bluuebunny/crossref_metadata_2025_split huggingface dataset:
Microbial communities in iron‐silica‐rich microbial mats at deep‐sea hydrothermal fields of the Southern Mariana Trough
Authors: Kato Shingo , Kobayashi Chiyori , Kakegawa Takeshi , Yamagishi Akihiko 
Published: April 2009

SummaryThe abundance, diversity and composition of bacterial and archaeal communities in the microbial mats at deep‐sea hydrothermal fields were investigated, using culture‐independent 16S rRNA and functional gene analyses combined with mineralogical analysis. Microbial mats were collected at two hydrothermal areas on the ridge of the back‐arc spreading centre in the Southern Mariana Trough. Scanning electron microscope and energy dispersive X‐ray spectroscopic (SEM‐EDS) analyses revealed that the mats were mainly composed of amorphous silica and contained numerous filamentous structures of iron hydroxides. Direct cell counting with SYBR Green I staining showed that the prokaryotic cell densities were more than 108 cells g−1. Quantitative polymerase chain reaction (Q‐PCR) analysis revealed that Bacteria are more abundant than Archaea in the microbial communities. Furthermore, zetaproteobacterial cells accounted for 6% and 22% of the prokaryotic cells in each mat estimated by Q‐PCR with newly designed primers and TaqMan probe. Phylotypes related to iron‐oxidizers, methanotrophs/methylotrophs, ammonia‐oxidizers and sulfate‐reducers were found in the 16S rRNA gene clone libraries constructed from each mat sample. A variety of unique archaeal 16S rRNA gene phylotypes, several pmoA, dsrAB and archaeal amoA gene phylotypes were also recovered from the microbial mats. Our results provide insights into the diversity and abundance of microbial communities within microbial mats in deep‐sea hydrothermal fields.
The role of pH in determining the species composition of the human colonic microbiota
Authors: Duncan Sylvia H. , Louis Petra , Thomson John M. , Flint Harry J. 
Published: April 2009

SummaryThe pH of the colonic lumen varies with anatomical site and microbial fermentation of dietary residue. We have investigated the impact of mildly acidic pH, which occurs in the proximal colon, on the growth of different species of human colonic bacteria in pure culture and in the complete microbial community. Growth was determined for 33 representative human colonic bacteria at three initial pH values (approximately 5.5, 6.2 and 6.7) in anaerobic YCFA medium, which includes a mixture of short‐chain fatty acids (SCFA) with 0.2% glucose as energy source. Representatives of all eight Bacteroides species tested grew poorly at pH 5.5, as did Escherichia coli, whereas 19 of the 23 Gram‐positive anaerobes tested gave growth rates at pH 5.5 that were at least 50% of those at pH 6.7. Growth inhibition of B. thetaiotaomicron at pH 5.5 was increased by the presence of the SCFA mix (33 mM acetate, 9 mM propionate and 1 mM each of iso‐valerate, valerate and iso‐butyrate). Analysis of amplified 16S rRNA sequences demonstrated a major pH‐driven shift within a human faecal bacterial community in a continuous flow fermentor. Bacteroides spp. accounted for 27% of 16S rRNA sequences detected at pH 5.5, but 86% of sequences at pH 6.7. Conversely, butyrate‐producing Gram‐positive bacteria related to Eubacterium rectale represented 50% of all 16S rRNA sequences at pH 5.5, but were not detected at pH 6.7. Inhibition of the growth of a major group of Gram‐negative bacteria at mildly acidic pH apparently creates niches that can be exploited by more low pH‐tolerant microorganisms.
Paediatric testicular cancer: an updated review of incidence and conditional survival from the Surveillance, Epidemiology and End Results database
Authors: Alanee Shaheen , Shukla Aseem 
Published: April 2009

