bluuebunny/crossref_metadata_2025_split huggingface dataset:
Does the time from biopsy to surgery affect biochemical recurrence after radical prostatectomy?
Authors: Boorjian Stephen A. , Bianco Fernando J. , Scardino Peter T. , Eastham James A. 
Published: September 2005

In a large urological oncology section this month the topics of cancer of the prostate, bladder, kidney and testis are covered. To mention but a few of these, authors from New York report that the time from biopsy to surgery in the case of prostate cancer did not influence the probability of biochemical recurrence for men who had a radical prostatectomy within a year of diagnosis. A paper from Boston reports several pregnancies which occurred after brachytherapy for prostate cancer. Incidentally, there is a letter to the Editor at the end of this month's issue, from a UK author, which deals with the same topic. There are two papers from the USA presenting data on the use of nilutamide in hormone‐refractory prostate cancer, and a third from Japan using flutamide in the same setting. A report from New York correlates urine cytology findings before and after flexible cystoscopy, finding that cytology immediately after flexible cystoscopy correlates well with that before cystoscopy.OBJECTIVETo evaluate whether the time from biopsy to radical prostatectomy (RP) predicts the biochemical recurrence (BCR) after RP, as men diagnosed with clinically localized prostate cancer have several available treatment options and investigating these alternatives may delay the initiation of definitive therapy.PATIENTS AND METHODSWe identified 3969 consecutive patients who had RP for clinically localized prostate cancer from 1987 to 2002; those eligible for the study had RP within a year of diagnosis. The interval between biopsy and RP was analysed both as a continuous and as a dichotomous variable (divided at 3 months). Multivariate analysis was used to evaluate the impact of time to RP on BCR. Subsets were also analysed for the effect of time to RP in patients considered to be at high risk of recurrence, with group 1 having a prostate specific antigen (PSA) level of ≥ 20 ng/mL, a biopsy Gleason score of ≥ 8, or clinical stage ≥ T2c; and group 2 assessed as having a >40% probability of BCR using a preoperative nomogram.RESULTSIn all, 3149 patients met the inclusion criteria and had a mean (interquartile range) follow‐up after RP of 5.4 (2.2–7.9) years. Multivariate analysis showed that the year of biopsy, PSA level before biopsy, clinical stage and biopsy Gleason score (all P < 0.001) were significantly associated with BCR after RP. The time to RP, treated either as a continuous variable (P = 0.252) or when categorized at 3 months (P = 0.939), failed to predict BCR. Further, the time to RP was not an independent predictor of BCR for patients at high risk of recurrence in group 1 (P = 0.147) or group 2 (P = 0.548).CONCLUSIONSThe time from biopsy to RP did not influence the probability of BCR for men who had RP within a year of diagnosis, even for those considered to be at high risk of BCR. Instead, the clinical and pathological features of the cancer provided the best estimate of the risk of BCR.
New life after prostate brachytherapy? Considering the fertile female partner of the brachytherapy patient
Authors: Grocela Joseph , Mauceri Thomas , Zietman Anthony 
Published: September 2005

OBJECTIVESTo examine several cases of unusual and unexpected pregnancy in the female partners of men treated with brachytherapy for cancer of the prostatePATIENTS AND METHODSSelf‐reported pregnancy of partners of patients who had had prostate brachytherapy was assessed. The dosimetry to the testicles and sperm counts were used to examine the feasibility of pregnancy in the partners.RESULTSThree reported cases of pregnancy showed the men to have viable counts of within several or all of the parameters of the World Health Organisation criteria for normal semen analysis.CONCLUSIONSThese cases provide a cautionary tale and suggest that all men being treated with prostate brachytherapy should be counselled about the possibility of continued fertility. Documentation of this ‘risk’ on the consent form will allow for proper discussion of this issue in a clinical and medicolegal context. The key to addressing this problem is to propagate much better patient information. The topic should be addressed clearly in information booklets for the patients. Prostate brachytherapy may allow for pregnancy to be achieved in the fertile partners of patients, even after full radiation treatment of the patient.
A phase II study of nilutamide in men with prostate cancer after the failure of flutamide or bicalutamide therapy
Authors: Davis Nancy B. , Ryan Christopher W. , Stadler Walter M. , Vogelzang Nicholas J. 
Published: September 2005

