bluuebunny/crossref_metadata_2025_split huggingface dataset:
Variation in plant species richness of different life forms along a subtropical elevation gradient in the Himalayas, east Nepal
Authors: Bhattarai Khem Raj , Vetaas Ole R. 
Published: June 2003

ABSTRACTAim To explore the variation in species richness along a subtropical elevation gradient, and evaluate how climatic variables explain the richness of the different life forms such as trees, shrubs, climbers, herbs and ferns.Location The study was made in a subtropical to warm temperate region in the south‐eastern part of Nepal, between 100 and 1500 m above sea level (a.s.l.).Methods The number of species was counted in six plots (50 × 20 m) in each of the 15 100 m elevation bands covering the main physiognomic structures along an imaginary transect. Each species recorded was assigned to a life form. Potential evapotranspiration (PET, i.e. energy), mean annual rainfall (MAR), and their ratio (MI = moisture index) were evaluated as explanatory variables by means of generalized linear models (GLM). Each variable was tested individually, and in addition MAR and PET were used to test the water‐energy dynamics model for each life form.Results The richness of herbaceous species, including herbaceous climbers, was unrelated to any of the climate variables. PET was strongly negatively correlated with elevation, and the following relationships were found between increasing PET and richness: (i) shrubs, trees and total species (sum of all life forms) showed unimodal responses (ii) ferns decreased monotonically, and (iii) woody climbers increased monotonically. Richness of all woody groups increased monotonically with MAR and MI. The water‐energy dynamics model explained 63% of the variation in shrubs, 67% for trees and 70% for woody species combined.Main conclusions For the various herbaceous life forms (forbs, grasses, and herbaceous climbers) we found no significant statistical trends, whereas for woody life forms (trees, shrubs, and woody climbers) significant relationships were found with climate. E.M. O’Brien's macro‐scale model based on water‐energy dynamics was found to explain woody species richness at a finer scale along this elevational‐climatic gradient.
Intrastriatal Methylmalonic Acid Administration Induces Convulsions and TBARS Production, and Alters Na+,K+‐ATPase Activity in the Rat Striatum and Cerebral Cortex
Authors: Malfatti Carlos Ricardo Maneck , Royes Luiz Fernando Freire , Francescato Leandro , Sanabria Emílio Rafael Garrido , Rubin Maribel Antonello , Cavalheiro Esper Abrão , Mello Carlos Fernando 
Published: June 2003

Summary:  Purpose: Methylmalonic acid (MMA) inhibits succinate dehydrogenase (SDH) and β‐hydroxybutyrate dehydrogenase activity in vitro. Acute intrastriatal administration of MMA induces convulsions through glutamatergic mechanisms probably involving primary adenosine triphosphate (ATP) depletion and free radical generation. In this study we investigated whether the intrastriatal administration of MMA causes lipoperoxidation and alteration in Na+, K+‐ATPase activity ex vivo and characterized the electrographic changes elicited by the intrastriatal administration of this organic acid. Methods: MMA‐induced lipoperoxidation, alterations in Na+, K+‐ATPase activity and electrographic changes were measured by measuring total thiobarbituric acid‐reacting substances and inorganic phosphate release by spectrophotometry, and by depth electrode recording, respectively. Results: We demonstrated that intrastriatal MMA (6 mmol) injection causes convulsive behavior and electrographically recorded convulsions that last ∼2 h. Concomitant with the increase of thiobarbituric acid–reacting substances (TBARS) content, we observed a significant inhibition of Na+,K+‐ATPase activity in the striatum, and activation of Na+,K+‐ATPase activity in the ipsilateral cerebral cortex. Intrastriatal MMA injection increased the content of TBARS in the striatum measured 30 min (32.4 ± 12.0%, compared with the noninjected contralateral striatum) and 3 h (39.7 ± 5.1%, compared with the noninjected contralateral striatum) after MMA injection. TBARS content of the ipsilateral cerebral cortex increased after MMA injection at 30 min (42.1 ± 6.0%) and 3 h (40.4 ± 20.2%), and Na+,K+‐ATPase activity in the ipsilateral cerebral cortex increased during ictal activity (113.8 ± 18%) and returned to basal levels as electrographic convulsions vanished in the cortex. Interestingly, intrastriatal MMA administration induced a persistent decrease in Na+,K+‐ATPase activity only in the injected striatum (44.9 ± 8.1% at 30 min and 68.7 ± 9.4 at 3 h). Conclusions: These data suggest that MMA induces lipoperoxidation associated with Na+,K+‐ATPase inhibition or activation, depending on the cerebral structure analyzed. It is suggested that Na+,K+‐ATPase inhibition may play a primary role in generating MMA‐induced convulsions.
The Spectrum of Long‐term Epilepsy–associated Tumors: Long‐term Seizure and Tumor Outcome and Neurosurgical Aspects
Authors: Luyken Cordelia , Blümcke Ingmar , Fimmers Rolf , Urbach Horst , Elger Christian E. , Wiestler Otmar D. , Schramm Johannes 
Published: June 2003

