bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neuroendocrine Regulation of Nutrient Partitioning
Authors: ROHNER‐JEANRENAUD FRANÇOISE 
Published: February 2006

ABSTRACT: Leptin is a satiety factor which acts within the hypothalamus to decrease the levels of several neuropeptides stimulating food intake (among them, neuropeptide Y [NPY]), while increasing those that inhibit food intake. These effects of leptin bring about decreased body weight. In vivo, leptin potentiates basal and insulin‐stimulated glucose utilization, presumably its oxidation, and decreases fat storage. Leptin increases sympathetic‐mediated energy dissipation, and the expression of uncoupling proteins‐1, ‐2, and ‐3. In peripheral tissues (muscles, adipose, others), leptin decreases triglyceride content by increasing fatty acid oxidation, decreasing the activity/expression of esterification and lipogenic enzymes, and favoring lipolysis. It decreases the lipogenic activity of insulin. Ultimately, leptin depletes fat stores and promotes leanness. NPY, taken as one example of what an orexigenic agent may produce, increases food intake and body weight. It favors fat storage in adipose tissue by stimulating lipogenic activity. It decreases glucose utilization by muscles, making more glucose carbon available for lipogenesis. Effects of NPY result from vagus nerve‐mediated hyperinsulinemia and overactivity of the hypothalamo‐pituitary‐adrenal axis. Thus, NPY favors fat stores, and ultimately obesity.Glucocorticoids are necessary for NPY effects to occur, because central administration of the neuropeptide in adrenalectomized animals is ineffective. Glucocorticoids also have genuine effects when administered centrally to normal rats. They increase the hypothalamic content of NPY and decrease that of CRH. This double neuropeptidic change stimulates food intake, insulin output, adipose tissue storage ability, decreases the expression of uncoupling proteins‐1 and ‐3, and increases body weight. Body weight homeostasis appears to require a finely tuned regulation of both leptin and glucocorticoids, with their respective opposite effects.
Hypothalamic Origin of the Metabolic Syndrome X
Authors: BJÖRNTORP PER , ROSMOND ROLAND 
Published: February 2006

ABSTRACT:The conspicuous similarities between Cushing's syndrome and the Metabolic Syndrome X open up the possibility that hypercortisolemia is involved also in the latter. Salivary cortisol is possible to measure during undisturbed conditions including perceived stressful events during everyday life. Such measurements clearly show that normally regulated cortisol secretion is associated with excellent health in anthropometric, metabolic, and hemodynamic variables. Upon perceived stress cortisol secretion is increased and followed by the Metabolic Syndrome X (insulin resistance, abdominal obesity, elevated lipids, and blood pressure). In a minor part of the population a defect, “burned‐out” cortisol secretion, occurs with decreased sex steroid and growth hormone secretions, and strong, consistent associations with the Metabolic Syndrome X. Psychosocial and socioeconomic handicaps with tendencies to abuse and depressive‐anxious mood changes are consistently associated. The feedback control of cortisol secretion by central glucocorticoid receptors (GR) is blunted, and the function of the GR is abnormal. This corresponds to a polymorphism early in the GR gene locus, which is also associated with abdominal obesity and insulin resistance and is found in 14% of the Swedish male population.We suggest that the Metabolic Syndrome X is due to a discretely elevated cortisol secretion, discoverable during reactions to perceived stress in everyday life. This is based on environmental factors and expressed with different impact depending on genetic susceptibility.
Tachykinin‐like Peptides and Their Receptors: A Review
Authors: VANDEN BROECK JOZEF , TORFS HERBERT , POELS JEROEN , VAN POYER WENDY , SWINNEN ELFRIEDE , FERKET KATHELIJNE , DE LOOF ARNOLD 
Published: February 2006

Abstract: Tachykinin‐like peptides have been identified in many vertebrate and invertebrate species. On the basis of the data reviewed in this paper, these peptides can be classified into two distinct subfamilies, which are recognized by their respective sequence characteristics. All known vertebrate tachykinins and a few invertebrate ones share a common C‐terminal sequence motif, ‐FXGLMa. The insect tachykinins, which have a common ‐GFX1GX2Ra C‐terminus, display about 30% of sequence homology with the first group.Tachykinins are multifunctional brain/gut peptides. In mammals and insects, various isoforms play an important neuromodulatory role in the central nervous system. They are involved in the processing of sensory information and in the control of motor activities. In addition, members of both subfamilies elicit stimulatory responses on a variety of visceral muscles. The receptors for mammalian and insect tachykinins show a high degree of sequence conservation and their functional characteristics are very similar. In both mammals and insects, angiotensin‐converting enzyme (ACE) plays a prominent role in tachykinin peptide metabolism.
The Use of Collagen‐GAG Membranes in Reconstructive Surgery
Authors: ORGILL DENNIS P. , STRAUS FRANCIS H. , LEE RAPHAEL C. 
Published: February 2006

