bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Sesamoid Bones of the Hand and their Pathology
Authors: WOOD VIRCHEL E. 
Published: August 2005

Three cases of sesamoid bone pathology are presented, including two cases of sesamoid fracture and a case of sesamoid periostitis. The literature is reviewed. Sesamoid bones probably function in the body as pulleys. Most people have five sesamoid bones in each hand. Two at the thumb metacarpophalangeal joint, one at the interphalangeal joint of the thumb, one at the metacarpophalangeal joint of the index finger on the radial side, and one at the metacarpophalangeal joint of the little finger on the ulnar side. Sesamoid bones have been seen with periostitis in Reiter’s syndrome. The medial sesamoid bone of the thumb metacarpophalangeal is frequently enlarged in acromegaly. The sesamoid bones of the thumb have been fractured or trapped inside the joint during injury to the thumb metacarpophalangeal joint. The treatment of disabling pain in a sesamoid bone is enucleation of the bone.
Clinical Differences Between Typical and Atypical Cleft Hand
Authors: MIURA T. , SUZUKI M. 
Published: August 2005

To clarify the clinical features of the cleft hand and to differentiate the typical cleft hand from the atypical, hand pattern profiles were used. In cases of typical cleft hand, the metacarpal or the proximal phalanx on either side of the cleft are longer than on the unaffected side. Conversely, in cases of atypical cleft hand, the hand pattern profile shows a dysplastic bone formation. There was an obvious difference in the metacarpal pattern between typical cleft hand and failure of formation. The metacarpal pattern of typical cleft hand is like that in webbing of normal fingers, and the metacarpal pattern of failure of formation is like the pattern in symbrachydactyly.
Axon Regeneration and Vascularisation of Nerve Grafts an Experimental Study
Authors: McCULLOUGH C. J. , GAGEY O. , HIGGINSON D. W. , SANDIN B. M. , CROW J. C. , SEBILLE A. 
Published: August 2005

An experimental model has been designed to assess the effect of vascularisation on axon regeneration in nerve grafts. The vascular status of the grafts has been demonstrated by microangiography and histology. Rat sciatic nerve grafts in which the vascular pedicles were left intact retained a normal vascular pattern which was not adversely affected by wrapping the graft in a polythene sleeve. In devascularised grafts, revascularisation commenced at three days and was complete at nine days. If the devascularised grafts were wrapped in a polythene sleeve, revascularisation was impeded and at fifteen days the middle segment of the graft was avascular and infarcted. The rate of axon regeneration was measured electrophysiologically in the above four groups of nerve grafts. There was a linear relationship between the rate of axon regeneration with time post-graft, axon growth proceeding at a mean rate of 1.150mm/day (S.E. ± 0.084) after a mean delay of 4.85 days. There was no significant difference in the rate of axon regeneration in the four groups.
Subungual Melanoma Following a Single Injury
Authors: ROBERTS A. H. N. 
Published: August 2005

Subungual melanoma is an uncommon disease. This paper presents eight cases where a subungual melanoma followed a single injury to the digit after an interval of between nine months and seven years (average 2.9 years).Although most injuries to the nail bed have no long term problems and subungual melanomata do arise in apparently normal nail beds, it is felt that there is increasing evidence that a direct causal relationship between the injury and the melanoma exists in some cases. This evidence includes case histories, statistical studies, the incidence of melanoma in coloured races and the distribution between the various digits.
Flexor Digitorum Profundus Avulsion through Enchondroma
Authors: FROIMSON A. I. , SHALL L. 
Published: August 2005

A flexor digitorum profundus tendon avulsion occurring at the site of a pathological fracture through an enchondroma is reported. The avulsion appears to be the result of direct trauma crush to the distal phalanx of the little finger. The lesion was curetted and grafted using autogenous bone, the fracture was stabilized with a K-wire and the tendon was advanced and secured using Bunnell pullout wire technique. The lesion healed and function was restored.
Neuro‐hormonal activation predicts ventilatory response to exercise and functional capacity in patients with heart failure
Authors: Passino Claudio , Poletti Roberta , Bramanti Francesca , Prontera Concetta , Clerico Aldo , Emdin Michele 
Published: August 2005

