bluuebunny/crossref_metadata_2025_split huggingface dataset:
Significance of platelet‐activating factor acetylhydrolase in patients with non‐insulin‐dependent (type 2) diabetes mellitus
Authors: Serban M. , Tanaseanu Cristina , Kosaka T. , Vidulescu Cristina , Stoian Irina , Marta Daciana S. , Tanaseanu S. , Moldoveanu Elena 
Published: May 2007

Abstract Background: Non‐insulin dependent diabetes mellitus (NIDDM) represents an independent risk factor for cardiovascular diseases (CVD), being characterized by a continnous low‐grade inflammation and endothelial activation state. Plasma platelet ‐ activating factor ‐ acetylhydrolases (PAF‐AHs) are a subgroup of Ca2+ ‐independent phospholipase A2 family (also known as lipoprotein‐associated phospholipases A2) that hydrolyze and inactivate the lipid mediator platelet‐activating factor (PAF) and/or oxidized phospholipids. This enzyme is considered to play an important role in inflammatory diseases and atherosclerosis. The present study aims to investigate the relations between the levels of PAF‐AH activity and LDL‐cholesterol/HDL‐cholesterol (LDL‐ch/HDL‐ch) ratio in NIDDM patients as compared to controls. Methods: serum PAF‐AH activity was measured in 50 patients with dyslipidemia, in 50 NIDDM patients and in 50 controls (normal lipid and glucose levels). Total cholesterol, LDL‐ch, HDL‐ch, triglyceride and blood glucose were determined in all subjects. Results: All NIDDM patients display hiperlipidemia, with increased LDL‐ch and triglyceride levels. There is a significant correlation between LDL‐ch levels (especially LDL‐ch / HDL‐ch ratio) and PAF‐AH activity in dyslipidemic and NIDDM patients. Conclusion: Diabetic and dyslipidemic patients have an increased plasma PAF‐AH activity correlated with their LDL‐ch levels and mainly with LDL‐ch / HDL‐ch ratio. Plasma PAF‐AH high levels appear to be important as a risk marker for endothelial dysfunction in patients with NIDDM.
Multiorgan dysfunction syndrome: how water might contribute to its progression
Authors: Lange H. 
Published: May 2007

AbstractMulitorgan dysfunction syndrome (MODS) is one of the most frequent conditions encountered in intensive‐care medicine. MODS is defined as total r partial loss oftwo or more organs with vital functions. The development of acute renal failure (ARF) in MODS leads to an additional aggravation with considerably higher hospital mortality than in other ICU patients with MODS. Whereas dissolved substances involved in the regulation of regional blood flow, endothelial cell injury, microvascular permeability, oxygnation, and nutrition of cells are at the focus of interest in MODS, hardly any scientific attention is paid to their main solvent water. An impaired renal water excretion and an icreased metabolic water volunme requiring exceetion interfere with diffusive and convective oxygen transport through the different fluid compartments. It will be shown first that the ratio of Uosm/Posm appears to be a reliable tools to assess overhydration in ARF. Secondly, the limits of urinary output in response to water intake will be considered. Furthermore, the metabolic water formation by an enhanced degradation of endogenous protein and fat will be discussed. Finally, the daily caloric intake is questioned with respect to energy expenditure and metabolic water formation.
Protein folding in the post‐genomic era
Authors: Yon Jeannine M. 
Published: May 2007

AbstractProtein folding is a topic of fundamental interest since it concerns the mechanisms by which the genetic message is translated into the three‐dimensional and functional structure of proteins. In these post‐genomic times, the knowledge of the fundamental principles are required in the exploitation of the information contained in the increasing number of sequenced genomes. Protein folding also has practical applications in the understanding of different pathologies and the development of novel therapeutics to prevent diseases associated with protein misfolding and aggregation. Significant advances have been made ranging from the Anfinsen postulate to the “new view” which describes the folding process in terms of an energy landscape. These new insights arise from both theoretical and experimental studies. The problem of folding in the cellular environment is briefly discussed. The modern view of misfolding and aggregation processes that are involved in several pathologies such as prion and Alzheimer diseases. Several approaches of structure prediction, which is a very active field of research, are described.
Biomedical applications of protein chips
Authors: Ng Jocelyn H. , Ilag Leodevico L. 
Published: May 2007