OBJECTIVESTo determine, using the Surveillance, Epidemiology, and End Results (SEER) population‐based database, the epidemiological variables and update the understanding of testicular tumours in children, as knowledge of their incidence and survival is predicated upon multi‐institutional cooperation.PATIENTS AND METHODSUsing the SEER database, we ascertained the incidence rate, 5‐year survival by disease stage at diagnosis, and 5‐year conditional survival after surviving for 1–3 years for cases recorded between 1973 and 2005. We stratified the incidence rate by race and histology to examine if these factors affect disease characteristics.RESULTSWe identified 195 cases of testicular tumours in children from birth to age 14 years, and 785 for children aged 15–18 years. Yolk sac tumour was the most common testicular tumour, and overall, Caucasian children were most at risk and four times more likely to be affected than African‐American children. The incidence rate of testicular tumour overall has not increased significantly since 1973. Conditional survival is excellent for all testicular malignancies, with a 1‐year conditional survival (chance of surviving 5‐years after having survived the first year) of 99.6%.CONCLUSIONSWe present an updated analysis of the SEER database for the incidence and survival of testicular tumours, and revisit the issue of whether the incidence of testicular tumours in children is increasing. We also present to our knowledge, the first calculation of conditional survival in children for this malignancy. There has been no significant increase in the incidence of testicular tumours for children aged <14 years. By contrast, the postpubertal group aged 15–18 years showed a reversal in this trend.
Precursor of prostate‐specific antigen expression in prostatic intraepithelial neoplasia and adenocarcinoma: a study of 90 cases
Authors: Hull David , Ma Jun , Singh Harpreet , Hossain Deloar , Qian Junqi , Bostwick David G. 
Published: April 2009

OBJECTIVETo assess the expression of the precursor of prostate‐specific antigen (pro‐PSA), a distinct molecular form of serum‐free PSA that includes native and truncated forms, in benign epithelium, high‐grade prostatic intraepithelial neoplasia (PIN) and prostatic adenocarcinoma.MATERIALS AND METHODSWe immunohistochemically evaluated 90 formalin‐fixed, paraffin‐embedded prostate needle biopsies using monoclonal antibodies against [−2] pro‐PSA, native [−5/−7] pro‐PSA, prostate‐specific membrane antigen (PSMA), PSA and racemase. Staining intensity was recorded using a scale of 0–3 (0, no staining; 3, highest staining). The percentage of immunoreactive cells in benign epithelium, high‐grade PIN and adenocarcinoma was estimated in increments of 10%.RESULTSAll cases had [−5/−7] pro‐PSA immunoreactivity. There was weak focal perinuclear cytoplasmic immunoreactivity for [−5/−7] pro‐PSA in 62% (range 0–90%) of benign epithelial cells, whereas there was strong diffuse cytoplasmic staining in 83% (range 10–90%) of high‐grade PIN and 87% (range 40–90%) of cancer cells. Almost all (99%) cases were immunoreactive for [−2] pro‐PSA. The median (range) proportion of cells expressing [−2] pro‐PSA was lower in benign epithelium, at 17 (0–80)%, than in high‐grade PIN, at 55 (0–90)% (P < 0.001) and adenocarcinoma, at 55 (0–100)% (P < 0.001). The intensity of immunoreactivity for both isoforms increased from benign to neoplastic (high‐grade PIN and adenocarcinoma) epithelium. A total of 31% of high‐grade PIN and 11% of cancer cases with negative racemase staining showed strong staining for [−5/−7] pro‐PSA.CONCLUSIONThe expression of [−5/−7] pro‐PSA in benign and neoplastic cells might be used in combination with high molecular weight keratin, p63, and racemase to distinguish benign epithelium from high‐grade PIN and adenocarcinoma, particularly when racemase staining is negative. Both isoforms are sensitive markers for prostatic epithelium, making them possible candidates for investigating carcinoma with an unknown primary, particularly in cases in which PSA staining is negative and the level of suspicion is high.
Receptor‐induced phasic activity of newborn mouse bladders is inhibited by protein kinase C and involves T‐type Ca2+ channels
Authors: Ekman Mari , Andersson Karl‐Erik , Arner Anders 
Published: April 2009

