bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anorectal function following low anterior resection
Authors: Rasmussen O. O. , Petersen I. K. , Christiansen J. 
Published: May 2003

AbstractIntroduction Rectal function following rectal resection for carcinoma was studied in 43 patients.Methods Sixteen women and 27 men with a median age of 66 years (range 41–79 years) were included. Twenty‐three patients had a diverting ileostomy at the time of resection. Eight patients had a 6‐cm colonic J‐pouch. Ten patients had anastomotic leakage including two patients without diverting ileostomy. One patient had pre‐operative radiation with 25 Gy. The patients were studied at a median 12 months (range 3–30) after rectal resection. Distance from anal verge to the anastomosis was a median 7 cm (range 3–12 cm). Clinical data, anal manometry and rectal compliance were analysed.Results Stool frequency was 3 per day (range 1–10). Twenty‐two (51%) patients were continent, 11 (26%) were incontinent for flatus, and 10 (23%) were incontinent for faeces (three for liquid and seven for solid stool). Fourteen (33%) patients had constipation, two of whom also had incontinence for solid or liquid stool. The level of the anastomosis for patients with postoperative constipation was 5 cm (range 3–12 cm), while it was 7 cm (range 3–10 cm) for nonconstipated patients (NS). Anal manometry was normal. Rectal compliance was lower in patients with incontinence for liquid or solid faeces than in patients with flatus incontinence only (P < 0.01), and rectal volume tolerability was lower in incontinent patients compared with continent patients (P < 0.05). The rectoanal reflex was present in 31 (72%) patients. There was a negative correlation between maximal rectal volume and stool frequency and between level of the anastomosis and degree of incontinence. Age did not affect functional outcome.Conclusion Many patients had a poor functional result following low anterior resection. One in four suffered from incontinence to liquid or solid faeces and one third of the patients experienced constipation. A low level of anastomosis tended to increase stool frequency and carried a higher risk of incontinence. Patients with faecal incontinence tended to have lower rectal compliance and volume tolerability than patients who were continent, while there was no difference in anal pressures.
A prospective randomized trial of diltiazem and glyceryltrinitrate ointment in the treatment of chronic anal fissure
Authors: Bielecki K. , Kolodziejczak M. 
Published: May 2003

AbstractObjective The aim of this study was to compare prospectively diltiazem with GTN ointment in the treatment of anal fissure.Patients and methods Of 43 outpatients with chronic anal fissure, 22 patients were randomized to topical diltiazem (2%) ointment and 21 patients to glyceryltrinitrate (GTN) (0.5%) ointment twice daily for 8 weeks. During the course of treatment each patient was seen three times. Side‐effects and healing were recorded.Results Healing occurred in 19 of 22 patients treated with diltiazem and 18 of 21 patients were cured with GTN (P = 0.95). Those who were treated with nitroglycerin ointment developed headache and dizzness developed after GTN in 33.3% of cases while no patient had any side‐effects after diltiazem.Conclusions Diltiazem and glyceryltrinitrate (GTN) were equally effective in healing anal fissure but the former resulted in fewer side‐effects.
The correlation between quality of life and functional outcome in ulcerative colitis patients after proctocolectomy ileal pouch anal anastomosis
Authors: Carmon E. , Keidar A. , Ravid A. , Goldman G. , Rabau M. 
Published: May 2003

AbstractObjective  The aim of this study was to evaluate functional outcome and quality of life (QOL) in patients undergoing proctocolectomy ileal pouch anal anastomosis (IPAA), to assess the correlation between functional outcome and QOL, and to identify factors influencing functional outcome and QOL in these patients.Background  IPAA is now considered the procedure of choice for ulcerative colitis. Functional outcome and QOL are important factors in evaluating operative outcome.Methods  All patients with UC who had undergone IPAA at our institute during the period 1990–2001 were included. QOL and functional outcome were evaluated by mailed questionnaires. QOL was scored using the Short Form 36 (SF‐36). Global Assessment of Function Scale was used to evaluate functional outcome.Results  Data were obtained in 77 of 99 patients (78%), with the median age of 38 years. Median follow up time was 4.25 years. The QOL in patients after pelvic pouch procedure was excellent, with scores equal to published norms for the Israeli general population in most scales. Functional outcome and QOL scores correlated strongly (r > 0.5; P < 0.0001) in all dimensions. Older age was associated with lower scores in both functional outcome and QOL scales (P < 0.0001).Conclusions  This study demonstrates a strong association between functional outcome and QOL in patients after IPAA. These patients, however, have a QOL that is comparable with the general population. Age at time of surgery strongly influences both functional outcome and QOL. This finding has to be taken into consideration in pre‐operative counseling.
Pathological staging of epidermoid anal carcinoma for the new era
Authors: Hill J. , Meadows H. , Haboubi N. , Talbot I. C. , Northover J. M. A. 
Published: May 2003

