bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evidence of occult dysautonomia in Fowler's syndrome: alteration of cardiovascular autonomic function tests in female patients presenting with urinary retention
Authors: AMARENCO GERARD , RAIBAUT PATRICK , ISMAEL SAMER SHEIKH , RENE‐CORAIL PATRICK , HAAB FRANCOIS 
Published: January 2006

OBJECTIVETo assess the hypothesis that an occult impairment of the autonomic system might represent one of the mechanisms of urinary disturbance in Fowler's syndrome (FS), in which the pathophysiology of urinary retention is the predominant feature.PATIENTS AND METHODSWe prospectively investigated 10 women (mean age 43.7 years) with FS, diagnosed by assessing both voiding‐phase dysfunction (complete or incomplete retention with a residual urine volume of >150 mL, and a maximum flow rate of <15 mL/s), abnormalities of striated urethral sphincter electromyography (decelerating bursts and complex repetitive discharges), the presence of polycystic ovaries and absence of any apparent usual causes (obstructive, neurological diseases). The women had a urodynamic investigation, electromyographic examination, cystoscopy, brain and spinal cord magnetic resonance imaging (MRI) and cardiovascular autonomic function tests (CAFTs, i.e. heart rate variability to deep breathing, cold‐pressor test, Valsalva ratio, blood pressure response to standing, and sympathetic skin responses), for parasympathetic and sympathetic functions. Evidence of dysautonomia, as classically described, was defined by two or more positive CAFTs.RESULTSThe mean duration of symptoms was 7.9 years; there was urinary retention in six patients (one complete and five incomplete) and the other four complained of straining to void, diminished stream and hesitancy. Five patients were using intermittent self‐catheterization. Six patients had two or more positive CAFTs and were considered to have dysautonomia. In all 10 women the clinical neurological and urological examinations were normal with no apparent clinical symptoms of dysautonomia (blurred vision, pupil abnormalities, clinical manifestations of postural hypotension, gastrointestinal symptoms). Brain and spinal cord MRI, cystoscopy, bladder and kidney ultrasonography, sacral‐evoked latencies and cortical‐evoked responses after pudendal nerve stimulation were normal.CONCLUSIONThere was an occult impairment of the autonomic system in women with FS; this condition might be a pure bladder expression of a generalized but occult dysautonomia, which in some cases might be diagnosed using CAFTs.
Venogenic erectile dysfunction in Klippel–Trenaunay syndrome
Authors: AGRAWAL VINEET , MINHAS SUKS , RALPH DAVID J. 
Published: January 2006

OBJECTIVETo report the management of erectile dysfunction (ED) secondary to Klippel–Trenaunay syndrome (KTS), a rare congenital vascular disease.PATIENTS AND METHODSThree men (mean age 33 years) with vasogenic ED secondary to KTS underwent venous ligation surgery of the affected veins. These men had tried various treatments for their ED, including phosphodiesterase type 5 inhibitors and intracavernosal injection therapy, with little success.RESULTSThere was abnormal penile venous drainage in all three men, probably associated with congenital vascular malformation from KTS. After venous ligation the men were followed for 5 years and all reported good quality erections satisfactory for sexual intercourse.CONCLUSIONED in men with KTS may be due to venous drainage anomalies and if confirmed, venous ligation surgery should be performed as this gives the best chance of a complete resolution.
Prostate tissue and leukocyte levels of n‐3 polyunsaturated fatty acids in men with benign prostate hyperplasia or prostate cancer
Authors: CHRISTENSEN JEPPE HAGSTRUP , FABRIN KNUD , BORUP KIRSTEN , BARBER NEIL , POULSEN JOHAN 
Published: January 2006

