bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reaction of Melon (Cucumis meloL.) Cultivars toMonosporascus cannonballus(Pollack &Uecker) and their Effect on Total Phenol, Total Protein and Peroxidase Activities
Authors: Salari Mohammad , Panjehkeh Naser , Nasirpoor Zahra , Abkhoo Javad 
Published: December 2012

AbstractEighteen melon cultivars were screened for resistance toMonosporascus cannonballusunder greenhouse conditions. The melon cultivars were grown in pasteurized sand, which had been inoculated with a high level (60CFUs/g of soil) ofM. cannonballusmycelium from culture. CultivarsNabijani,Sfidak khatdar,Sfidak bekhat,Ghandak,Mollamosai,Chappat,Hajmashallahi andShadgan were moderately resistant toM. cannonballusbut all other melon cultivars were moderately to highly susceptible (HS) to this pathogen. A second screening was performed for resistance toM. cannonballusunder greenhouse conditions. In the second screening, cultivarsNabijani,Sfidak khatdar,Sfidak bekhat,Ghandak,Mollamosai,Chappat,Hajmashallahi andShadgan were moderately resistant toM. cannonballus. To examine the melon resistance mechanism againstM. cannonballus,the activities of total phenol, total protein and peroxidase in two melon cultivarsNabijani (as resistant) and Khaghani (as susceptible) were determined at 0, 24, 48 and 72 h after inoculation. Inoculated resistant cultivar roots had always higher content of total phenol, total protein and peroxidase than the corresponding inoculated susceptible cultivar roots. The results indicated that there was a relationship between resistance inNabijani and accumulation of total phenol, total protein and peroxidase.
Hepatitis viruses (other than hepatitis B and C viruses) as causes of hepatocellular carcinoma: an update
Authors: Kew M. C. 
Published: December 2012

SummaryChronic hepatitis B and C virus infections are universally accepted as causes of hepatocellular carcinoma in humans. Hepatitis A and E viruses cause only acute self‐limiting infections of the liver. Of the remaining hepatitis viruses ‐ Delta hepatitis, hepatitis G (GB‐C), TT and SEN ‐ all have at some time been incriminated as causes of hepatocellular carcinoma. Delta hepatitis virus requires helper functions from hepatitis B virus to become invasive. Chronic Delta/hepatitis B viral co‐infection runs a more severe course than that resulting from chronic hepatitis B virus infection alone, with progression to cirrhosis being more likely and more rapid. A substantial majority of the early studies did not find an increased incidence of hepatocellular carcinoma in co‐infected individuals. But more recently, an increased incidence of the tumour has been recorded more often than no increase. Further studies are needed to draw a firm conclusion with regard to the hepatocarcinogenic effect of dual Delta/hepatitis B virus co‐infection. With one exception, no published study (of 13) has incriminated chronic infection with hepatitis G virus as a cause of hepatocellular carcinoma. The dissenting study, published in 1999, was the only one performed in the United States. Fewer studies of the hepatocarcinogenic effect of TT virus have been performed. Apart from one study, published in 1999, no convincing evidence is available that supports a causal role for TT virus in hepatocarcinogenesis. The exception was in Japanese patients with high hepatitis C viral loads but independent of chronic hepatitis C virus infection. No evidence has been produced to indicate that SEN virus causes hepatocellular carcinoma.
The 2‐methylcitrate cycle is implicated in the detoxification of propionate in Toxoplasma gondii
Authors: Limenitakis Julien , Oppenheim Rebecca D. , Creek Darren J. , Foth Bernardo J. , Barrett Michael P. , Soldati‐Favre Dominique 
Published: December 2012