Summary:  Purpose: To describe the histologic spectrum and clinical characteristics of patients with neuroepithelial tumors and drug‐resistant epilepsy and to analyze clinical data and treatment related to seizure outcome and survival. Methods: Data were analyzed from 207 consecutive patients with intractable epilepsy (aged 2–54 years), who between 1988 and 1999 had ≥50% resection of supratentorial, neuroepithelial tumors. Extent of resection was assessed on postoperative magnetic resonance imaging (MRI); seizure outcome was classified according to Engel's outcome scale; and follow‐up data were prospectively updated. Results: Median follow‐up was eight years (range, 2–14 years). Histologic examination revealed 154 classic epilepsy‐associated tumors (ganglioglioma, dysembryoplastic neuroepithelial tumor, pleomorphic xanthoastrocytoma, and pilocytic astrocytomas) and 53 others (astrocytomas and oligodendrogliomas). Four World Health Organization (WHO) grade III tumors were found (astrocytoma, n = 3; ganglioglioma, n = 1). After surgery, 82% of the patients were seizure free (class I). The following factors were associated with improved seizure outcome: Short duration of epilepsy before surgery, single EEG focus, absence of additional hippocampal sclerosis or cortical dysplasia, transsylvian approach, other than astrocytomas, and complete tumor resection. After 5 years, only nine (4%) patients had tumor recurrence, four (2%) with malignant transformation and death. None of the four patients with anaplastic tumors died. Even patients with astrocytomas of WHO grade II or III showed 10‐year recurrence of only 25% and 10‐year survival of 90%. Conclusions: Tumors associated with long‐term epilepsy should be removed early for two different reasons: high rate of seizure freedom and rare but potential risk of malignant tumor progression. The unexpected long survival of these astrocytomas should be investigated by using immunohistochemistry and molecular biology.
Acute Postoperative Seizures after Frontal Lobe Cortical Resection for Intractable Partial Epilepsy
Authors: Tigaran Simona , Cascino Gregory D. , McClelland Robyn L. , So Elson L. , Richard Marsh W. 
Published: June 2003

Summary:  Purpose: To evaluate the incidence and prognostic importance of acute postoperative seizures (APOSs) occurring in the first week after a focal corticectomy in patients with partial epilepsy of frontal lobe origin. Methods: We retrospectively evaluated 65 patients who underwent a frontal lobe cortical resection for intractable partial epilepsy between April 1987 and December 2000. All patients were followed up for a minimum of 1 year after surgery. Results: APOSs occurred in 17 (26%) patients. None of the following factors was shown to be significantly associated with the occurrence of APOSs: gender, duration of epilepsy, etiology for seizure disorder, use of subdural or depth electrodes, surgical pathology, or postoperative risk factor for seizures. Patients with APOSs were older at seizure onset and at the time of surgery (p = 0.003 and p = 0.05, respectively). At last follow‐up, patients who had APOSs had a seizure‐free outcome similar to that of individuals without APOSs (47.1% vs. 50.0%; p = 0.77). Patients with APOSs appeared less likely to have a favorable outcome [i.e., fewer than three seizures per year and >95% decrease in seizure activity (58.8 vs. 70.8%; p = 0.35)]. This result may not have reached statistical significance because of the sample size. No evidence suggested that precipitating factors or the timing of APOSs was an important prognostic factor. Conclusions: The presence of APOSs after frontal lobe surgery for intractable epilepsy does not preclude a significant reduction in seizure tendency. These findings may be useful in counseling patients who undergo surgical treatment for frontal lobe epilepsy.
Pathobiology and Genetics of Neural Tube Defects
Authors: Finnell Richard H. , Gould Amy , Spiegelstein Ofer 
Published: June 2003

