bluuebunny/crossref_metadata_2025_split huggingface dataset:
Participation in the National Flood Insurance Program: An Empirical Analysis for Coastal Properties
Authors: Kriesel Warren , Landry Craig 
Published: August 2004

AbstractA perennial question about the National Flood Insurance Program is: how can participation be increased? An empirical analysis of individual‐level data reveals that in a sample of coastal areas the participation rate is 49 percent of eligible properties. Participation responsiveness to price is inelastic, but it has been increased by the mandatory purchase requirements for mortgage borrowers. Easing conditions for participation in the program would probably not reduce flood control measures, such as seawalls, which may degrade beach conditions and coastal ecosystems.
Reinsurance Arrangements Maximizing Insurer's Survival Probability
Authors: Gajek Lesław , Zagrodny Dariusz 
Published: August 2004

AbstractThe article concerns the problem of purchasing a reinsurance policy that maximizes the survival probability of the insurer. Explicit forms of the contracts optimal for the insurer are derived which are stop loss or truncated stop loss depending on the initial surplus, a quota to be spend on reinsurance and pricing rules of both the insurer and the reinsurer.
On the Cost Structure of the Japanese Property‐Casualty Insurance Industry
Authors: Hirao Yukiko , Inoue Tomoo 
Published: August 2004

AbstractThis article tests economies of scale and economies of scope for the property‐casualty insurance companies in Japan. We fit a composite cost function to a set of Japanese firms over the period from 1980 to 1995 and employ an error components model. Our main findings are as follows. First, statistically significant economies of scale are observed in both Japanese firms and foreign firms operating in Japan. Second, economies of scope are also statistically significant for Japanese firms and most of the foreign insurers between the “third sector” products and the rest of the property‐casualty insurance lines.
Turnip yellow mosaic virus: transfer RNA mimicry, chloroplasts and a C‐rich genome
Authors: DREHER THEO W. 
Published: August 2004

SUMMARYTaxonomy:  Turnip yellow mosaic virus (TYMV) is the type species of the genus Tymovirus, family Tymoviridae. TYMV is a positive strand RNA virus of the alphavirus‐like supergroup.Physical properties:  Virions are non‐enveloped 28‐nm T = 3 icosahedrons composed of a single 20‐kDa coat protein that is clustered in 20 hexameric and 12 pentameric subunits. Infectious particles and empty capsids coexist in infected tissue. The genomic RNA is 6.3 kb long, with a 5′m7GpppG cap and a 3′ untranslated region ending in a tRNA‐like structure to which valine can be covalently added. The genome has a distinctive skewed C‐rich, G‐poor composition (39% C, 17% G).Viral proteins:  Two proteins, whose open reading frames extensively overlap, are translated from the genomic RNA. p206, which contains sequences indicative of RNA capping, NTPase/helicase and polymerase activities, is the only viral protein that is necessary for genome replication in single cells. It is produced as a polyprotein and self‐cleaved to yield 141‐ and 66‐kDa proteins. p69 is required for virus movement within the plant and is also a suppressor of gene silencing. The coat protein is expressed from the single subgenomic RNA.Hosts and symptoms:  TYMV has a narrow host range almost completely restricted to the Cruciferae. Experimental host species are Brassica pekinensis (Chinese cabbage) or B. rapa (turnip), in which diffuse chlorotic local lesions and systemic yellow mosaic symptoms appear. Arabidopsis thaliana can also be used. Clumping of chloroplasts and the accumulation of vesicular invaginations of the chloroplast outer membranes are distinctive cytopathological symptoms. High yields of virus are produced in all leaf tissues, and the virus is readily transmissible by mechanical inoculation. Localized transmission by flea beetles may occur in the field.
Homologous soybean and Arabidopsis genes share responsiveness to cyst nematode infection
Authors: MAZAREI MITRA , LENNON KRISTEN A. , PUTHOFF DAVID P. , RODERMEL STEVEN R. , BAUM THOMAS J. 
Published: August 2004