ABSTRACT: Porous collagen‐glycosaminoglycan (PCG) membranes with a porous silicone elastomer coating have been useful as a scaffold for dermal replacement in burn victims. Critical physicochemical parameters of these membranes include pore size, cross‐link density, the percentage of glycosaminoglycan, and the degree of banding of the collagen. These factors govern the immunobiological response. Optimizing these parameters can reduce inflammation, scarring, and contraction of wounds grafted with PCG membranes. PCG membranes are currently commercially manufactured (Integra®, Integra Life Sciences, New Jersey) and available for clinical use.Because clinical outcomes have improved using these membranes for burn wound coverage, other skin reconstruction problems including scar resurfacing, keloids, treatment of donor sites, and treatment of chronic wounds can be considered as potential applications. This manuscript illustrates our early experience using Integra® as a CG membrane for dermal replacement in reconstructive surgery. Our results indicate that CG membranes can lead to improved compliance and appearance compared to a meshed graft and may be sequentially placed in multiple layers to correct contour deformities. Also, in one case, we observed that, if placed on a wound bed with embedded skin epithelial cells, the PCG promotes epithelialization through the PCG matrix. The use of this material results in a supple integument with many similarities to normal skin.
Study on the Distribution Pattern of Skin Temperature in Normal Chinese and Detection of the Depth of Early Burn Wound by Infrared Thermography
Authors: ZHU WEI‐PING , XIN XIANG‐RONG 
Published: February 2006

ABSTRACT: Objective Conduct basic research of the distribution pattern of skin temperature and estimate the wound depth in normal Chinese in the early stage of burn injury by using technical thermography.Methods (1) Two hundred twenty‐three volunteers from the electrical power system were randomly chosen: 138 males and 85 females, mean age 42.5 ± 8.8, and mean weight 65.37 ± 9.7 kg. (2) Thermovisionr 470 Pro camera of AGEMA Corporation, Sweden, was used. (3) A total of 29,882 values of skin temperature from all over the body were classified, compared, and statistically analyzed.Results The difference in temperature on the y‐axis of the body is relatively significant, from 0 to 9 °C. The difference in temperature on the x‐axis of the body is relatively invariable.Conclusions The depth of early burn wound can be detected by using infrared thermography, which is an objective, fast, nontouching, and noninvasive method.
Ion Channel Modulation as the Basis for Neuroprotective Action of MS‐153
Authors: UENISHI HIROAKI , HUANG CHAO‐SHENG , SONG JIN‐HO , MARSZALEC WILLIAM , NARAHASHI TOSHIO 
Published: February 2006

ABSTRACT:MS‐153, (R)‐(‐)‐5‐methyl‐1‐nicotinoyl‐2‐pyrazoline, is a new neuroprotective durg. Recent data in the literature suggest that it inhibits glutamate accumulation occurring during ischemia and the translocation of protein kinase C gamma (PKCγ). The present study was undertaken to prove the hypothesis that MS‐153 blocks neuroreceptors and ion channels involved in glutamate accumulation. Neurons isolated from rat dorsal root ganglia and frontal cortex were used for recording channel currents by the whole‐cell patch clamp technique. The effects of bath‐applied MS‐153 were examined on tetrodotoxin‐sensitive and tetrodotoxin‐resistant sodium channels and high voltage‐gated calcium channels of dorsal root ganglion neurons, and channels activated by glutamate,N‐methyl‐d‐aspartate (NMDA), kainate, α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxarole propionic acid (AMPA), γ‐aminobutyric acid (GABA) and acetyloholine (ACH) in cortical neurons.MS‐153 at a concentration of 300 μM had no effect on either tetrodotoxin‐sensitive or tetrodotoxin‐resistant sodium channels. High voltage‐gated calcium channels were either suprressed or not affected by 1–300 μM MS‐153. The variable blocking effect of MS‐153 was due to the variable activity of intracellular components in individual neurons, especially that of PKC, whose translocation is known to be inhibited by MS‐153. When 100 nM phorbol 12‐Myristate‐13‐acetate (PMA) was applied to neurons, MS‐153 suppressed the calcium channel current more frequently. Calphostin C (0.5 μM), a specific PKC inhibitor, applied intracellularly via recording patch pipette, completely abolished MS‐153 suppression of the calcium channel current. Currents induced by glutamate, NMDA, kainate, AMPA, GABA or ACH were not affected by MS‐153 at 300 μM. It was concluded that MS‐153 inhibited high voltage‐gated calcium channels through interactions with PKC, thereby preventing massive release of glutamate from nerve terminals in ischemic conditions.
Further Characterization of CD34‐Low/Negative Mouse Hematopoietic Stem Cells
Authors: NAKAUCHI HIROMITSU , TAKANO HINA , EMA HIDEO , OSAWA MASATAKE 
Published: February 2006

