bluuebunny/crossref_metadata_2025_split huggingface dataset:
Milk feeding and dietary patterns predict weight and fat gains in infancy
Authors: Baird Janis , Poole Jason , Robinson Sian , Marriott Lynne , Godfrey Keith , Cooper Cyrus , Inskip Hazel , Law Catherine ,   The Southampton Women's Survey Study Group
Published: August 2008

SummaryCurrent guidelines recommend that infants are exclusively breast fed for the first 6 months of life, with particular solid foods being gradually introduced from 6 months. Our objective was to compare the growth of infants whose feeding most closely followed current guidelines with the growth of infants with other feeding practices.Participants were 1740 infants in a prospective cohort study in Southampton, UK. At 6 and 12 months, infants’ milk feeding was recorded, diets assessed using food frequency questionnaires (FFQ), and anthropometry performed. Principal components analysis was used to identify patterns of foods in the diet using the food intakes assessed by the FFQs. Two patterns (‘infant guidelines’ and ‘adult foods’) explained most variance in infant diet at 6 and 12 months of age. The main outcomes were conditional growth in weight, length and skinfold thickness from 0–6 and 6–12 months.Infants who were breast fed from 0–6 months gained weight, length and adiposity more slowly than formula‐fed infants, independent of age at introduction of solids and maternal factors: compared with infants who were breast fed from 0–6 months, formula‐fed infants gained 0.21 standard deviation scores (SDS) in weight [95% confidence interval (CI) 0.00, 0.42]. Infants whose dietary pattern was most similar to current feeding guidelines, with high frequencies of fresh fruit and vegetables, home‐prepared foods and breast milk, gained weight and skinfold thickness more rapidly from 6 to 12 months than other infants, independent of milk feeding, age at introduction of solids and maternal factors. Compared with infants in the lowest quarter, infants in the highest ‘infant guidelines’ score quarter gained 0.24 SDS [95% CI 0.06, 0.43] in weight and 0.26 SDS [95% CI 0.07, 0.45] in skinfold thickness. Conversely, infants whose diets had the highest frequencies of breads and processed foods gained weight less rapidly from 6 to 12 months than other infants.The extent to which the patterns of diet and growth we have described will influence the current or later health of infants is unknown. We are following up the infants in this study to assess the impact of these patterns beyond the first year of life. These associations should also be examined in other settings and populations.
Nitric oxide production occurs after cytosolic alkalinization during stomatal closure induced by abscisic acid
Authors: GONUGUNTA VIJAY K. , SRIVASTAVA NUPUR , PULI MALLIKARJUNA R. , RAGHAVENDRA AGEPATI S. 
Published: August 2008

ABSTRACTAbscisic acid (ABA) raised the cytosolic pH and nitric oxide (NO) levels in guard cells while inducing stomatal closure in epidermis of Pisum sativum. Butyrate (a weak acid) reduced the cytosolic pH/NO production and prevented stomatal closure by ABA. Methylamine (a weak base) enhanced the cytosolic alkalinization and aggravated stomatal closure by ABA. The rise in guard cell pH because of ABA became noticeable after 6 min and peaked at 12 min, while NO production started at 9 min and peaked at 18 min. These results suggested that NO production was downstream of the rise in cytosolic pH. The ABA‐induced increase in NO of guard cells and stomatal closure was prevented by 2‐phenyl‐4,4,5,5‐tetramethyl imidazoline‐1‐oxyl 3‐oxide (cPTIO, a NO scavenger) and partially by N‐nitro‐L‐Arg‐methyl ester (L‐NAME, an inhibitor of NO synthase). In contrast, cPTIO or L‐NAME had only a marginal effect on the pH rise induced by ABA. Ethylene glycol tetraacetic acid (EGTA, a calcium chelator) prevented ABA‐induced stomatal closure while restricting cytosolic pH rise and NO production. We suggest that during ABA‐induced stomatal closure, a rise in cytosolic pH is necessary for NO production. Calcium may act upstream of cytosolic alkalinization and NO production, besides its known function as a downstream component.
Host–parasite coevolution and patterns of adaptation across time and space
Authors: GANDON S. , BUCKLING A. , DECAESTECKER E. , DAY T. 
Published: August 2008

