Miracle-dz/UniFAR-FTUs huggingface dataset:
Paleoceanographic Events and Deep-Sea Ostracodes

Eight recognized or theorized paleoceanographic events during the past 70 million years were tested against changes in the global deep-sea benthic ostracode fauna. Two events, the sudden Cretaceous-Tertiary boundary event at 66 million years ago and the more gradual 40-million-year event (formation of the psychrosphere), show up most dramatically. Before the 40-million-year event, ostracodes freely radiated into the deeper water regions but were provincial. The development of thermal stratification isolated these deep-water taxa, mostly the survivors of the Cretaceous-Tertiary boundary event, which adapted to a new, free-flowing but more frigid ecosystem and spread rapidly throughout the world.
An application of the Hopfield model to Huffman codes

An application of the neural Hopfield model to the source (optimal) coding problem is presented. This application gives the structure of a Hopfield network, capable of calculating the lengths of the codewords that must be associated to a source alphabet so as to minimize their average length. The case of a stationary and memoryless block-to-variable-length source coding is discussed. >
Cyclin D1 and p21 is elevated in the giant cells of giant cell tumors

Alterations of cell cycle regulatory proteins, especially those that regulate G1 to S transition, have been implicated in the pathogenesis of a wide variety of human tumors. In previous studies we showed that that there is overexpression of cyclin D1 protein predominately in the giant cell component of giant cell tumors of bone. The purpose of this study was to investigate the mechanisms that may be responsible for cyclin D1 accumulation in giant cell tumors. Giant cell tumors have high levels of cyclin D1 mRNA and the giant cell‐enriched population of these tumors have significantly more mRNA and protein expression of cyclin D1 than the mononuclear cell population. The giant cells also expressed higher levels of p21 protein and more p21 bound to cyclin D1 than the mononuclear cells. It is possible that p21 may be contributing to the cyclin D1 accumulation that occurs in the giant cells and perhaps even giant cell formation in these tumors. Additional studies are required to confirm the role of p21 in the pathogenesis of these tumors. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:428–437, 2006
From Farming to Fishing : Marine Resource Conservation and a New Generation of Fishermen

This paper examines the arrival of a new group of fishermen on the Kenyan coast and what this has meant for the state of fishery resources. It reviews four subject areas: access and the number of fishermen; the fishermen’s identity; the choice of fishing gear; and the fishing grounds selected. Data were collected from a small number of fishing households in the villages of Uyombo and Takaungu in Kilifi District, using mainly qualitative research methods. Local households on the Kenyan coast face increasing pressure on land as well as on marine resources. The declining economic situation and greater pressure on land have made people turn to fishing as an income-generating activity. This group of fishermen is referred to as the ‘new’ generation of fishermen as they have been involved in fishing for only one or two generations (including the current one) in contrast to the ‘old’ generation from families who have been fishing or in fishingrelated activities for much longer. The old generation of fishermen and their households have also diversified their incomes, with many fishing households turning to farming, for example, with women and grown-up children involved in various activities. The new generation of fishermen, mainly of the Mijikenda population group, has often been blamed for the loss of traditional access regulations and for using harmful fishing gear. This paper discusses the new generation of fishermen and their identity as they perceive it and relates this to employment generation as a policy measure for marine conservation.
Attention-deficit/hyperactivity disorder and comorbidities in 18 Paisa Colombian multigenerational families.

