bluuebunny/crossref_metadata_2025_split huggingface dataset:
Suicide in Cyprus 1988–1999
Authors: Zacharakis CA , Hadjivassilis V. , Madianos MG , Papadimitriou GN , Stefanis CN 
Published: February 2005

AbstractSuicide is a universally observed human behavior related to bio-psychological, social and cultural factors. The aim of the present study was to examine suicide in Cyprus, an island that has known many civilizations and cultures. All completed suicide cases in the Christian population of Cyprus during the years 1988–1999 were included in the study and they were analyzed according to age, gender, reported reasons for suicide and suicide methods. The main results indicate that: 1. The mean age-standardized suicide rate is the lowest in Europe, in males (3.08/100,000) and also in females (1.05/100,000). 2. Mean suicide rates increase significantly with age in males only. 3. Female suicide rates are highest in the 15–24 age group. 4. Statistically significant rising trends of male and female suicide rates in the all-ages group. 5. Suicide methods were mostly violent. Among males, the most common methods were poisoning, firearms-explosives, and hanging, while in females, jumping, hanging and poisoning. 6. Mental disorders, physical illness, interpersonal and financial problems were the main reported reasons for suicide. The epidemiological characteristics of suicide in Cyprus might be attributed to a combined effect of social and cultural factors and probably reflect influences from countries to which Cyprus is ethnically, historically or geographically related.
Making and breaking serotonin neurons and autism
Authors: Scott Michael M. , Deneris Evan S. 
Published: February 2005

AbstractDysfunction of brain serotonin system development is hypothesized to contribute to autistic behaviors. The testing of this hypothesis will likely depend on a better understanding of the genes and mechanisms involved in serotonin neuron cell fate specification. In this review we summarize the main features of vertebrate serotonin neuroanatomical development and recent studies that have revealed critical steps in the molecular genetic program that controls serotonin neuron phenotype. We then discuss the potential relevance of these findings to advances in autism research and to new molecular genetic tools under development that will impact future testing of the hypothesis.
The Jeffords Switch and Public Support for Divided Government
Authors: NICHOLSON STEPHEN P. 
Published: February 2005

On 24 May 2001, US Senator James M. Jeffords of Vermont formally announced that he intended to leave the Republican party to become an Independent. Although congressional party switches in the United States are noteworthy because of their infrequency, the Jeffords switch was especially significant because he would caucus with the Democratic party, handing the Democratic party control of the Senate by a one-vote margin. When Jeffords formally left the Republican party on 5 June 2001, it was the first time that partisan control of the US Senate changed hands mid-session. Perhaps most importantly, with the House and presidency under Republican control, the Jeffords move ushered in the return of divided government – split party control of the executive and legislative branches. Indeed, Jeffords' switch received vast amounts of media attention precisely for this reason. The scant attention given to other recent party defectors in the US Senate such as Ben Nighthorse Campbell of Colorado or Robert (Bob) Smith of New Hampshire suggests that the Jeffords switch was much larger than a senator simply changing his party affiliation.Over the last twenty years, split partisan control of the executive and legislative branches occurred in American government roughly two-thirds of the time. Given the frequency of divided government, especially in the post-war era, scholars have written much about its causes. The focus of much of this research concerns voting behaviour, especially ticket-splitting and voting against the president's party at the midterm (midterm voting). Some scholars advocate ‘cognitive madisonianism’ or ‘policy-balancing’ explanations, which posit that a subset of voters with moderate policy preferences intentionally, but not necessarily consciously, engage in ticket-splitting or midterm voting to bring about policy moderation or ‘balance’ among the parties. Others contend that ticket splitting and midterm voting is unintentional, a by-product of factors that shape voting behaviour such as candidates, partisanship and campaigns.
Partitioning, bioavailability and effects of oestrogens and xeno-oestrogens in the aquatic environment
Authors: Langston W.J. , Burt G.R. , Chesman B.S. , Vane C.H. 
Published: February 2005

This review provides insights into the distribution and impact of oestrogens and xeno-oestrogens in the aquatic environment and highlights some significant knowledge gaps in our understanding of endocrine disrupting chemicals. Key areas of uncertainty in the assessment of risk include the role of estuarine sediments in mediating the fate and bioavailability of environmental (xeno)oestrogens (notably their transfer to benthic organisms and estuarine food chains), together with evidence for endocrine disruption in invertebrate populations.Emphasis is placed on using published information to interpret the behaviour and effects of a small number of ‘model compounds’ thought to contribute to oestrogenic effects in nature; namely, the natural steroid 17β-oestradiol (E2) and the synthetic hormone 17α-ethinyloestradiol (EE2), together with the alkylphenols octyl- and nonyl-phenol (OP, NP) as oestrogen mimics. Individual sections of the review are devoted to sources and concentrations of (xeno)oestrogens in waterways, sediment partitioning and persistence, bioaccumulation rates and routes, assays and biomarkers of oestrogenicity, and, finally, a synopsis of reproductive and ecological effects in aquatic species.
Degradation of antifouling booster biocides in water
Authors: Harino Hiroya , Kitano Masaaki , Mori Yoshiaki , Mochida Kazuhiko , Kakuno Akira , Arima Satoshi 
Published: February 2005