AbstractBackground:Heart failure (HF) is characterised by reduced tolerance to effort, associated with progressive fatigue and dyspnoea. Neuro‐hormonal activation is a hallmark of HF and influences its clinical evolution.Aim:To evaluate the relationship between neuro‐hormonal activation, exercise capacity and ventilatory efficiency.Methods and results:154 HF patients (127 males, 62±1 years) underwent cardiopulmonary exercise testing and resting blood sampling for assay of plasma brain natriuretic peptide (BNP), NT‐proBNP, norepinephrine, epinephrine, aldosterone and plasma renin activity (PRA). BNP and NT‐proBNP levels correlated with peak oxygen consumption (VO2) (both R=−0.53, p<0.001), VE/VCO2 slope (R=0.56; p<0.001 and R=0.58; p<0.001, respectively) and maximum workload (R=−0.49; p<0.001 and R=−0.47; p<0.001, respectively). Norepinephrine correlated slightly less with peak VO2 (R=−0.38, p<0.001), VE/VCO2 (R=0.45; p<0.001) and maximum workload (R=−0.35; p<0.001). There was a significant inverse correlation between left ventricular ejection fraction and BNP (R=−0.48, p<0.001), NT‐proBNP (R=−0.42; p<0.001) and norepinephrine (R=−0.43; p<0.001). Weaker correlations were found for PRA, exercise parameters and ejection fraction. ROC curves showed that BNP was able to identify patients with peak VO2<14 ml/min/kg (cut‐off 98 pg/ml, AUC 0.775) and a VE/VCO2>35 (cut‐off 183 pg/ml, AUC 0.797), as well as NT‐proBNP (cut‐off 537 pg/ml, AUC 0.799 and cut‐off 1010 pg/ml, AUC 0.768, respectively) and norepinephrine (cut‐off 454 pg/ml, AUC 0.716 and cut‐off 575 pg/ml, AUC 0.783, respectively).Conclusion:Haemodynamic impairment (as indicated by BNP and NT‐proBNP plasma values) and sympathetic activation predict exercise capacity and ventilatory efficiency in HF patients.
Circulating levels of tumor necrosis factor‐α correlate positively with severity of peripheral oedema in patients with right heart failure
Authors: Odeh Majed , Sabo Edmond , Oliven Arie 
Published: August 2005

AbstractBackground:Several previous studies have shown that circulating levels of tumor necrosis factor‐α (TNF) are elevated in patients with advanced congestive heart failure. However, the relationship between circulating levels of TNF and severity of peripheral oedema in these patients has not been previously evaluated.Aims:To investigate the relationship between circulating levels of TNF, and severity of peripheral oedema in patients with right‐sided heart failure (RHF).Methods and results:Circulating levels of TNF were measured in 15 healthy volunteers, and in 83 patients with RHF with various levels of peripheral oedema. At presentation, 13 patients had no peripheral oedema (grade 0), 22 patients had mild peripheral oedema (grade 1), 23 patients had moderate peripheral oedema (grade 2), and 25 patients had severe peripheral oedema (grade 3). The values of circulating TNF levels (mean±S.E.M.) at presentation in the control group and in the RHF patients (oedema grades 0—3) were 2.98±0.21, 4.22±0.55, 4.67±0.29, 7.66±0.44, and 10.94±0.67 pg/mL respectively. There was a significant difference between the groups (p<0.0001, ANOVA), and a significant positive correlation was found between circulating TNF levels and severity of peripheral oedema (r=0.77, p<0.0001).Conclusion:A significant relationship is present between circulating levels of TNF and severity of peripheral oedema in patients with RHF.
Activation of the NF‐κB system in peripheral blood leukocytes from patients with chronic heart failure
Authors: Jankowska Ewa A. , von Haehling Stephan , Czarny Anna , Zaczynska Ewa , Kus Agnieszka , Anker Stefan D. , Banasiak Waldemar , Ponikowski Piotr 
Published: August 2005