SUMMARYWe previously isolated a partial soybean cDNA clone (D17.1) whose corresponding transcript increases in susceptible roots 1 day post inoculation (dpi) with the soybean cyst nematode, Heterodera glycines. Here we isolated the corresponding full‐length cDNA from a soybean cDNA library and designated this gene of unknown function Gm17.1. Time course RNA gel blot analyses revealed that Gm17.1 mRNA steady‐state levels were elevated in soybean roots following H. glycines infection up to at least 6 dpi. For further in‐depth study we identified a homologous Arabidopsis thaliana gene and designated this gene At17.1. Arabidopsis is successfully infected by the sugar beet cyst nematode (H. schachtii), a close relative of H. glycines. We isolated the At17.1 promoter, fused it to the β‐glucuronidase (GUS) reporter gene, and transformed this construct into Arabidopsis plants as well as soybean hairy roots. Histochemical analysis of plant materials containing the At17.1::GUS construct revealed that the At17.1 promoter is functional in Arabidopsis as well as in soybean and that during normal plant development the At17.1 promoter directs GUS expression predominantly to the vascular tissues and root tips of both plant species. When At17.1::GUS Arabidopsis plants and soybean hairy roots were inoculated with cyst nematodes, strong GUS activity was detected within the cyst nematode‐induced feeding structures. Further tests of At17.1 promoter activity in Arabidopsis revealed that this promoter was induced by auxin, jasmonic acid, mannitol and dehydration. Quantitative real‐time reverse transcription‐polymerase chain reaction assays of At17.1 expression confirmed the observed promoter characteristics. Based on our expression data and the observation that both the soybean and the Arabidopsis homologues behaved in a similar fashion following cyst nematode infection, it is likely that these genes are closely associated with cyst nematode parasitism of plants, potentially with hormone and osmotic changes occurring in the developing nematode feeding cells. Furthermore, these data provide additional insights into the strengths of the Arabidopsis–H. schachtii pathosystem to study cyst nematode–plant interactions in lieu of less tractable pathosystems. This finding is supported by the fact that the Arabidopsis promoter tested here produced similar results in Arabidopsis and soybean.
The jasmonate‐insensitive mutant jin1 shows increased resistance to biotrophic as well as necrotrophic pathogens
Authors: NICKSTADT ANJA , THOMMA BART P. H. J. , FEUSSNER IVO , KANGASJÄRVI JAAKKO , ZEIER JUERGEN , LOEFFLER CHRISTIANE , SCHEEL DIERK , BERGER SUSANNE 
Published: August 2004

SUMMARYJasmonic acid and related oxylipin compounds are plant signalling molecules that are involved in the response to pathogens, insects, wounding and ozone. To explore further the role of jasmonates in stress signal transduction, the response of two jasmonate‐signalling mutants, jin1 and jin4, to pathogens and ozone was analysed in this study. Upon treatment with the biotrophic bacterial pathogen Pseudomonas syringae, endogenous jasmonate levels increased in jin1 and jin4 similar to wild‐type, demonstrating that these mutants are not defective in jasmonate biosynthesis. Jin1 but not jin4 is more resistant to P. syringae and this higher resistance is accompanied by higher levels of salicylic acid. Jin1 is also more resistant to the necrotrophic fungal pathogen Botrytis cinerea and shows wild‐type sensitivity to ozone whereas jin4 is more susceptible to B. cinerea and ozone. These results indicate that the mutations in jin1 and jin4 affect different branches of the jasmonate signalling pathway. Additionally, in this combination of phenotypes, jin1 is unique among all other jasmonate‐related mutants described thus far. These data also provide support for a crosstalk between the jasmonate and salicylate pathways.
Pathogen‐induced resistance and alarm signals in the phloem
Authors: VAN BEL AART J. E. , GAUPELS FRANK 
Published: August 2004

SUMMARYDespite a long‐standing notion of long‐distance signals triggering systemic acquired resistance (SAR), the translocation pathway and the identity of the signals involved have not been determined with any degree of certainty. A critical assessment indicates that, in parallel to signalling via the phloem, alternative modes for SAR induction such as signalling via the xylem or air‐borne signalling by volatile substances may occur. This review further evaluates several classes of compounds as being functional in systemic resistance signalling. Evidence in favour of SAR involvement of phloem‐mobile substances such as salicylic acid, lipid‐derived molecules, reactive oxygen species and components of the antioxidant machinery is contradictory, circumstantial or inconclusive, at best. Nitric oxide bound to proteins or thiols seems a good candidate for signalling, but has not been found in phloem sap thus far. No convincing support of the involvement in SAR of phloem‐mobile substances such as calcium, oligosaccharides, peptides or RNA species, which function in other systemic signalling cascades, has yet been produced. Nevertheless, phloem‐mobile macromolecules are considered as potential tools for SAR given their pivotal role in remote gene expression under stress conditions. In this framework, the existence of several cascades for signal generation along the phloem pathway is envisaged. Finally, recent methods for detection of molecular signals in phloem sap and their expression in companion cells are presented.
The AoPR10 promoter and certain endogenous PR10 genes respond to oxidative signals in Arabidopsis
Authors: MUR LUIS A. J. , STURGESS FAYE J. , FARRELL GILLIAN G. , DRAPER JOHN 
Published: August 2004