The concentrations of booster compounds were surveyed in the port of Osaka, Japan. The concentrations of Sea-Nine 211, Diuron and Irgarol 1051 in water samples from the port of Osaka were in the ranges <0·30–0·55 ng l−1, 13–350 ng l−1, 1·3–77 ng l−1, respectively. Pyrithiones were not detected in water samples. The levels of Diuron and Irgarol 1051 in the port of Osaka were high in the mooring area for small and medium-hull vessels with poor flushing.Susceptibility of bacterial populations in estuarine water to antifouling biocides was studied. Sea-Nine 211, Diuron, Irgarol 1051 and Copper pyrithione dissolved in dimethyl sulfoxide (DMSO) were added to estuarine water and number of colony forming units (CFU) of bacteria in estuarine water was counted using R2A agar plate. The CFU was not decreased at the concentration less than 1·0 mg/l of Diuron, Irgarol 1051 and Copper pyrithione. However, CFU was decreased at 0·1 mg/l of Sea-Nine 211. Degradation of Sea-Nine 211, Diuron, Irgarol 1051 and Copper pyrithione by bacteria in estuarine water was studied using a die-away method. At an initial concentrations of 0·1 mg/l, observed half-lives of Sea-Nine 211 and Copper pyrithione were 10 and 20 days, respectively. In contrast, Diuron and Irgarol 1051 were degraded scarcely during 60 days of culture.Photodegradation of these booster biocides by sunlight and UV light were studied. Under UV, all biocides were below detection limit after one day of irradiation. Under sunlight, Copper pyrithiones were also below detection limits after one day. Drastic decrease of Sea-Nine 211 concentration was observed after one day. Diuron and Irgarol 1051 scarcely decreased during 17 days of sunlight irradiation.
The dextromethorphan analog dimemorfan attenuates kainate‐induced seizures via σ1 receptor activation: comparison with the effects of dextromethorphan
Authors: Shin Eun‐Joo , Nah Seung‐Yeol , Kim Won‐Ki , Ko Kwang Ho , Jhoo Wang‐Kee , Lim Yong‐Kwang , Cha Joo Young , Chen Chieh‐Fu , Kim Hyoung‐Chun 
Published: February 2005

In a previous study, we demonstrated that a dextromethorphan analog, dimemorfan, has neuroprotective effects.
Dextromethorphan and dimemorfan are high‐affinity ligands at σ1 receptors. Dextromethorphan has moderate affinities for phencyclidine sites, while dimemorfan has very low affinities for such sites, suggesting that these sites are not essential for the anticonvulsant actions of dimemorfan.
Kainate (KA) administration (10 mg kg−1, i.p.) produced robust convulsions lasting 4–6 h in rats. Pre‐treatment with dimemorfan (12 or 24 mg kg−1) reduced seizures in a dose‐dependent manner. Dimemorfan pre‐treatment also attenuated the KA‐induced increases in c‐fos/c‐jun expression, activator protein (AP)‐1 DNA‐binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus. These effects of dimemorfan were comparable to those of dextromethorphan.
The anticonvulsant action of dextromethorphan or dimemorfan was significantly counteracted by a selective σ1 receptor antagonist BD 1047, suggesting that the anticonvulsant action of dextromethorphan or dimemorfan is, at least in part, related to σ1 receptor‐activated modulation of AP‐1 transcription factors.
We asked whether dimemorfan produces the behavioral side effects seen with dextromethorphan or dextrorphan (a phencyclidine‐like metabolite of dextromethorphan). Conditioned place preference and circling behaviors were significantly increased in mice treated with phencyclidine, dextrorphan or dextromethorphan, while mice treated with dimemorfan showed no behavioral side effects.
Our results suggest that dimemorfan is equipotent to dextromethorphan in preventing KA‐induced seizures, while it may lack behavioral effects, such as psychotomimetic reactions.