OBJECTIVE Eighteen extended multigenerational families were recruited from the genetically isolated Paisa community in Colombia to conduct genetic studies of attention-deficit/hyperactivity disorder (ADHD). This report describes the inclusion strategy and clinical features of participants to facilitate comparisons with other data sets. METHOD Families were selected through a fixed-sampling scheme beginning with child probands referred for clinical evaluation for ADHD. Direct structured psychiatric interviews were conducted with 433 informative individuals, including 92 children aged 4 to 11, 57 adolescents aged 12 to 17, and 284 adults. Best estimate ADHD diagnoses were established for each informative pedigree member. RESULTS These families contained a high proportion of individuals affected with ADHD (32.8%), which was highly comorbid with conduct disorder (50%; odds ratio 11.5, 95% confidence interval = 6.4-20.9), oppositional defiant disorder (25.4%; odds ratio 2.7, confidence interval = 1.5-4.8), and associated conditions including nicotine dependence and alcohol abuse and/or dependence. CONCLUSIONS ADHD in these extended Paisa families is highly comorbid with conduct and oppositional defiant disorders. This pattern of comorbidity, as well as the large dense pedigrees of the sample, suggests that it will be particularly useful for molecular genetic studies that are currently under way.
Substrate specificity of soluble and membrane‐associated ADP‐ribosyltransferase ART2.1

ADP‐ribosyltransferases (ARTs) are a family of enzymes that catalyze the covalent transfer of an ADP‐ribose moiety, derived from NAD, to an amino acid of an acceptor protein, thereby altering its function. To date, little information is available on the protein target specificity of different ART family members. ART2 is a T‐cell‐specific transferase, attached to the cell surface by a glycosylphosphatidylinositol (GPI) anchor, and also found in serum. Here we investigated the role of ART2 localization in serum or on the cell surface, or solubilized with detergents or enzymes, on its target protein specificity. We found that detergent solubilization of cell membranes, or release of ART2 by phosphoinositide‐specific phospholipase C treatment, altered the ability of ART2 to ADP‐ribosylate high or low molecular weight histone proteins. Similarly, soluble recombinant ART2 (lacking the GPI anchor) showed a different histone specificity than did cell‐bound ART2. When soluble ART2 was incubated with serum proteins in the presence of [32P]‐labeled NAD, several serum proteins were ADP‐ribosylated in a thiol‐specific manner. Mass spectrometry of labeled proteins identified albumin and transferrin as ADP‐ribosylated proteins in serum. Collectively, these studies reveal that the membrane or solution environment of ART2 plays a pivotal role in determining its substrate specificity. J. Cell. Biochem. 98: 851–860, 2006. © 2006 Wiley‐Liss, Inc.
Cross sections, relic abundance, and detection rates for neutralino dark matter.

Neutralino annihilation and elastic scattering cross sections are derived which differ in important ways from previous work. These are applied to relic abundance calculations and to direct detection of neutralino dark matter from the galactic halo. Assuming the neutralino is the lightest supersymmetric particle and that it is less massive than the ${Z}^{0}$, we find relic densities of neutralinos greater than 4% of critical density for almost all values of the supersymmetric parameters. We constrain the parameter space by using results from the DESY ${e}^{+}$${e}^{\mathrm{\ensuremath{-}}}$ storage ring PETRA (chargino mass less than 23 GeV) and the ASP detector at the SLAC storage ring PEP, and then assuming a critical density of neutralinos, display event rates in a cryogenic detector for a variety of models. A new term implies ``spin-independent'' elastic scattering even for these Majorana particles and inclusion of propagator momenta increases detection rates by 10\char21{}300 % even for pure photinos. ${Z}^{0}$-squark interference leads to very low detection rates for some values of the parameters. The new term in the elastic cross section dominates for heavy, mostly spinless materials and mitigates the negative interference cancellations in light materials, except for the pure photino or pure Higgsino cases where it does not contribute. In general, the rates can be substantially different from the pure photino and pure Higgsino special cases usually considered.
Re: High frequency of multiple melanomas and breast and pancreas carcinomas in CDKN2A mutation-positive melanoma families.

we have previ-ously suggested such an interaction ofbreast cancer and melanoma genotypes.This database has been recently updated,providing the opportunity to increase thepower of our statistical analysis. Thepresent database includes persons bornin Sweden after 1934 (“offspring”) andtheir biological parents, totaling morethan 9.6 million individuals
Impact of renin-angiotensin system polymorphisms on development of systolic dysfunction in hypertrophic cardiomyopathy. Evidence from a study of genotyped patients.

