cancers but more often metastasized to the liver. Venous invasion was more common in medullary than scirrhous or well‐differentiated adenocarcinomas. Postoperative survival for patients with poorly differentiated medullary cancers was significantly better than for patients with scirrhous‐type cancers but did not differ significantly from survival with well‐differentiated adenocarcinoma. The most common cause of death was hematogenous metastasis in patients with medullary or well‐differentiated adenocarcinomas, whereas in patients with scirrhous cancer peritoneal metastasis was the most frequent cause. In conclusion, the biologic behavior of poorly differentiated medullary gastric adenocarcinoma was similar to that of well‐differentiated adenocarcinoma.
Meckel’s Diverticulum: Comparison of Incidental and Symptomatic Cases
Authors: Bani‐Hani Kamal E. , Shatnawi Nawaf J. 
Published: September 2004

AbstractAlthough Meckel’s diverticulum is the commonest congenital gastrointestinal anomaly, there is still debate concerning the proper management of asymptomatic diverticula. Records of all patients whose Meckel’s diverticulum was resected at our hospitals between 1990 and 2002 were reviewed. Clinical characteristics, mode of presentations, and management for all patients were analyzed. Meckel’s diverticula were resected in 68 patients. Patients were divided into two groups: the incidental group included 40 patients (24 males) in whom the diagnosis of diverticula was incidental. The symptomatic group included 28 patients (20 males) who presented with diverticulum‐related complications. Preoperative diagnosis was possible in only four cases. In four patients from the symptomatic group, Meckel’s diverticula were found and left untouched during a previous laparotomy. There was no significant difference between the two groups with respect to gender (p = 0.48). Patients in the symptomatic group were significantly younger than patients in the incidental group (p = 0.002). The diverticula in the symptomatic group tended to be longer (p = 0.001) with a narrower base (p = 0.001) than the diverticula in the incidental group. A diameter of ≤ 2 cm was significantly associated with more complications (p = 0.01). Heterotopic tissue was present more significantly in the symptomatic group than the incidental group (p = 0.01). There was no significant difference in the morbidity rate between the two groups (p = 0.71), and there was no mortality in either group. Preoperative diagnosis of Meckel’s diverticulum is difficult and should be kept in mind in cases of acute abdomen. Resection of incidentally found diverticula is not associated with increased operative morbidity or mortality.
Liver delivery of NO by NCX‐1000 protects against acute liver failure and mitochondrial dysfunction induced by APAP in mice  THIS ARTICLE HAS BEEN RETRACTED
Authors: Fiorucci Stefano , Antonelli Elisabetta , Distrutti Eleonora , Mencarelli Andrea , Farneti Silvana , Soldato Piero Del , Morelli Antonio 
Published: September 2004

NCX‐1000, (3α, 5β, 7β)‐3,7‐dihydroxycholan‐24oic acid[2‐methoxy‐4‐[3‐[4‐(nitroxy)butoxy]‐3‐oxo‐1‐propenyl]phenyl ester, is a nitric oxide (NO)‐derivative of ursodeoxyxholic acid (UDCA) that selectively release NO in the liver.
Here, we demonstrated that administering mice with 40 μmol kg−1 NCX‐1000, but not UDCA, improves liver histopathology and reduces mortality caused by 330 μmol kg−1 APAP from 60 to 25% (P<0.01). Administration of NCX‐1000, in a therapeutic manner, that is, 2 h after acetaminophen (APAP) intoxication reduced mortality, improved liver histopathology and prevented liver IFN‐γ, TNF‐α, Fas/Fas ligand and inducible nitric oxide synthase (iNOS) mRNA accumulation caused by APAP.
In vitro exposure of primary cultures of mouse hepatocytes to APAP, 6.6 mM, resulted in apoptosis followed by necrosis. Loss of cell viability correlates with early mitochondrial membrane potential (Δψm) hyperpolarization followed by depolarization and cytochrome c translocation from mitochondria to cytosol. APAP‐induced apoptosis associated with procaspase‐3 and ‐9 cleavage, appearance of truncated Bid and activation of poly(ADP‐ribose) polymerase (PARP).
Treating primary culture of hepatocytes with 5 μM cyclosporine and 10 μM trifluoperazine for eight resulted in significant reduction of apoptosis induced by APAP suggesting that loss of Δψm was mechanistically involved in apoptosis induced by APAP in vitro.
NCX‐1000, but not UDCA, concentration‐dependently (ED50=16 μM) protected against Δψm depolarization and reduced transition from apoptosis to necrosis caused by 6.6 mM APAP.
Treating primary cultures of hepatocytes with the NO‐donor DETA‐NO, 100 μM, reduced apoptosis induced by APAP and prevented caspase activation.
In conclusion, NCX‐1000 is effective in protecting against APAP‐induced hepatotoxicity when administered in a therapeutic manner. This protection may involve the inhibition of apoptosis and the maintenance of mitochondrial integrity.

