65 research outputs found
Analysis of Production, Impact, and Scientific Collaboration on Difficult Airway Through the Web of Science and Scopus (1981–2013)
No full textBackground: Bibliometrics, the statistical analysis of written publications, is an increasingly popular approach to the assessment of scientific activity. Bibliometrics allows researchers to assess the impact of a field, or research area, and has been used to make decisions regarding research funding. Through bibliometric analysis, we hypothesized that a bibliometric analysis of difficult airway research would demonstrate a growth in authors and articles over time.
Methods: Using the Web of Science (WoS) and Scopus databases, we conducted a search of published manuscripts on the difficult airway from January 1981 to December 2013. After removal of duplicates, we identified 2412 articles. We then analyzed the articles as a group to assess indicators of productivity, collaboration, and impact over this time period.
Results: We found an increase in productivity over the study period, with 37 manuscripts published between 1981 and 1990, and 1268 between 2001 and 2010 (P 9% for both WoS and Scopus, and CAGR for anesthesiology as a whole =0.64% in WoS, and =3.30% in Scopus. Furthermore, we found a positive correlation between the number of papers published per author and the number of coauthored manuscripts (P < .001). We also found an increase in the number of coauthored manuscripts, in international cooperation between institutions, and in the number of citations for each manuscript. For any author, we also identified a positive relationship between the number of citations per manuscript and the number of papers published (P < .001).
Conclusions: We found a greater increase over time in the number of difficult airway manuscripts than for anesthesiology research overall. We found that collaboration between authors increases their impact, and that an increase in collaboration increases citation rates. Publishing in English and in certain journals, and collaborating with certain authors and institutions, increases the visibility of manuscripts published on this subject.Depto. de MedicinaFac. de MedicinaTRUEpu
2008 Author Recognition Bibliography
No full texthttps://scholarworks.gvsu.edu/authorrecognition/1006/thumbnail.jp
The helix-loop-helix transcriptional regulator Id4 is required for terminal differentiation of luminal epithelial cells in the prostate
No full textInhibitor of differentiation 4 (Id4), a member of the helix-loop-helix family of transcriptional regulators has emerged as a tumor suppressor in prostate cancer. In this study we investigated the effect of loss of Id4 (Id4-/-) on mouse prostate development. Histological analysis was performed on prostates from 25 days, 3 months and 6 months old Id4-/- mice. Expression of Amacr, Ck8, Ck18, Fkbp51, Fkbp52, androgen receptor, Pten, sca-1 and Nkx3.1 was investigated by immunohistochemistry. Results were compared to the prostates from Nkx3.1-/-mice. Id4-/- mice had smaller prostates with fewer and smaller tubules. Subtle PIN like lesions were observed at 6mo. Decreased Nkx3.1 and Pten and increased stem cell marker sca-1, PIN marker Amacr and basal cell marker p63 was observed at all ages. Persistent Ck8 and Ck18 expression suggested that loss of Id4 results in epithelial commitment but not terminal differentiation in spite of active Ar. Loss of Id4 attenuates normal prostate development and promotes hyperplasia/ dysplasia with PIN like lesions. The results suggest that loss of Id4 maintains stem cell phenotype of �luminal committed basal cells�, identifying a unique prostate developmental pathway regulated by Id4
Knowledge, attitudes, and perceptions towards waterpipe tobacco smoking amongst college or university students: a systematic review
No full textBackground
Despite evidence for the harms of waterpipe tobacco smoking (WTS), its use is increasing amongst college and university students worldwide. This systematic review aims to assess the knowledge of, attitudes towards and perceptions of WTS among college or university students.
Methods
We electronically searched MEDLINE, EMBASE, CINAHL, PSYCHINFO and ISI the Web of Science in October 2018, restricting our search to studies published since January 1990. We included studies among university or college students that used qualitative or quantitative methods, and addressed either knowledge, attitudes, or perceptions towards WTS. We excluded studies where WTS could not be distinguished from other forms of tobacco use and studies reported as abstracts where the full text could not be identified. Data were synthesised qualitatively and analysed data by region (global north/ south), and by reasons for use, knowledge of health hazards, how knowledge influences use, perceptions towards dependence, and policy knowledge.