OBJECTIVETo investigate the mechanisms involved in the phasic contractile activity after muscarinic receptor activation of newborn urinary bladders and to compare neonatal and adult bladders.MATERIALS AND METHODSDetrusor muscle strips were isolated from newborn mice (aged 0–2 days) and compared with preparations from adult mice (aged 10–12 weeks). The effects of an activator (phorbol 12,13‐dibutyrate, PDBu) and an inhibitor (GF109203X) of protein kinase C (PKC) on contractions were investigated. T‐type Ca2+ channels were blocked with NiCl2.RESULTSThe newborn urinary bladders responded with prominent phasic contractile activity in response to carbachol (1 µm). GF109203X (3 µm) reduced carbachol‐induced force by ≈60% in the newborn, compared with 30% in the adult. PDBu (1 µm) enhanced the muscarinic receptor‐mediated contraction in adult bladder muscle, whereas it completely abolished the responses in the newborn. There was no inhibition after activation with depolarization (high‐K+) or purinergic agonists (ATP, α,β‐methylene ATP). NiCl2 (>30 µm) inhibited the peak responses to carbachol in the newborn and at 300 µm it completely abolished the phasic contractile response. The responses of the adult bladder muscle were only marginally affected by NiCl2.CONCLUSIONSMuscarinic receptor stimulation recruits the PKC signalling pathway in both the adult and neonatal urinary bladder. Potent PKC activation is inhibitory on carbachol‐induced activation in the newborn and stimulatory in the adult bladder. Furthermore, muscarinic receptor stimulation activates T‐type Ca2+ channels in the newborn, but not the adult bladder.
Robot‐assisted laparoscopic prostatectomy is not associated with early postoperative radiation therapy
Authors: Chino Junzo , Schroeck Florian R. , Sun Leon , Lee W. Robert , Albala David M. , Moul Judd W. , Koontz Bridget F. 
Published: April 2009

OBJECTIVETo compare open radical prostatectomy (RP) and robot‐assisted laparoscopic prostatectomy (RALP), and to determine whether RALP is associated with a higher risk of features that determine recommendations for postoperative radiation therapy (RT).PATIENTS AND METHODSPatients undergoing RP from 2003 to 2007 were stratified into two groups: open RP and RALP. Preoperative (PSA level, T stage and Gleason score), pathological factors (T stage, Gleason score, extracapsular extension [ECE] and the status of surgical margins and seminal vesicle invasion [SVI]) and early treatment with RT or referral for RT within 6 months were compared between the groups. Multivariate analysis was used to control for selection bias in the RALP group.RESULTSIn all, 904 patients were identified; 368 underwent RALP and 536 underwent open RP (retropubic or perineal). Patients undergoing open RP had a higher pathological stage with ECE present in 24.8% vs 19.3% in RALP (P = 0.05) and SVI in 10.3% vs 3.8% (P < 0.001). In the RALP vs open RP group, there were positive surgical margins in 31.5% vs 31.9% (P = 0.9) and there were postoperative PSA levels of3 0.2 ng/mL in 5.7% vs 6.3% (P = 0.7), respectively. On multivariate analysis to control for selection bias, RALP was not associated with indication for RT (odds ratio (OR) 1.10,P = 0.55), or referral for RT (OR 1.04,P = 0.86).CONCLUSIONRALP was not associated with an increase in either indication or referral for early postoperative RT.
One‐sided anterior urethroplasty: a new dorsal onlay graft technique
Authors: Kulkarni Sanjay , Barbagli Guido , Sansalone Salvatore , Lazzeri Massimo 
Published: April 2009

OBJECTIVETo investigate the feasibility, tolerability, safety and efficacy of using a new surgical technique for the repair of anterior urethral strictures to preserve vascular supply to the urethra and its entire muscular and neurogenic support.PATIENTS AND METHODSIn all, 24 patients (mean age 46 years) underwent a new one‐sided anterior dorsal oral mucosal graft urethroplasty while preserving the lateral vascular supply to the urethra, the central tendon of the perineum, the bulbospongiosum muscle and its perineal innervation. The cause of stricture was instrumentation in three cases (12%), unknown in five (21%), infection in four (17%), and lichen sclerosus in 12 (50%). The stricture site was bulbar in 12 cases (50%) and panurethral in 12 (50%). The mean stricture length was 4.2 cm in patients with bulbar strictures and 10 cm in patients with panurethral strictures. Of 24 patients, 20 patients (83%) had received previous treatments. Clinical outcome was considered a failure when any postoperative instrumentation was needed, including dilatation.RESULTSThe overall mean (range) follow‐up was 22 (12–55) months. Of the 24 patients, 22 (92%) had a successful outcome and two (8%) were failures. One failure was treated using definitive perineal urethrostomy and another failure underwent successful internal urethrotomy.CONCLUSIONSThe preservation of the one‐sided vascular supply to the urethra and its entire muscular and neurogenic support should represent a slight but significant step toward perfecting the surgical technique of urethral reconstruction using a minimally invasive approach.
Plasma phospholipid transfer protein (PLTP): review of an emerging cardiometabolic risk factor
Authors: Tzotzas T. , Desrumaux C. , Lagrost L. 
Published: April 2009