AbstractAim:To evaluate the activation of transcriptional nuclear factor kappa‐B (NF‐κB) in peripheral blood leukocytes (PBL) from patients with chronic heart failure (CHF). In vitro experiments were used to elucidate the role of lipopolysaccharide (LPS) as a stimulus for the NF‐κB system in PBL.Methods and results:We examined 46 CHF patients (age: 62±1 years, LVEF: 31±1%, NYHA class: 2.7±0.1), 11 coronary artery disease (CAD) patients without CHF, and 13 healthy young subjects. The immunocytochemical localisation of NF‐κB in PBL was assessed using a polyclonal rabbit IgG anti‐c‐Rel‐subunit antibody. NF‐κB activation was expressed as the percentage of PBL nuclei stained positively for c‐Rel (NF‐κB(+)cell). PBL from healthy controls were exposed in vitro to the following concentrations of LPS from Escherichia coli (strain O111:B4): 0.1, 10 and 5000 ng/mL. CHF patients demonstrated the highest NF‐κB activation in PBL (NF‐κB(+)cells [%]: 37.1±1.5) as compared to CAD patients (29.1±3.0%) and controls (12.6±1.5%) (all p<0.05). There were three main clinical determinants of NF‐κB activation in PBL from CHF patients: peak oxygen consumption (r=0.53, p=0.025), presence of peripheral oedema (r=0.37, p<0.05) and serum C‐reactive protein (r=0.40, p=0.02). In PBL from healthy subjects, LPS at all concentrations increased NF‐κB activity towards the pattern detected in CHF.Conclusions:The NF‐κB system is highly overactive in PBL from CHF patients. LPS at low concentrations in peripheral blood may be involved in NF‐κB activation in PBL, and is a potential target for future therapeutic applications.
Novel CIPK1-Associated Proteins in Arabidopsis Contain an Evolutionarily Conserved C-Terminal Region That Mediates Nuclear Localization
Authors: Ok Sung Han , Jeong Hye Jin , Bae Jung Myung , Shin Jeong-Sheop , Luan Sheng , Kim Kyung-Nam 
Published: August 2005

Abstract
Environmental stimuli, including light, pathogens, hormones, and abiotic stresses, elicit changes in the cytosolic Ca2+ signatures of plant cells. However, little is known about the molecular mechanisms by which plants sense and transmit the specific cytoplasmic Ca2+ signal into the nucleus, where gene regulation occurs to respond appropriately to the stress. In this study, we have identified two novel Arabidopsis (Arabidopsis thaliana) proteins specifically associated with Calcineurin B-Like-Interacting Protein Kinase1 (CIPK1), a member of Ser/Thr protein kinases that interact with the calcineurin B-like Ca2+-binding proteins. These two proteins contain a very similar C-terminal region (180 amino acids in length, 81% similarity), which is required and sufficient for both interaction with CIPK1 and translocation to the nucleus. Interestingly, the conserved C-terminal region was also found in many proteins from various eukaryotic organisms, including humans. However, none of them have been characterized so far. Taken together, these findings suggest that the two proteins containing the evolutionarily conserved C-terminal region (ECT1 and ECT2) may play a critical role in relaying the cytosolic Ca2+ signals to the nucleus, thereby regulating gene expression.
An Auxilin-Like J-Domain Protein, JAC1, Regulates Phototropin-Mediated Chloroplast Movement in Arabidopsis
Authors: Suetsugu Noriyuki , Kagawa Takatoshi , Wada Masamitsu 
Published: August 2005

Abstract
The ambient-light conditions mediate chloroplast relocation in plant cells. Under the low-light conditions, chloroplasts accumulate in the light (accumulation response), while under the high-light conditions, they avoid the light (avoidance response). In Arabidopsis (Arabidopsis thaliana), the accumulation response is mediated by two blue-light receptors, termed phototropins (phot1 and phot2) that act redundantly, and the avoidance response is mediated by phot2 alone. A mutant, J-domain protein required for chloroplast accumulation response 1 (jac1), lacks the accumulation response under weak blue light but shows a normal avoidance response under strong blue light. In dark-adapted wild-type cells, chloroplasts accumulate on the bottom of cells. Both the jac1 and phot2 mutants are defective in this chloroplast movement in darkness. Positional cloning of JAC1 reveals that this gene encodes a J-domain protein, resembling clathrin-uncoating factor auxilin at its C terminus. The amounts of JAC1 transcripts and JAC1 proteins are not regulated by light and by phototropins. A green fluorescent protein-JAC1 fusion protein showed a similar localization pattern to green fluorescent protein alone in a transient expression assay using Arabidopsis mesophyll cells and onion (Allium cepa) epidermal cells, suggesting that the JAC1 protein may be a soluble cytosolic protein. Together, these results suggest that JAC1 is an essential component of phototropin-mediated chloroplast movement.
Differential effects of trans‐crotononitrile and 3‐acetylpyridine on inferior olive integrity and behavioural performance in the rat
Authors: Seoane A. , Apps R. , Balbuena E. , Herrero L. , Llorens J. 
Published: August 2005