SUMMARYThe PR10 class of genes has been associated with plant defence. Previous studies with an asparagus PR10 gene (AoPR1) promoter in heterologous plants suggested that the AoPR10‐GUS transgene was responsive to oxidative signals/stresses. Arabidopsis thaliana AoPR10‐GUS transgenics allowed expression to be compared with that of a close homologue from the large family of PR10 class genes within the Arabidopsis genome. AoPR10‐GUS was induced developmentally at sites of phenylpropanoid accumulation and by wounding, pathogen challenge and treatment with H2O2 but not with salicylic acid (SA), ethylene, methyljasmonate or NO donors. Both wound‐ and pathogen‐associated AoPR10‐GUS expression could be suppressed by superoxide dismutase and the NADPH oxidase inhibitor, diphenylene iodonium. Northern blotting using an Arabidopsis PR10 homologue as a probe revealed transcript up‐regulation by oxidative species generated by glucose oxidase and xanthine oxidase. In Arabidopsis, the AoPR10‐GUS transgene was potentiated by SA and expressed systemically following wounding or challenge with avirulent bacteria. AoPR10‐GUS × npr1‐1 crosses revealed that potentiation and systemic expression was NPR1‐independent. Systemic AoPR10‐GUS expression following elicitation of a hypersensitive response but not wounding was abolished in NahG crosses, suggesting an SA‐mediated potentiating action during SAR (systemic acquired resistance). These data suggest that the AoPR10 promoter reports the expression of reactive oxygen species‐responsive PR10 genes and may indicate systemic changes in oxidative status following either wounding and/or the elicitation of a hypersensitive response in Arabidopsis.
An Arabidopsis mutant with altered hypersensitive response to Xanthomonas campestris pv. campestris, hxc1, displays a complex pathophenotype
Authors: LUMMERZHEIM MARIE , KROJ THOMAS , FERREIRA MARCIO , TRONCHET MAURICE , GODARD FRANÇOIS , VAN MONTAGU MARK , ROBY DOMINIQUE 
Published: August 2004

SUMMARYThe hxc1 mutant was identified by screening an EMS (ethylmethane sulphonate) mutagenized population of Arabidopsis Col‐0 plants for an altered hypersensitive response (HR), after spray inoculation with an HR‐inducing isolate of Xanthomonas campestris pv. campestris (Xcc) (strain 147). The hxc1 mutant shows a susceptible phenotype several days after initiation of the interaction with the avirulent strain. This macroscopically observed phenotype was confirmed by measurement of in planta bacterial growth and by microscopical analysis. Interestingly, the hxc1 mutation acts very specifically. Hxc1 displays a pathophenotype identical to that observed in the wild‐type with several extensively characterized avirulent and virulent bacteria, except in response to Pseudomonas syringae pv. tomato strain DC3000/avrRpm1, for which a partial loss of resistance was observed. Finally, the mutation causes an attenuation of expression of several defence markers regulated through different signalling pathways. Together, these data underline the complexity of this novel defence mutant, and support the hypothesis of a mutation affecting a key component acting during the first steps of the plant defence response leading to resistance to Xcc147 and Pseudomonas syringae pv. tomato containing the avr gene, avrRpm1.
Downstream targets of the Phytophthora infestans Gα subunit PiGPA1 revealed by cDNA‐AFLP
Authors: DONG WUBEI , LATIJNHOUWERS MAITA , JIANG RAYS H. Y. , MEIJER HAROLD J. G. , GOVERS FRANCINE 
Published: August 2004

