bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Burning Mirrors of Diocles: Reflections On the Methodology and Purpose of the History of Pre-Modern Science
Authors: Hogendijk Jan P. 
Published: December 2007

AbstractMuch has been done on the publication of original sources in Arabic during the past 30 years, but much more remains to be done. Some of the recent multiple editions are unnecessary duplication of work and therefore waste of energy. This energy could be better spent on the publication of unpublished sources, and on studies involving the contextualization of Islamic sciences. Furthermore, historians of pre-modern science should work on the popularization of their wonderful subject. This exoteric work is as important as esoteric research, because the survival of the field depends on its image among various audiences outside the community of historians of science.
Geometry in Context in the Sixteenth Century: the View From the Museum
Authors: Bennett Jim 
Published: December 2007

AbstractThis paper examines the discrepancy between the attitudes of many historians of mathematics to sixteenth-century geometry and those of museum curators and others interested in practical mathematics and in instruments. It argues for the need to treat past mathematical practice, not in relation to timeless criteria of mathematical worth, but according to the agenda of the period. Three examples of geometrical activity (cartography, surveying and warfare) are used to illustrate this, and two particular contexts (the wider world of human affairs and the discipline of natural philosophy) are presented in which mathematical practice localised in the sixteenth century takes on a special historical significance.
The Language of Demonstration: Translating Science and the Formation of Terminology in Arabic Philosophy and Science
Authors: Endress Gerhard 
Published: December 2007

AbstractThe reception of the rational sciences, scientific practice, discourse and methodology into Arabic Islamic society proceeded in several stages of exchange with the transmitters of Iranian, Christian-Aramaic and Byzantine-Greek learning. Translation and the acquisition of knowledge from the Hellenistic heritage went hand in hand with a continuous refinement of the methods of linguistic transposition and the creation of a standardized technical language in Arabic: terminology, rhetoric, and the genres of instruction. Demonstration more geometrico, first introduced by the paradigmatic sciences-mathematics, astronomy, mechanics-and adopted by philosophers embracing the cosmology of Neoplatonism, was complemented and superseded by the methods of syllogistic demonstration. Faced with the establishment of philosophy as a demonstrative science, which claimed absolute and universal knowledge, even the hermeneuti
Criticism of Authority in the Writings of Moses Maimonides and Fakhr Al-Din Al-Razi
Authors: Tzvi Langermann Y. 
Published: December 2007

AbstractCriticism of authority was a prominent feature of medieval philosophical writing. In this study the critiques of two contemporaneous scholars, Moses Maimonides and Fakhr al-Dīn al-Rāzī, are compared. Maimonides criticized Hellenistic authorities, mainly Aristotle. However, the starting point for his critique was Aristotle's admission of the limitations of his own inquiries. Maimonides admired Aristotle's questioning of his own conclusions; indeed, his own thought was characterized by constant self-doubt. Al-Rāzī criticized an earlier Muslim scholar, Ibn Sīnā (Avicenna), an intellectual giant whose imprint was strongly felt in philosophy and medicine. Al Rāzī used his commentaries on a number of Ibn Sīnā's books as a stage for criticizing the master and for arguing for his own, alternative viewpoints.
Certainty, Doubt, Error: Comments On the Epistemological Foundations of Medieval Arabic Science1
Authors: Gutas Dimitri 
Published: December 2007

AbstractThe article comments on the epistemological foundations of medieval Arabic science and philosophy, as presented in five earlier communications, and attempts to draw some guidelines for the study of its social history. At the very beginning the notion of "Islam" is discounted as a meaningful explanatory category for historical investigation. A first part then looks at the applied sciences and notes three major characteristics of their epistemological approach: (a) they were functionalist and based on (b) experience and (c) observation. The second part looks at the theoretical sciences and notes that their epistemology was based on (a) geo
Evolution of allostery in the cyclic nucleotide binding module
Authors: Kannan Natarajan , Wu Jian , Anand Ganesh S , Yooseph Shibu , Neuwald Andrew F , Venter J Craig , Taylor Susan S 
Published: December 2007

Abstract
Background
The cyclic nucleotide binding (CNB) domain regulates signaling pathways in both eukaryotes and prokaryotes. In this study, we analyze the evolutionary information embedded in genomic sequences to explore the diversity of signaling through the CNB domain and also how the CNB domain elicits a cellular response upon binding to cAMP.