SummaryPlasma phospholipid transfer protein (PLTP) is a lipid transfer glycoprotein that binds to and transfers a number of amphipathic compounds. In earlier studies, the attention of the scientific community focused on the positive role of PLTP in high‐density lipoprotein (HDL) metabolism. However, this potentially anti‐atherogenic role of PLTP has been challenged recently by another picture: PLTP arose as a pro‐atherogenic factor through its ability to increase the production of apolipoprotein B‐containing lipoproteins, to decrease their antioxidative protection and to trigger inflammation. In humans, PLTP has mostly been studied in patients with cardiometabolic disorders. Both PLTP and related cholesteryl ester transfer protein (CETP) are secreted proteins, and adipose tissue is an important contributor to the systemic pools of these two proteins. Coincidently, high levels of PLTP and CETP have been found in the plasma of obese patients. PLTP activity and mass have been reported to be abnormally elevated in type 2 diabetes mellitus (T2DM) and insulin‐resistant states, and this elevation is frequently associated with hypertriglyceridemia and obesity. This review article presents the state of knowledge on the implication of PLTP in lipoprotein metabolism, on its atherogenic potential, and the complexity of its implication in obesity, insulin resistance and T2DM.
PRIVACY, THE INDIVIDUAL AND GENETIC INFORMATION: A BUDDHIST PERSPECTIVE
Authors: HONGLADAROM SORAJ 
Published: April 2009

ABSTRACTBioinformatics is a new field of study whose ethical implications involve a combination of bioethics, computer ethics and information ethics. This paper is an attempt to view some of these implications from the perspective of Buddhism. Privacy is a central concern in both computer/information ethics and bioethics, and with information technology being increasingly utilized to process biological and genetic data, the issue has become even more pronounced. Traditionally, privacy presupposes the individual self but as Buddhism does away with the ultimate conception of an individual self, it has to find a way to analyse and justify privacy that does not presuppose such a self. It does this through a pragmatic conception that does not depend on a positing of the substantial self, which is then found to be unnecessary for an effective protection of privacy. As it may be possible one day to link genetic data to individuals, the Buddhist conception perhaps offers a more flexible approach, as what is considered to be integral to an individual person is not fixed in objectivity but depends on convention.
A Novel Application of a Bivariate Regression Model for Binary and Continuous Outcomes to Studies of Fetal Toxicity
Authors: Najita Julie S. , Li Yi , Catalano Paul J. 
Published: April 2009

Summary
Public health concerns over the occurrence of birth defects and developmental abnormalities that may occur as a result of prenatal exposure to drugs, chemicals and other environmental factors has led to an increasing number of developmental toxicity studies. Because fetal pups are commonly evaluated for multiple outcomes, data analysis frequently involves a joint modelling approach. We focus on modelling clustered binary and continuous outcomes in the setting where both outcomes are potentially observable in all offspring but, owing to practical limitations, the continuous outcome is only observed in a subset of offspring. The subset is not a simple random sample but is selected by the experimenter under a prespecified probability model. Although joint models for binary and continuous outcomes have been developed when both outcomes are available for every fetus, many existing approaches are not directly applicable when the continuous outcome is not observed in a simple random sample. We adapt a likelihood-based approach for jointly modelling clustered binary and continuous outcomes when the continuous response is missing by design and missingness depends on the binary trait. The approach takes into account the probability that a fetus is selected in the subset. Through the use of a partial likelihood, valid estimates can be obtained by a simple modification to the partial likelihood score. Data involving the herbicide 2,4,5-trichlorophenoxyacetic-acid are analysed. Simulation results confirm the approach.
Direct evidence for axonal transport defects in a novel mouse model of mutant spastin‐induced hereditary spastic paraplegia (HSP) and human HSP patients
Authors: Kasher Paul R. , De Vos Kurt J. , Wharton Stephen B. , Manser Catherine , Bennett Ellen J. , Bingley Megan , Wood Jonathan D. , Milner Roy , McDermott Christopher J. , Miller Christopher C. J. , Shaw Pamela J. , Grierson Andrew J. 
Published: April 2009

