Miracle-dz/UniFAR-FTUs huggingface dataset:
Unscheduled DNA synthesis in rat adult myenteric neurons: an immunohistochemical study

Unscheduled DNA synthesis refers to DNA synthesis not followed by cell division. Previous studies have suggested that this phenomenon may occur in neurons from peripheral myenteric ganglia in conditions of functional hyperstimulation. In order to verify these observations, we have carried on an immunohistochemical study on myenteric neurons from the hypertrophic intestinal loops upstream from a partial obstruction (an experimental condition that induces a relevant increase of the neuronal workload) after labelling with two different markers: the proliferating cell nuclear antigen (PCNA), that is specifically expressed in cell nuclei during the S-phase, and the protein gene product 9.5 (PGP 9.5), a specific marker of nerve cells. While no myenteric neuron immunopositive for the anti-PCNA antibody was found in the control intestine, in the hypertrophic myenteric ganglia some neurons were positive for PCNA. These results provide an unequivocal evidence on the existence of unscheduled DNA synthesis in myenteric neurons from the hypertrophic intestine.
Regulation of Tissue Inhibitor of Metalloproteinase 1 Gene Transcription by RUNX1 and RUNX2*

Tissue inhibitor of metalloproteinase 1 (TIMP1) is a contributory factor to fibrosis of a variety of organs including the liver. UTE-1 is a regulatory DNA motif essential for TIMP1 promoter activity in a variety of cell types including hepatic stellate cells (HSC), the key profibrogenic cells of the liver. In this study we identify RUNX1 and RUNX2 as UTE-1-binding proteins that are induced at the post-transcriptional level during activation of HSC. RUNX1 is expressed in at least two major isoforms, RUNX1B and RUNX1A. Overexpression of full-length RUNX1B isoform in HSC repressed TIMP1 promoter activity, whereas the truncated RUNX1A isoform and RUNX2 functioned as stimulators. To gain further understanding of the way in which RUNX1 isoforms differentially regulate TIMP1 transcription, we investigated the relationship between the UTE-1 site and its adjacent upstream serum-response element (SRE) in the promoter. The UTE-1 and SRE sites cooperate in a synergistic fashion to stimulate transcription of a heterologous minimal active promoter providing that they are in close proximity. The key regulatory sequence within the SRE is an AP-1 site that in HSC directs high level transcription via its interaction with JunD. RUNX1A was shown to interact directly with JunD, and by contrast RUNX1B failed to interact with JunD. Co-expression studies showed that RUNX1B can repress JunD-stimulated TIMP1 promoter activity. From these observations we propose that JunD and RUNX factors assemble at the adjacent SRE and UTE-1 sites in the TIMP1 promoter and form functional interactions that stimulate transcription. However, RUNX1B is unable to interact with JunD, and as such its occupancy at the UTE-1 site disrupts the optimal assembly of transcriptional activators required for directing high level TIMP1 promoter function.
Splenic sequestration associated with sickle cell trait and hereditary spherocytosis

Coexistence of sickle cell trait and hereditary spherocytosis (HS) is unusual, and only 16 cases have been reported in the literature. These patients have the same clinical and hematological features as individuals having HS alone. We report a serious complication, acute splenic sequestration crisis (ASSC), occurring in two patients with sickle cell trait and HS. One patient experienced four episodes of ASSC during an 11‐year span, while the other had two episodes of this complication during a 4‐year period. Red blood cell studies and membrane protein analysis confirmed the diagnosis of HS as a consequence of spectrin deficiency. Splenectomy resulted in marked clinical and hematological improvement in both patients. Histological examination of spleens following splenectomy confirmed that significant erythrostasis and sickling had indeed occurred. ASSC can occur in patients with coexistence of sickle cell trait and HS, and this potentially life‐threatening complication should be considered in this condition. © 1992 Wiley‐Liss, Inc.
HIV prevalence, risk behaviors, and high-risk sexual and injection networks among young women injectors who have sex with women.