AbstractThe development of microchips involving proteins has accelerated within the past few years. Although DNA chip technologies formed the precedent, many different strategies and technologies have been used because proteins are inherently a more complex type of molecule. This review covers the various biomedical applications of protein chips in diagnostics, drug screening and testing, disease monitoring, drug discovery (proteomics), and medical research. The proteomics and drug discovery section is further subdivided to cover drug discovery tools (on‐chip separations, expression profiling, and antibody arrays), molecular interactions and signaling pathways, the identification of protein function, and the identification of novel therapeutic compounds. Although largely focused on protein chips, this review includes chips involving cells and tissues as a logical extension of the type of data that can be generated from these microchips.
Targeting apoptosis in neurological disease using the herpes simplex virus
Authors: Perkins Dana 
Published: May 2007

AbstractHerpes Simplex Viruses type 1 (HSV‐1) and 2 (HSV‐2) cause central nervous system (CNS) disease ranging from benign aseptic meningitis to fatal encephalitis. In adults, CNS infection with HSV‐2 is most often associated with aseptic meningitis while HSV‐1 frequently produces severe, focal encephalitis associated with high mortality and morbidity. Recent studies suggested that the distinct neurological outcome of CNS infection with the two viruses may be due to their distinct modulation of apoptotic cell death: HSV‐1 triggers neuronal apoptosis, while HSV‐2 is neuroprotective. Apoptosis also occurs in the etiology of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and Down's syndrome, and determines the loss of specific neuronal populations and the decline in cognitive functions. Notwithstanding, the therapy of these disorders may rely on the use of replication‐defective HSV‐1 vectors to deliver anti‐apoptotic transgenes to the CNS. However, the recent discovery of a neuroprotective activity innate to the HSV‐2 genome (the ICP10 PK gene) suggests that: i) ICP10 PK may constitute a novel therapeutic approach by targeting both the apoptotic cell death and the cognitive decline, and ii) HSV‐2 may be more suitable than HSV‐1 as a vector for targeting neuronal disease.
Effects of oral supplement of L‐glutamine on diverted colon wall
Authors: Paulo F. L. 
Published: May 2007

AbstractDiverted colorectal segments can present trophic and inflammatory changes. These alterations are of special importance in the patients whose colostomy becomes permanent, as well as in the differential diagnosis with other inflammatory diseases. This study was accomplished to quantify these alterations and to determine if oral supplement of L‐glutamine would avoid them. Twenty‐six adult male Wistar rats were distributed in three groups: control, colostomized and colostomized+L‐glutamine. The colostomized group received a loop colostomy. The colostomized+L‐glutamine group received a colostomy similar to the previous group and oral supplement of L‐glutamine. Partial volumes of all layers of the colonic wall were measured by image analysis stereology. The diversion caused a decrease of partial volumes of the mucosa and the epithelium as well, and also of the height of the intestinal crypts (p<0.05). There was an increase of partial volumes of the lamina propria, of the submucosa and of the muscularis mucosae vs controls (p<0.05). The partial volume of the muscularis propria didn't show significant alteration. The supplementation of L‐glutamine was effective in preventing the atrophy of mucosa and epithelium (p<0.05), also avoiding the increase of partial volumes of the submucosa and lamina propria (p<0.05). This supplement didn't change significantly the muscular layers. In conclusion, colostomy causes the atrophy of the colon wall, mainly due to the atrophy of the epithelium. The supplementation of L‐glutamine is able to avoid these changes.
Relationship between chromosomal changes complexity and disease aggressiveness in myeloid and lymphoid disorders
Authors: Lungeanu Agripina , Arghir Aurora , Lupu Anca , Popescu Delia Mut , Berbec Nicoleta 
Published: May 2007