AbstractThe description of coevolutionary dynamics requires a characterization of the evolutionary dynamics of both the parasite and its host. However, a thorough description of the underlying genetics of the coevolutionary process is often extremely difficult to carry out. We propose that measures of adaptation (mean population fitness) across time or space may represent a feasible alternative approach for characterizing important features of the coevolutionary process. We discuss recent experimental work in the light of simple mathematical models of coevolution to demonstrate the potential power of this phenotypic experimental approach.
NON‐L‐TYPE VOLTAGE‐DEPENDENT CALCIUM CHANNELS CONTROL VASCULAR TONE OF THE RAT BASILAR ARTERY
Authors: Navarro‐Gonzalez Manuel F , Grayson T Hilton , Meaney Kate R , Cribbs Leanne L , Hill Caryl E 
Published: August 2008

SUMMARYConstriction of cerebral arteries is considered to depend on L‐type voltage‐dependent calcium channels (VDCCs); however, many previous studies have used antagonists with potential non‐selective actions. Our aim was to determine the expression and function of VDCCs in the rat basilar artery.The relative expression of VDCC subtypes was assessed using quantitative polymerase chain reaction and immunohistochemistry. Data were correlated with physiological studies of vascular function. Domains I–II of the T channel subtypes expressed in the rat basilar artery were cloned and sequenced.Blockade of L‐type channels with nifedipine had no effect on vascular tone. In contrast, in the presence of nifedipine, hyperpolarization of short arterial segments produced relaxation, whereas depolarization of quiescent segments evoked constriction.The mRNA and protein for L‐ and T‐type VDCCs were strongly expressed in the main basilar artery and side branches, with CaV3.1 and CaV1.2 the predominant subtypes.T‐Type VDCC blockers (i.e. 1 µmol/L mibefradil, 10 µmol/L pimozide and 100 µmol/L flunarizine) decreased intracellular calcium in smooth muscle cells, relaxed and hyperpolarized arteries, whereas nickel chloride (100 µmol/L) had no effect. In contrast with nifedipine, 10 µmol/L nimodipine produced hyperpolarization and relaxation.When arteries were relaxed with 10 µmol/L U73122 (a phospholipase C inhibitor) in the presence of nifedipine, 40 mmol/L KCl evoked depolarization and constriction, which was significantly reduced by 1 µmol/L mibefradil.Sequencing of domains I–II revealed splice variants of CaV3.1, which may impact on channel activity.We conclude that vascular tone of the rat basilar artery results from calcium influx through nifedipine‐insensitive VDCCs with pharmacology consistent with CaV3.1 T‐type channels.
Microarray analysis of mitogenic effects of T3 on the rat liver
Authors: Bungay Anton , Selden Clare , Brown David , Malik Raza , Hubank Mike , Hodgson Humphrey 
Published: August 2008

AbstractBackground and Aim:  A single dose of the thyroid hormone tri‐iodothyronine, T3, can enhance both size and function of normal rodent liver, which is potentially of value in the treatment of liver disease. However the mechanism of this has not been fully elucidated, and it cannot be modeled in vitro. We therefore investigated the transcriptome response to T3 in rat liver in vivo.Methods:  After adult rats were administered 5 µg T3 subcutaneously, a whole rat genome microarray comparing global hepatic gene expression against vehicle‐only treated liver after 3 h was performed.Results:  Informative transcripts which had identifiable gene ontology biological processes were grouped according to function, broadly reflecting general metabolic effects and those linked to cell‐proliferation control. We then compared the transcriptome response after 5‐µg T3 initiating hepatocyte DNA synthesis (mitogenic) with that after 0.1 µg T3, a supraphysiological amount not initiating hepatocyte DNA synthesis.Conclusions:  We compared the results with published results of the response to other primary mitogens, and identified the Gadd45beta/MyD118 gene as a common early factor upregulated during proliferation.
Early upregulation of cyclooxygenase‐2 in human papillomavirus type 16 and telomerase‐induced immortalization of human esophageal epithelial cells
Authors: Zhuang Ze‐Hao , Tsao Sai‐Wah , Deng Wen , Wang Ji‐De , Xia Harry Hua‐Xiang , He Hua , Feng Hui‐Chen , Wang Li‐Dong , Gu Qing , Lam S‐K , Lin Marie C‐M , Kung Hsiang‐Fu , Wong Benjamin C‐Y 
Published: August 2008