British Journal of Pharmacology (2005) 144, 908–918. doi:10.1038/sj.bjp.0705998
ClC‐3 chloride channel is upregulated by hypertrophy and inflammation in rat and canine pulmonary artery
Authors: Dai Yan‐Ping , Bongalon Shaner , Hatton William J , Hume Joseph R , Yamboliev Ilia A 
Published: February 2005

Cl− channels have been implicated in essential cellular functions including volume regulation, progression of cell cycle, cell proliferation and contraction, but the physiological functions of the ClC‐3 channel are controversial. We tested the hypothesis that the ClC‐3 gene (ClCn‐3) is upregulated in hypertensive pulmonary arteries of monocrotaline‐treated rats, and upregulated ClC‐3 channel aids viability of pulmonary artery smooth muscle cells (PASMCs).
Experimental pulmonary hypertension was induced in rats by a single subcutaneous administration of monocrotaline (60 mg kg−1). Injected animals developed characteristic features of pulmonary hypertension including medial hypertrophy of pulmonary arteries and right ventricular hypertrophy.
Reverse transcriptase–polymerase chain reaction (RT–PCR), immunohistochemistry and Western immunoblot analysis indicated that histopathological alterations were associated with upregulation of the ClC‐3 mRNA and protein expression in both smooth muscle cells of hypertensive pulmonary arteries and in cardiac myocytes.
RT–PCR analysis of mRNA, extracted from canine cultured PASMCs, indicated that incubation with the inflammatory mediators endothelin‐1 (ET‐1), platelet‐derived growth factor (PDGF), interleukin‐1beta (IL‐1β) and tumor necrosis factor alpha (TNFα), but not transforming growth factor beta (TGFβ), upregulated ClC‐3 mRNA.
Adenovirus‐mediated delivery and overexpression of ClC‐3 in canine PASMCs improved cell viability against increasing concentrations of hydrogen peroxide (H2O2, range 50–250 μM).
In conclusion, upregulation of ClC‐3 in rat hypertensive lung and heart is a novel observation. Our functional data suggest that upregulation of ClC‐3 is an adaptive response of inflamed pulmonary artery, which enhances the viability of PASMCs against reactive oxygen species.

British Journal of Pharmacology (2005) 145, 5–14. doi:10.1038/sj.bjp.0706135
The role of joint nerves and mast cells in the alteration of vasoactive intestinal peptide (VIP) sensitivity during inflammation progression in rats
Authors: McDougall Jason J , Barin Ali Kursat 
Published: February 2005

The present study examined the peripheral effects of vasoactive intestinal peptide (VIP) on rat knee joint blood flow during acute and chronic inflammation. The involvement of joint nerves and synovial mast cells on these effects was also investigated.
Prior to blood flow assessment, animals were deeply anaesthetised with ethyl carbamate (urethane; 2 mg kg−1 i.p.). Local application of VIP (10−13–10−9 mol) onto the capsular surface of normal rat knee joints caused a dose‐dependent increase in synovial perfusion with an ED50 of 1.2 × 10−11 mol. The dilator effect of the peptide was transient with the maximal response occurring approximately 1 min after drug administration.
VIP‐induced vasodilatation was blocked by co‐administration of the VIP receptor antagonist VIP6–28 (10−9 mol). The inhibitory effect of the antagonist was consistent across the entire VIP dose range (P=0.01).
The vasoresponsiveness to VIP was significantly attenuated in acutely inflamed joints; however, surgical denervation of acutely inflamed knees re‐established the vasodilator effect of the neuropeptide.
Topical application of VIP to 1‐ and 3‐week adjuvant monoarthritic knees produced a hyperaemic response, which was not significantly different from normal (P=0.06 and 0.73 for 1‐ and 3‐week adjuvant treated joints, respectively).
Stabilisation of synovial mast cells by disodium cromoglycate (cromolyn) pretreatment did not alter the vasoresponsiveness to VIP in acute or chronically inflamed joints.
The vasodilatatory effect of VIP is lost during acute knee joint inflammation and this abrogated effect is neurally dependent. In the chronic phase of knee joint inflammation, VIP‐mediated hyperaemia recovers to normal levels. Synovial mast cells do not influence the vasomotor effects of exogenously applied VIP in inflamed knee joints.