OBJECTIVETo determine the prostate‐specific antigen (PSA) response and time to PSA or radiographic progression in men with prostate cancer refractory to bicalutamide and/or flutamide therapy.PATIENTS AND METHODSMen with histologically confirmed prostate cancer not amenable to curative surgery or radiation therapy were eligible for the study if they had radiographic or PSA progression on at least one antiandrogen (not nilutamide) despite continued androgen suppression and standard antiandrogen withdrawal periods. All men received nilutamide 150 mg/day orally for ≥ 8 weeks unless there was unacceptable toxicity or disease progression. All men were evaluated for response, safety and toxicity. Baseline PSA levels, chest X‐ray, bone scan and abdominopelvic computed tomography studies were obtained; the re‐evaluation included PSA levels every 4 weeks and repeated imaging every 8 weeks in those with baseline abnormalities. The chest X‐ray was repeated if there were pulmonary symptoms. Nineteen men were consented and 16 were evaluable for response.RESULTSThe median (range) Gleason score was 7 (6–9) and the median number of previous second‐line therapies was 2 (1–4). Bicalutamide therapy had failed in all patients. At baseline, 13 (of 16 men) had radiographically evident disease, nine with diffuse osseous and four with radiographically measurable metastases. There was no grade 3/4 toxicity; the commonest grade 1/2 toxicities were constipation (three), sensory neuropathy (four), fatigue (six), and visual changes (two) involving transiently altered colour vision and sensitivity to light, respectively. Responses included three partial and 13 with progressive disease.CONCLUSIONSThe study was discontinued after a planned interim analysis because nilutamide had no apparent activity. Although well tolerated, nilutamide offers benefit to few men with prostate cancer in whom bicalutamide has failed.
Clinical outcome of maximum androgen blockade using flutamide as second‐line hormonal therapy for hormone‐refractory prostate cancer
Authors: Miyake Hideaki , Hara Isao , Eto Hiroshi 
Published: September 2005

OBJECTIVESTo investigate the efficacy of maximum androgen blockade (MAB) using flutamide as second‐line hormonal therapy for advanced hormone‐refractory prostate cancer (HRPC).PATIENTS AND METHODSThe study included 55 patients with HRPC who were treated with MAB using flutamide (375 mg daily) as second‐line hormonal therapy. All patients had previously received bicalutamide combined with either surgical or medical castration as first‐line hormonal therapy, which failed. The effect of the second‐line therapy was evaluated by serum prostate‐specific antigen (PSA) level alone, and the response defined as a decrease of >50% from the baseline PSA at the start of second‐line therapy.RESULTSOn initiating second‐line hormonal therapy there was a reduction in the PSA level in 25 of the 55 patients (45%), among whom 12 (22%) were regarded as responders, while the PSA level continued to increase in the remaining 30 (55%). The median (range) duration of the PSA response was 6 (1–13) months. During the observation period there were no severe side‐effects from the second‐line MAB therapy. Patients without bone metastases or whose disease progressed >1 year after first‐line therapy had a significantly higher incidence of PSA response to second‐line therapy, despite no significant effect of other factors examined on the PSA response to second‐line therapy. Furthermore, the cause‐specific survival in responders to second‐line therapy was significantly better than that in nonresponders; however, multivariate analysis showed that no factors, including response to second‐line therapy, could be used as independent predictors of cause‐specific survival.CONCLUSIONSMAB using flutamide as second‐line hormonal therapy can give a comparatively favourable PSA response with no severe side‐effects; therefore, this therapy may be suitable for patients with HRPC after primary MAB using bicalutamide has failed, particularly in those with no bone metastases or whose disease has progressed for >1 year after first‐line therapy.
Labour Market Trends and Structures in ASEAN and the East Asian NIEs
Authors: Manning Chris , Fong Pang Eng 
Published: September 2005

The paper reviews the literature on labour markets in the region with special emphasis on the impact of economic growth and structural change on employment and wages. It deals with labour supply trends, employment creation outside agriculture (especially export orientated industrialization and new high‐tech industries), labour absorption in agriculture, wage differentials and the functioning of rural and urban labour markets.The creation of efficient and equitable labour market institutions and labour market flexibility have emerged as dominant issues in the NIEs. In the ASEAN‐4, because of concentration of employment in low productivity and low wage jobs and underutilization of labour, the rate of modern sector labour absorption remains the major policy concern.
Trade Policy Issues in the Asian‐Pacific Region:
Authors: Yamazawa Ippei 
Published: September 2005