AbstractBackground and Aim:  Cyclooxygenase‐2 (COX‐2) plays an important role in the carcinogenesis of esophageal squamous cell carcinoma (ESCC). However, it is not clear whether COX‐2 is involved in the early or late stage of the development of ESCC. The aim of this study was to investigate the role of COX‐2 in the carcinogenesis of ESCC by an immortalized esophageal epithelial cell line.Methods:  Human papillomavirus type 16 (HPV16)–E6/E7 and human telomerase reverse transcriptase (hTERT) transfection were used for immortalization of esophageal epithelial cells. COX‐2‐specific RNA interference was used for the inhibition of COX‐2 expression.Results:  An immortalized esophageal epithelial cell line, NE6‐E6E7/hTERT, was established, which had high proliferation activity but failed to induce colony formation in soft agar. COX‐2 expression was upregulated in the early process of immortalization, while COX‐2 small interfering RNA (siRNA) decreased the Bcl‐2 expression, increased the expression of Bax, and induced cell‐cycle arrest at the G0/G1 phase in NE6‐E6E7/hTERT cells. Expressions of p53, cyclinD1, and the ratio of hyperphosphorylated‐RB/hypophosphorylated‐RB were progressively increased after E6E7 and the subsequent hTERT transfections. These changes were accompanied by the alteration of COX‐2 expression, but could be reversed by COX‐2 siRNA (P < 0.05). P16 expression was significantly downregulated in NE6‐E6E7 or NE6‐E6E7/hTERT cells (P < 0.05), and was not affected by COX‐2 siRNA.Conclusions:  Our results suggest that induction of cyclooxygenase‐2 is essential in the human papillomavirus type 16 and hTERT‐induced immortalization of human esophageal epithelial cells, and that COX‐2 inhibition may be a potential target to block the carcinogenesis of ESCC at the precancerous stage.
Use of health care by young Asian New Zealanders: Findings from a national youth health survey
Authors: Ameratunga Shanthi , Tin Sandar Tin , Rasanathan Kumanan , Robinson Elizabeth , Watson Peter 
Published: August 2008

Aim:  To examine the use of health services and perceived barriers to accessing health care among young Asian New Zealanders.Methods:  Secondary analysis of data from Youth2000, a cross‐sectional survey of secondary school students in New Zealand (NZ) conducted in 2001. Of the 9567 survey participants (aged 12–18 years), this study was restricted to students who identified with an ‘Asian’ ethnic category (n = 922).Results:  Chinese and Indian students (the largest Asian ethnic groups in NZ) reported levels of overall health comparable to NZ European (NZE) students. However, relative to NZE students, Chinese students were more likely to report (i) not having a usual location for health care (adjusted OR 3.28; 95% CI: 2.51–4.43); and (ii) having problems getting health care when they needed it (adjusted OR 1.61; 95% CI: 1.32–1.96). Asian students who had been in NZ for 5 years or less (compared with NZ‐born students), as well as those who did not speak English at home (compared with those who did) were less likely to report having a usual source of health care, even after adjusting for their overall health (adjusted OR 2.13, 95% CI: 1.27–3.56; and adjusted OR 1.69, 95% CI: 1.11–2.56, respectively).Conclusion:  Young Asian New Zealanders are less likely to access health care than their NZE counterparts. The perceived barriers require explicit attention within the broader platforms of health‐care quality, and professional and cultural competence of health‐care services.
Epidemiology and outcome of acute kidney injury in New Zealand children
Authors: Ball Emma F , Kara Tonya 
Published: August 2008

Objectives:  To determine the aetiology, incidence and short‐term outcomes of New Zealand children with acute kidney injury (AKI) requiring renal replacement therapy (RRT) over a 6‐year period.Methods:  A retrospective chart review of all children requiring RRT for AKI from January 2001 to December 2006 at Starship Children's Hospital, Auckland, New Zealand was conducted. The primary outcome was survival to discharge.Results:  A total of 226 children required RRT for AKI over the 6‐year study period. The annual incidence was 4.0 per 100 000 total population under 15 years of age. The commonest causes of AKI were post cardiac surgery (58%), haemolytic uraemic syndrome (17%), sepsis (13%) and glomerulonephritis (4%). The survival rate to hospital discharge was 89%. A total of 40% of all surviving children had one or more abnormalities at the time of discharge suggestive of ongoing renal dysfunction (hypertension, continuing need for antihypertensive medication, reduced estimated glomerular filtration rate or abnormal urinalysis). More Maori and Pacific Island children were treated for AKI than would be expected from population data (P < 0.0001). Sepsis and glomerulonephritis were seen more commonly as causes of AKI in Maori and Pacific Island children compared with New Zealand European children.Conclusion:  In our study, 40% of surviving children had evidence of short‐term renal dysfunction at discharge following AKI. This suggests that all children should undergo a period of follow‐up after any episode of AKI to look for resolution or further development of signs of renal injury.
Anthropometry and renal size of children suffering under sustained conflict in Sri Lanka
Authors: Whitehall John 
Published: August 2008