Results
Identification and classification of CNB domains in Global Ocean Sampling and other protein sequences reveals that they typically are fused to a wide variety of functional domains. CNB domains have undergone major sequence variation during evolution. In particular, the sequence motif that anchors the cAMP phosphate (termed the PBC motif) is strikingly different in some families. This variation may contribute to ligand specificity inasmuch as members of the prokaryotic cooA family, for example, harbor a CNB domain that contains a non-canonical PBC motif and that binds a heme ligand in the cAMP binding pocket. Statistical comparison of the functional constraints imposed on the canonical and non-canonical PBC containing sequences reveals that a key arginine, which coordinates with the cAMP phosphate, has co-evolved with a glycine in a distal β2-β3 loop that allosterically couples cAMP binding to distal regulatory sites.

Conclusion
Our analysis suggests that CNB domains have evolved as a scaffold to sense a wide variety of second messenger signals. Based on sequence, structural and biochemical data, we propose a mechanism for allosteric regulation by CNB domains.
Early Exposure to General Anesthesia Causes Significant Neuronal Deletion in the Developing Rat Brain
Authors: NIKIZAD H. , YON J‐H. , CARTER L. B. , JEVTOVIC‐TODOROVIC V. 
Published: December 2007

AbstractFrequent exposure of children to general anesthesia is common practice in modern medicine. Although previously unrecognized, recent in vitro and in vivo animal studies suggest that exposure to clinically relevant general anesthetics at the peak of brain development could be detrimental to immature mammalian neurons, as demonstrated by massive and widespread apoptotic neurodegeneration. The survival of the developing neurons presumably depends on proper and timely formation of synapses, for which synaptic proteins (e.g., synaptophysin, synaptobrevin, amphiphysin, synaptosomal‐associated protein 25 [SNAP‐25], and Ca2+/calmodulin‐dependent protein kinase II [CaM kinase II]) are crucially important. Overinhibition of developing neurons impairs synaptic protein function and activity‐induced synaptic plasticity, which could in turn result in permanent neuronal loss. To examine the effects of general anesthesia, the pharmacological agents known to cause extensive neuronal inhibition, on synaptic proteins, and neuronal survival at the peak of synaptogenesis, we exposed 7‐day‐old rat pups to general anesthesia (midazolam, 9 mg/kg of body weight, subcutaneously, followed by 6 h of nitrous oxide 75 vol% and isoflurane 0.75 vol%). We found that this general anesthesia causes permanent neuronal deletion in the most vulnerable brain regions—the cerebral cortex and the thalamus—while transiently modulating protein levels of synaptophysin, synaptobrevin, amphiphysin, SNAP‐25, and CaM kinase II.
Brain‐Derived Neurotrophic Factor in Neuronal Survival and Behavior‐Related Plasticity
Authors: LIPSKY ROBERT H. , MARINI ANN M. 
Published: December 2007

AbstractNeurotrophins are critical to the development and maintenance of the mammalian central nervous system. Among them is brain‐derived neurotrophic factor (BDNF), whose synthesis and release is targeted by activation of glutamate receptors. Perturbation of this process probably underlies neurodegenerative and psychiatric disorders. A naturally occurring variation in humans, in the form of a common single‐nucleotide polymorphism in the pro region of the polypeptide at codon 66 (Val66→Met), affects processing of the pro‐BDNF polypeptide and its activation‐dependent release. This variant is associated with differences in the volume of the hippocampal formation and with anxiety and depression‐related phenotypes. Convergent findings supporting a role for BDNF in alterations to hippocampal structure and behavior are found in a “humanized” BDNF transgenic mouse. Also, recent human genetic studies have supported a role of BDNF signaling in addictive behaviors by allele‐, genotype‐, and haplotype‐based association of the TrkB gene, which encodes the cognate receptor for BDNF, with alcohol dependence. A better understanding of the influence of BDNF‐mediated pathways in cell survival and plasticity will aid in developing new approaches to restoring normal function in disease states.
Induction of Neurotrophic Factors GDNF and BDNF Associated with the Mechanism of Neurorescue Action of Rasagiline and Ladostigil
Authors: WEINREB ORLY , AMIT TAMAR , BAR‐AM ORIT , YOUDIM MOUSSA B.H. 
Published: December 2007