SummaryThroughout the 1980s the Asian‐Pacific region (and especially fast Asian countries) has achieved rapid economic growth accompanied by drastic changes in industrial production and trade. In the textile and clothing industry (‘textile’ industry hereafter), exporting countries display the ‘flying geese’ pattern. The first‐tier exportec Japan, had retreated by the mid‐ 1970s. The second‐tier exporters, the East Asian newly industrializing economies (NIEs, consisting of South Korea, Taiwan and Hong Kong), are now being replaced by the third‐tier, ASEAN and Chinese exporters. The drastic changes in production and trade have resulted from the spread of modern textile production techniques in response to changing comparative advantage. This has been caused by increased labour costs and exchange rate alignment in the first‐and second‐tier exporters, but it has also been affected by the trade policies of industrial importer countries.The textile industry trade has been tightly managed under the Multi‐Fibre Arrangement (MFA), and individual trade flows have been restricted by quota allocation under the MFA. At the current GATT Uruguay Round negotiations the major contracting parties agreed, in the Dunkel text of December 7997, on the gradual phasing out of the MFA restrictions over ten years. How will textile industry trade develop in the absence of the MFA restrictions? This paper focuses on the trade and production of textiles and clothing, but the case of this industry exemplifies important trade policy issues arising from the rapidly changing industrial structure in the Asian‐Pacific region.In discussing textile trade policy issues, economists often focus on the MFA. However, the MFA has not produced a watertight regime. Textile production and trade have changed through product and process innovation, new management styles, and the ever‐changing tastes of consumers. The MFA restrictions have effected these innovative changes, but the policy issues need to be discussed in this context of industrial change.1
Parents, Power and Public Participation: Sure Start, an Experiment in New Labour Governance
Authors: Gustafsson Ulla , Driver Stephen 
Published: September 2005

Abstract This paper examines parent participation in local Sure Start partnerships within the broader context of public involvement in policy‐making processes. Public participation is set against a background where an emphasis on participatory democracy is seen as a solution to shortcomings identified with policy‐making and implementation. However, the meaning of public participation is by no means straightforward and gives rise to problems at several levels. Many of these problems emanate from concerns with power and legitimation. While these concerns highlight important aspects of public participation in public and social administration, this paper, drawing on Foucault's concept of “pastoral power”, examines whether public participation is better viewed as a predictable part of governance in modern Western democracies where subjects need to be recruited to exercise power over themselves.
How not to become a museum piece
Authors: Beck Ulrich 
Published: September 2005

AbstractIn this essay I want to address two question marks which arose during my reading of Michael Burawoy's inspiring piece. First, sharing his spirit of recreating the sociological enlightenment by differentiating between different types of public sociologies, I do not share his optimism that sociology can easily become an integral part of public discourse and practice. Second, I don’t think that mainstream sociology is really prepared for this adventure. My argument points in the opposite direction: all the different forms of public and non‐public sociology are in danger of becoming museum pieces. Thus, sociology not only needs a public voice, it also needs to be reinvented first – in order to have a public voice at all!
Effects of creatine treatment on survival and differentiation of GABA‐ergic neurons in cultured striatal tissue
Authors: Andres R. H. , Ducray A. D. , Huber A. W. , Pérez‐Bouza A. , Krebs S. H. , Schlattner U. , Seiler R. W. , Wallimann T. , Widmer H. R. 
Published: September 2005

AbstractHuntington's disease (HD) is an autosomal dominant neurodegenerative disorder, characterized by a prominent loss of GABA‐ergic medium‐sized spiny neurons in the caudate putamen. There is evidence that impaired energy metabolism contributes to neuronal death in HD. Creatine is an endogenous substrate for creatine kinases and thereby supports cellular ATP levels. This study investigated the effects of creatine supplementation (5 mm) on cell survival and neuronal differentiation in striatal cultures. Chronic creatine treatment resulted in significant increased densities of GABA‐immunoreactive (‐ir) neurons, although total neuronal cell number and general viability were not affected. Similar effects were seen after short‐term treatment, suggesting that creatine acted as a differentiation factor. Inhibitors of transcription or translation did not abolish the creatine‐mediated effects, nor did omission of extracellular calcium, whereas inhibition of mitogen‐activated protein kinase and phosphatidylinositol‐3‐kinase significantly attenuated the creatine induced increase in GABA‐ir cell densities. Creatine exhibited significant neuroprotection against toxicity instigated either by glucose‐ and serum deprivation or addition of 3‐nitropropionic acid. In sum, the neuroprotective properties in combination with promotion of neuronal differentiation suggest that creatine has potential as a therapeutic drug in the treatment of neurodegenerative diseases, like HD.
Modulation of the homophilic interaction between the first and second Ig modules of neural cell adhesion molecule by heparin
Authors: Kulahin Nikolaj , Rudenko Olga , Kiselyov Vladislav , Poulsen Flemming M. , Berezin Vladimir , Bock Elisabeth 
Published: September 2005