AbstractChemoradiotherapy is the standard treatment for most patients with epidermoid anal cancer. Pre‐treatment staging is based on size for T1‐T3 lesions and clinical and radiological assessment of adjacent organ invasion for T4 lesions. For patients with residual or recurrent carcinoma, anorectal excision offers the best chance of oncological salvage. Pathological staging systems for anorectal excision specimens were validated at the time when surgical treatment was first line therapy. A validated staging system is necessary for salvage surgical excision specimens following an attempt to cure by radiotherapy and chemotherapy for the purpose of prognosis and further treatment planning.
Can umbilical cord blood‐derived progenitors behave like neural cells after exposure to neurogenic signals?
Authors: Zigova T. , Sanberg P. R. 
Published: May 2003

Previous studies have suggested that human umbilical cord blood (HUCB) may serve as a rich source of hematopoietic and nonhematopoietic stem cells and that conditions exist that can coax hematopoietic cells to express neural characteristics. In our laboratory, these cells were tested for several models of neurodegenerative diseases and spinal cord injuries. Through a series of transplantation studies we have begun to uncover the properties of HUCB‐derived cells in neuropoietic regions of the neonatal (1) and aging rodent brain. The systematic application of phenotyping approaches to characterize survival, migratory potential and morphologic properties of the differentiated HUCB progeny within normal/unaffected brain will serve as a base for understanding the potential effect of these cells in the diseased brain.Acknowledgements:  Supported in part by R01 6155039 (TZ). HUCB cells were obtained from Saneron CCEL Therapeutics, Inc. and BioWhittaker, Inc.
PKC is involved in arachidonic acid‐induced choline acetyltransferase activity in spinal cord neurons
Authors: Chalimoniuk M. , Pederson W. A. , Mattson M. P. , Toborek M. 
Published: May 2003

Arachidonic acid (AA) may affect cholinergic neuronal circuits in spinal cord. To test this hypothesis, activity of choline acetyltransferase (ChAT) was studied in cultured spinal cord neurons treated with AA (0.1–10 mm). AA increased ChAT activity in dose‐ and time‐dependent manners. These effects were mimicked by exposure to PMA but inhibited by a coexposure to PKC inhibitors. AA‐mediated increase in ChAT activity also was prevented by treatments with EGTA, indicating the role of calcium. In contrast, cotreatments with 7‐nitroindazole, sodium vanadate, and N‐acetyl‐cysteine had no influence on AA‐induced changes in ChAT activity. These results indicate that the AA‐evoked increase in ChAT activity in spinal cord neurons is mediated by PKC, most likely, at the post‐transcriptional level.Acknowledgements: Supported by grants from KSCHIRT and Philip Morris Research Program.
Developmental pattern of synapsin I expression in mouse somatosensory cortex
Authors: Liguz‐Lecznar M. , Nowicka D. , Skangiel‐Kramska J. 
Published: May 2003

Synapsin I is a member of a synapsin family which are phosphoproteins associated with synaptic vesicles. It is thought to be involved in neuronal development and plasticity. We have shown the existence of two distinct patterns of synapsin I immunostaining in adult mice primary somatosensory cortex (SI). The first consisted of small, dispersed immunoreactive puncta in neuropil. The second is confined to the perikarya and proximal dendrites of the specific class of neurons present in layers IV and VI of SI, probably reflecting the expression of a novel isoform of synapsin I. The aim of this study was to examine the developmental pattern of synapsin I expression in mouse SI cortex. Using immunocytochemistry and Western blot analysis we found that this unique pattern of synapsin I expression in SI appeared between the 2nd and 3rd postnatal week and probably coincides with the increase in the number of synaptic contacts and the development of inhibitory circuits in SI.Acknowledgement: Supported by KBN grant no. 3P04C 008 22.
Can the developing striatum effect the dopaminergic features of hNT neurons in vitro?
Authors: Misiuta I. , McGrogan M. , Willing A. , Sanberg P. , Zigova T. 
Published: May 2003