SummaryToxoplasma gondii belongs to the coccidian subgroup of the Apicomplexa phylum. The Coccidia are obligate intracellular pathogens that establish infection in their mammalian host via the enteric route. These parasites lack a mitochondrial pyruvate dehydrogenase complex but have preserved the degradation of branched‐chain amino acids (BCAA) as a possible pathway to generate acetyl‐CoA. Importantly, degradation of leucine, isoleucine and valine could lead to concomitant accumulation of propionyl‐CoA, a toxic metabolite that inhibits cell growth. Like fungi and bacteria, the Coccidia possess the complete set of enzymes necessary to metabolize and detoxify propionate by oxidation to pyruvate via the 2‐methylcitrate cycle (2‐MCC). Phylogenetic analysis provides evidence that the 2‐MCC was acquired via horizontal gene transfer. In T. gondii tachyzoites, this pathway is split between the cytosol and the mitochondrion. Although the rate‐limiting enzyme 2‐methylisocitrate lyase is dispensable for parasite survival, its substrates accumulate in parasites deficient in the enzyme and its absence confers increased sensitivity to propionic acid. BCAA is also dispensable in tachyzoites, leaving unresolved the source of mitochondrial acetyl‐CoA.
Interocular differences in visual latency induced by reduced‐aperture monovision
Authors: Plainis Sotiris , Petratou Dionysia , Giannakopoulou Trisevgeni , Radhakrishnan Hema , Pallikaris Ioannis G , Charman W Neil 
Published: December 2012

AbstractPurposeTo explore the interocular differences in the temporal responses of the eyes induced by the monocular use of small‐aperture optics designed to aid presbyopes by increasing their depth‐of‐focus.MethodsMonocular and binocular pattern‐reversal visual evoked potentials (VEPs) were measured at a mean photopic field luminance of 30 cd/m2 in seven normal subjects with either natural pupils or when the non‐dominant eye wore a small‐aperture contact lens (aperture diameter 1.5, 2.5 or 3.5 mm, or an annular opaque stop of inner and outer diameters 1.5 and 4.0 mm respectively). Responses were also measured with varying stimulus luminance (5, 13.9, 27.2 and 45 cd/m2) and a fixed 3.0 mm artificial pupil.ResultsMean natural pupil diameters were 4.7 and 4.4 mm under monocular and binocular conditions respectively. The small‐aperture contact lenses reduced the amplitude of the P100 component of the VEP and increased its latency. Inter‐ocular differences in latency rose to about 20–25 ms when the pupil diameter of the non‐dominant eye was reduced to 1.5 mm. The measurements with fixed pupil and varying luminance suggested that the observed effects were explicable in terms of the changes in retinal illuminance produced by the restrictions in pupil area.ConclusionsThe anisocoria induced by small‐aperture approaches to aid presbyopes produces marked interocular differences in visual latency. The literature of the Pulfrich effect suggests that such differences can lead to distortions in the perception of relative movement and, in some cases, to possible hazard.
Reducing saturated fatty acids in Arabidopsis seeds by expression of a Caenorhabditis elegans 16:0–specific desaturase
Authors: Fahy Deirdre , Scheer Barbara , Wallis James G. , Browse John 
Published: December 2012

SummaryPlant oilseeds are a major source of nutritional oils. Their fatty acid composition, especially the proportion of saturated and unsaturated fatty acids, has important effects on human health. Because intake of saturated fats is correlated with the incidence of cardiovascular disease and diabetes, a goal of metabolic engineering is to develop oils low in saturated fatty acids. Palmitic acid (16:0) is the most abundant saturated fatty acid in the seeds of many oilseed crops and in Arabidopsis thaliana. We expressed FAT–5, a membrane‐bound desaturase cloned from Caenorhabditis elegans, in Arabidopsis using a strong seed‐specific promoter. The FAT‐5 enzyme is highly specific to 16:0 as substrate, converting it to 16:1∆9; expression of fat‐5 reduced the 16:0 content of the seed by two‐thirds. Decreased 16:0 and elevated 16:1 levels were evident both in the storage and membrane lipids of seeds. Regiochemical analysis of phosphatidylcholine showed that 16:1 was distributed at both positions on the glycerolipid backbone, unlike 16:0, which is predominately found at the sn‐1 position. Seeds from a plant line homozygous for FAT–5 expression were comparable to wild type with respect to seed set and germination, while oil content and weight were somewhat reduced. These experiments demonstrate that targeted heterologous expression of a desaturase in oilseeds can reduce the level of saturated fatty acids in the oil, significantly improving its nutritional value.
Orphan Rocker Tracks: A Variant of Friction Melanosis in an Institutionalized Child
Authors: Diamond Gary , Amitai Dan Ben 
Published: December 2012

AbstractFriction melanosis is an acquired pigmentary disorder consisting of diffuse, brown pigmentation resulting from repeated rubbing of affected areas of the skin. An institutionalized child whose lower back was subjected to intense and repeated rocking displayed the characteristic lesions.
Predictive value of clinical chorioamnionitis in extremely premature infants
Authors: Tokumasu Hironobu , Hinotsu Shiro , Kita Fumiyo , Kawakami Koji 
Published: December 2012