AbstractThe second Ig module (IgII) of the neural cell adhesion molecule (NCAM) is known to bind to the first Ig module (IgI) of NCAM (so‐called homophilic binding) and to interact with heparan sulfate and chondroitin sulfate glycoconjugates. We here show by NMR that the heparin and chondroitin sulfate‐binding sites (HBS and CBS, respectively) in IgII coincide, and that this site overlaps with the homophilic binding site. Using NMR and surface plasmon resonance (SPR) analyses we demonstrate that interaction between IgII and heparin indeed interferes with the homophilic interaction between IgI and IgII. Accordingly, we show that treatment of cerebellar granule neurons (CGNs) with heparin inhibits NCAM‐mediated outgrowth. In contrast, treatment with heparinase III or chondroitinase ABC abrogates NCAM‐mediated neurite outgrowth in CGNs emphasizing the importance of the presence of heparan/chondroitin sulfates for proper NCAM function. Finally, a peptide encompassing HBS in IgII, termed the heparin‐binding peptide (HBP), is shown to promote neurite outgrowth in CGNs. These observations indicate that neuronal differentiation induced by homophilic NCAM interaction is modulated by interactions with heparan/chondroitin sulfates.
Novel multifunctional neuroprotective iron chelator‐monoamine oxidase inhibitor drugs for neurodegenerative diseases.In vivoselective brain monoamine oxidase inhibition and prevention of MPTP‐induced striatal dopamine depletion
Authors: Gal Shunit , Zheng Hailin , Fridkin Mati , Youdim Moussa B. H. 
Published: September 2005

AbstractSeveral multifunctional iron chelators have been synthesized from hydroxyquinoline pharmacophore of the iron chelator, VK‐28, possessing the monoamine oxidase (MAO) and neuroprotectiveN‐propargylamine moiety. They have iron chelating potency similar to desferal. M30 is a potent irreversible rat brain mitochondrial MAO‐A and ‐B inhibitorin vitro(IC50, MAO‐A, 0.037 ± 0.02; MAO‐B, 0.057 ± 0.01). Acute (1–5 mg/kg) and chronic [5–10 mg/kg intraperitoneally (i.p.) or orally (p.o.) once daily for 14 days]in vivostudies have shown M30 to be a potent brain selective (striatum, hippocampus and cerebellum) MAO‐A and ‐B inhibitor. It has little effects on the enzyme activities of the liver and small intestine. Its N‐desmethylated derivative, M30A is significantly less active. Acute and chronic treatment with M30 results in increased levels of dopamine (DA), serotonin(5‐HT), noradrenaline (NA) and decreases in DOPAC (dihydroxyphenylacetic acid), HVA (homovanillic acid) and 5‐HIAA (5‐hydroxyindole acetic acid) as determined in striatum and hypothalamus. In the mouse MPTP (N‐methy‐4‐phenyl‐1,2,3,6‐tetrahydropyridine) model of Parkinson's disease (PD) it attenuates the DA depleting action of the neurotoxin and increases striatal levels of DA, 5‐HT and NA, while decreasing their metabolites. As DA is equally well metabolized by MAO‐A and ‐B, it is expected that M30 would have a greater DA neurotransmission potentiation in PD than selective MAO‐B inhibitors, for which it is being developed, as MAO‐B inhibitors do not alter brain dopamine.
Immobilization stress causes increases in tetrahydrobiopterin, dopamine, and neuromelanin and oxidative damage in the nigrostriatal system
Authors: Kim Sung Tae , Choi Ji Hyun , Chang Jin Woo , Kim Seong Who , Hwang Onyou 
Published: September 2005