AbstractParkinson's disease (PD) and Alzheimer's disease (AD) are the most common neurodegenerative disorders, although there is no drug or therapeutic treatment to demonstrate disease‐modifying effects. Previous work has proposed that neurodegeneration is linked to a lack of trophic support in those neurons and brain areas associated with PD and AD. Indeed, previous studies have found that neurotrophic factors (NTFs) support neuronal survival in various cellular and animal models of PD and AD. Thus, attention has begun to turn to the possibility of NTF neuroprotective–neurorescue therapies for these diseases, indicating that NTFs may be of significant clinical importance as exogenously supplied or endogenously induced elements that obliterate neuronal deficits and degeneration.
We have recently reported that the anti‐PD drug rasagiline, the anti‐AD drug ladostigil, and their propargyl moiety, propargylamine, enhanced the expression levels of brain‐derived neurotrophic factor and glial cell line–derived neurotrophic factor, endogenous NTFs associated with activation of phosphatidylinositol 3‐kinase, protein kinase, and mitogen‐activated protein kinase cell signaling/survival pathways. These studies indicate that the induction of NTFs by rasagiline and ladostigil might suppress apoptosis and induce neurorescue in neurodegenerative disorders and may support the drugs' possible disease‐modifying mechanism of action.
Effect of Methylene Blue and Related Redox Dyes on Monoamine Oxidase Activity; Rat Pineal Content of N‐Acetylserotonin, Melatonin, and Related Indoles; and Righting Reflex in Melatonin‐Primed Frogs
Authors: OXENKRUG G.F. , SABLIN S.O. , REQUINTINA P.J. 
Published: December 2007

AbstractThe ability of methylene blue (MB) to inhibit the nitric oxide–induced stimulation of N‐methyl‐d‐aspartate receptors has been suggested as a possible mechanism of MB's clinical antidepressant action. This study evaluated the alternative/additional mechanisms of the antidepressant effect of MB on biochemical and behavior levels. Selective inhibition of monoamine oxidase type A (MAO‐A) is widely accepted as a major mechanism of the clinical antidepressant effect. MB and the related redox dyes toluidine blue O (TBO), thionine (TN), brilliant cresyl blue (BCB), and toluylene blue (TB) were reversible competitive inhibitors of both MAO‐A and MAO‐B and were highly selective toward MAO‐A. TBO was the most potent inhibitor, followed by TN, BCB, MB, and TB. The dyes studied increased rat pineal N‐acetylserotonin (NAS) and melatonin content, in accordance with our previous observations of the stimulating effect of selective inhibition of MAO‐A on pineal melatonin biosynthesis. The redox dyes exerted antidepressant‐like activity in frogs; that is, they suppressed the righting reflex in melatonin‐primed frogs. This study's results indicate that selective inhibition of MAO‐A might mediate the clinical antidepressant effect of MB through NAS stimulation and melatonin biosynthesis.
Effect of Luzindole and Other Melatonin Receptor Antagonists on Iron‐ and Lipopolysaccharide‐Induced Lipid Peroxidation in Vitro
Authors: REQUINTINA PURA J. , OXENKRUG GREGORY F. 
Published: December 2007

AbstractMelatonin and its precursor, N‐acetylserotonin (NAS), have been shown in in vivo and in vitro studies to inhibit iron‐ and lipopolysaccharide (LPS)‐induced lipid peroxidation in rats and mice. Using in vitro studies, we examined whether these effects will be affected by the melatonin receptor antagonists luzindole (a competitive MT1/MT2 antagonist), DH 97 (MT2), prazosin (MT3), and 4‐P‐PDOT (MT2). Lipid peroxidation in the form of malondialdehyde (MDA) was assayed by measuring thiobarbituric acid–reactive substances. The antagonists did not affect the melatonin and NAS effect on iron‐ and LPS‐induced peroxidation. However, luzindole alone, but not the other antagonists, inhibited the iron‐ and LPS‐induced peroxidation in the rat brain and kidney homogenates. At a dose of 50 μM, luzindole reduced iron‐induced MDA levels by 80% in the brain and 84% in the kidney, whereas LPS‐induced MDA levels were reduced by 85% in both brain and kidney. A dose of 800 μM prevented lipid peroxidation, bringing the MDA levels to values of samples untreated by iron or LPS.
Antibodies to Serotonin Attenuate Closed Head Injury Induced Blood–Brain Barrier Disruption and Brain Pathology
Authors: SHARMA H.S. , PATNAIK R. , PATNAIK S. , MOHANTY S. , SHARMA A. , VANNEMREDDY P. 
Published: December 2007