BACKGROUND Although the renin-angiotensin system (RAS) can affect the development of left ventricular (LV) hypertrophy, few data exist regarding the relationships between RAS polymorphisms and alteration of LV function. The effect of RAS polymorphisms on LV function in genotyped hypertrophic cardiomyopathy (HCM) was examined in the present study. METHODS AND RESULTS The study group comprised 126 carriers with sarcomere gene mutations from 49 HCM families (64 males, mean age 51±21 years). LV morphology and function were evaluated by echocardiography. In angiotensin-converting enzyme (ACE) insertion/deletion (I/D), the D allele (n=81) exhibited significantly larger LV end-systolic dimension (LVDs) (32±11mm) and lower ejection fraction (56±15%) than those with the II genotype (28±7mm and 62±12%, respectively, P<0.05; n=45). Although angiotensin II type 1 receptor (AT(1)-R) A/C(1166) polymorphism did not affect echocardiographic parameters, the presence of the ACE D allele with the AT(1)-R C(1166) allele (n=9) was associated with larger LVDs (37±17mm) and lower ejection fraction (48±20%) compared with other genotypes (30±9mm and 58±14%, respectively, P<0.05; n=117). Under these conditions, severe LV hypertrophy was frequently associated with LV wall thinning. CONCLUSIONS The presence of both the ACE D and AT(1)-R C(1166) allele is associated with LV dilation with systolic dysfunction in genotyped HCM. In addition to the severity of LV hypertrophy, screening for these RAS polymorphisms could contribute to further risk stratification of patients with HCM, although other genetic polymorphisms should be further examined.
Vitreous surgery combined with internal limiting membrane peeling for traumatic macular hole with severe retinal folds.

PURPOSE To report a case of a traumatic macular hole with severe retinal folds in which vitreous surgery combined with internal limiting membrane (ILM) peeling was beneficial. To demonstrate that the area from which the ILM was peeled can be clearly differentiated by scanning laser ophthalmoscopy. METHODS A posterior hyaloid detachment was created during vitreous surgery on a 34 year old man with a traumatic macular hole. The remaining vitreous was resected and the ILM was peeled. The fundus was examined through a scanning laser ophthalmoscope before and after the surgery. RESULTS The retinal folds disappeared concurrently with the detachment of the ILM, resulting in closure of the macular hole. The area from which the ILM was peeled was clearly observed through the scanning laser ophthalmoscope. CONCLUSION In this patient, it was helpful to perform not only posterior hyaloid detachment but also ILM peeling. The scanning laser ophthalmoscope was highly useful for observing the area from which the ILM was peeled.
Short‐term Effects of Ambient Gaseous Pollutants and Particulate Matter on Daily Mortality in Shanghai, China

Short‐term Effects of Ambient Gaseous Pollutants and Particulate Matter on Daily Mortality in Shanghai, China: Guohai Chen, et al. Shanghai Environmental Monitoring Center, China—Identification of the specific pollutants contributing most to the health hazard of the air pollution mixture may have important implications for environmental and social policies. In the current study, we conducted a time‐series analysis to examine the specific effects of major air pollutants [particulate matter less than 10 microns in diameter (PM10), sulfur dioxide (SO2), and nitrogen dioxides (NO2)] on daily mortality in Shanghai, China, using both single‐pollutant and multiple‐pollutant models. In the single‐pollutant models, PM10, SO2, and NO2 were found to be associated with mortality from both all non‐accidental causes and from cardiopulmonary diseases. Unlike some prior studies in North America, we found a significant effect of gaseous pollutants (SO2 and NO2) on daily mortality even after adjustment for PM10 in the multiple‐pollutant models. Our findings, combined with previous Chinese studies showing a consistent, significant effect of gaseous pollutants on mortality, suggest that the role of outdoor exposure to SO2 and NO2 should be investigated further in China.
Cyclin-dependent kinase inhibitors: a survey of recent patent literature