SUMMARYIn many plant pathogens heterotrimeric G‐proteins are essential signalling components involved in development and pathogenicity. In the late blight oomycete pathogen Phytophthora infestans the G‐protein α subunit PiGPA1 controls zoospore motility and is required for virulence. To identify G‐protein targets and signalling pathways downstream of PiGPA1, we used an optimized cDNA‐AFLP protocol for analysing gene expression profiles in hypovirulent P. infestans strains that were previously generated by silencing the Pigpa1 gene. First, expression profiles in sporangia and mycelium of the wild‐type strain were compared, and this revealed a substantial number of mycelium‐ or sporangia‐specific transcript derived fragments (TDFs). Subsequently, profiles in sporangia of wild‐type, Pigpa1‐silenced mutants and of a strain expressing a constitutively active form of PiGPA1 were compared. From a total of 2860 TDFs, 92 were down‐ and 19 up‐regulated in the Pigpa1‐silenced mutants. A subset of the differential TDFs was cloned and sequenced, and homology searches were carried out against Phytophthora EST and genomic databases and the NCBI database. cDNA‐AFLP expression profiles were verified by Northern blot analysis or RT‐PCR. The power of cDNA‐AFLP for the identification of target genes in knock‐down or gain‐of‐function mutants is discussed.
Gastrointestinal side‐effects of traditional non‐steroidal anti‐inflammatory drugs and new formulations
Authors: Lazzaroni M. , Bianchi Porro G. 
Published: August 2004

SummaryAlthough adverse effects of non‐steroidal anti‐inflammatory drugs (NSAIDs) occur in only a small proportion of users, the widespread use of these drugs has resulted in a substantial overall number of affected persons who experience serious gastrointestinal complications. Dyspeptic symptoms are estimated to occur in 10–60% of NSAID users and lead to discontinuation of treatment in 5–15% of rheumatoid arthritis patients taking NSAIDs. It is now well established that the point prevalence of peptic ulcer disease in patients receiving conventional NSAID therapy ranges between 10 and 30%, representing a 10–30‐fold increase over that found in the general population. One of 175 users of conventional NSAIDs in the USA will be hospitalized each year for NSAID‐induced gastrointestinal damage. The mortality of hospitalized patients remains about 5–10%, with an expected annual death rate of 0.08%. The selective COX‐II inhibitors (rofecoxib, celecoxib, parecoxib, etoricoxib, valdecoxib, lumiracoxib) show consistently comparable efficacy to that of conventional non‐steroidal anti‐inflammatory drugs (NSAIDs) in patients with rheumatoid arthritis and osteoarthritis, but have a significantly reduced propensity to cause gastrointestinal toxicity. In many cases, the gastric effects of therapeutically active doses of COX‐II inhibitors are indistinguishable from placebo. The safety benefits of COX‐2 inhibitors given alone appear similar to combined therapy with conventional NSAIDs and gastroprotective agents. These findings warrant the consideration of COX‐II inhibitors as first‐line therapy in patients requiring long‐term pain control.
Diagnosis and therapy of irritable bowel syndrome
Authors: De Giorgio R. , Barbara G. , Stanghellini V. , Cremon C. , Salvioli B. , De Ponti F. , Corinaldesi R. 
Published: August 2004

SummaryIrritable bowel syndrome (IBS) is one of the most common gut functional diseases, affecting 10–20% of people worldwide. Although most patients do not seek medical help, the disease accounts for huge costs for both patients and health‐care systems and worsens significantly patients' quality of life. Diagnosis is based on the identification of symptoms according to Manning, Rome I and Rome II criteria and exclusion of alarm indicators. IBS symptoms overlap with those of coeliac disease, lactose intolerance, food allergies and bile salt malabsorption. The treatment of IBS is centred on an excellent doctor–patient relationship along with drugs targeting the predominant symptom, especially during exacerbations. Current pharmacological remedies are unsatisfactory due to the high number of patients complaining of lack of response and/or symptom recurrence. Although useful in some IBS patients, the validity of psychotherapy deserves further investigation. A wide array of potentially useful drugs are currently under consideration in pre‐clinical trials. A better understanding of the pathogenetic mechanisms underlying IBS may help to develop more effective drugs for this disease.
Non‐steroidal anti‐inflammatory drugs: who should receive prophylaxis?
Authors: Hawkey C. J. 
Published: August 2004

SummaryNon‐steroidal anti‐inflammatory drugs (NSAIDs) are the major recognized cause of iatrogenic disease, and may cause 100 000 deaths per annum through peptic ulcer complications. A number of risk factors can be identified that indicate patients at high risk. These patients can be managed by substitution of a COX‐2 inhibitor or by prophylaxis with a proton pump inhibitor (PPI). Because risk factors that render patients at high risk of ulcer complications also act in the absence of NSAID use, PPI prophylaxis (or Helicobacter pylori eradication where H. pylori is the risk factor) have much to offer and controlled studies show that the incidence of recurrent peptic ulcer bleeding can be reduced substantially by PPI co‐administration. Substitution of COX‐2 inhibitors also has much to offer, arguably most in those without risk factors (although regulatory authorities do not accept this argument). Recent data show that PPI and COX‐2 inhibitors can play complementary roles in the management of patients with moderate to severe dyspepsia and at high risk of ulcer complications.
What the physician needs to know for correct management of gastro‐oesophageal reflux disease and dyspepsia
Authors: Talley N. J. 
Published: August 2004