OBJECTIVETo compare the levels of n‐3 polyunsaturated fatty acids (PUFAs) in leukocytes and prostate tissue in men with prostate cancer or benign prostatic hyperplasia (BPH), as dietary intake of n‐3 PUFAs has been linked to the risk of prostate cancer; the prostate‐specific antigen (PSA) level was also compared to prostate tissue levels of n‐3 PUFAs.PATIENTS AND METHODSProstate tissue was obtained and leukocytes isolated from 20 men with prostate cancer and 35 with BPH. The n‐3 PUFAs α‐linolenic acid (ALA), eicosapentanoic acid (EPA) and docosahexaenoic acid (DHA) were measured in prostate tissue and in peripheral blood leukocytes using gas chromatography. PSA levels were measured in all of the men.RESULTSThere was a strong positive correlation between EPA and DHA in leukocytes and in prostate tissue (EPA: r = 0.80, DHA: r = 0.53, both P < 0.001) in all the men, whereas there was no association between the content of ALA in leukocytes and in prostate tissue (r = −0.15). Men with BPH had similar levels of ALA in leukocytes and in prostate tissue, but men with prostate cancer had more ALA in prostate tissue than in leukocytes. The PSA level was significantly positively correlated with ALA level in prostate tissue (r = 0.42, P < 0.01) but there was no significant correlation between PSA level and EPA and DHA levels. There were no significant correlations between PSA level and n‐3 PUFA levels in leukocytes.CONCLUSIONDietary intake of the marine n‐3 PUFAs reflected in EPA and DHA levels in leukocytes are also reflected in EPA and DHA levels in prostate tissue in men with and without prostate cancer. However, there is a discrepancy between the levels of ALA in leukocytes and in prostate tissue, with higher levels in men with prostate cancer. This is in accordance with the strong positive association between PSA and ALA levels in prostate tissue. This study therefore does not support the hypothesis that intake of marine n‐3 PUFAs might protect against prostate cancer, but lends support to the deleterious role of ALA in the development of prostate cancer.
Site of local anaesthesia in transrectal ultrasonography‐guided 12‐core prostate biopsy: does it make a difference?
Authors: PHILIP JOE , MCCABE JOHN E. , DUTTA ROY SUBHAJIT , SAMSUDIN AZIZAN , CAMPBELL IAIN M. , JAVLÉ PRADIP 
Published: January 2006

OBJECTIVETo prospectively compare the efficacy of bi‐basal vs bi‐apical periprostatic nerve block (PPNB) during 12‐core prostate biopsy guided by transrectal ultrasonography (TRUS), and to evaluate the pain experienced on inserting the probe compared to the biopsy procedure, as PPNB with lignocaine local anaesthesia has been used for over a decade for minimizing pain during prostatic biopsy.PATIENTS AND METHODSIn all, 143 men who were to have a TRUS‐guided prostate biopsy were systematically randomized to two groups, to receive PPNB at the apex or base. A 10‐cm visual analogue score was used to record the pain experienced during probe insertion, the biopsy and just before to leaving the department .RESULTSThe mean pain score on biopsy in the apical group was similar to that of the basal group (apex 1.9, base 1.6, P = 0.36). Probe introduction produced a significantly higher pain score (probe 2.2, biopsy 1.7, P < 0.001) than at the biopsy.CONCLUSIONSPatients who experienced greater pain with the introduction of the probe also reported more pain with the biopsy procedure. The site of local anaesthetic before prostatic biopsy showed no significant difference in pain scores. Older men tolerated the procedure better. Analgesia after PPNB at near either the apex or base appears equal, regardless of the site of injection. We suggest that topical perianal anaesthetic agents could significantly reduce not only pain perception, but also improve tolerance.
Genetic analysis of rice domestication syndrome with the wild annual species, Oryza nivara
Authors: Li Changbao , Zhou Ailing , Sang Tao 
Published: January 2006

Summary

With a small and sequenced genome, rice provides an excellent system for studying the genetics of cereal domestication.
We conducted a quantitative trait locus (QTL) analysis of key domestication traits using an F2 population derived from a cross between the cultivated rice, Oryza sativa, and the annual wild species, O. nivara.
We found that the QTL of large phenotypic effects were targeted by domestication selection for effective harvest and planting, including a reduction in seed shattering and seed dormancy and the synchronization of seed maturation. Selection for higher yield was probably responsible for the fixation of mutations at a cluster of QTL on chromosome 7 and a few other chromosomal locations that could have substantially improved plant architecture and panicle structure, resulting in fewer erect tillers and longer and more highly branched panicles in cultivated rice.
In comparison with the wild perennial species, O. rufipogon, rice domestication from O. nivara would have involved QTL with a greater degree of chromosomal co‐localization and required little genetic change associated with life history or mating system transitions. The genetic analyses of domestication traits with both wild relatives will open opportunities for the improvement of rice cultivars utilizing natural germplasm.
Nitric oxide down‐regulates caveolin‐1 expression in rat brains during focal cerebral ischemia and reperfusion injury
Authors: Shen Jiangang , Ma Stephanie , Chan Puishan , Lee Waisin , Fung Peter C. W. , Cheung Raymond T. F. , Tong Yao , Liu Ke Jian 
Published: January 2006