Our laboratory is investigating the dopaminergic (DA) characteristics of the human, neuronally committed hNT cells for the DA replenishment therapies, like Parkinson's disease. Recent in vitro experiments indicated that hNT cells express markers typical of DA neurons in the substania nigra (SN) including tyrosine hydroxylase (TH), aldehyde dehydrogenase and transcription factor Nurr1. Even though up to 50% of cultured hNT neurons express TH, the long‐term maintenance of DA phenotype may depend on additional factors. Since the striatum is a target tissue for DA neurons in the SN, the goal of the present study is to examine the effect of the developing striatum on the TH expression of hNT neurons in a simplified coculture system.Acknowledgement: Supported by the Shimberg Scholar Award.
Nicotine indirectly increases acetylcholine release in rat striatum
Authors: Machová E. , Žemličková V. , Doležal V. 
Published: May 2003

We investigated the influence of nicotine on the release of ACh from rat striatal slices in the presence of domperidone to remove dopamine inhibition of ACh release. In medium facilitating glutamatergic transmission (with glycine and without Mg) nicotine increased the release of ACh evoked by mild potassium depolarization. This effect of nicotine was not present in resting conditions or when the tissue was fully depolarized. Enhancement of the release of ACh was prevented by tetrodotoxine, nicotinic antagonist mecamylamine, and glutamate NMDA antagonist MK 801. Our results suggest that nicotine increases ACh release indirectly by stimulation of nicotinic receptors on glutamatergic nerve terminals leading to the enhancement of glutamate release. Released glutamate in turn increases firing of cholinergic interneurons and ACh release. Nicotinic receptors on striatal glutamatergic nerve terminals perhaps play a role in the mechanism of striatal cholinergic hyperactivity observed in Parkinson's disease.Acknowledgements: Supported by grants GACR 305/01/0283 and GAAV 5011206.
Effects of NGF on different phenotypes and genotypes of cholinergic murine SN56 cells
Authors: Bielarczyk H. , Szutowicz A. , Madziar B. , Jankowska A. 
Published: May 2003

Nerve growth factor (NGF) is important for differentiation and maintenance of septal cholinergic neurons. It caused concentration‐dependent increase of choline acetyltransferase (ChAT) activity ([EC50%] 1 ng/mL), acetylcholine (ACh) content and morphologic maturation of SN56TrkA(+)p75(+) but not TrkA(–)p75(+) cells. NGF added with cyclic AMP altered significantly differential effects of the latter neither in TrkA(–) nor TrkA(+). However, when cyclic AMP‐predifferentiated cells were treated with NGF alone, it caused suppression of the cholinergic phenotype in both cell lines. Anti‐p75 antibodies totally reversed inhibitory effects of NGF on ChAT activity. Differentiation was accompanied by increase whereas its reversal by decrease of intracellular Ca content. These data indicate that NGF may exert opposite effects on phenotype of cholinergic neurons by p75 receptor signaling pathways and changes in intracellular Ca.Acknowledgement: Supported by KBN project 6P05A 01020.
Protein aggregation in postsynaptic density after transient brain ischemia
Authors: Beręsewicz M. , Zabłocka B. , Domańska‐Janik K. 
Published: May 2003

Brief cerebral ischemia causes changes in synaptic transmission and in consequence in neuronal function manifested in delayed cell death of CA1 hippocampal region. Postsynaptic density (PSD) is composed by a network of interacting proteins, including scaffolding proteins, neurotransmitter receptors, cytoskeletal proteins and protein kinases. PSD dynamically modulates signal transduction what influence the cell fate. We investigated the composition of the PSD network and effect of ischemia on its complexity. Two experimental procedures were applied. The interaction between PSD‐95 and Src, Fyn, Raf‐1, paxilin or NMDA receptor subunits were explored using coimmunoprecipitation method. In addition, the effect of ischemia‐reperfusion on the density of PSD were evaluated by measurement of is solubility. We find out the decrease in solubility of the PSD‐95, NR2A, NR2B and Raf‐1. Of interest, the latter was restricted to surviving regions of hippocampus.Acknowledgement:  Financed by PBZ‐KBN‐002/CD/P05/2000.
Tumor necrosis factor‐alpha aggravates hippocampal damage in rat induced by amyloid beta‐peptide (25–35)
Authors: Stepanichev M. , Yakovlev A. , Onufriev M. , Lazareva N. , Zarubenko I. , Gulyaeva N. 
Published: May 2003