British Journal of Pharmacology (2005) 145, 104–113. doi:10.1038/sj.bjp.0706169
Validation of IKKβ as therapeutic target in airway inflammatory disease by adenoviral‐mediated delivery of dominant‐negative IKKβ to pulmonary epithelial cells
Authors: Catley Matthew C , Chivers Joanna E , Holden Neil S , Barnes Peter J , Newton Robert 
Published: February 2005

Asthma is an inflammatory disease of the lungs and the transcription factor NF‐κB regulates the production of numerous inflammatory mediators that may have a role in the pathogenesis of asthma. Hence, the signalling pathways leading to NF‐κB activation are considered prime targets for novel anti‐inflammatory therapies. The prevention of NF‐κB activity in mice, through the knockout of IKKβ or p65, causes fatal liver degeneration in utero making it difficult to determine the full implications of inhibiting NF‐κB activity in tissues physiologically relevant to human diseases.
This study used adenovirus delivery of a dominant inhibitor of NF‐κB (IκBαΔN) and dominant‐negative IKKα (IKKα(KM)) and IKKβ (IKKβ(KA)) to investigate the role of the individual IKKs in NF‐κB activation and inflammatory gene transcription by human pulmonary A549 cells.
Overexpression of IKKβ(KA) or IκBαΔN prevented NF‐κB‐dependent transcription and DNA binding. IKKβ(KA) also prevented IκBα kinase activity. Similarly, IKKβ(KA) and IκBαΔN overexpression also inhibited IL‐1β‐ and TNFα‐dependent increases in ICAM‐1, IL‐8 and GM‐CSF in addition to IL‐1β‐mediated increases in cyclooxygenase‐2 expression, whereas IKKα(KM) overexpression had little effect on these outputs.
IKKβ(KA) also reduced cell viability and induced caspase‐3 and PARP cleavage regardless of the stimuli, indicating the induction of apoptosis. This effect seemed to be directly related to IKKβ kinase activity since IκBαΔN only induced PARP cleavage in TNFα‐treated cells.
These results demonstrate that inhibition of IKKβ and NF‐κB suppresses inflammatory mediator production and reduces A549 cell viability. Thus, novel therapies that target IKKβ could have potent anti‐inflammatory effects and may be beneficial in the treatment of certain cancers.

British Journal of Pharmacology (2005) 145, 114–122. doi:10.1038/sj.bjp.0706170
Elevated erythrocyte phosphoribosylpyrophosphate and ATP concentrations in Japanese sumo wrestlers
Authors: Nishida Y. , Akaoka I. , Hayashi E. , Miyamoto T. 
Published: February 2005

1. Japanese sumo wrestlers have a diet rich in energy, which results in marked obesity. Their plasma urate and triglyceride levels were significantly elevated.2. Erythrocyte phosphoribosylpyrophosphate (PRPP) and ATP concentrations in sumo wrestlers were significantly elevated when compared to the levels in control subjects.3. There were no significant differences in erythrocyte PRPP synthetase (EC2.7.6.1), purine nucleoside phosphorylase (EC2.4.2.1) and hypoxanthine guanine phosphoribosyl transferase (EC2.4.2.8) activities between sumo wrestlers and control subjects.4. Erythrocyte adenosine kinase (EC2.7.1.20), adenosine deaminase (EC3.5.4.4) and adenine phosphoribosyl transferase (EC2.4.2.7) activities in sumo wrestlers were significantly elevated.5. It seems that sumo wrestlers have an increased turnover of adenine nucleotides which may contribute to hyperuricaemia.
Excess energy intake promotes the development of hypoalbuminaemia in rats fed on low-protein diets
Authors: Lunn P. G. , Austin S. 
Published: February 2005

1. A group of rats were givenad lib.a diet with a protein-energy: total energy (P:E) value of 0·03. Other animals received the same protein intake (g/kg body-weight per d) as this group, but had their energy consumption reduced to either 90, 80. 70, 60 or 50% of thead lib.value.2. The restricted growth rate of rats fed on the P:E – 0·03 dietad lib.has been shown to be due entirely to their insufficient protein consumption. In contrast, energy intake was far in excess of that required for maintenance and the limited amount of growth.3. Carcass analysis demonstrated that some of the excess energy intake was stored as fat, but a greater part had been dissipated, presumably by diet-induced thermogenesis.4. The plasma concentration of triiodothyronine (T3) was elevated in all animals consuming excess energy and was significantly related to both the total surplus and the amount of energy dissipated.5. In the group of animals restricted to 50% of thead lib.intake, energy rather than protein appeared to be the factor limiting growth. Energy intake was below estimated requirements for maintenance and was associated with values for plasma T3that were lower than those found in well-fed control rats.6. Although all the animals had similar protein intakes, plasma albumin concentration differed between the groups and was found to be inversely proportional to the energy intake. Thus it was lowest in animals receiving foodad lib.and rose to near normal values in the most-severely-restricted rats.7. It is suggested that hypoalbuminaemia, and perhaps other features of protein deficiency, seen in animals fed on low-P:E diets may occur as an undesirable consequence of the metabolic response required to deal with excess energy consumption.
Dietary-induced obesity: effect of dietary fats on adipose tissue cellularity in mice
Authors: Bourgeois Francine , Alexiu Andre , Lemonnter Daniel 
Published: February 2005