AbstractThe inferior olive climbing fibre projection is key to cerebellar contributions to motor control. Here we present evidence for a novel tool, trans‐crotononitrile (TCN), to selectively inactivate the olive to study its functions. Anatomical, electrophysiological and behavioural techniques have been used in rats to assess the CNS effects of TCN, with a focus on the olivocerebellar projection. These findings were compared with those obtained with 3‐acetylpyridine (plus nicotinamide administered 3.5 h later, 3AP + 3.5 h). Fluoro‐Jade B cell labelling showed that TCN and 3AP + 3.5 h induce neurodegeneration primarily within the inferior olive, with no other targets in common. Recordings of evoked field potentials on the cerebellar cortical surface showed that both neurotoxins can reduce transmission in climbing fibre but not mossy fibre pathways. Both histological and electrophysiological differences suggest that TCN and 3AP have distinct mechanisms of action. Estimates of the numbers of surviving cells within individual subdivisions of the olive indicate that TCN and 3AP + 3.5 h cause different patterns of subtotal olivary lesion: most surviving neurons are present in the rostral (TCN) or caudal (3AP + 3.5 h) parts of the medial accessory olive, which are associated with two different cerebellar modules: the C2 and A modules, respectively. In behavioural studies, TCN and 3AP + 3.5 h produced differences in motor deficits consistent with the notion that these cerebellar modules have distinct functional responsibilities. Thus, studies using TCN as compared with 3AP + 3.5 h have the potential to shed light on the contributions of different cerebellar modules in motor control.
Tissue‐specific expression of tryptophan hydroxylase mRNAs in the rat midbrain: anatomical evidence and daily profiles
Authors: Malek Zeina S. , Dardente Hugues , Pevet Paul , Raison Sylvie 
Published: August 2005

AbstractSerotonin (5‐HT) is involved in both photic and non‐photic synchronization of the mammalian biological clock located in the suprachiasmatic nuclei (SCN). We have previously demonstrated that tryptophan hydroxylase protein (TPH), the rate‐limiting enzyme of 5‐HT synthesis, shows circadian rhythmicity in the pathways projecting from the raphe nuclei to the intergeniculate leaflets of the thalamus on one hand, and to the SCN on the other hand. In this study, we investigate whether the circadian rhythmicity in TPH protein could result from the rhythmic expression of tph gene in the raphe nuclei. We thus cloned specific tph1 and tph2 partial cDNAs and assessed the daily profiles of TPH mRNA levels by in situ hybridization in the rat raphe nuclei. Our results demonstrate that: (i) tph2 gene is exclusively expressed in the raphe nuclei, whereas tph1 gene is expressed in the pineal gland; (ii) under light–dark cycle (LD), TPH2 mRNA levels present daily variation within both median and dorsal raphe nuclei; (iii) under constant darkness TPH2 mRNA levels in both nuclei exhibit the same variation reported under LD cycle.These data show that the circadian 5‐HT synthesis within the serotonergic neurons projecting to the circadian system might be explained by the rhythmic transcription of the tph2 gene in raphe nuclei. Taking our result with previous data into consideration, we further suggest that 5‐HT synthesis and release within the circadian system could be directly or indirectly under the control of the SCN.
Impacts of lesion severity and tyrosine kinase receptor B deficiency on functional outcome of femoral nerve injury assessed by a novel single‐frame motion analysis in mice
Authors: Irintchev Andrey , Simova Olga , Eberhardt Kirsten A. , Morellini Fabio , Schachner Melitta 
Published: August 2005

AbstractFunctional recovery after peripheral nerve injury is often poor. Comprehension of cellular and molecular mechanisms limiting or promoting restoration of function and design of efficient therapeutic approaches remain serious challenges for neuroscience and medicine. Progress has been restricted by the lack of reliable methods for evaluation of motor functions in laboratory animals. We describe a novel approach for assessment of muscle function in mice after femoral nerve damage, an injury causing impairment of knee extension. The functional deficit can be precisely estimated by angle and distance measurements on single video frames recorded during movements of the animals with or without body weight support. Using this method we describe here the precise time‐course and degree of functional recovery after femoral nerve crush and transection. In addition, we show that restoration of function is considerably impaired in mice with a reduced expression level of the tyrosine kinase receptor B, a cognate receptor for the neurotrophin brain‐derived neurotrophic factor. This finding is consistent with known functions of brain‐derived neurotrophic factor and tyrosine kinase receptor B and demonstrates the potential of the method. The principles of the approach are highly relevant for the development of novel functional assays in other peripheral and, in particular, central nervous system injury paradigms.
Tetrodotoxin‐resistant Na+ channels in human neuroblastoma cells are encoded by new variants of Nav1.5/SCN5A
Authors: Ou Shao‐Wu , Kameyama Asako , Hao Li‐Ying , Horiuchi Masahisa , Minobe Etsuko , Wang Wu‐Yang , Makita Naomasa , Kameyama Masaki 
Published: August 2005