AbstractBackgroundClinical chorioamnionitis and histological chorioamnionitis are important risk factors for neonatal complications and neurodevelopmental impairment in premature infants. It is unclear, however, whether a diagnosis of clinical chorioamnionitis is sufficient to establish a diagnosis of histological chorioamnionitis. The aim of this study was to evaluate the predictive value of clinical chorioamnionitis in the diagnosis of histological chorioamnionitis in extremely premature infants.MethodsThis study was a secondary analysis of data from the Neonatal Research Network in Japan, a population‐based cohort study aimed at identifying the clinical characteristics and morbidity of very low‐birthweight infants. Data for extremely premature infants <28 weeks' gestational age from 2003 to 2007, were used. Subset analysis investigated positive predictive value by gestational age.ResultsOf the 2470 infants analyzed, 786 were diagnosed with clinical chorioamnionitis and 1129 with histological chorioamnionitis. The positive predictive value of clinical chorioamnionitis for histological chorioamnionitis was 86.6% (681/786; 95% confidence interval [CI]: 84.4–88.6%), sensitivity was 60.3% (681/1129; 95%CI: 58.8–61.7%), and specificity was 92.2% (1236/1341; 95%CI: 90.9–93.3%). In subset analysis, the positive predictive value was particularly high at 23 weeks of gestation (89.1%; 115/129), with sensitivity of 65.3% (115/176) and specificity of 89.6% (120/134).ConclusionsThe finding that clinical chorioamnionitis is a useful predictor of histological chorioamnionitis provides important insights into the relationship between these two diagnoses, and has important implications in determining the appropriate timing of delivery of extremely premature infants.
The modality‐specific contribution of peptidergic and non‐peptidergic nociceptors is manifest at the level of dorsal horn nociresponsive neurons
Authors: Zhang Jie , Cavanaugh Daniel J. , Nemenov Michael I. , Basbaum Allan I. 
Published: December 2012

Key points
Ablation of TRPV1+/peptidergic or of MrgprD+/non‐peptidergic nociceptors produces modality‐specific deficits in the behavioural responses to heat and mechanical stimuli, respectively. Noxious heat‐induced dorsal horn Fos expression is also eliminated, despite the heat responsiveness of the non‐peptidergic nociceptors.
To assess whether this modality‐specific contribution is manifest at the level of individual spinal neurons, we made extracellular recordings from mouse dorsal horn after selective ablation of the two nociceptor populations.
Intrathecal capsaicin, which ablated the TRPV1+ nociceptors, abolished responsiveness of superficial and deep dorsal horn neurons to noxious heat, with no change in response to noxious mechanical stimulation.
Ablation of MrgprD+ afferents did not alter the response to noxious heat but reduced the firing of dorsal horn neurons in response to noxious mechanical stimulation.
These findings argue strongly that TRPV1+ and MrgprD+ nociceptors provide modality‐specific contributions to the response properties of spinal cord neurons.
Abstract  We previously demonstrated that genetic and/or pharmacological ablation of the TRPV1+/peptidergic or the MrgprD+/non‐peptidergic subset of nociceptors produced selective, modality‐specific deficits in the behavioural responses to heat and mechanical stimuli, respectively. To assess whether this modality‐specific contribution is also manifest at the level of spinal cord neuron responsiveness, here we made extracellular recordings from lumbar dorsal horn neurons of the mouse in response to graded thermal and mechanical stimulation. We found that, following intrathecal injection of capsaicin to eliminate the central terminals of TRPV1+ nociceptors, neurons in the region of laminae I and V of the spinal cord lost responsiveness to noxious heat (whether generated by a contact heat probe or diode laser), with no change in their response to noxious mechanical stimulation. In contrast, ablation of MrgprD+ afferents did not alter the response to noxious heat, but reduced the firing of superficial dorsal horn nociceptive‐specific neurons in response to graded mechanical stimulation and decreased the relative number of wide dynamic range neurons that were exclusively mechanosensitive. Neither ablation procedure reduced the number of dorsal horn neurons that responded to noxious cold. These findings support the conclusion that TRPV1+ nociceptors are necessary and probably sufficient for noxious heat activation of dorsal horn neurons and that, despite their polymodal properties, TRPV1+ and MrgprD+ nociceptors provide modality‐specific contributions to the response properties of spinal cord neurons.
Effects of voluntary wheel running on the kidney at baseline and after ischaemia–reperfusion‐induced acute kidney injury: a strain difference comparison
Authors: Moningka Natasha C. , Cunningham, Jr Mark W. , Sterling Myrline , West Crystal A. , Verlander Jill W. , Croker Byron P. , Ahlgren Joslyn , Hayward Linda , Baylis Chris 
Published: December 2012