Women injection drug users who have sex with women (WSW IDUs) constitute 20% to 30% of American women IDUs.1 Compared with other women IDUs, WSW IDUs have higher HIV prevalence and incidence rates and a greater likelihood of engaging in high-risk injection and sexual practices with men.1–16 Previous reports suggested that WSW IDUs may be particularly likely to engage in drug injection and sex with men who have sex with men (MSM)1,2,5,6,9,17–19 and to be subordinated and isolated within drug users’ social milieus and more generally.1,20,21 Historical and generational factors may have changed some relationships as a consequence of the HIV epidemic itself, however. Ethnographic data from New York City and Boston, Mass, suggest that many older MSM IDUs and WSW IDUs who injected drugs together may have died earlier in the epidemic, which might reduce the extent to which WSW IDUs currently engage in drug injection and sex with MSM. To further examine HIV risk among WSW IDUs, we compared social situations, injection and sexual networks, and behaviors of young WSW IDUs with those of other young women IDUs.
Ca2+-dependent Localization of Integrin-linked Kinase to Cell Junctions in Differentiating Keratinocytes*

Integrin complexes are necessary for proper proliferation and differentiation of epidermal keratinocytes. Differentiation of these cells is accompanied by down-regulation of integrins and focal adhesions as well as formation of intercellular adherens junctions through E-cadherin homodimerization. A central component of integrin adhesion complexes is integrin-linked kinase (ILK), which can induce loss of E-cadherin expression and epithelial-mesenchymal transformation when ectopically expressed in intestinal and mammary epithelia. In cultured primary mouse keratinocytes, we find that ILK protein levels are independent of integrin expression and signaling, since they remain constant during Ca2+-induced differentiation. In contrast, keratinocyte differentiation is accompanied by marked reduction in kinase activity in ILK immunoprecipitates and altered ILK subcellular distribution. Specifically, ILK distributes in close apposition to actin fibers along intercellular junctions in differentiated but not in undifferentiated keratinocytes. ILK localization to cell-cell borders occurs independently of integrin signaling and requires Ca2+ as well as an intact actin cytoskeleton. Further, and in contrast to what is observed in other epithelial cells, ILK overexpression in differentiated keratinocytes does not promote E-cadherin down-regulation and epithelial-mesenchymal transition. Thus, novel tissue-specific mechanisms control the formation of ILK complexes associated with cell-cell junctions in differentiating murine epidermal keratinocytes.
Evaluation the compressive and diametric tensile strength of nano and hybrid composites

Madam, Over time several changes have been made in formulation to produce composite materials for adequate clinical success. The latest innovations are the development of dental composites based on nanotechnology. [1,2] So we decide to evaluate the physical properties Diametral Tensile Strength (DTS) and Compressive Strenghth (CS) of such new materials in this study. Four different light‐activated resin composite materials of A2 shades (10 samples in each group) were used.
Autopsy findings in a human immunodeficiency virus-infected population over 2 decades: influences of gender, ethnicity, risk factors, and time.