Summary:  Purpose: Neural tube defects (NTDs), including spina bifida and anencephaly, are common congenital malformations that occur when the neural tube fails to achieve proper closure during early embryogenesis. Based on epidemiological and clinical data obtained over the last few decades, it is apparent that these multifactorial defects have a significant genetic component to their etiology that interacts with specific environmental risk factors. The purpose of this review article is to synthesize the existing literature on the genetic factors contributing to NTD risk. Results: To date, there is evidence that closure of the mammalian neural tube initiates and fuses intermittently at four discrete locations. Disruption of this process at any of these four sites may lead to an NTD, possibly arising through closure site–specific genetic mechanisms. Candidate genes involved in neural tube closure include genes of the folate metabolic pathway, as well as those involved in folate transport. Conclusions: Although extensive efforts have focused on elucidating the genetic risk factors contributing to the etiology of NTDs, the population burden for these malformations remains unknown. One group at high risk for having children with NTDs is epileptic women receiving antiepileptic medications during pregnancy. Efforts to better understand the genetic factors that may contribute to their heightened risk, as well as the pathogenesis of neural tube closure defects, are reviewed herein.
McLeod phenotype associated with a XK missense mutation without hematologic, neuromuscular, or cerebral involvement
Authors: Jung Hans H. , Hergersberg Martin , Vogt Marco , Pahnke Jens , Treyer Valerie , Röthlisberger Benno , Kollias Spyros S. , Russo David , Frey Beat M. 
Published: June 2003

BACKGROUND: The X‐linked McLeod neuroacanthocytosis syndrome is a multisystem disorder with hematologic, neuromuscular, and central nervous system (CNS) manifestations. All carriers of the McLeod blood group phenotype examined so far had at least subclinical signs of systemic involvement.STUDY DESIGN AND METHODS: Evaluation of two brothers carrying the McLeod phenotype with neurologic examination, immunohematology, RBC membrane protein Western blotting, analysis of XK DNA sequence and RNA levels, muscle histology including XK/Kell immunohistochemistry, cerebral magnetic resonance imaging (MRI), and quantified positron emission tomography (PET).RESULTS: Immunohematology and Western blotting confirmed presence of the McLeod blood group phenotype. No acanthocytosis or other hematologic anomalies were found. XK gene sequence analysis revealed a missense mutation in exon 3 (E327K). WBC XK RNA levels were not decreased. There were no neuromuscular and CNS signs or symptoms. In addition, no subclinical involvement was discovered on the basis of normal muscle histology with a physiologic pattern of XK and Kell immunohistochemistry, normal cerebral MRI, and quantified PET.CONCLUSION: Known disease‐causing XK gene mutations comprised deletions, nonsense, or splice‐site mutations predicting absent or truncated XK protein devoid of the Kell‐protein binding site. Although the E327K missense mutation was associated with the immunohematologic characteristics of McLeod syndrome, the mutated XK protein seemed to be largely functional. These findings contribute to the understanding of the physiology of XK and Kell proteins, and the pathogenetic mechanisms of acanthocytosis, myopathy, and striatal neurodegeneration in McLeod syndrome.
Apoptotic markers are increased in platelets stored at 37°C
Authors: Bertino A.M. , Qi X.Q. , Li J. , Xia Y. , Kuter D.J. 
Published: June 2003

BACKGROUND: PLTs for transfusion lose viability during storage in blood banking. This loss of viability is accelerated at 37°C, as is the risk of bacterial contamination, and has led to the selection of 22°C as the routine storage temperature. Because PLTs contain an intact apoptotic mechanism, we sought to determine whether PLTs undergo apoptosis during storage and whether storage at 37°C accelerated this process.STUDY DESIGN AND METHODS: PLT‐rich plasma from PLT concentrates was stored at 37 or 22°C in small aliquots or whole bags, with and without cell‐permeable caspase inhibitors. Number of PLTs, pH, LDH level, and 3‐(4,5‐dimethylthiazol‐2‐yl)‐5‐(3‐carboxymethoxyphenyl)‐2‐(4‐sulfophenyl)‐2H‐tetrazolium activity were analyzed over time. PLT lysates were prepared and tested for the presence and activation of apoptotic proteins by enzyme assay and Western blotting.RESULTS: PLT viability was greatly reduced after 1 to 2 days of storage at 37°C; however, signs of apoptosis were evident by 3 hours after temperature shift. In temperature‐stressed PLTs only, a gradual rise in caspase‐3 activity was detected that correlated with the appearance of the 17‐ to 20‐kDa cleavage products of caspase‐3. Gelsolin, a caspase‐3 substrate, underwent cleavage within the same time frame. Bcl‐xL and caspase‐2 also declined significantly; caspase‐9 activity rose. Specific caspase inhibitors could prevent caspase activation but did not improve PLT cellular viability at 37°C.CONCLUSIONS: PLTs contain apoptotic proteins that are activated during PLT storage at 37°C and may account for the rapid decline in PLT cellular viability. Although ineffective here, inhibition of PLT apoptosis may improve PLT cellular viability.
Calcineurin Is Essential for
Candida albicans
Survival in Serum and Virulence
Authors: Blankenship Jill R. , Wormley Floyd L. , Boyce Molly K. , Schell Wiley A. , Filler Scott G. , Perfect John R. , Heitman Joseph 
Published: June 2003