AbstractAs a signalling molecule of the integral membrane protein family, caveolin participates in cellular signal transduction via interaction with other signalling molecules. The nature of interaction between nitric oxide (NO) and caveolin in the brain, however, remains largely unknown. In this study we investigated the role(s) of NO in regulating caveolin‐1 expression in rat ischemic brains with middle cerebral artery occlusion (MCAO). Exposure to 1 h ischemia induced the increases in neuronal nitric oxide synthase (nNOS) and NO concentration with concurrent down‐regulation of caveolin‐1 expression in the ischemic core of rat brains. Subsequent 24 h or more reperfusion time led to an increase in inducible NOS (iNOS) expression and NO production, as well as a decline of caveolin‐1 protein at the core and penumbra of the ischemic brain. Afterwards, NOS inhibitors and an NO donor were utilized to clarify the link between NO production and caveolin‐1 expression in the rats with 1 h ischemia plus 24 h reperfusion. NG‐nitro‐l‐arginine methyl ester (L‐NAME, a non‐selective NOS inhibitor), N6‐(1‐iminoethyl)‐lysine (NIL, an iNOS inhibitor), and 7‐nitroindazole (7‐NI, a nNOS inhibitor) prevented the loss of caveolin‐1 in the core and penumbra of the ischemic brain, whereas l‐N5‐(1‐iminoethyl)‐ornithine (L‐NIO, an endothelial NOS inhibitor) showed less effect than the other NOS inhibitors. S‐Nitroso‐N‐acetylpenicillamine (SNAP, a NO donor) down‐regulated the expression of caveolin‐1 protein in normal and ischemic brains. These results, when taken together, suggest that NO modulates the expression of caveolin‐1 in the brain and that the loss of caveolin‐1 is associated with NO production in the ischemic brain.
Intrinsic and extrinsic erythropoietin enhances neuroprotection against ischemia and reperfusion injury in vitro
Authors: Liu Ruiqin , Suzuki Asuka , Guo Zhiwei , Mizuno Yoshikuni , Urabe Takao 
Published: January 2006

AbstractThis study was designed to investigate the neuroprotective effect of intrinsic and extrinsic erythropoietin (EPO) against hypoxia/ischemia, and determine the optimal time‐window with respect to the EPO‐induced neuroprotection. Experiments were conducted using primary mixed neuronal/astrocytic cultures and neuron‐rich cultures. Hypoxia (2%) induces hypoxia‐inducible factor‐1α (HIF‐1α) activity followed by strong EPO expression in mixed cultures and weak expression in neuron‐rich cultures as documented by both western blot and RT–PCR. Immunoreactive EPO was strongly detected in astrocytes, whereas EPOR was only detected in neurons. Neurons were significantly damaged in neuron‐rich cultures but were distinctly rescued in mixed cultures. Application of recombinant human EPO (rhEPO) (0.1 U/mL) within 6 h before or after hypoxia significantly increased neuronal survival compared with no rhEPO treatment. Application of rhEPO after onset of reoxygenation achieved the maximal neuronal protection against ischemia/reperfusion injury (6 h hypoxia followed 24 h reoxygenation). Our results indicate that HIF‐1α induces EPO gene released by astrocytes and acts as an essential mediator of neuroprotection, prove the protective role of intrinsic astrocytic‐neuronal signaling pathway in hypoxic/ischemic injury and demonstrate an optimal therapeutic time‐window of extrinsic rhEPO in ischemia/reperfusion injury in vitro. The results point to the potential beneficial effects of HIF‐1α and EPO for the possible treatment of stroke.
Wild‐type huntingtin protects neurons from excitotoxicity
Authors: Leavitt Blair R. , van Raamsdonk Jeremy M. , Shehadeh Jacqueline , Fernandes Herman , Murphy Zoe , Graham Rona K. , Wellington Cheryl L. , Lynn A. Raymond  , Hayden Michael R. 
Published: January 2006