Key points
The impact of exercise on functional proteins critical for proper blood vessel health in the kidney is not well understood.
Using rats of different genetic backgrounds, we studied how chronic exercise affects the abundance of specific blood vessel proteins in the kidney, and whether this has any impact on the rat's susceptibility to acute kidney injury.
We found that the renal response to exercise is dependent on genetic background, and that in one strain exercise rendered the kidney more vulnerable to acute kidney injury.
The vulnerable rats exhibited exercise‐dependent loss of the protective renal proteins critical for proper blood vessel health, while the protected strain showed increases in these protective proteins.
Our findings are particularly relevant regarding exercise prescription to kidney disease patients.
Abstract  Exercise‐induced vascular endothelial adaptations in the kidney are not well understood. Therefore, we investigated the impact of voluntary wheel running (VWR) on the abundance of endothelial nitric oxide synthase (eNOS) and extracellular superoxide dismutase (EC SOD), in kidney and lung, and other SOD isoforms and total antioxidant capacity (TAC), in kidney. We also determined whether VWR influences susceptibility to acute kidney injury (AKI). Male Sprague–Dawley and Fisher 344 rats, VWR or sedentary for 12 weeks, were subjected to AKI (uninephrectomy (UNX) and 35 min of left kidney ischaemia–24 h reperfusion, IR). We measured glomerular filtration rate (GFR) and renal plasma flow (RPF), and analysed renal structural injury. Running was comparable between strains and VWR reduced body weight. In Sprague–Dawley rats, VWR reduced eNOS and EC SOD, but increased Mn SOD in kidney. Similar changes were seen after 6 weeks of VWR in Sprague–Dawley rats. In Fisher 344 rats, VWR increased eNOS, all SOD isoforms and TAC in kidney. Both strains increased eNOS and EC SOD in lung with VWR. Compared to UNX alone, UNX‐IR injury markedly reduced renal function for both strains; however, in the Sprague–Dawley rats, VWR exacerbated falls in GFR and RPF due to UNX‐IR, whereas in the Fisher 344 rats, GFR was unaffected by VWR. Some indices of renal structural injury due to UNX‐IR tended to be worse in SD vs. F344. Our study demonstrates that genetic background influences the effect of exercise on kidney eNOS and EC SOD, which in turn influence the susceptibility to AKI.
Gastric vagal afferent modulation by leptin is influenced by food intake status
Authors: Kentish Stephen J. , O'Donnell Tracey A. , Isaacs Nicole J. , Young Richard L. , Li Hui , Harrington Andrea M. , Brierley Stuart M. , Wittert Gary A. , Blackshaw L. Ashley , Page Amanda J. 
Published: December 2012