Male Wistar rats received intrahippocampal injections of 3 nmol aggregated Aβ (25–35), intracerebroventricular injections of 0.5 μg human recombinant TNFα or both. Aβ or Aβ + TNFα (but not TNFα alone) induced cell loss in the CA1 pyramidal cell layer, the extension of neuronal degeneration being significantly larger in Aβ + TNFα‐treated group. In hippocampi of both Aβ‐treated groups (but not in TNFα alone‐treated group) reactive gliosis and microglia activation (upregulation of GFAP and isolectin B4 expression) were demonstrated. TUNEL‐positive nuclei were found in the hippocampi of both Aβ‐treated groups. Caspase‐3 activity significantly increased in the ipsilateral hippocampus after the injection of Aβ. However, TNFα prevented Aβ‐induced caspase‐3 activation. The results are discussed from the perspective of dual (neuroprotective and neurodestructive) roles of TNF in the brain.Acknowledgement:  Supported by RBR F (grant # 01‐04‐449477).
HIV‐1 Tat protein disrupts the blood–brain barrier through the oxidative and inflammatory mechanisms
Authors: Toborek M. , Pu H. , Andras I. , Flora G. , Lee Y. W. 
Published: May 2003

Tat protein, which is released from HIV‐infected cells, may play a major role in HIV‐induced pathological processes in the CNS, including HIV‐associated dementia. Therefore, the aim of the present study was to examine the effects of Tat on vascular inflammatory responses as well as blood–brain barrier structure and function both in vitro and in vivo environments. Tat treatment induced cellular oxidative processes, activities of redox‐regulated transcription factors, and expression of inflammatory mediators. Most importantly, Tat disrupted the blood–brain barrier and stimulated monocyte infiltration of the CNS. Disruption tight junction protein integrity appeared to be the underlying mechanism of these effects. Among studied junctional proteins, claudin 5 expression was the most affected by Tat treatment. These data provide evidence that Tat can be involved in the blood–brain barrier breakdown and HIV entry into the brain.Acknowledgements:  Supported by NIH; NS39254, MH63022, and AA013843.
Zinc peptidases and Alzheimer's disease
Authors: Nalivaeva N. N. , Carson J. A. , Fisk L. , Turner A. J. 
Published: May 2003

We have investigated the role of zinc peptidases in metabolism of the amyloid precursor protein (APP) and the effects of hypoxia. Two peptidase families have been studied: the neprilysin (NEP) family which includes, in the brain: NEP, endothelin converting enzyme (ECE) and secreted endopeptidase (SEP). Reactive oxygen species can regulate enzyme activity via modulation of the zinc ion at the active site. Both NEP and ECE can prevent accumulation of amyloid beta peptide by hydrolyzing the peptide. As acute and chronic hypoxia can modulate APP processing, we have investigated the effects of hypoxia in cell culture on the expression and activity of NEP, ECE and SEP. In parallel, we have monitored the expression of another zinc peptidase, alpha‐secretase, that mediates the nonamyloidogenic processing of APP. Overall, zinc peptidases appear neuroprotective and modulation of these activities in pathological states could lead to neurodegeneration.Acknowledgements:  This work was supported by the UK MRC, The Royal Society, INTAS, The Biochemical Society.
The study of the creatine kinase in rat brain during ischemia by magnetization transfer and biochemical analysis
Authors: Dobrota D. , Likavčanová K. , Kašparová S. , Liptaj T. , Prónayová N. , Mlynárik V. , Belan V. 
Published: May 2003

Various methods are used to study the biochemical changes in the central nervous system under normal and pathological conditions. The magnetization transfer 31P magnetic resonance technique was used here to measure the creatine kinase (CK) reaction rate constant in vivo in rats with cerebral ischemia. The measurements indicated that the rate constant of the CK reaction was significantly reduced in the case of chronic brain ischemia in aged rats. The similar reduction of the creatine kinase activity was found in the ischemic rat brain homogenate measured by biochemical analysis. At the same time, corresponding conventional phosphorus magnetic resonance spectra showed negligible or no change in signal intensities of compounds containing macroergic phosphates.Acknowledgements: This work was supported by the Grant Category C and Comenius University Grant No. X/2003.
In vitro1H magnetic resonance spectroscopy differences between meningeoma and astrocytoma
Authors: Likavčanová K. , Dobrota D. , Liptaj T. , Prónayová N. , Galanda M. , Belan V. 
Published: May 2003