Importance of the field: Abnormalities in protein phosphorylation by cyclin-dependent kinases (CDKs) have been observed in numerous major human diseases, which has strongly encouraged the search for pharmacological inhibitors. Almost 10 years after the first compounds entered clinical studies, numerous CDK inhibitors with differing selectivity profiles are now undergoing preclinical and clinical evaluation. Nevertheless, these intensive searches have not yet resulted in drug approvals. Areas covered in this review: This paper reviews patent activity associated with these efforts during the 2005 – 2008 period. What the reader will gain: Readers will rapidly obtain an overview of the majority of CDK inhibitor scaffolds; they will discover which companies are the main players in the field and acquire information on products that have reached the clinical phases. Take home message: In most cases, applications have been claimed in the field of cancer; however, potential applications of CDK inhibitors in other therapeutic areas are regularly reported and could herald therapeutic introduction over the next few years.
Energetic asymmetry among hydrogen bonds in MHC class II⋅peptide complexes

Comparison of crystallized MHC class II⋅peptide complexes has revealed that, in addition to pocket interactions involving the peptide side chains, peptide binding to MHC class II molecules is characterized by a series of hydrogen bonds between genetically conserved amino acid residues in the class II molecule and the main chain of the peptide. Many class II⋅peptide structures have two sets of symmetrical hydrogen bonds at the opposite ends of the class II antigen-binding groove (β-His-81, β-Asn-82 vs. α-His-68, α-Asn-69). In this study, we alter these peripheral hydrogen bonds and measure the apparent contribution of each to the kinetic stability of peptide⋅class II complexes. Single conservative amino substitutions were made in the I-Ad protein to eliminate participation as a hydrogen bonding residue, and the kinetic stability of a diverse set of peptides bound to the substituted I-Ad proteins was measured. Although each hydrogen bond does contribute to peptide binding, our results point to the striking conclusion that those hydrogen bonds localized to the amino terminus of the peptide contribute profoundly and disproportionately to the stability of peptide interactions with I-Ad. We suggest that the peripheral hydrogen bonds at the amino terminus of the bound peptide that are conserved in all class II⋅peptide crystal structures solved thus far form a cooperative network that critically regulates peptide dissociation from the class II molecule.
Distinct gene expression signatures in the striata of wild‐type and heterozygous c‐fos knockout mice following methamphetamine administration: Evidence from cDNA array analyses

Methamphetamine (METH) is a drug of abuse which can cause apoptosis and degeneration of monoaminergic terminals in the mammalian brain. c‐fos appears to play a protective role against METH‐induced damage because METH toxicity is exacerbated in c‐fos heterozygous knockout mice. In the present study, we used the comprehensive technique of cDNA array to test the idea that heterozygous c‐fos knockout mice might show differential METH‐induced molecular responses in comparison to wild‐type (WT) animals. Of 1,176 genes examined, the expression of 195 genes in either of the two groups of mice was affected by at least 2‐fold at 2 or 12 h after METH treatment. More genes were either up‐ or downregulated in the WT mice. Moreover, there were substantial differences in the pattern of responses between the two genotypes, with more genes involved in DNA repair and protective processes being upregulated in WT mice after METH administration. These results support the idea that the c‐fos knockout genotype may render the animals unable to trigger multicomponent responses in order to protect against the multifaceted toxic effects of this illicit neurotoxin. Synapse 44:211–226, 2002. © 2002 Wiley‐Liss, Inc.
Phosphorylation of Rat Melanopsin at Ser-381 and Ser-398 by Light/Dark and Its Importance for Intrinsically Photosensitive Ganglion Cells (ipRGCs) Cellular Ca2+ Signaling