SummaryUpper gastrointestinal symptoms are highly prevalent; usually those consulting have multiple symptoms, confounding management. Here, common clinically relevant management issues are considered based on the best available evidence. Regardless of the presenting symptoms, determine if there are any alarm features; these have a low positive predictive value for malignancy but all patients with them should be referred for prompt upper gastrointestinal endoscopy. Ask about medications; of most importance are the non‐steroidal anti‐inflammatory drugs (NSAIDs), both non‐selective and COX‐2 selective. Try to ascertain if the symptom pattern suggests gastro‐oesophageal reflux disease (GERD) or not. Dominant heartburn, however, may be of limited value; if the background prevalence of GERD is 25% and the patient complains of dominant heartburn, then the likelihood that such a patient has GERD as identified by 24‐h oesophageal pH testing is only just over 50%. If reflux disease is strongly suspected and there are no alarm features, give an empirical trial of a proton pump inhibitor (PPI). Symptoms cannot separate adequately functional from organic dyspepsia. Endoscopy in dyspepsia with no alarm features is more costly than an empirical management approach. H. pylori testing and treatment remains in most settings the preferable initial choice for managing dyspepsia without obvious GERD. However, a PPI trial may offer a similar outcome and may be preferable in low H. pylori prevalence areas; head‐to‐head management trials in primary care are lacking.
Definition and diagnosis in portal hypertension – continued problems with the Baveno consensus?
Authors: De Franchis R. 
Published: August 2004

SummaryThe goals of the Baveno workshops were to develop consensus definitions of key events related to portal hypertension and variceal bleeding, and to produce guidelines to facilitate the conduct and reporting of clinical trials. The consensus definitions concern the diagnosis of active bleeding, failure to control bleeding, the criteria to distinguish continuing bleeding from rebleeding, and the means of assessing failure to prevent rebleeding. The guidelines concern the timing of diagnostic endoscopy, the policy for blood volume restitution, the measures to prevent infection and encephalopathy, and the treatment options for acute bleeding, as well as primary and secondary prophylaxis. The intention of the experts who developed the guidelines was that, as feedback from their practical application develops, they should be adapted to better fit the practical needs. The applicability of the Baveno definitions has been evaluated in a study where the definitions of clinically significant bleeding, failure to control bleeding, the time frame for the acute bleeding episode and the definition of rebleeding were tested. The main criticism raised in this study was that tachycardia, one of the criteria that define failure to control bleeding, was misleading in 15% of patients who had the symptom but were not bleeding.
Prognosis of hepatorenal syndrome – has it changed with current practice?
Authors: Angeli P. 
Published: August 2004

SummaryThe Consensus Conference on Hepatorenal Syndrome (HRS) organized by the International Ascites Club in 1994 redefined HRS, introduced new diagnostic criteria that are now widely accepted, and proposed the distinction between two types of HRS: type 1 and type 2. Before the introduction of the new therapeutic options, the median survival of patients with type 1 HRS was only 1.7 weeks, and 6–12 months in patients with type 2 HRS. Liver transplantation (LT) was the first therapeutic option to change the prognosis of cirrhotic patients with HRS and 5‐year survival after LT in patients with HRS is only slightly less than that of transplanted patients without HRS and markedly increased when compared to survival in nontransplanted patients with HRS. Nevertheless, a large proportion of patients die before LT is possible because of the poor prognosis of HRS and the prolonged waiting times in most transplant centres. Other therapeutic approaches were therefore developed to increase survival in patients with HRS. Vasoconstrictors and transjugular intrahepatic portosystemic shunt (TIPS) are the most promising. The administration of vasoconstrictors together with albumin has been shown to reverse type 1 HRS and even to completely normalize renal function in 60–70% of treated patients. To date, four studies assessing TIPS in the management of type 1 HRS have been reported and TIPS insertion was technically successful in all of them. Given the shortage of donors for LT, vasoconstrictor therapy and TIPS strategies may be considered as a bridge to LT in patients with type 1 HRS.