OBJECTIVES To examine autopsy pathology in an urban population infected with the human immunodeficiency virus (HIV) and to determine if age at death and disease frequencies are associated with gender, HIV risk factors, ethnicity, and therapeutic era. DESIGN AND METHODS Retrospective analysis of autopsy data from 394 HIV-infected adults. The population was divided into 3 therapeutic eras for analysis: group A, 1979-1986; group B, 1987-1995; and group C, 1996-2000. RESULTS Women died at significantly younger ages than men (mean +/- SEM age, 38.9 +/- 1.0 years vs 42.5 +/- 0.64 years), even after adjustment for risk factors, ethnicity, and therapeutic era. This age discrepancy occurred despite a lower prevalence of arteriosclerosis, cachexia, and hepatitis B in women and no significant differences in the frequencies of other infectious diseases. Whites had a longer survival than patients of other ethnicities (mean age at death, 44.7 +/- 1.2 years for whites, 39.9 +/- 0.80 years for blacks, and 41.3 +/- 0.87 years for Hispanic individuals). Renal, cardiac, and splenic pathologies, Mycobacterium avium-intracellulare (MAI) infection, and cachexia were more common in blacks than in whites and/or Hispanic individuals, and cytomegalovirus and systemic lymphoma were more common in whites and Hispanic individuals than in blacks. Diseases associated with intravenous drug use were hepatitis C, cirrhosis, and tuberculosis; those with all sexual risk factors, cytomegalovirus infection, herpes simplex virus infection, and Pneumocystis carinii pneumonia; and those with homosexual risk, Kaposi sarcoma and MAI infection. The prevalence of many disease entities changed over time: compared with the other groups, group C had lower prevalences of many viral and fungal illnesses, MAI infection, systemic lymphoma, cachexia, and Kaposi sarcoma and higher prevalences of hepatitis, cirrhosis, arteriosclerosis, staphylococcal and streptococcal infections, and traumatic lesions. When the data were adjusted for changing demographic and risk composition, the only significant changes in disease frequency for period C were decreased prevalences of PCP and Kaposi sarcoma and increased prevalences of cirrhosis and arteriosclerosis. CONCLUSIONS Significant gender- and ethnicity-related differences in age of death occurred in this HIV-infected population, and these differences were not explained by the frequencies of diseases. The lower prevalences of PCP and Kaposi sarcoma in group C are likely a reflection of the impact of potent therapies on causes of mortality. The higher prevalences of cirrhosis and arteriosclerosis suggest that entities not targeted by antiretroviral reconstitution of immunity will play an increasingly important role in HIV-related mortality in the future.
A maternal-effect selfish genetic element in Caenorhabditis elegans

Selfish genetic interactions in nematodes Identifying the effects and evolution of selfish genetic elements can be difficult because of their biased inheritance. Ben-David et al. identified a selfish genetic element that drives maternal-effect lethality in the nematode Caenorhabditis elegans (see the Perspective by Phadnis). This incompatibility stems from the interaction between a maternally deposited toxin and a zygotically expressed antidote. Interestingly, the antidote is encoded by the gene pha-1, which has been described as an essential gene in embryonic development. Science, this issue p. 1051; see also p. 1013 A gene thought to be essential for nematode worm development is, in fact, a toxin antidote and part of a selfish genetic element. Selfish genetic elements spread in natural populations and have an important role in genome evolution. We discovered a selfish element causing embryonic lethality in crosses between wild strains of the nematode Caenorhabditis elegans. The element is made up of sup-35, a maternal-effect toxin that kills developing embryos, and pha-1, its zygotically expressed antidote. pha-1 has long been considered essential for pharynx development on the basis of its mutant phenotype, but this phenotype arises from a loss of suppression of sup-35 toxicity. Inactive copies of the sup-35/pha-1 element show high sequence divergence from active copies, and phylogenetic reconstruction suggests that they represent ancestral stages in the evolution of the element. Our results suggest that other essential genes identified by genetic screens may turn out to be components of selfish elements.
Sodium Hydrogen Exchange 1 ( NHE-1 ) Regulates Connexin 43 Expression in Cardiomyocytes via Reverse Mode Sodium Calcium Exchange and JNK Dependent Pathways

Connexin 43, the major connexin isoform in gap junctions of cardiac ventricular myocytes, undergoes changes in distribution and expression in cardiac diseases. The Na-H exchanger (NHE-1), a key mediator of hypertrophy and heart failure has been shown to be localized in the cardiomyocyte gap junctional regions, however whether NHE-1 regulates gap junction proteins in the hypertrophied cardiomyocyte is not known. To address this question neonatal rat ventricular myocytes were treated with phenylephrine (PE) for 24 hours to induce hypertrophy. Increased Cx43 expression observed with PE treatment (132.4 ± 6.3 % compared to control; P<0.05) was further significantly augmented by the specific NHE-1 inhibitor EMD87580 (173.2 ± 8.7 % increase compared to control; P<0.05 vs PE), an effect which was mimicked by another NHE-1 inhibitor cariporide. PE-induced hypertrophy was associated with MAPK JNK1/2 activation whereas inhibition of JNK1/2 with either SP60015 or using siRNA significantly increased PE-induced upregulation of Cx43 protein levels. Inhibition of reverse mode Na-Ca exchange (NCX) with KB-R7943 partially reversed JNK1/2 activation (195.2 ± 21.4 % vs 143.7 ± 14.4 % with KB-R7943; P<0.05) and augmented upregulation of Cx43 protein (121.1 ± 8.3 % vs 215.9 ± 25.6 % with KB-R7943; P<0.05) in the presence of PE. Our results demonstrate that NHE-1 negatively regulates Cx43 protein expression in PE-induced cardiomyocyte hypertrophy via a JNK1/2 dependent pathway which is likely activated by reverse mode NCX activity. This article has not been copyedited and formatted. The final version may differ from this version. JPET Fast Forward. Published on July 23, 2008 as DOI: 10.1124/jpet.108. 140228 at A PE T Jornals on N ovem er 3, 2017 jpet.asjournals. org D ow nladed from
Catastrophic Failure in Highly Scaled Commercial NAND Flash Memories