Abstract: We have previously reported that in adult mouse bone marrow, CD34low/− c‐kit+ Sca‐1+ lineage markers negative (Lin−) (CD34−KSL) cells represent hematopoietic stem cells with long‐term marrow repopulating ability whereas CD34+ c‐kit+ Sca‐1+ Lin− (CD34+KSL) cells are progenitors with short‐term reconstitution capacity. To further characterize cells in those two populations, relative expression of various genes wereee examniend by reverse transcriptase polymerase chain reaction (RT‐PCR). In CD34−KSL Cells, none of the genes sturied was found to be expressed with the exception of GATA‐2, IL‐1Rα, IL‐2Rγ, AIC‐2B, c‐kit, EPO‐R, and c‐mpl. In contrast, expression of GATA‐1 and all cytokine receptor genes examined except IL‐2Rβ, IL‐7Rα and IL‐9Rα were found in CD34+KSL.The difference between these two populations was also shown in single cell culture analysis of these cells. when cells were clone sorted and cultured in the presence of SCF, IL‐3 and EPO, CD34−KSL cells required much more time to undergo the first cell division than CD34+KSL cells. dormancy and random fashion of cell division by CD34−KSL cells were also evident by the analysis of the second cell division, which was found to be delayed and unsynchronous comapred with CD34+KSL cells. Clonal culture analusis showed that CD34−KSL cells were more potent in proliferation and multilineage differentiation capacities than CD34+KSL cells. In a paired‐daughter cell experiment, 75% of CD34−KSL and 50% of CD34+KSL paired‐daughter‐derived colonies were nonidentical wiht wide vairety of lineage combinations. Taken together, these data support our previous notion that CD34−KSL cells are at higher rank in hematopoietic hierarchy than CD34+KSL cells. In addition, our results using highly enriched stem cell population directly obtained from mouse bone marrow support the proposed stochastic nature of lineage commitment.
Free Radicals and Hearing: Cause, Consequence, and Criteria
Authors: EVANS PATRICIA , HALLIWELL BARRY 
Published: February 2006

ABSTRACT: Reactive oxygen and nitrogen species, including free radicals, are produced in the human body in both health and disease. In health, they may arise as regulatory mechanisms, intercellular signaling species, or as bacteriocidal agents. Their production is normally controlled by the antioxidant defense mechanisms that include intracellular enzymes‐for example, glutathione peroxidase and superoxide dismutase‐and low molecular‐mass compounds such as vitamin E or ascorbic acid. Although repair mechanisms exist, some steady‐state basal oxidative damage occurs in all individuals.Oxidative stress arises when there is a marked imbalance between the production and removal of reactive oxygen and nitrogen species. This may originate from an overproduction of these substances or from a depletion in the antioxidant defenses. Certain drugs may induce oxidative stress by forming drug‐derived radicals that can not only deplete the antioxidant defenses but can also react directly with biomolecules. To be able to assess whether oxidative stress is occurring in a particular tissue, reliable biomarkers of oxidative damage are required. Since oxidative stress can damage all major biomolecules in vitro and probably in vivo, biomarkers for DNA, protein, and lipid damage are being developed which, when taken with an assessment of the antioxidant status of the individual, will allow evaluation of the involvement of oxidative stress in the etiology of disease and in the side effects of drugs. There is some evidence to suggest that free radical‐mediated damage may be involved in the ototoxicity of aminoglycosides and cisplatin derivatives. Whether this is a cause or consequence of the toxic insult to the sensory hair cells of the inner ear remains to be determined.
Genetic Factors in Aminoglycoside Toxicity
Authors: FISCHEL‐GHODSIAN NATHAN 
Published: February 2006