ABSTRACT

Calcineurin is a calcium-activated protein phosphatase that is the target of the immunosuppressants cyclosporin A and FK506. In T cells, calcineurin controls nuclear import of the NF-AT transcription factor and gene activation. In plants and fungi, calcineurin functions in stress responses (e.g., temperature, cations, and pH) and is necessary for the virulence of the fungal pathogen
Cryptococcus neoformans
. Here we show that calcineurin is also required for the virulence of another major fungus that is pathogenic to humans,
Candida albicans. C. albicans
calcineurin mutants had significantly reduced virulence in a murine model of systemic infection. In contrast to its role in
C. neoformans
, calcineurin was not required for
C. albicans
survival at 37°C. Moreover,
C. albicans
calcineurin mutant strains exhibited no defects in known
Candida
virulence traits associated with host invasion, including filamentous growth, germ tube formation, and adherence to and injury of mammalian cells.
C. albicans
calcineurin mutant strains failed to colonize and grow in the kidneys of infected animals and were unable to survive when exposed to serum in vitro. Our studies illustrate that calcineurin has evolved to control aspects of the virulence of two divergent fungal pathogens via distinct mechanisms that can be targeted to achieve broad-spectrum antifungal action.
Ady4p and Spo74p Are Components of the Meiotic Spindle Pole Body That Promote Growth of the Prospore Membrane in
Saccharomyces cerevisiae
Authors: Nickas Mark E. , Schwartz Cindi , Neiman Aaron M. 
Published: June 2003

ABSTRACT

Spore formation in
Saccharomyces cerevisiae
occurs via the de novo synthesis of the prospore membrane during the second meiotic division. Prospore membrane formation is triggered by assembly of a membrane-organizing center, the meiotic outer plaque (MOP), on the cytoplasmic face of the spindle pole body (SPB) during meiosis. We report here the identification of two new components of the MOP, Ady4p and Spo74p. Ady4p and Spo74p interact with known proteins of the MOP and are localized to the outer plaque of the SPB during meiosis II. MOP assembly and prospore membrane formation are abolished in
spo74
Δ/
spo74
Δ cells and occur aberrantly in
ady4
Δ/
ady4
Δ cells. Spo74p and the MOP component Mpc70p are mutually dependent for recruitment to SPBs during meiosis. In contrast, both Ady4p and Spo74p are present at SPBs, albeit at reduced levels, in cells that lack the MOP component Mpc54p. Our findings suggest a model for the assembled MOP in which Mpc54p, Mpc70p, and Spo74p make up a core structural unit of the scaffold that initiates synthesis of the prospore membrane, and Ady4p is an auxiliary component that stabilizes the plaque.
TmkA, a Mitogen-Activated Protein Kinase of
Trichoderma virens
, Is Involved in Biocontrol Properties and Repression of Conidiation in the Dark
Authors: Mukherjee Prasun K. , Latha Jagannathan , Hadar Ruthi , Horwitz Benjamin A. 
Published: June 2003