AbstractIn this paper are presented four cases, with unusual chromosomal abnormalities, identified at the first presentation, among over 100 patients with myeloid and lymphoid acute and chronic leukemias cytogenetically investigated. The complexity and nature of cytogenetic abnormalities was in direct relationship with the disease evolution. The first case, a 22 years old man with acute lymphoblastic leukemia type L3, exhibited many structural changes in bone marrow cells with diploid number of chromosomes: del(3)(q26); del (5)(p13); t(8;14) (q24;q32); del(9)(p11q11);inv(15)(p12qter). The second case, a 62 years old woman, diagnosed as poorly differentiated acute leukemia, refractory to treatment, showed hiperdiploidy (48–54 chromosomes) and 3–4 markers derived from chromosomes 5 and 12. The third case, a young man of 27 years old, diagnosed as acute myeloid leukemia, apart of Philadelphia chromosome, presented trisomy 16, both in diploid and aneuploid cells. None of these three patients did respond to any medical therapy. Their rapid death was a powerful proof of the correlation between the complexity of genome changes and disease aggressiveness. In the fourth case, a constitutional translocation t(3;5)(q26.3;q21) identified in a 72 years old woman with essential thrombocythemia, appeared not to be involved in the etiology of the disease. In this case, the treatment with hydroxyurea was successful and the disease evolution was favourable. In conclusion, we appreciate that in the three cases of myeloid and lymphoid leukemias it was a direct relationship between the complexity of genomic changes and the aggressiveness of the disease.
Evaluation of the cholesterol influence in type II collagen‐induced arthritis in DBA/1J mice: an autoradiographic study
Authors: Hamer Erica R. , Apfel M.I.R. , Carvalho J.J. , Pereira M.J.S. , Levy R.A. 
Published: May 2007

AbstractIn order to verify the cholesterol influence in RA severity in DBA/1J mice, we quantified the cholesterol present in the knee joints of normal (N) and with collagen II induced arthritis (CIA). Forty male DBA/1J mice, were divided in normal (n=20) and CIA group (n=20). Mice in CIA group were injected with 100 μg of collagen II emulsified in Freund's complete adjuvant. Sixteen DBA/1J (8 N and 8 CIA) received an injection of 2.96 × 106 Bq of 3H‐cholesterol and were anesthetized and sacrificed. Semi‐fine sections were covered with LM‐1 emulsion, exposed for six weeks and developed. Collagen induced edema, erythema and dysfunction of knee joints in CIA group. Radioactive cholesterol was located more on the synovial membrane, where we found the greatest density of silver grains, significantly (P<0.0001) higher in group CIA vs. controls (61±2.3 × 18±0.7). We conclude that the cholesterol deposits on the synovial membrane is related to CIA severity.
Selective protection by phosphatidic acid against staurosporine‐induced neuronal apoptosis
Authors: Popescu A.T. , Vidulescu Cristina , Stanciu Cristina L. , Popescu B.O. , Popescu L.M. 
Published: May 2007

AbstractPhosphatidic acid, the main product of lipid breakdown through phospholipase D activation, has been implicated in important signal transduction pathways able to influence cell fate in many ways. The purpose of this work was to determine possible effects of phosphatidic acid on neuronal cell death pathways. Here we used cerebellar granular cell cultures and cell death was triggered with either staurosporine or H2O2. Cell viability was quantified by spectrophotometry, using the 3‐ (4, 5‐dimethylthiazol‐2‐y1)‐2, 5‐diphenyl‐tetrazolium bromide (MTT) test. Staurosporine (1‐3 μM) or H2O2 (50‐800 μM) induced cell death in a dose‐dependent manner. Using fluorescent staining (propidium iodide or annexin V‐Cy3/6‐carboxyfluorescein) we showed that cell death was mostly apoptotic in staurosporine treated cells and mostly non‐apoptotic (necrotic) in H2O2 treated cells. Phosphatidic acid was able to increase cell viability in staurosporine‐, but not in H2O2 ‐ treated cells. We therefore conclude that phosphatidic acid has neuroprotective potential in neurons exposed to stimuli that trigger apoptosis.
Heart failure: a hemodynamic disorder complicated by maladaptive proliferative responses
Authors: Katz A. M. 
Published: May 2007