ABSTRACT: Ototoxicity is the major irreversible toxicity of aminoglycosides, and occurs both in a dose‐dependent and idiosyncratic fashion. The idiosyncratic pathway is presumably due to genetic predispositions, and in 1993 we identified an inherited mutation that predisposes to aminoglycoside ototoxicity, the A1555G mutation in the mitochondrial 12S ribosomal RNA gene. Seventeen‐33% of patients with aminoglycoside ototoxicity carry this mutation.In a search for additional susceptibility mutations, a dual strategy of yeast genetics and candidate genes was employed. Through yeast genetics 8 genes that by overexpression prevent aminoglycoside toxicity were identified. The human homologues of these genes may harbor aminoglycoside susceptibility mutations. Another candidate gene is the mitochondrial ribosomal protein S12, which interacts with the ribosomal RNA gene and in bacteria can harbor aminoglycoside resistance mutations. Analysis of this gene in 41 patients with aminoglycoside ototoxicity did not reveal any mutations in the coding regions. However, an Italian family with five maternally related family members who went deaf after aminoglycosides led to the identification of the second susceptibility mutation in the mitochondrial 12S ribosomal RNA gene, ΔT961Cn.While these findings have immediate clinical implications for prevention of aminoglycoside‐induced ototoxicity, they have not yet led to a clear understanding of the pathophysiology of aminoglycoside toxicity or the development of therapeutic options after the onset of symptoms.
Protection and Spontaneous Recovery from Cisplatin‐Induced Hearing Loss
Authors: SMOORENBURG GUIDO F. , DE GROOT JOHN C. M. J. , HAMERS FRANK P. T. , KLIS SJAAK F. L. 
Published: February 2006

ABSTRACT: Cisplatin [cis‐diamminechloroplatinum(II)] has proved itself as a potent antineoplastic agent. However, nephrotoxicity, neurotoxicity, gastrointestinal toxicity, myelosuppression, and ototoxicity interfere with its therapeutical efficacy. Forced diuresis reduces nephrotoxicity, effectively leaving neurotoxicity and ototoxicity as the major side effects of concern, and gastrointestinal toxicity and myelosuppression as the secondary side effects.So far, attempts to reduce these side effects by developing equally potent platinum analogs have been unsuccessful. Some success has been achieved, however, by cotreatment with protective agents. Nearly all these agents are sulfuror sulfhydryl‐containing compounds (thio compounds), known as antioxidants and potent heavy metal chelators. These thio compounds may provide protection from cisplatin toxicity either (1) by direct interaction between the cisplatin and the thio moiety, (2) by displacing platinum from its site of toxic action, (3) by preventing platinum from interfering with superoxide dismutase, or (4) by scavenging of cisplatin‐induced free radicals. In particular the first two protective mechanisms bear the risk of reducing the antineoplastic activity of cisplatin.Since nephrotoxicity can be controlled effectively by forced diuresis, a more specific approach of coping with ototoxicity by focusing on protection at the sensorineural level was chosen. Being familiar with the neuroprotective and neurotrophic properties of ACTH‐related neuropeptides, specifically against cisplatin‐induced peripheral neuropathies, it was judged expedient to test for a possible otoprotective action of these neuropeptides. The results were positive, although tainted with high interanimal variability.When testing for the possibility that the neuropeptides would merely delay cisplatin‐induced ototoxicity rather than reduce it, it was discovered in control series without neuropeptide cotreatment that the ear can recover spontaneously from cisplatin‐induced hearing loss. This was found both electrophysiologically and in outer hair cell (OHC) counts. Although these preliminary findings require further investigation, they strongly suggest that spontaneous recovery of cochlear injury can occur in the mature mammalian cochlea. Moreover, the otoprotective action of the ACTH‐related neuropeptides suggests that it may be possible to stimulate recovery from acute hearing loss using neuropeptides.
Transient Phenomena in d.c. Plasma‐Spray Torches
Authors: COUDERT Jean François , FAUCHAIS Pierre 
Published: February 2006