Aim:  To measure anthropometry, blood pressure and renal lengths of children in a war torn region of Sri Lanka and compare results with local and international standards.Methods:  Measurements of 147 Tamil children in Kilinochchi, north‐east Sri Lanka, were compared with the World Health Organization standards using Anthro 2005 software in a period of relative peace in December 2005. Renal lengths were measured by ultrasound and compared with Australian and Indian data.Results:

2–5 years of age. The weight‐to‐height ratio for combined sexes revealed 13.9% were <−3 standard deviations (SD) and 33.3% <−2 SD. The height‐to‐age ratio revealed 5.6% <−3 SD and 22.2% <−2 SD. The weight‐to‐age ratio revealed 13.9% <−3 SD and 38.9% <−2 SD. The body mass index of 13.9% of children was <−3 SD, of 25% it was <−2 SD. Stunting and wasting is prevalent, and worse than in other areas of Sri Lanka, except in tea estates.
5–12 years. The height‐to‐age ratio for combined sexes revealed 15.7% were <−3 SD and 38.5% <−2 SD. The weight‐to‐age ratio revealed 6.1% were <−3 SD and 47.3% <−2 SD. The body mass index of 64.0% of children was <5th percentile. More children are stunted and wasted in this older group. Girls are more affected than boys.
Renal lengths fell progressively below −2 SD for both age and height when compared with Australian and Indian children.

Conclusion:  Tamil children in Kilinochchi are more stunted and wasted than others in Sri Lanka, except those in the tea estates. Progressive renal stunting because of under‐nutrition may be a mechanism for later disease. The loss of potential for human development can only be addressed by long‐term improvement in access to nutrition.
Transient middle cerebral artery occlusion disrupts the forelimb movement representations of rat motor cortex
Authors: Gharbawie Omar A. , Williams Preston T. J. A. , Kolb Bryan , Whishaw Ian Q. 
Published: August 2008

AbstractInfarcts from proximal middle cerebral artery (MCA) stroke can produce impairments in motor function, particularly finger movements in humans and digit flexion in rats. In rats, the extent of neural damage may be limited to basal ganglia structures or may also include portions of the frontal and parietal cortex in severe cases. Although the primary motor cortex (M1) is anatomically spared in proximal MCA occlusion, its functional integrity is suspect because even a small subcortical infarct can damage neural circuits linking M1 with basal ganglia, brainstem, and spinal cord. This motivated the present study to investigate the neurophysiological integrity of M1 after transient proximal MCA occlusion. Rats, preoperatively trained and non‐preoperatively trained to reach for food, received extensive reach training/testing with the contralateral‐to‐lesion paw for several weeks after MCA occlusion. The forelimb movement representations were assayed from the ipsilateral‐to‐lesion M1 with intracortical microstimulation approximately 10 weeks after MCA occlusion. Digit flexion was impaired during food grasping in rats with relatively small subcortical infarcts and was completely abolished in rats that sustained at least moderate subcortical damage. Corresponding forelimb movement representations ranged from abnormally small to absent. The results suggest that ischemia in subcortical territories of the MCA does not spare the neurophysiological properties of M1 despite its apparent anatomical intactness, probably because of damage sustained to its descending fibers. Thus, M1 dysfunction contributes to the impairments that ensue from proximal MCA occlusion, even when the infarct is limited to subcortical regions.
Clinical heterogeneity and genotype‐phenotype correlations in hereditary spastic paraplegia because of Spatacsin mutations (SPG11)
Authors: Paisan‐Ruiz C. , Nath P. , Wood N. W. , Singleton A. , Houlden H. 
Published: August 2008

Background:  Autosomal recessive hereditary spastic paraplegia (ARHSP) with thin corpus callosum is a distinct and usually severe form of complex hereditary spastic paraplegia classified as SPG11. Recently mutations on SPG11 gene (KIAA1840), which is localized to chromosome 15q13‐q15, were shown to cause the majority of SPG11 cases.Methods:  We analysed the 40 coding exons of this gene in the probands from eight families with complex ARHSP, four of these families had a thin corpus callosum and two has mild thinning.Results:  Three families were identified with novel mutations in the SPG11 gene. One family was of Asian origin with a homozygous nonsense mutation and had a very severe phenotype but only very mild thinning of the corpus callosum. In the other two English families the parents were unrelated and the mutations were compound heterozygotes. In these two families the phenotype was mild and both probands had a thin corpus callosum.Conclusion:  Given the probable mechanism of action of the mutations in the Spatacsin gene, we discuss the probable genotype phenotype correlations in these families. This study confirms the frequent occurrence of Spatacsin mutations in complex ARHSP with genotype phenotype effects and exposes the spectrum of clinical heterogeneity in SPG11.
Activation of nociceptin/orphanin FQ‐NOP receptor system inhibits tyrosine hydroxylase phosphorylation, dopamine synthesis, and dopamine D1 receptor signaling in rat nucleus accumbens and dorsal striatum
Authors: Olianas Maria C. , Dedoni Simona , Boi Marianna , Onali Pierluigi 
Published: August 2008