AbstractBoth tetrodotoxin‐sensitive (TTX‐S) and TTX‐resistant (TTX‐R) voltage‐dependent Na+ channels are expressed in the human neuroblastoma cell line NB‐1, but a gene encoding the TTX‐R Na+ channel has not been identified. In this study, we have cloned cDNA encoding the α subunit of the TTX‐R Na+ channel in NB‐1 cells and designated it hNbR1. The longest open reading frame of hNbR1 (accession no. AB158469) encodes 2016 amino acid residues. Sequence analysis has indicated that hNbR1 is highly homologous with human cardiac Nav1.5/SCN5A with > 99% amino acid identity. The presence of a cysteine residue (Cys373) in the pore‐loop region of domain I is consistent with the supposition that hNbR1 is resistant to TTX. Analysis of the genomic sequence of SCN5A revealed a new exon encoding S3 and S4 of domain I (exon 6A). In addition, an alternative splicing variant, lacking exon 18, that encodes 54 amino acids in the intracellular loop between domains II and III was found (hNbR1‐2; accession no. AB158470). Na+ currents in human embryonic kidney cells (HEK293) transfected with hNbR1 or hNbR1‐2 showed electrophysiological properties similar to those for TTX‐R INa in NB‐1 cells. The IC50 for the TTX block was ≈ 8 µm in both variants. These results suggest that SCN5A has a newly identified exon for alternative splicing and is more widely expressed than previously thought.
Timed hypocaloric feeding and melatonin synchronize the suprachiasmatic clockwork in rats, but with opposite timing of behavioral output
Authors: Caldelas Ivette , Feillet Celine A. , Dardente Hugues , Eclancher Françoise , Malan André , Gourmelen Sylviane , Pévet Paul , Challet Etienne 
Published: August 2005

AbstractTemporal organization of the molecular clockwork and behavioral output were investigated in nocturnal rats housed in constant darkness and synchronized to nonphotic cues (daily normocaloric or hypocaloric feeding and melatonin infusion) or light (light–dark cycle and daily 1‐h light exposure). Clock gene (Per1, Per2 and Bmal1) and clock‐controlled gene (Vasopressin) expression in the suprachiasmatic nuclei was assessed over 24 h. Light and exogenous melatonin synchronized the molecular clock, signaling, respectively, ‘daytime’ and ‘nighttime’, without affecting temporal organization of behavioral output (rest/activity rhythm). By contrast, synchronization to hypocaloric feeding led to a striking temporal change between gene expression in the suprachiasmatic clock and waveform of locomotor activity rhythm, rats then becoming active during the subjective day (diurnal‐like temporal organization). When the time of feeding coincided with activity offset, normocaloric feeding also synchronized the locomotor activity rhythm with no apparent switch in temporal organization. Peak of Per2 expression in the piriform cortex occurred between the beginning and the middle of the activity/feeding period, depending on the synchronizer. These data demonstrate that even though the suprachiasmatic clockwork can be synchronized to nonphotic cues, hypocaloric feeding likely acts downstream from clock gene oscillations in the suprachiasmatic nuclei to yield a stable yet opposite organization of the rest/activity cycle.
Extracellular signal‐regulated kinases (ERKs) modulate cocaine‐induced gene expression in the mouse amygdala
Authors: Radwanska Kasia , Caboche Jocelyne , Kaczmarek Leszek 
Published: August 2005

AbstractIt is known that acute cocaine administration activates the extracellular signal‐regulated kinase (ERK) pathway in the striatum, and results in transcription and translation of immediate early genes (IEGs). In the present study we investigated a possible involvement of ERK in the regulation of IEG expression in the amygdala, another brain structure known to be related to an addicted state. The patterns of cocaine‐induced c‐Fos, JunB and Zif268 protein expression were investigated, using an immunohistochemical approach, within distinct nuclei of the amygdala, either in the presence or absence of a selective inhibitor of the ERK pathway, SL327. Although these IEGs were similarly activated in the various nuclei of the amygdala after acute administration of cocaine, they showed different patterns after chronic injections. They also showed selective sensitivities to ERK inhibition. In particular, whereas c‐Fos and JunB expressions were augmented following chronic cocaine treatment, as compared with acute treatment, Zif268 expression was decreased by this chronic treatment. Additionally, chronic blocking of ERK activation affected cocaine‐induced c‐Fos and JunB but not Zif268 expression. Thus, the differential involvement of ERK in chronic vs. acute regulation of IEGs may account for its specific role in addiction‐related behavioral alterations, such as sensitization and tolerance.