ABSTRACT: D.c. plasma torches have been involved for many years in industrial applications such as welding, cutting or deposit elaboration by plasma spraying or plasma assisted vapor deposition. These techniques use specific properties of plasmas produced by d.c. arcs where high temperatures (up to 25000 K) and high flow velocities (up to few km/s) are available. A considerable amount of experimental work was devoted, in the past, to characterize the properties of arc jets as a function of arc current, torch design and configuration, plasma forming gas thermophysical properties and flowrate. In the same time models approached more and more accurately the behavior of arc jets, testifying of a real advance in both knowledge and understanding of the different implicated processes and mechanisms.Nevertheless, and mainly because of experimental difficulties, transient phenomena due to arc instabilities have been less intensively studied and their interest has only been underlined the last decade, although they were mentioned more than thirty years ago.Due to the extraordinary progress accomplished in the field of instrumentation, new diagnostic techniques have become available, accompanied by powerful signal processing methods which are now easy to apply thanks to the development of computers and associated software. It has been experimentally demonstrated in plasma torches that the arc is submitted to gas dynamic forces which give rise to two different modes of instability among which two major cases can be distinguished. The first one is the so‐called “take‐over” mode, characterized by rather low fluctuations of arc voltage compared to the mean value, the second one being the “restrike” mode, for which the fluctuations of arc voltage are about the same in amplitude than the mean value. The restrike mode is clearly identified as the result of the stretching of the arc by the cold gas flow, followed by electrical breakdown of the cold gas layer which gives rise to a new arc‐anode attachment. The stretching‐rearcing sequences are repeated at a frequency which is governed by experimental conditions and give a sawtooth shaped voltage signal, the analysis of which provides clear information about the arc dynamics. The fluctuations of arc length generate strong voltage variations which are correlated to the electrical power supplied to the gas and, as a consequence, to the variations of the arc jet temperature and velocity. The amplitude and frequency of voltage fluctuations can be related to the torch working and geometrical parameters and dimensional analysis allow to establish reliable semi‐empirical correlations. Temperature and velocity distributions are strongly correlated to the torch working conditions and the resulting fluctuations. It will be illustrated for different operating conditions of a d.c. spray torch.
Stimulus Processing by Type II Hair Cells in the Mouse Utricle
Authors: HOLT JEFFREY R. , VOLLRATH MELISSA A. , EATOCK RUTH ANNE 
Published: February 2006

Abstract: In type II and neonatal hair cells in the mouse utricle, the receptor potentials evoked by low‐frequency sinusoidal deflections of the hair bundle are attenuated by adaptation of the mechanoelectrical transduction current and the voltage‐dependent activation of a large potassium (K)‐selective outwardly rectifying conductance, gDR. These processes may contribute to high‐pass filtering of the responses of some utricular afferents to sinusoidal linear accelerations below 2 Hz. Depolarizing receptor potentials are more attenuated by gDR than are hyperpolarizing receptor potentials. It may therefore reduce nonlinear distortion introduced by mechanoelectrical transduction, which generates larger depolarizing currents than hyperpolarizing currents.The discharge properties of utricular afferents vary according to whether they innervate the striolar or extrastriolar zones of the sensory epithelium. Regional variation in hair‐cell properties is likely to contribute. Preliminary results suggest that the outwardly rectifying K conductances of type II cells are slower and larger in the striola than in the extrastriola, consistent with regional variation in the relative numbers of delayed rectifier and A‐current K channels.
A Review of Otolith Pathways to Brainstem and Cerebellum
Authors: BÜTTNER‐ENNEVERA J. A. 
Published: February 2006

Abstract: Our knowledge of otolith pathways is developing rapidly, but is still far from complete. Primary afferents from the sacculus and utricle terminate mainly in the lateral, inferior and caudal superior vestibular nuclei, and the ventral cerebellum, in particular the nodulus. Otolith signals descend via reticulo‐ and vestibulospinal pathways in the spinal cord to influence neck motoneurons and ascending proprioceptive afferents. Utricular information can reach the extraocular eye muscles via mono‐, di‐, and multisynaptic pathways, but saccular afferents probably only by multisynaptic pathways.The otolith signals are relayed from the vestibular nuclei, medullary reticular formation, inferior olive, and lateral reticular nucleus to sagittal zones in the caudal cerebellar vermis (nodulus and uvula), and influence the deep cerebellar nuclei. The graviceptive information could be channeled by the cerebellar efferents back to the vestibular and inferior olive complex, or fed into ascending pathways that would innervate the mescencephalon, the thalamus, and cerebral cortex.