Tumor transformation of the human brain cells causes different biochemical changes. Here we employed 1H magnetic resonance spectroscopy to compare the presence of low molecular weight metabolites in meningeoma and astrocytoma tumors by measuring perchloric acid extracts of the cells. In 1H spectra of meningeoma we detected high signal from lactate but were unable to detect any signal of NAA and creatine. In contrast, astrocytoma samples revealed significantly higher level of inositol and glycine and significant decrease in glutamate and glutamine compared with meningeoma but no presence of taurine. Our results suggest that 1H MRS can provide useful information about biochemical changes in different types of brain tumors.Acknowledgements: This work was supported by the Grant Category C and Comenius University Grant No. X/2003.
High‐efficiency transfection of human endothelial cells mediated by cationic lipids
Authors: Kaiser S. , Toborek M. 
Published: May 2003

Cellular transfections provide powerful experimental tools to study gene regulation. However, endothelial cells are difficult to transfect. Therefore, the present studies were performed to optimize transfection techniques in human endothelial cells. To study transfection rates, endothelial cells were transfected with the pGL3 vector, containing the luciferase reporter gene, complexed with several currently available liposomes, such as different Perfect Lipid (pFx) mixtures, DMRIE‐C, or lipofectin. The optimal transfection rate was achieved in cells transfected for 1.5 h with 5 mg/mL of DNA plasmid in the presence of 36 mg/mL of pFx‐7. Transfections mediated by other liposomes were less efficient. Usefulness of the optimized transfection technique was confirmed in cells transfected with NF‐kB or AP‐1‐responsive constructs. We conclude that among several currently available liposomes, pFx‐7 appears to be the most suitable for transfections of cultured human endothelial cells.Acknowledgements: Supported by NIH; NS39254, MH63022, and AA013843.
Nicotine up‐regulates expression of neurotrophic factors and attenuates apoptosis of spinal cord neurons
Authors: Garrido R. , Toborek M. 
Published: May 2003

Nicotine may induce neuroprotection in spinal cord injury; however, the mechanisms of these effects are not fully understood. The present study focused on the effects of nicotine on expression of neurotrophic factors, such as brain‐derived neurotrophic factor (BDNF) and basic fibroblast growth factor (FGF‐2) in a model of spinal cord injury. In this model, cultured spinal cord neurons are exposed to 10 mm arachidonic acid (AA). Exposure to AA diminished expression of BDNF and FGF‐2; however, pretreatment with nicotine protected against these effects. Mecamylamine and α‐bungarotoxin inhibited nicotine‐mediated up‐regulation of BDNF and FGF‐2. Moreover, nicotine, BDNF and FGF‐2 protected against AA‐induced apoptosis of spinal cord neurons. These results suggest that AA can induce apoptosis of spinal cord neurons by depletion of neurotrophic factors and that nicotine can protect against these effects through the alpha7 receptor‐mediated pathway.Acknowledgements:  Supported by grants from Philip Morris Research Program and KSCHIRT.
Nonapoptotic functions of ‘apoptotic’ cascades: caspase‐3 is involved in hippocampal synaptic plasticity
Authors: Kudryashov I. , Kudryashova I. , Gulyaeva N. 
Published: May 2003

Numerous studies establish caspases as essential mediators of cell death. However, many of the same signals that are involved in neuronal death in both physiological and pathological settings may be also involved in developmental and synaptic plasticity in the nervous system. Here we present the experimental data demonstrating the correlation of caspase‐3 activity with population spike amplitude modification in early postnatal ontogenesis suggesting that caspase‐3 is involved in developmental hippocampal synaptic plasticity not related to apoptosis. We also demonstrate that inhibition of caspase‐3 activity in hippocampal slices time‐dependently blocks NMDA‐dependent long‐term potentiation in CA1 region. These results confirm the involvement of caspase‐3 in modulating synaptic plasticity through the cleavage‐dependent alterations in structural proteins and components of signal transduction systems.Acknowledgement:  Supported by RBR F (grant # 01‐04‐449476).