Background: Melanopsin is a retinal light-sensitive receptor involved in non-image forming functions including circadian timing. Results: The intracellular C-terminal part of melanopsin was shown to be phosphorylated at distinct functional sites in response to light and dark. Conclusion: Phosphorylation status of melanopsin influences its functions. Significance: Distinct sites of phosphorylation are important in determining the signaling properties of melanopsin. The G protein-coupled light-sensitive receptor melanopsin is involved in non-image-forming light responses including circadian timing. The predicted secondary structure of melanopsin indicates a long cytoplasmic tail with many potential phosphorylation sites. Using bioinformatics, we identified a number of amino acids with a high probability of being phosphorylated. We generated antibodies against melanopsin phosphorylated at Ser-381 and Ser-398, respectively. The antibody specificity was verified by immunoblotting and immunohistochemical staining of HEK-293 cells expressing rat melanopsin mutated in Ser-381 or Ser-398. Using the antibody recognizing phospho-Ser-381 melanopsin, we demonstrated by immunoblotting and immunohistochemical staining in HEK-293 cells expressing rat melanopsin that the receptor is phosphorylated in this position during the dark and dephosphorylated when light is turned on. On the contrary, we found that melanopsin at Ser-398 was unphosphorylated in the dark and became phosphorylated after light stimulation. The light-induced changes in phosphorylation at both Ser-381 and Ser-398 were rapid and lasted throughout the 4-h experimental period. Furthermore, phosphorylation at Ser-381 and Ser-398 was independent of each other. The changes in phosphorylation were confirmed in vivo by immunohistochemical staining of rat retinas during light and dark. We further demonstrated that mutation of Ser-381 and Ser-398 in melanopsin-expressing HEK-293 cells affected the light-induced Ca2+ response, which was significantly reduced as compared with wild type. Examining the light-evoked Ca2+ response in a melanopsin Ser-381 plus Ser-398 double mutant provided evidence that the phosphorylation events were independent.
Retrograde signalling with nitric oxide at neocortical synapses

Long‐term changes of synaptic transmission in slices of rat visual cortex were induced by intracellular tetanization: bursts of short depolarizing pulses applied through the intracellular electrode without concomitant presynaptic stimulation. Long‐term synaptic changes after this purely postsynaptic induction were associated with alterations of release indices, thus providing a case for retrograde signalling at neocortical synapses. Both long‐term potentiation and long‐term depression were accompanied by presynaptic changes, indicating that retrograde signalling can achieve both up‐ and down‐regulation of transmitter release. The direction and the magnitude of the amplitude changes induced by a prolonged intracellular tetanization depended on the initial properties of the input. The inputs with initially high paired‐pulse facilitation (PPF) ratio, indicative of low release probability, were most often potentiated. The inputs with initially low PPF ratio, indicative of high release probability, were usually depressed or did not change. Thus, prolonged postsynaptic activity can lead to normalization of the weights of nonactivated synapses. The dependence of polarity of synaptic modifications on initial PPF disappeared when plastic changes were induced with a shorter intracellular tetanization, or when the NO signalling pathway was interrupted by inhibition of NO synthase activity or by application of NO scavengers. This indicates that the NO‐dependent retrograde signalling system has a relatively high activation threshold. Long‐term synaptic modifications, induced by a weak postsynaptic challenge or under blockade of NO signalling, were nevertheless associated with presynaptic changes. This suggests the existence of another retrograde signalling system, additional to the high threshold, NO‐dependent system. Therefore, our data provide a clear case for retrograde signalling at neocortical synapses and indicate that multiple retrograde signalling systems, part of which are NO‐dependent, are involved.
Genotype analysis of the VNTR polymorphism in the SMYD3 histone methyltransferase gene: Lack of correlation with the level of histone H3 methylation in NSCLC tissues or with the risk of NSCLC

Fabrice Barl esi, Giuseppe Giaccone*, Marielle I. Gallegos-Ruiz, Simone W. Span, Pierre Lefesvre, Frank A.E. Kruyt and Jose Antonio Rodriguez Department of Medical Oncology, VU University Medical Center, Amsterdam, The Netherlands Universit e de la M editerran ee, Assistance Publique Hopitaux de Marseille, Thoracic Oncology, Marseille, France Medical Oncology Branch, CCR, National Cancer Institute, NIH, Bethesda, MD Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands Department of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country, Leioa, Spain