AbstractHeart failure has traditionally been viewed as a hemodynamic syndrome characterized by fluid retention, high venous pressure, and low cardiac output. Over the past decade, however, it has become clear that because of deterioration and progressive dilatation (remodeling) of the diseased heart, this is also a rapidly fatal syndrome. The importance of prognosis came to be appreciated when clinical trials showed that therapy which initially improves such functional abnormalities, as high venous pressure and low cardiac output, often fail to improve survival, and that some drugs which improve hemodynamics worsen long‐term prognosis. The latter is true for most vasodilators which, in spite of alleviating the adverse short‐term consequences of high afterload, shorten survival. Notable exceptions are ACE inhibitors, whose vasodilator effects do not explain their ability to prolong survival; instead, these drugs slow both deterioration and remodeling of the failing heart. Inotropic agents, while providing immediate relief of symptoms, generally shorten long‐term survival, whereas β‐blockers slow deterioration and remodeling, and reduce mortality. Aldosterone antagonists exert beneficial effects on prognosis that are not easily explained by their diuretic effects, but instead can be explained by their ability to inhibit signaling pathways that stimulate maladaptive hypertrophy, remodeling, apoptosis and other deleterious responses that cause deterioration of the failing heart. These and other findings demonstrate that heart failure is more than a hemodynamic disorder; these patients suffer from maladaptive proliferative responses that cause cardiac cell death and progressive dilatation that play a key role in determining the poor progressive in this syndrome.
Phospholipase A2 modulates respiratory burst developed by neutrophils in patients with rheumatoid arthritis
Authors: Bostan Marinela , Galatiuc C. , Hirt M. , Constantin M.C. , Brasoveanu L.I. , Iordachescu Dana 
Published: May 2007

AbstractActivated by bacterial peptides, phorbol esters, calcium ionophores and other agonists, neutrophils (PMNs) release the proinflammatory mediator, arachidonic acid (AA) via the intervention of phospholipase A2 (PLA2). AA may play an essential role in activation of NADPH‐oxidase, which is involved in the generation of superoxide anion by neutrophils. The present study is focused on the involvement of PLA2 in the respiratory burst developed by PMNs isolated from patients with rheumatoid arthritis (RA). PLA2 exists in very high levels in diseases such as rheumatoid arthritis and may cause acute inflammatory and proliferative changes in synovial structures. The respiratory burst was evaluated as superoxide anion release, using an amplified chemiluminiscence method. The assays were performed using PMNs untreated or treated with different doses of stimulatory reagents (phorbol 12‐myristate‐13‐acetate (PMA), calcium ionophore (A23187)). Our data suggested that PMA stimulated the production of superoxid anion in a dose‐response manner, as compared with A23187, which did not induce a significant release of superoxide anion in PMNs‐RA. The exogenous addition of AA significantly amplified the superoxide anion release by PMNs‐RA stimulated with PMA and to a lesser extent, by PMNs stimulated with A23187. AA has also reversed the inhibitory effect of arachidonyl‐trifluorometylketone and E‐6‐(bromomethylene)tetrahydro‐3‐(1‐naph‐thalenyl)2H‐pyran‐2‐one (BEL) on the superoxide anion release by PMNs‐RA. In conclusion, the differential responses to these two agents suggested that different isoforms of PLA2 were activated by A23187 or PMA, and support the idea that activation of these different PLA2 served distinct functions of PMNs. Therefore, the inhibition of PLA2 enzymes might be of great importance in the immunotherapy of rheumatoid arthritis.
Expression and significance of new tumor suppressor gene PTEN in primary liver cancer
Authors: Dong‐Dong Lu , Xi‐Ran Zhang , Xiang‐Rong Cao 
Published: May 2007

Abstract Objective: To investigate expression and significance of PTEN gene in primary hepatocellular carcinoma (HCC). Methods: Immunohistochemical peroxidase‐conjugated streptavidin (SP) method was used to detect expression of PTEN gene in 120 cases of primary HCC and its adjacent tissue 10 cases of normal liver tissue. The relationship between expression of tumor suppressor gene of PTEN and the percentage of lymph node metastasis of HCC was analyzed. Results: It was shown that PTEN gene was expressed in all 10 cases of normal liver tissues and paracancerous liver tissues. The staining was localized mainly in cytoplasm. Expression of PTEN in 120 cases of HCC were as follows: 12.5% were negative, 17.5% were weak positive, and 70% were strong positive. At time of diagnosis, 33/120 (27.5%) presented lymph node metastasis. Lymph node metastases were present in 80% (12 out of 15) PTEN negative HCC, 57.14% (12 out of 21) PTEN weak positive HCC and only 10.71% (9 out of 84) PTEN intense positive HCC, (P<0.05). Therefore, PTEN tumor suppresor gene malfunction seems to be involed in mtastasing capacity of HCC. Conclusion: This study suggests that PTEN gene was deleted or weakly expressed in primary hepatocellar carcinoma, which is probably related to its tumorigenesis.
Plasma membrane potential interferes with the respiratory burst of peripheral granulocytes
Authors: Livescu Alexandra , Manda Gina , Constantin Carolina , Neagu Monica , Iordachescu Dana 
Published: May 2007