1. Male and female mice, 4 weeks old, were fedad lib.diets containing various amounts of lard (0–300 g/kg) or various kinds of dietary fats (300 g/kg) for 13 weeks. Fat cell number and size were determined by a histological method in three different adipose sites.2. Lard at 200 g/kg diet (43% energy from lipids) was sufficient to promote fat cell hyperplasia in the parametrial fat. Hyperplasia was also observed in the subcutaneous fat in males. The relationship between fat cell hypertrophy and the level of lard in the diet was dependent on site and sex.3. Obesity was produced whatever the kind of dietary fat eaten: lard, beef tallow, sunflower oil or soya-bean oil. In the subcutaneous depot of males given lard, fat cell size and number were increased, but only cell hypertrophy was observed in those given soya-bean oil. In the female groups of mice fat cell hyperplasia or hypertrophy or both were related to the adipose site but not the kind of dietary fat.4. It is concluded that dietary fats of different origin can induce obesity in mice. The effects on adipose tissue cellularity depend on the levels and kind of fat eaten, the adipose site and sex.
Effect of pharmacological doses of ascorbic acid on the hepatic microsomal haemoproteins in the guinea-pig
Authors: Sutton Judith L. , Basu T. K. , Dickerson J. W. T. 
Published: February 2005

1. Ascorbic acid deficiency results in a reduction in the activity of the hepatic mixed function oxidase systems in the guinea-pig. In this study, male Dunkin-Hartley guinea-pigs were given 0, 50, 100, 200 or 300 mg ascorbic acid/d in two equal doses in buffered sucrose solution (200 g/l) for 4 d. Controls received an equal volume of sucrose solution.2. A dose of 50 mg ascorbic acid/d resulted in a significant rise in the specific activities of both cytochromes P-450 and b5. At doses of 200 and 300 mg ascorbic acid/d the concentration of both haemoproteins was significantly lower than the control values. These effects were mirrored by total microsomal haem concentration.3. These results suggest that when given in large doses, ascorbic acid ceases to act simply as a vitamin and should be considered a drug competing for substrates and cofactors with co-administered drugs and endogenous substrates such as cholesterol.
Artificial rearing of pigs
Authors: Newport M. J. , Keal H. D. 
Published: February 2005

1. Pigs weaned at 2 d of age were given diets in which a functional fish-protein concentrate (FFPC) supplied 0 (diet U), 350 (diet H), 525 (diet I) or 700 (diet G) g crude protein (nitrogen × 6·25, CP)/kg total CP. The remainder of the CP was supplied by dried skim-milk and whey. The diets were reconstituted (200 g dry matter (DM)/l), from two spray-dried powders (diets U and G) and these were mixed in the proportions 1:1 and 1:3 (v/v) to give diets H and I respectively. All four diets were given at hourly intervals on a scale based on live weight, and supplemented with vitamins and minerals. All diets contained the same amounts of calcium, phosphorus, sodium and potassium.2. In an experiment to 28 d of age with ten pigs/diet, performance was inversely related to the amount of FFPC in the diet. One pig (diet I) and four pigs (diet G) died after scouring. In healthy pigs, N retention (g/d per kg live weight) was not affected by partial replacement of dried skim-milk (diet H).3. Digestion of protein was studied in a further experiment with eight pigs/diet, killed at 7 d of age and at 1 h after a feed. The amount, pH, DM and total N contents of the digesta in the stomach were also inversely related to the amount of FFPC in the diet.4. FFPC had no consistent effect on proteolytic enzymes. Greater amounts of trypsin and chymotrypsin were present in the distal compared with the proximal region of the small intestine, but source of dietary protein had no effect.5. The proportion of non-protein-N in the total N in digesta from the small intestine was lower in pigs receiving FFPC suggesting that this protein may be more resistant to proteolysis than milk proteins. The apparent absence of an increase in enzyme secretion when FFPC was given could, therefore, explain the decrease in performance.6. Some general effects of non-milk proteins from this series of experiments in the baby pig are discussed. It is suggested that performance may be inversely related to the rate of gastric emptying, as indicated by the amount of DM in the stomach. Unlike milk, other sources of protein did not coagulate in the stomach, and reduced the pH, DM and total N contents of the digesta. Giving diets containing a single-cell protein did appear to stimulate proteolytic enzyme secretion, unlike fish or soya-bean proteins.