Key points
Obesity occurs when energy intake exceeds expenditure, and the excess energy is stored as fat.
We show that, after a 14 h food deprivation or 12 weeks consumption of a high‐fat diet, gastric vagal afferent responses to mechanical stimulation in the presence of the satiety peptide leptin are altered.
Leptin has an excitatory effect on gastric mucosal vagal afferents, which is abolished after food restriction or prolonged excess.
In contrast, leptin has an inhibitory effect on gastric tension‐sensitive afferents, but only after food restriction or energy excess conditions.
These changes in the response to leptin in the stomach, after food restriction or prolonged high‐fat feeding, occur in such a manner as to facilitate an increase in food intake in both conditions.
Abstract  Energy intake is strongly influenced by vagal afferent signals from the stomach, and is also modulated by leptin. Leptin may be secreted from gastric epithelial cells, so we aimed to determine the direct effect of leptin on gastric vagal afferents under different feeding conditions. Female C57BL/6 mice were fed standard laboratory diet, high‐fat diet or were food restricted. The expression of leptin receptor (Lep‐R) and its signal transduction molecules in vagal afferents was determined by retrograde tracing and reverse‐transcription polymerase chain reaction, and the relationship between leptin‐immunopositive cells and gastric vagal afferent endings determined by anterograde tracing and leptin immunohistochemistry. An in vitro preparation was used to determine the functional effects of leptin on gastric vagal afferents and the second messenger pathways involved. Leptin potentiated vagal mucosal afferent responses to tactile stimuli, and epithelial cells expressing leptin were found close to vagal mucosal endings. After fasting or diet‐induced obesity, potentiation of mucosal afferents by leptin was lost and Lep‐R expression reduced in the cell bodies of gastric mucosal afferents. These effects in diet‐induced obese mice were accompanied by a reduction in anatomical vagal innervation of the gastric mucosa. In striking contrast, after fasting or diet‐induced obesity, leptin actually inhibited responses to distension in tension receptors. The inhibitory effect on gastric tension receptors was mediated through phosphatidylinositol 3‐kinase‐dependent activation of large‐conductance calcium‐activated potassium channels. The excitatory effect of leptin on gastric mucosal vagal afferents was mediated by phospholipase C‐dependent activation of canonical transient receptor potential channels. These data suggest the effect of leptin on gastric vagal afferent excitability is dynamic and related to the feeding state. Paradoxically, in obesity, leptin may reduce responses to gastric distension following food intake.
Infant satiety depends on transient expression of cholecystokinin‐1 receptors on ependymal cells lining the third ventricle in mice
Authors: Ozaki Tomoya , Mohammad Shahid , Morioka Eri , Takiguchi Soichi , Ikeda Masayuki 
Published: December 2012

Key points
In mammals, satiety‐controlling mechanisms develop before the switch from ingestive behaviour from milk suckling to regular food intake; however, the underlying mechanisms are currently unknown.
We show that absence of the cholecystokinin‐1 (CCK‐1) receptor gene significantly increases suckling pup weight, regardless of maternal genotype in mice.
CCK‐1 receptor expression was observed in satiety‐controlling regions such as the hypothalamus, caudal brainstem, nodose ganglion and pylorus, which is consistent with suggested receptor function in adults, whereas corresponding receptor expression was low to non‐existent at pre‐weanling stages.
Third ventricle ependymal tanycyte‐like cells transiently expressed CCK‐1 receptors at critical developmental stages, and gastrointestinal milk filling upregulated cFos expression in these cells.
Localized blocking of ependymal CCK‐1 receptors was sufficient to produce overweight pups, suggesting that the ependymal CCK‐1 receptor is an infant‐specific satiety controller.
Abstract  Cholecystokinin (CCK) is a hypothetical controller for suckling and infancy body weight, although the underlying mechanisms remain unclear. Therefore, the present study analysed the mechanisms using mice lacking the CCK‐1 receptor (CCK1R–/–). Although CCK1R–/– mice displayed normal weights at birth and adulthood, CCK1R–/– pups had enlarged adipocytes and were overweight from the first to second week after birth, regardless of maternal genotype. The lacZ reporter gene assay and/or calcium imaging analysis demonstrated that CCK‐1 receptors were abundant in satiety‐controlling regions such as the hypothalamus, brainstem, nodose ganglion and pylorus in adults, whereas these signals were few to lacking at pre‐weanling stages. At postnatal day (PD) 6, the increase in cFos expression in the medullary nucleus tractus solitarius was similarly triggered by gastrointestinal milk‐ or saline filling in both genotypes, further indicating immature CCK‐1 receptor function in an ascending satiety‐controlling system during infancy. Conversely, third ventricle ependymal tanycyte‐like cells expressed CCK‐1 receptors with expression peaking at PD6. At PD6, wild‐type but not CCK1R–/– mice had increased cFos immunoreactivity in ependymal cells following gastrointestinal milk filling whereas the response became negligible at PD12. In addition, ependymal cFos was not increased by saline filling, indicating that these responses are dependent on CCK‐1 receptors, developmental stage and nutrients. Furthermore, body weights of wild‐type pups were transiently increased by blocking ependymal CCK receptor function with microinjection of a CCK‐1 antagonist, but not a CCK‐2 antagonist. Hence, we demonstrate de novo functions of ependymal CCK‐1 receptors and reveal a new aspect of infant satiety‐controlling mechanisms.