AbstractHuntingtin is a caspase substrate, and loss of normal huntingtin function resulting from caspase‐mediated proteolysis may play a role in the pathogenesis of Huntington disease. Here we tested the hypothesis that increasing huntingtin levels protect striatal neurons from NMDA receptor‐mediated excitotoxicity. Cultured striatal neurons from yeast artificial chromosome (YAC)18 transgenic mice over‐expressing full‐length wild‐type huntingtin were dramatically protected from apoptosis and caspase‐3 activation compared with cultured striatal neurons from non‐transgenic FVB/N littermates and YAC72 mice expressing mutant human huntingtin. NMDA receptor activation induced by intrastriatal injection of quinolinic acid initiated a form of apoptotic neurodegeneration within the striatum of mice that was associated with caspase‐3 cleavage of huntingtin in neurons and astrocytes, decreased levels of full‐length huntingtin, and the generation of a specific N‐terminal caspase cleavage product of huntingtin. In vivo, over‐expression of wild‐type huntingtin in YAC18 transgenic mice conferred significant protection against NMDA receptor‐mediated apoptotic neurodegeneration. These data provide in vitro and in vivo evidence that huntingtin may regulate the balance between neuronal survival and death following acute excitotoxic stress, and that the levels of huntingtin may modulate neuronal sensitivity to excitotoxic neurodegeneration. We suggest that further study of huntingtin's anti‐apoptotic function will contribute to our understanding of the pathogenesis of Huntingdon's disease and provide insights into the selective vulnerability of striatal neurons to excitotoxic cell death.
Copper (II) ions potently inhibit purified PrPres amplification
Authors: Orem Nicholas R. , Geoghegan James C. , Deleault Nathan R. , Kascsak Richard , Supattapone Surachai 
Published: January 2006

AbstractThe structural conversion of a host protein, PrPC, into a protease‐resistant isoform, PrPres, is the central event in the pathogenesis of infectious prion diseases. Purification of native PrPC molecules from hamster brain by either cation exchange or immobilized chelator chromatographic resins yielded preparations that supported efficient amplification of scrapie‐induced PrPres in vitro. Using these purified preparations, we determined that in vitro PrPres amplification was inhibited by CuCl2 and ZnCl2 at IC50 concentrations of ∼400 nm and 10 μm, respectively. In contrast, 100 μm MnCl2 did not directly inhibit PrPres amplification or block Cu2+‐mediated inhibition. Additionally, the inhibition of PrPres amplification by Cu2+ ions could be reversed by addition of either neocuproine or imidazole. Cu2+ inhibited PrPres amplification in both the presence and absence of stimulatory polyanion molecules. These biochemical findings support the hypothesis that Cu2+ ions might regulate the pathogenesis of prion diseases in vivo.
Ectopic expression of tyrosine hydroxylase in the pigmented epithelium rescues the retinal abnormalities and visual function common in albinos in the absence of melanin
Authors: Lavado Alfonso , Jeffery Glen , Tovar Victoria , de la Villa Pedro , Montoliu Lluís 
Published: January 2006

AbstractAlbino mammals have profound retinal abnormalities, including photoreceptor deficits and misrouted hemispheric pathways into the brain, demonstrating that melanin or its precursors are required for normal retinal development. Tyrosinase, the primary enzyme in melanin synthesis commonly mutated in albinism, oxidizes l‐tyrosine to l‐dopaquinone using l‐3,4‐dihydroxyphenylalanine (L‐DOPA) as an intermediate product. L‐DOPA is known to signal cell cycle exit during retinal development and plays an important role in the regulation of retinal development. Here, we have mimicked L‐DOPA production by ectopically expressing tyrosine hydroxylase in mouse albino retinal pigment epithelium cells. Tyrosine hydroxylase can only oxidize l‐tyrosine to L‐DOPA without further progression towards melanin. The resulting transgenic animals remain phenotypically albino, but their visual abnormalities are corrected, with normal photoreceptor numbers and hemispheric pathways and improved visual function, assessed by an increase of spatial acuity. Our results demonstrate definitively that only early melanin precursors, L‐DOPA or its metabolic derivatives, are vital in the appropriate development of mammalian retinae. They further highlight the value of substituting independent but biochemically related enzymes to overcome developmental abnormalities.
Isolation and characterization of polymorphic microsatellite markers for Alternaria alternata
Authors: TRAN‐DINH NAI , HOCKING AILSA 
Published: January 2006

Abstract Alternaria alternata is of major significance as a food and feed contaminant and is able to produce a range of mycotoxins that may elicit adverse effects in both animals and humans. We describe the isolation and characterization of five microsatellite markers for studying A. alternata. Marker polymorphism was screened in 64 isolates of A. alternata. The number of alleles per locus ranged from eight to 24, and allelic diversity ranged from 0.425 to 0.882. These markers will be useful in the study of relationships and population genetics amongst isolates of A. alternata.
Ethical Issues in Dialysis Aaron SpitalSeries Editor: Soliciting Kidneys on Web Sites: Is it Fair?
Authors: Wright Linda , Campbell Michael 
Published: January 2006