AbstractMembrane potential is involved in the regulation of several immune functions developed by granulocytes. The Na+/K+ gradient across the plasma membrane, mainly generated by the Na+/K+ pump, plays a key role in the maintenance of membrane potential. This study is focused on the correlation between plasma membrane potential and the in vitro receptor ‐ triggered respiratory burst of normal human peripheral granulocytes. The respiratory burst was measured as superoxide anion release by the cytochrome c reduction test and plasma membrane potential was modulated by experimental changes of the extracellular potassium concentration. Results show a differentiated cellular response, depending on the in vivo activation state and on the signals received in vitro by granulocytes via CR3 or FcγR. Alteration of the membrane potassium gradient modulates the respiratory burst of unstimulated and CR3‐activated cells, whilst it does not seem to significantly interfere with the signals delivered by FcγR.
Inflammatory mechanisms associated with brain damage induced by kainic acid with special reference to the interleukin‐1 system
Authors: Oprica M. , Eriksson C. , Schultzberg M. 
Published: May 2007

AbstractThe evidence of inflammatory processes in the clinical manifestations and neuropathological sequelae of epilepsy have accumulated in the last decade. Administration of kainic acid, an analogue of the excitatory amino acid glutamate, induces a characteristic behavioural syndrome and a reproducible pattern of neurodegeneration in several brain areas, closely resembling human temporal lobe epilepsy. Results from studies using the kainic acid model indicate that manipulation of pro‐ and anti‐inflammatory cytokines can modify the outcome with regard to the behavioural syndrome as well as the neuropathological consequences. Interleukin‐1 is one of the most important cytokines and has several actions in the brain that are critical for the host defense against injury and infection, and it is involved in the initiation of early stages of inflammation. It is believed that interleukin‐1 plays a pivotal role in the neuroinflammation associated with certain forms of neurodegeneration, including cerebral ischemia, trauma and excitotoxic brain injury. In this review, we have summarized the experimental data available with regard to the involvement of the interleukin‐1 system in kainic acid‐induced changes in the brain and emphasized the modulatory role of interleukin‐1β in this model of epilepsy.
Immunohistochemical analysis of differentiation in static and mixed prostate cancer spheroids
Authors: Song Hong , O'Connor Kim C. , David Odile , Giordano Carrie L. , Pappas‐LeBeau Helena , Clejan Sanda 
Published: May 2007

AbstractNeoplastic multicellular spheroids are in vitro models of solid tumors employed in drug testing and basic research. This study compares differentiation in static and mixed prostate cancer spheroids. Staining intensity of prostate specific antigen (PSA) was down‐regulated upon mixing from 0.21 ± 0.03 to 0.13 ± 0.03 in LNCaP multicellular spheroids, and from 0.13 ± 0.04 to 0.03 ± 0.02 in DU 145 multicellular spheroids. This was accompanied by 65% increase in the expression of cytokeratins 8 and 18 in DU 145 spheroids. PSA expression extended 60 μm within static spheroids and was disrupted in mixed culture. Diminished PSA expression and spatial organization suggests a more aggressive cancer. Higher cytokeratin expression could result from either differentiation towards a luminal phenotype or activation of the Ras pathway during dedifferentiation. THus, the existing paradigm of differentiation established for normal tissue does not apply for our neoplastic spheroids. Cell dedifferentiation is attributed to improved interstitial transport and synthesis of extracellular matrix.
Cyclooxygenase‐2 modulates cellular growth and promotes tumorigenesis
Authors: Trifan O. C. , Hla T. 
Published: May 2007

AbstractCyclooxygenase (COX)‐2 and the prostaglandins resulting from its enzymatic activity have been shown to play a role in modulating cell growth and development of human neoplasia. Evidence includes a direct relationship between COX‐2 expression and cancer incidence in humans and animal models, increased tumorigenesis after genetic manipulation of COX‐2, and significant anti‐tumor properties of non‐steroidal anti‐inflammatory drugs in animal models and in some human cancers. Recent data showed that COX‐2 and the derived prostaglandins are involved in control of cellular growth, apoptosis, and signal through a group of nuclear receptors named peroxisome proliferator‐activated receptors (PPARs). In this article we will review some of the findings suggesting that COX‐2 is involved in multiple cellular mechanisms that lead to tumorigenesis.