Heavy ion single-event measurements on a variety of high density commercial NAND flash memories are reported. Three single event effect (SEE) phenomena were investigated: single effect upsets (SEUs), single effect functional interrupts (SEFIs), and a new high current phenomenon which at high LETs results in catastrophic loss of ability to erase and program the device.
What Matters? Shaping Meaningful Learning through Teaching Information Literacy

The point of departure for this article is an assumed gap between the different communities concerned with the practices of teaching or researching information literacy. Its purpose is to discuss some critical features of teaching information literacy identified in three previous research studies with a view toward understanding how they support meaningful learning outcomes and what the implications of this understanding are for information literacy education. The analysis is framed by a sociocultural perspective of learning that views information seeking and learning as social practices set within the discursive practice of school. The findings indicate that teacher/student interaction with a focus on learning goals and content is a vital condition for students' meaningful learning. Focus on the object of teaching, away from information seeking skills toward an emphasis on the quality of students' research questions, on negotiating learning goals between pedagogues and students, and on the critical evaluation of information sources related to the knowledge contents of students' assignments improves learning. The conclusions are that observing such critical features of information literacy in teaching may allow the discursive practice of school to be reshaped in favour of more genuine research-based learning. A second conclusion is that there are mutual benefits in a closer interaction between the communities of teaching and researching information literacy.
Aspects of the biological redox chemistry of cysteine: from simple redox responses to sophisticated signalling pathways

Abstract The last decade has witnessed an increased interest in cysteine modifications such as sulfenic and sulfinic acids, thiyl radicals, sulfenyl-amides and thiosulfinates, which come together to enable redox sensing, activation, catalysis, switching and cellular signalling. While glutathionylation, sulfenyl-amide formation and disulfide activation are examples of relatively simple redox responses, the sulfinic acid switch in peroxiredoxin enzymes is part of a complex signalling system that involves sulfenic and sulfinic acids and interacts with kinases and sulfiredoxin. Although the in vivo evaluation of sulfur species is still complicated by a lack of appropriate analytical techniques, research into biological sulfur species has gained considerable momentum and promises further excitement in the future.
Bacterial adhesion on smooth and rough titanium surfaces after treatment with different instruments.

BACKGROUND Newly formed biofilm after implant debridement may challenge the long-term stability of peri-implant therapy. This in vitro study aimed to assess the roughness and adherence of Streptococcus sanguinis after treatment of smooth and rough titanium surfaces with an erbium-doped:yttrium, aluminum, and garnet (Er:YAG) laser, metal and plastic curets, and an air-powder abrasive system. METHODS Forty titanium disks with smooth-machined surfaces and 40 with sand-blasted and acid-etched surfaces were divided into the following treatment groups: Er:YAG laser; plastic curet; metal curet, and air-powder abrasive system. The surface roughness (roughness average [Ra]) before and after treatments was determined using a profilometer. S. sanguinis (American Type Culture Collection 10556) was grown on treated and untreated specimens, and the amounts of retained bacteria on the surfaces were measured by the culture method. Rough and smooth surfaces with and without a suspension of S. sanguinis were also analyzed using scanning electron microscopy (SEM). RESULTS For smooth surfaces, the roughest surfaces were produced by metal curets (repeated-measures analysis of variance [ANOVA] and Tukey test; P <0.05). The rough-surface profile was not altered by any of the treatments (repeated-measures ANOVA; P >0.05). Rough surfaces treated with metal curets and air-powder abrasion showed the lowest level of bacterial adhesion (two-way ANOVA and Tukey test; P <0.05). SEM analysis revealed distinct surface profiles produced by all devices. CONCLUSIONS Metal curets are not recommended for smooth titanium surface debridement due to severe texture alteration. Rough surfaces treated with a metal curet and the air-powder abrasive system were less susceptible to bacterial adhesion, probably due to texture modification and the presence of abrasive deposits.
The relationship between non-injection drug use behaviors on progression to AIDS and death in a cohort of HIV seropositive women in the era of highly active antiretroviral therapy use.