ABSTRACTThe Internet serves as a meeting place where people in need of kidney transplants can find strangers willing to donate. While Good Samaritan donors located via the Internet increase the number of kidneys available for transplantationthey also raise ethical issues. This practice alters the pattern for distributing kidneys from unrelated living donors and raises questions of justice in the allocation of organs. It is unclear if commercial forces are at play in the arrangements made between potential donors and recipients via the Internet. While it is unfair that some recipients do not have suitablewilling living donorsWeb sites help to balance the inequity by increasing the opportunity to find a living donor; they also benefit other potential recipients by reducing the waiting list. Howeveralthough these Web sites are probably here to stayInternet donor–recipient matches can have negative consequences that we need to minimize. Suggested strategies include regulatedmonitored Web sites and the development of more anonymous organ donor programs.
Vascular Calcifications in Uremia: Old Concepts and New Insights
Authors: Derici Ulver , El Nahas A. Meguid 
Published: January 2006

ABSTRACTThe annual mortality rate in uremic patientscorrected for agesexand raceis significantly higher than in the general population. This is primarily due to cardiovascular events. Vascular calcifications play a vital role in the development of cardiovascular morbidity and subsequent increased mortality. Vascular calcification affects both vascular intima and media layers and its mechanism remains poorly understood. Over the last few years it has been shown thatin addition to traditional cardiovascular risk factorsdisturbances in mineral metabolism in the uremic milieucalcium‐containing phosphate bindersand vitamin D treatment of secondary hyperparathyroidism may contribute to the pathogenesis of vascular calcifications. Other uremia‐related risk factors (e.g.increased oxidized low‐density lipoprotein cholesteroluremic toxinsincreased oxidative stressdialysis and dialysate‐related factorshemodynamic overloadhyperhomocysteinemia) may also play a role. In uremic patientsapart from these facilitating factorsdecreased levels of endogenous calcification inhibitors such as fetuin‐Amatrix Gla proteinosteoprotegerinand osteopontin have also been associated with increased calcium‐phosphate precipitation in extraskeletal tissues. Finallyvascular calcification is the outcome of the active and dynamic balance of procalcifying and anticalcifying influences. For the prevention and treatment of vascular calcificationsit is essential to avoid treatment modalities that lead to calcium overloadachieve good metabolic controland optimize dialysis.
Pulse High‐Volume Hemofiltration in Critically Ill Patients: A New Approach for Patients with Septic Shock
Authors: Ratanarat Ranistha , Brendolan Alessandra , Ricci Zaccaria , Salvatori Gabriella , Nalesso Federico , de Cal Massimo , Cazzavillan Stefania , Petras Dimitris , Bonello Monica , Bordoni Valeria , Cruz Dinna , Techawathanawanna North , Ronco Claudio 
Published: January 2006

ABSTRACTMortality rates in septic shock remain unacceptably high despite advances in our understanding of the syndrome and its treatment. Humoral factors are increasingly recognized to participate in the pathogenesis of septic shockgiving a biological rationale to therapies that might remove varied and potentially dangerous humoral mediators. While plasma water exchange in the form of hemofiltration can remove circulating cytokines in septic patientsthe procedureas routinely performeddoes not have a substantial impact on their plasma levels. More intensive plasma water exchangeas high‐volume hemofiltration (HVHF)can reduce levels of these mediators and potentially improve clinical outcomes. Howeverthere are concerns about the feasibility and costs of HVHF as a continuous modality—very high volumes are difficult to maintain over 24 hours and solute kinetics are not optimized by this regimen. We propose pulse HVHF (PHVHF)—HVHF of 85 ml/kg/hr for 6–8 hours followed by continuous venovenous hemofiltration (CVVH) of 35 ml/kg/hr for 16–18 hours—as a new method to combine the advantages of HVHFimprove solute kineticsand minimize logistic problems. We treated 15 critically ill patients with severe sepsis and septic shock using daily PHVHF in order to evaluate the feasibility of the techniqueits effects on hemodynamicsand the impact of the treatment on pathologic apoptosis in sepsis. Hemodynamic improvements were obtained after 6 hours of PHVHF and were maintained subsequently by standard CVVHas demonstrated by the reduction in norepinephrine dose. PHVHFbut not CVVHsignificantly reduces apoptotic plasma activity within 1 hour and the pattern was maintained in the following hours. PHVHF appears to be a feasible modality that may provide the same or greater benefits as HVHFwhile reducing the workload and cost.