British Journal of Pharmacology (2004) 143, 33–42. doi:10.1038/sj.bjp.0705780
Nephroprotection in Zucker diabetic fatty rats by vasopeptidase inhibition is partly bradykinin B2 receptor dependent
Authors: Schäfer Stefan , Schmidts Hans‐Ludwig , Bleich Markus , Busch Andreas E , Linz Wolfgang 
Published: September 2004

Vasopeptidase inhibition (i.e., the simultaneous inhibition of both angiotensin‐converting enzyme (ACE) and neutral endopeptidase) can ameliorate diabetic nephropathy. We investigated whether this nephroprotection is mediated by the bradykinin B2 receptor.
In all, 43 obese Zucker diabetic fatty (ZDF/Gmi‐fa/fa) rats aged 21 weeks were separated into four groups and treated for 26 weeks with either placebo, the bradykinin B2 receptor antagonist icatibant (500 μg kg−1 day−1 s.c. infusion), the vasopeptidase inhibitor AVE7688 (45 mg kg−1 day−1 in chow), or AVE7688 plus icatibant. Nephropathy was assessed as albuminuria at age 31 and 39 weeks, and by histopathologic scoring at the end of the treatment period.
All animals had established diabetes mellitus (blood glucose >20 mmol l−1) and marked albuminuria at baseline. Blood glucose was not influenced by any treatment. Icatibant alone did not influence albuminuria (8.6±1.6 vs placebo 9.5±1.3 mg kg−1 h−1). AVE7688 reduced albuminuria at week 31 markedly to 1.1±0.1 mg kg−1 h−1 and reduced glomerular and tubulo‐interstitial kidney damage at week 47. In the AVE7688 plus icatibant group, proteinuria was significantly higher than in the AVE7688 only group (2.0±0.6 mg kg−1 h−1), but still reduced compared to placebo. In addition, icatibant partly antagonized the tubulo‐interstitial protection mediated by AVE7688.
We conclude that vasopeptidase inhibition provides nephroprotection in rats with type II diabetic nephropathy, which is partly mediated by bradykinin B2 receptor activation.

British Journal of Pharmacology (2004) 143, 27–32. doi:10.1038/sj.bjp.0705884
Nitric oxide donors inhibit 5‐hydroxytryptamine (5‐HT) uptake by the human 5‐HT transporter (SERT)
Authors: Bryan‐Lluka Lesley J , Papacostas Marisa H , Paczkowski Filip A , Wanstall Janet C 
Published: September 2004

The aim was to test the hypothesis that nitric oxide (NO) donor drugs can inhibit the 5‐hydroxytryptamine (5‐HT) transporter, SERT.
The NO donors, MAHMA/NO (a NONOate; (Z)‐1‐[N‐methyl‐N‐[6‐(N‐methylammoniohexyl)‐amino]]diazen‐1‐ium‐1,2‐diolate), SIN‐1 (a sydnonimine; 5‐amino‐3‐(4‐morpholinyl)‐1,2,3‐oxadiazolium chloride), FK409 (an oxime; (±)‐(4‐ethyl‐2E‐(hydroxyimino)‐5‐nitro‐3E‐hexenamide)) and peroxynitrite, but not Angeli's salt (source of nitroxyl anion) or sodium nitrite, caused concentration‐dependent inhibition of the specific uptake of [3H]‐5‐HT in COS‐7 cells expressing human SERT.
Superoxide dismutase (150 U ml−1) plus catalase (1200 U ml−1), used to remove superoxide and hence prevent peroxynitrite formation, prevented the inhibitory effect of SIN‐1 (which generates superoxide) but not of MAHMA/NO or FK409.
The inhibitory effects of the NO donors were not affected by the free radical scavenger, hydroxocobalamin (1 mM) or the guanylate cyclase inhibitor, ODQ (1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one; 3 μM).
L‐Cysteine (1 mM; source of excess thiol residues) abolished or markedly reduced the inhibitory effects of MAHMA/NO, SIN‐1, FK409 and peroxynitrite.
It is concluded that inhibition of SERT by the NO donors cannot be attributed exclusively to NO free radical nor to nitroxyl anion. It does not involve guanosine‐3′,5′‐cyclic monophosphate, but may involve nitrosation of cysteine residues on the SERT protein. Peroxynitrite mediates the effect of SIN‐1, but not the other drugs.
Data in mice with hypoxic pulmonary hypertension suggest that SERT inhibitors may attenuate pulmonary vascular remodelling. Thus, NO donors may be useful in pulmonary hypertension, not only as vasodilators, but also because they inhibit SERT, provided they display this effect in vivo at appropriate doses.