AbstractClosed head injury (CHI) often results in profound brain swelling and instant death of the victims due to compression of the vital centers. However, the neurochemical basis of edema formation in CHI is still obscure. Previous studies from our laboratory show that blockade of serotonin synthesis prior to CHI in a rat model attenuates brain edema, indicating a prominent role for serotonin in head injury. Thus, neutralization of endogenous serotonin activity and/or blocking of its receptors will induce neuroprotection in CHI. Since serotonin has more than 14 receptors and selective serotonin antagonists are still not available, we used serotonin antiserum to neutralize its in vivo effects before or after CHI in a rat model. CHI was produced by an impact of 0.224 N on the right parietal skull bone under Equithesin anesthesia by dropping a weight of 114.6 g from a height of 20 cm through a guide tube. This concussive brain injury resulted in blood–brain barrier (BBB) disruption, brain edema formation, and volume swelling at 5 h that were most pronounced in the contralateral cerebral hemisphere. The plasma and brain serotonin levels were increased several‐fold at this time. Intracerebroventricular administration of serotonin antiserum (1:20, monoclonal) into the left lateral cerebral ventricle (30 μL in PBS) 30 min before or 30 min (but not 60 min) after CHI significantly attenuated BBB disruption, brain edema formation, volume swelling, and brain pathology. The plasma and brain serotonin levels continued to remain high. These observations are the first to suggest that antiserum to serotonin when administered into the CSF during the early phase of CHI are capable of inducing neuroprotection.
Rab‐Mediated Endocytosis
Authors: BASKYS ANDRIUS , BAYAZITOV ILDAR , ZHU ERCHENG , FANG LIWEI , WANG RONG 
Published: December 2007

AbstractRab proteins are small GTPases involved in endocytosis and recycling of cell surface molecules. Recently they have been implicated in the etiopathogenesis of several neurodegenerative disorders including Alzheimer's and Lewy body disease. In experiments on organotypic hippocampal cultures, upregulation of Rab protein family member Rab5b after group I metabotropic glutamate receptor (mGluR) stimulation was associated with reduced neuronal vulnerability to excitotoxic injury. This mGluR‐mediated neuroprotection was abolished by antisense‐induced deficiency of Rab5b. Electrophysiological measurements of excitatory synaptic transmission in the Schaffer collateral–CA1 pathway revealed that mGluR activation that induces neuroprotection also induced long‐term depression (LTD) of synaptic transmission. Similar to the neuroprotection, Rab5b deficiency abolished dihydroxyphenylglycine‐induced LTD. Together, these findings support the idea that Rab proteins, and the Rab5b protein in particular, may provide a link between neurodegenerative disease, neuroprotection, and synaptic plasticity, as well as possibly being a useful target for pharmacological interventions.
The Association between Hyperglycemia and Fracture Risk in Middle Age. A Prospective, Population-Based Study of 22,444 Men and 10,902 Women
Authors: Holmberg A. H. , Nilsson P. M. , Nilsson J-Å. , Åkesson K. 
Published: December 2007

Abstract
Aims: Type 1 diabetes mellitus is associated with increased fracture risk, whereas the risk associated with type 2 diabetes is less obvious. Elevated fasting blood glucose and high 2-h glucose during an oral glucose tolerance test indicate impaired glucose tolerance or diabetes. The associations among fasting blood glucose, 2-h glucose, and the risk of fracture were investigated.
Methods: The Malmö Preventive Project consists of 22,444 men (44 ± 6.6 yr) and 10,902 women (50 ±7.4 yr), with a follow-up of 19 yr (±3.9) and 15 yr (±4.5) for incident fractures. Baseline assessment included multiple examinations and lifestyle information. A logistic regression model was used. Adjustments were made for age, body mass index (BMI), and smoking.
Results: Low-energy fractures were recorded in 1246 men and 1236 women. A 2-h glucose measurement between 4.3 and 6.2 mmol/liter in men (second and third quartile), and above 6.5 mmol/liter in women (third and fourth quartile), adjusted for age, BMI, and smoking, was significantly associated with a decreased risk of multiple fractures, in men [odds ratios (ORs) 0.57–0.71] and women (ORs 0.38–0.66). In women, a 2-h glucose measurement above 7.5 mmol/liter was associated with a decreased risk of osteoporotic fractures (OR 0.57, 95% confidence interval 0.44–0.74).
Conclusions: In middle-aged men and women, elevated 2-h glucose levels were associated with decreased risks of multiple and osteoporotic fractures, independent of age, BMI, and smoking. A high 2-h glucose level is characterized by peripheral insulin resistance with a high insulin level. Our findings indirectly suggest a positive effect on bone from hyperglycemia.
Type 2 Deiodinase Polymorphism (Threonine 92 Alanine) Predicts l-Thyroxine Dose to Achieve Target Thyrotropin Levels in Thyroidectomized Patients
Authors: Torlontano Massimo , Durante Cosimo , Torrente Isabella , Crocetti Umberto , Augello Giovanni , Ronga Giuseppe , Montesano Teresa , Travascio Laura , Verrienti Antonella , Bruno Rocco , Santini Stefano , D’Arcangelo Palmina , Dallapiccola Bruno , Filetti Sebastiano , Trischitta Vincenzo 
Published: December 2007