ABSTRACT

Trichoderma virens
is a mycoparasitic fungus used in biocontrol of soilborne plant pathogens. It inhibits or kills plant-pathogenic fungi through production of antifungal antibiotics and parasitism of hyphae and sclerotia. Conidiation, or the production of asexual spores, an inducible process triggered by light or nutrient stress, is an important trait in survival and also development of formulation products. In many fungi, signaling pathways, including mitogen-activated protein kinase (MAPK) cascades, have been implicated in parasitism of host plants as well as in the production of asexual spores. Here, we have studied the role of a MAPK gene, that for TmkA, in conidiation and antagonistic properties of a biocontrol strain of
T. virens
. Through single- and double-crossover recombination, we obtained three
tmkA
loss-of-function mutants. The TmkA transcript was not detectable in these mutants. The mutants conidiated in the dark, although photoinduction was normal and the light sensitivities of the wild type and the mutant were the same. The mutants had, overall, normal colony morphology, but their radial growth rate was reduced by about 16%, with no decrease in biomass production. Against
Rhizoctonia solani
hyphae, the knockout mutants exhibited mycoparasitic coiling and lysis of host hyphae similar to that of the wild type. The mutants, however, were less effective in colonizing the sclerotia of
R. solani
. On
Sclerotium rolfsii
, the MAPK loss-of-function mutants had reduced antagonistic properties in confrontation assays and failed to parasitize the sclerotia. TmkA-dependent and -independent pathways are thus involved in antagonism against different hosts. Finally, in contrast to the case for other filamentous fungi studied so far, signaling through a MAPK represses, rather than induces, asexual sporulation.
Roles of Tyrosine-Rich Precursor Glycoproteins and Dityrosine- and 3,4-Dihydroxyphenylalanine-Mediated Protein Cross-Linking in Development of the Oocyst Wall in the Coccidian Parasite
Eimeria maxima
Authors: Belli Sabina I. , Wallach Michael G. , Luxford Catherine , Davies Michael J. , Smith Nicholas C. 
Published: June 2003

ABSTRACT

The oocyst wall of apicomplexan parasites protects them from the harsh external environment, preserving their survival prior to transmission to the next host. If oocyst wall formation could be disrupted, then logically, the cycle of disease transmission could be stopped, and strategies to control infection by several organisms of medical and veterinary importance such as
Eimeria
,
Plasmodium
,
Toxoplasma
,
Cyclospora
, and
Neospora
could be developed. Here, we show that two tyrosine-rich precursor glycoproteins, gam56 and gam82, found in specialized organelles (wall-forming bodies) in the sexual stage (macrogamete) of
Eimeria maxima
are proteolytically processed into smaller glycoproteins, which are then incorporated into the developing oocyst wall. The identification of high concentrations of dityrosine and 3,4-dihydroxyphenylalanine (DOPA) in oocyst extracts by high-pressure liquid chromatography, together with the detection of a UV autofluorescence in intact oocysts, implicates dityrosine- and possibly DOPA-protein cross-links in oocyst wall hardening. In addition, the identification of peroxidase activity in the wall-forming bodies of macrogametes supports the hypothesis that dityrosine- and DOPA-mediated cross-linking might be an enzyme-catalyzed event. As such, the mechanism of oocyst wall formation in
Eimeria
, is analogous to the underlying mechanisms involved in the stabilization of extracellular matrices in a number of organisms, widely distributed in nature, including insect resilin, nematode cuticles, yeast cell walls, mussel byssal threads, and sea urchin fertilization membranes.
RacB Regulates Cytoskeletal Function in
Dictyostelium
spp
Authors: Lee Eunkyung , Seastone David J. , Harris Ed , Cardelli James A. , Knecht David A. 
Published: June 2003

ABSTRACT

Thus far, 14 homologues of mammalian Rac proteins have been identified in
Dictyostelium.
It is unclear whether each of these genes has a unique function or to what extent they play redundant roles in actin cytoskeletal organization. To investigate the specific function of RacB, we have conditionally expressed wild-type (WT-RacB), dominant negative (N17-RacB), and constitutively activated (V12-RacB) versions of the protein. On induction, cells expressing V12-RacB stopped growing, detached from the surface, and formed numerous spherical surface protrusions while cells overexpressing WT-RacB became flattened on the surface. In contrast, cells overexpressing N17-RacB did not show any significant morphological abnormalities. The surface protrusions seen in V12-RacB cells appear to be actin-driven protrusions because they were enriched in F-actin and were inhibitable by cytochalasin A treatment. The protrusions in V12-RacB cells did not require myosin II activity, which distinguishes them from blebs formed by wild-type cells under stress. Finally, we examined the functional consequences of expression of wild-type and mutant RacB. Phagocytosis, endocytosis, and fluid phase efflux rates were reduced in all cell lines expressing RacB proteins but the greatest decrease was observed for cells expressing V12-RacB. From these results, we conclude that like other members of the Rho family, RacB induces polymerization of actin but the consequences of activation appear to be different from other
Dictyostelium
Rac proteins so far investigated, resulting in different morphological and functional changes in cells.