British Journal of Pharmacology (2004) 143, 63–70. doi:10.1038/sj.bjp.0705904
Influence of agonist intrinsic activity on the desensitisation of β2‐adrenoceptor‐mediated responses in mast cells
Authors: Scola Anne‐Marie , Chong Lee K , Chess‐Williams Russell , Peachell Peter T 
Published: September 2004

The aim of the present study was to determine whether the intrinsic activity of an agonist influences the extent of desensitisation of β2‐adrenoceptor‐mediated responses in human lung mast cells.
The effects of a wide range of β‐adrenoceptor agonists (10−10–10−5M) on the IgE‐mediated release of histamine from mast cells were determined. The intrinsic activity of agonists was established by comparing the maximal inhibitory response (Emax) of an agonist relative to the maximal response obtained with the full agonist, isoprenaline. The intrinsic activity order for the inhibition of histamine release was isoprenaline (1.0)>formoterol (0.94)>fenoterol (0.89)>terbutaline (0.84)>salbutamol (0.69)>clenbuterol (0.65)>salmeterol (0.30)>dobutamine (0.20).
There was a significant (P<0.05) positive correlation (r=0.81) between the extent to which β‐adrenoceptor agonists inhibited histamine release and the degree to which the agonists caused elevations in cAMP in mast cells.
Further studies investigated the effects of long‐term (24 h) incubation of mast cells with β‐adrenoceptor agonists on the subsequent ability of isoprenaline to inhibit histamine release. At concentrations of agonists selected to occupy a large percentage (88%) of β2‐adrenoceptors, there was a significant (P<0.05) correlation (r=0.73) between the relative intrinsic activity of agonists as inhibitors of histamine release and the extent of functional desensitisation induced by the agonists. At lower receptor occupancies, however, there was no correlation between the relative intrinsic activity of agonists and the extent of agonist‐induced desensitisation.
These data indicate that, under experimental conditions where high receptor occupancies prevail, agonist intrinsic activity influences the extent of desensitisation of β2‐adrenoceptor‐mediated responses in mast cells.

British Journal of Pharmacology (2004) 143, 71–80. doi:10.1038/sj.bjp.0705905
P2Y2‐receptor‐mediated activation of a contralateral, lanthanide‐sensitive calcium entry pathway in the human airway epithelium
Authors: Bahra Parmjit , Mesher Jonathan , Li Su , Poll Christopher T , Danahay Henry 
Published: September 2004

Receptor‐mediated calcium entry (RMCE) was examined in well‐differentiated cultures of normal human bronchial epithelial cells (HBECs). Changes in intracellular free Ca2+ ([Ca2+]i) were quantified using fluorescence ratio imaging of Fura‐2‐loaded cells during perfusion with Ca2+ mobilizing agonists.
Initial studies revealed an agonist potency of ATP=uridine triphosphate (UTP) >ADP=uridine diphosphate, consistent with purinergic activation of an apical P2Y2‐receptor mediating the increase in [Ca2+]i in HBECs.
Apical UTP (30 μM) induced a sustained period of elevated [Ca2+]i between 300 and 600 s following agonist stimulation that extracellular Ca2+ free studies indicated was dominated by Ca2+ influx.
RMCE was inhibited by 100 nM La3+ (83±3%) or Gd3+ (95±7%) (P<0.005, n=4–11) and was partially attenuated by Ni2+ (1 mM) (58.7±5.0%, P<0.005, n=9).
RMCE was also partially sensitive (< 25% inhibition, P<0.01) to the cation channel blockers SKF96365 (30 μM) and econazole (30 μM), but was insensitive to both verapamil (1 μM) and ruthenium red (10 μM).
Using either a sided Ca2+ readdition protocol or unilateral La3+, established that the RMCE pathway was located exclusively on the basolateral membrane.
The pharmacological sensitivity of the P2Y2‐receptor activated Ca2+ entry pathway in the human airway epithelium is inconsistent with the established profile of TRP channel families and is therefore likely to be of an as‐yet uncharacterized molecular identity.

British Journal of Pharmacology (2004) 143, 91–98. doi:10.1038/sj.bjp.0705913