AbstractNociceptin/orphanin FQ (N/OFQ) has been reported to inhibit dopamine (DA) release in basal ganglia mainly by acting on NOP receptors in substantia nigra and ventral tegmental area. We investigated whether N/OFQ could affect DA transmission by acting at either DA nerve endings or DA‐targeted post‐synaptic neurons. In synaptosomes of rat nucleus accumbens and striatum N/OFQ inhibited DA synthesis and tyrosine hydroxylase (TH) phosphorylation at Ser40 via NOP receptors coupled to inhibition of the cAMP/protein kinase A pathway. Immunofluorescence studies showed that N/OFQ preferentially inhibited phospho‐Ser40‐TH in nucleus accumbens shell and that in this subregion NOP receptors partly colocalized with either TH or DA D1 receptor positive structures. In accumbens and striatum N/OFQ inhibited DA D1 receptor‐stimulated cAMP formation, but failed to affect either adenosine A2A or DA D2 receptor regulation of cAMP. In accumbens slices, N/OFQ inhibited DA D1‐induced phosphorylation of NMDA and α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate glutamate receptors, whereas in primary cultures of accumbal cells, which were found to coexpress NOP and DA D1 receptors, N/OFQ curtailed DA D1 receptor‐induced cAMP‐response element‐binding protein phosphorylation. Thus, in accumbens and striatum N/OFQ exerts an inhibitory constraint on DA transmission by acting on either pre‐synaptic NOP receptors inhibiting TH phosphorylation and DA synthesis or post‐synaptic NOP receptors selectively down‐regulating DA D1 receptor signaling.
The co‐presence of Na+/Ca2+‐K+ exchanger and Na+/Ca2+ exchanger in bovine adrenal chromaffin cells
Authors: Pan Chien‐Yuan , Tsai Ling‐Ling , Jiang Jhih‐Hang , Chen Lih‐Woan , Kao Lung‐Sen 
Published: August 2008

AbstractWe have previously shown that there is high Na+/Ca2+ exchange (NCX) activity in bovine adrenal chromaffin cells. In this study, by monitoring the [Ca2+]i change in single cells and in a population of chromaffin cells, when the reverse mode of exchanger activity has been initiated, we have shown that the NCX activity is enhanced by K+. The K+‐enhanced activity accounted for a significant proportion of the Na+‐dependent Ca2+ uptake activity in the chromaffin cells. The results support the hypothesis that both NCX and Na+/Ca2+‐K+ exchanger (NCKX) are co‐present in chromaffin cells. The expression of NCKX in chromaffin cells was further confirmed using PCR and northern blotting. In addition to the plasma membrane, the exchanger activity, measured by Na+‐dependent 45Ca2+ uptake, was also present in membrane isolated from the chromaffin granules enriched fraction and the mitochondria enriched fraction. The results support that both NCX and NCKX are present in bovine chromaffin cells and that the regulation of [Ca2+]i is probably more efficient with the participation of NCKX.
Truck schedule recovery for solid waste collection in Porto Alegre, Brazil
Authors: Li Jing‐Quan , Borenstein Denis , Mirchandani Pitu B. 
Published: August 2008

AbstractThis paper considers a truck schedule recovery problem in the context of solid waste collection in the city of Porto Alegre, Brazil. When a truck on a scheduled trip breaks down, a backup truck needs to be selected to serve the cargo on that trip and other trucks might be rescheduled in order to gain the minimum operating and delay costs. The problem consists of designing, in the case of a severe disruption in a trip, new schedules taking into account the existing trucks in the system and a set of unfinished and not initiated collection trips, on which the trucks collect the solid waste in fixed routes and empty the loads in one of the several operational recycling facilities. The main objective is to minimize the total distances traveled and delay costs, as well as to obtain balanced assignments of truck unloads into the recycling facilities, due to the social benefits of the solid waste program. We modeled the problem as a mixed‐integer linear problem and used CPLEX to solve it. Finally, computational experiments are conducted on real‐world data. The results show that our approach successfully reduces the distances traveled and delays, simultaneously balancing the number of trucks unloading at each recycling facility, in comparison with the current manual strategy.