AbstractMutations in spastin are the most common cause of hereditary spastic paraplegia (HSP) but the mechanisms by which mutant spastin induces disease are not clear. Spastin functions to regulate microtubule organisation, and because of the essential role of microtubules in axonal transport, this has led to the suggestion that defects in axonal transport may underlie at least part of the disease process in HSP. However, as yet there is no direct evidence to support this notion. Here we analysed axonal transport in a novel mouse model of spastin‐induced HSP that involves a pathogenic splice site mutation, which leads to a loss of spastin protein. A mutation located within the same splice site has been previously described in HSP. Spastin mice develop gait abnormalities that correlate with phenotypes seen in HSP patients and also axonal swellings containing cytoskeletal proteins, mitochondria and the amyloid precursor protein (APP). Pathological analyses of human HSP cases caused by spastin mutations revealed the presence of similar axonal swellings. To determine whether mutant spastin influenced axonal transport we quantified transport of two cargoes, mitochondria and APP‐containing membrane bound organelles, in neurons from mutant spastin and control mice, using time‐lapse microscopy. We found that mutant spastin perturbs anterograde transport of both cargoes. In neurons with axonal swellings we found that the mitochondrial axonal transport defects were exacerbated; distal to axonal swellings both anterograde and retrograde transport were severely reduced. These results strongly support a direct role for defective axonal transport in the pathogenesis of HSP because of spastin mutation.
Normal protein composition of synapses in Ts65Dn mice: a mouse model of Down syndrome
Authors: Fernandez Fabian , Trinidad Jonathan C. , Blank Martina , Feng Dong‐Dong , Burlingame Alma L. , Garner Craig C. 
Published: April 2009

AbstractDown syndrome (DS) is the most prevalent form of intellectual disability caused by the triplication of ∼230 genes on chromosome 21. Recent data in Ts65Dn mice, the foremost mouse model of DS, strongly suggest that cognitive impairment in individuals with DS is a consequence of reduced synaptic plasticity because of chronic over‐inhibition. It remains unclear however whether changes in plasticity are tied to global molecular changes at synapses, or are due to regional changes in the functional properties of synaptic circuits. One interesting framework for evaluating the activity state of the DS brain comes from in vitro studies showing that chronic pharmacological silencing of neuronal excitability orchestrates stereotyped changes in the protein composition of synaptic junctions. In the present study, we use proteomic strategies to evaluate whether synapses from the Ts65Dn cerebrum carry signatures characteristic of inactive cortical neurons. Our data reveal that synaptic junctions do not exhibit overt alterations in protein composition. Only modest changes in the levels of synaptic proteins and in their phosphorylation are observed. This suggests that subtle changes in the functional properties of specific synaptic circuits rather than large‐scale homeostatic shifts in the expression of synaptic molecules contribute to cognitive impairment in people with DS.
Health Insurance Coverage and Mortality Revisited
Authors: Kronick Richard 
Published: April 2009

Objective. To improve understanding of the relationship between lack of insurance and risk of subsequent mortality.Data Sources. Adults who reported being uninsured or privately insured in the National Health Interview Survey from 1986 to 2000 were followed prospectively for mortality from initial interview through 2002. Baseline information was obtained on 672,526 respondents, age 18–64 at the time of the interview. Follow‐up information on vital status was obtained for 643,001 (96 percent) of these respondents, with approximately 5.4 million person‐years of follow‐up.Study Design. Relationships between insurance status and subsequent mortality are examined using Cox proportional hazard survival analysis.Principal Findings. Adjusted for demographic, health status, and health behavior characteristics, the risk of subsequent mortality is no different for uninsured respondents than for those covered by employer‐sponsored group insurance at baseline (hazard ratio 1.03, 95 percent confidence interval [CI], 0.95–1.12). Omitting health status as a control variable increases the estimated hazard ratio to 1.10 (95 percent CI, 1.03–1.19). Also omitting smoking status and body mass index increases the hazard ratio to 1.20 (95 percent CI, 1.15–1.24). The estimated association between lack of insurance and mortality is not larger among disadvantaged subgroups; when the analysis is restricted to amenable causes of death; when the follow‐up period is shortened (to increase the likelihood of comparing the continuously insured and continuously uninsured); and does not change after people turn 65 and gain Medicare coverage.Conclusions. The Institute of Medicine's estimate that lack of insurance leads to 18,000 excess deaths each year is almost certainly incorrect. It is not possible to draw firm causal inferences from the results of observational analyses, but there is little evidence to suggest that extending insurance coverage to all adults would have a large effect on the number of deaths in the United States.