Abstract
Context: Type 2 deiodinase (D2) converts T4 in T3 in several human tissues, including hypothalamus and pituitary, and, therefore, plays a pivotal role in the negative feedback regulation of TSH secretion. A common variant of the gene, threonine (Thr) 92 alanine (Ala), has been identified and associated with decreased D2 enzymatic activity.
Objective: Our objective was to investigate whether this polymorphism predicts the T4 dosage needed to obtain target TSH levels in thyroidectomized patients.
Setting: Ambulatory patients were included in the study.
Patients: A total of 191 consecutive thyroid cancer patients, previously treated by near total thyroidectomy and radioiodine ablation, were studied. They were on stable T4 dose treatment aimed at obtaining either suppressed (supp) (n = 117, &lt; 0.1 mU/liter) or near-supp (n = 74, ≥ 0.1 &lt; 0.5 mU/liter) serum TSH levels.
Main Outcome Measures: DNA genotyping for D2 Thr92Ala variant and evaluation of T4 dose (μg/kg) needed to obtain target TSH levels were determined.
Results: Ala/Ala homozygous patients needed a higher T4 dose as compared with patients carrying the Thr92 variant (X/Thr patients) according to a recessive genetic model (2.08 ± 0.43 vs. 1.90 ± 0.35 μg/kg; P &lt; 0.05). This difference was observable in the near-supp group (P = 0.002), but not in the supp group (P = 0.4).
Conclusions: D2 Thr92Ala polymorphism seems to predict the need for higher T4 intake in thyroidectomized patients. If this finding is confirmed in additional studies, it may predict the T4 requirement to suppress TSH on the basis of the individual genetic background.
The G53D Mutation in Kir6.2 (KCNJ11) Is Associated with Neonatal Diabetes and Motor Dysfunction in Adulthood that Is Improved with Sulfonylurea Therapy
Authors: Koster Joseph C. , Cadario Francesco , Peruzzi Cinzia , Colombo Carlo , Nichols Colin G. , Barbetti Fabrizio 
Published: December 2007

AbstractContext: Mutations in the Kir6.2 subunit (KCNJ11) of the ATP-sensitive potassium channel (KATP) underlie neonatal diabetes mellitus. In severe cases, Kir6.2 mutations underlie developmental delay, epilepsy, and neonatal diabetes (DEND). All Kir6.2 mutations examined decrease the ATP inhibition of KATP, which is predicted to suppress electrical activity in neurons (peripheral and central), muscle, and pancreas. Inhibitory sulfonylureas (SUs) have been used successfully to treat diabetes in patients with activating Kir6.2 mutations. There are two reports of improved neurological features in SU-treated DEND patients but no report of such improvement in adulthood.Objective: The objective of the study was to determine the molecular basis of intermediate DEND in a 27-yr-old patient with a KCNJ11 mutation (G53D) and the patient’s response to SU therapy.Design: The G53D patient was transferred from insulin to gliclazide and then to glibenclamide over a 160-d period. Motor function was assessed throughout. Electrophysiology assessed the effect of the G53D mutation on KATP activity.Results: The G53D patient demonstrated improved glycemic control and motor coordination with SU treatment, although glibenclamide was more effective than gliclazide. Reconstituted G53D channels exhibit reduced ATP sensitivity, which is predicted to suppress electrical activity in vivo. G53D channels coexpressed with SUR1 (the pancreatic and neuronal isoform) exhibit high-affinity block by gliclazide but are insensitive to block when coexpressed with SUR2A (the skeletal muscle isoform). High-affinity block by glibenclamide is present in G53D channels coexpressed with either SUR1 or SUR2A.Conclusion: The results demonstrate that SUs can resolve motor dysfunction in an adult with intermediate DEND and that this improvement is due to inhibition of the neuronal but not skeletal muscle KATP.