AbstractOxidative stress is believed to contribute to the pathophysiology of Parkinson's disease, in which nigrostriatal dopaminergic (DA) neurons undergo degeneration. Identification of endogenous molecules that contribute to generation of oxidative stress and vulnerability of these cells is critical in understanding the etiology of this disease. Exposure to tetrahydrobiopterin (BH4), the obligatory cofactor for DA synthesis, was observed previously to cause oxidative damage in DA cells. To demonstrate the physiological relevance of this observation, we investigated whether an overproduction of BH4 and DA might actually occur in vivo, and, if it did, whether this might lead to oxidative damage to the nigrostriatal system. Immobilization stress (IMO) elevated BH4 and DA and their synthesizing enzymes, tyrosine hydroxylase and GTP cyclohydrolase I. This was accompanied by elevation of lipid peroxidation and protein‐bound quinone, and activities of antioxidant enzymes. These increases in the indices of oxidative stress appeared to be due to increased BH4 synthesis because they were abolished following administration of the BH4 synthesis inhibitor, 2,4‐diamino‐6‐hydroxy‐pyrimidine. IMO also caused accumulation of neuromelanin and degeneration of the nigrostriatal system. These results demonstrate that a severe stress can increase BH4 and DA and cause oxidative damages to the DA neurons in vivo, suggesting relevance to Parkinson's disease.
β‐Arrestin1 and β‐arrestin2 are differentially required for phosphorylation‐dependent and ‐independent internalization of δ‐opioid receptors
Authors: Zhang Xiaoqing , Wang Feifei , Chen Xiaoqing , Li Jiali , Xiang Bin , Zhang Yu‐Qiu , Li Bao‐Ming , Ma Lan 
Published: September 2005

Abstractβ‐Arrestins are key negative regulators and scaffolds of G protein‐coupled receptor (GPCR) signalling. β‐Arrestin1 and β‐arrestin2 preferentially bind to the phosphorylated GPCRs in response to agonist stimulation, resulting in receptor internalization and desensitization. The critical roles of GPCR kinases (GRKs)‐catalyzed receptor phosphorylation and interaction of β‐arrestins with the phosphorylated receptor in receptor internalization are well established. However, emerging evidence suggests that an agonist‐stimulated internalization mechanism that is independent of receptor phosphorylation may also be employed in some cases, although the molecular mechanism for the phosphorylation‐independent GPCR internalization is not clear. The current study investigated the role of receptor phosphorylation and the involvement of different β‐arrestin subtypes in agonist‐induced δ‐opioid receptor (DOR) internalization in HEK293 cells. Results from flow cytometry, fluorescence microscopy, and surface biotin labelling experiments showed that elimination of agonist‐induced DOR phosphorylation by mutation GRK binding or phosphorylation sites only partially blocked agonist‐induced receptor internalization, indicating the presence of an agonist‐induced, GRK‐independent mechanism for DOR internalization. Fluorescence and co‐immunoprecipitation studies indicated that both the wild‐type DOR and the phosphorylation‐deficient mutant receptor could bind and recruit β‐arrestin1 and β‐arrestin2 to the plasma membrane in an agonist‐stimulated manner. Furthermore, internalization of both the wild‐type and phosphorylation‐deficient receptors was increased by overexpression of either type of β‐arrestins and blocked by dominant‐negative mutants of β‐arrestin‐mediated internalization, demonstrating that both phosphorylation‐dependent and ‐independent internalization require β‐arrestin. Moreover, double‐stranded RNA‐mediated interference experiments showed that either β‐arrestin1 or β‐arrestin2 subtype‐specific RNAi only partially inhibited agonist‐induced internalization of the wild‐type DOR. However, agonist‐induced internalization of the phosphorylation‐deficient DOR was not affected by β‐arrestin1‐specific RNAi but was blocked by RNAi against β‐arrestin2 subtype. These data indicate that endogenous β‐arrestin1 functions exclusively in the phosphorylation‐dependent receptor internalization, whereas endogenous β‐arrestin2, but not β‐arrestin1, is required for the phosphorylation‐independent receptor internalization. These results thus provide the first evidence of different requirement for β‐arrestin isoforms in the agonist induced phosphorylation‐dependent and ‐independent GPCR internalization.