AIMS To evaluate the effects of longitudinal patterns and types of non-injection drug use (NIDU) on HIV progression in the highly active antiretroviral therapy (HAART) era. DESIGN Women's Interagency HIV Study (WIHS), a prospective cohort study conducted at six US sites. METHODS Data were collected semi-annually from 1994 to 2002 on 1046 HIV(+) women. Multivariate Cox proportional hazards modeling was used to estimate relative hazards for developing AIDS and for death by pattern and type of NIDU. FINDINGS During follow-up, 285 AIDS events and 287 deaths, of which 177 were AIDS-related, were reported. At baseline, consistent and former NIDU was associated with CD4(+) counts of < 200 cells/microl (43% and 46%, respectively) and viral load > 40,000 copies/ml (53% and 55%, respectively). Consistent NIDU reported less HAART use (53%) compared with other NIDU patterns. Stimulant use was associated with CD4(+) cell counts of < 200 cells/microl (53%) and lower HAART initiation (63%) compared with other NIDU types. In multivariate analyses, progression to AIDS was significantly higher among consistent (RH = 2.52), inconsistent (RH = 1.63) and former (RH = 1.56) users compared with never users; and for stimulant (RH = 2.04) and polydrug (RH = 1.65) users compared with non-users. Progression to all-cause death was higher only among former users (RH = 1.48) compared with never users in multivariate analysis. NIDU behaviors were not associated with progression to AIDS-related death. CONCLUSIONS In this study, pattern and type of NIDU were associated with HIV progression to AIDS and all-cause mortality. These differences were associated with lower HAART utilization among consistent NIDU and use of stimulants, and poor baseline immunological and virological status among former users.
Can pre-placement health assessments predict subsequent sickness absence?

BACKGROUND Sickness absence is a growing economic problem, due largely to the financial losses it incurs. The ability to identify employees likely to take greater than average sickness absence may provide managers with useful information at the pre-placement stage. AIM To confirm whether specific risk factors identified at the pre-placement health assessment could predict subsequent sickness absence. METHODS A total of 400 National Health Service pre-placement health questionnaires were analysed to allocate employees to low-, medium- or high-risk categories for subsequent sickness absence, using the risk table developed by C. J. M. Poole (Can sickness absence be predicted at the pre-placement health assessment? Occup Med (Lond) 1999; 49:337-339) [1]. Subsequent sickness absence was analysed to assess if there was an association between the allocated category and sickness absence taken. RESULTS Mean sickness absence hours per 1000 h worked were 22.5 (95% CI 18.2-27.2) in the low-risk group, 33.6 (27.2-40.7) in the medium-risk group and 44.7 (25.1-69.9) in the high-risk group (analysis of variance, P <or= 0.002), demonstrating a statistically significant difference in sickness absence taken in subsequent years. CONCLUSIONS The results confirmed Poole's hypothesis that future sickness absence can be predicted at the pre-placement health assessment. Certain risk factors, namely female sex, age, smoking, history of at least two previous episodes of low-back pain and previous days sickness absence identified at pre-placement assessment, predict a greater than average subsequent sickness absence. However, the best model using identified risk factors only predicted 10-12% of the variation in sickness absence.