Results
Eighty-six studies were included; 45 from the global north and 41 from the global south. Socio-cultural and peer influences were major contributing factors that encouraged students to initiate WTS. Furthermore, WTS dependence had two components: psychological and social. This was compounded by the general perception that WTS is a less harmful, less addictive and more sociable alternative to cigarette smoking. Knowledge of WTS harms failed to correlate with a reduced risk of WTS use, and some students reported symptoms of WTS addiction. A large proportion of students believed that quitting WTS was easy, yet few were able to do so successfully. Finally, students believed current public health campaigns to educate on WTS harms were inadequate and, particularly in the global north, were not required.
Conclusion
Reasons for WTS amongst university students are multi-faceted. Overall, interventions at both the individual and community level, but also policy measures to portray a message of increased harm amongst students, are required. Additional studies are necessitated to understand temporal changes in students’ beliefs, thus allowing for better targeted interventions
TYPIFICATION OF TECTARIA PARADOXA (POLYPODIACEAE SUB-FAM. TECTARIOIDEAE)
No full textMAZUMDAR, J. 2017. Typification of Tectaria paradoxa (Polypodiaceae subfam. Tectarioideae). Reinwardtia 16(2): 93?95. — Aspidium paradoxum has not yet been lectotypified, because the original material is ambiguous. A specimen from the collections of A. Fée, the author of the species, was located in the herbarium of Montpellier (MPU), which is here designated as the lectotype for this species. It is now known as Tectaria paradoxa, a fern species widely distributed across tropical Asia.</jats:p
-174G/C Polymorphism in the Interleukin-6 Promoter Is Differently Associated with Prostate Cancer Incidence Depending on Race
No full textInterleukin-6 (IL-6), a pro-inflammatory cytokine, is involved in prostate cancer progression, including androgen independence. Serum IL-6 levels also correlate with prostate tumor burden, prostate-specific antigen levels and metastasis. Since circulating cytokine levels vary considerably inter-individually, such variation could be linked to genetic factors, including genetic polymorphism. The -174G>C/rs1800795 polymorphism in the IL-6 promoter is functionally relevant in terms of transcriptional regulation and disease association. We investigated a possible association of the -174G/C polymorphism with prostate cancer. Since significant racial disparities exist in prostate cancer incidence, we also investigated this association between the -174G/C polymorphism and prostate cancer in Caucasians and African-Americans, separately. Direct sequencing of the PCR amplicon from genomic DNA was used for genotyping rs1800795 in all subjects [age-matched controls (N = 140) and prostate cancer patients (N = 164)]. Sample size and power was calculated using the PGA software. We found the GG genotype to be associated with increased risk of prostate cancer in Caucasian subjects, whereas the CC genotype was associated with increased risk in the African-American sample set. Such a dimorphic genotypic association with cancer and race is unique and suggests a complex gene-gene and gene-environment interaction
A Modified Coupled Spectrophotometric Method to Detect 2-5 Oligoadenylate Synthetase Activity in Prostate Cell Lines
No full textBackground: 2-5 oligoadenylate synthetases (OAS) are interferon inducible enzymes that polymerizes ATP to 2-5-linked oligomers of adenylate (2-5As). As part of the innate immune response, these enzymes are activated by viral double stranded RNA or mRNAs with significant double stranded structure. The 2-5As in turn activate RNaseL that degrade single stranded RNAs. Three distinct forms of OAS exist in human cells (OAS1, 2 and 3) with each form having multiple spliced variants. The OAS enzymes and their spliced variants have different enzyme activities. OAS enzymes also play a significant role in regulating multiple cellular processes such as proliferation and apoptosis. Moreover, Single nucleotide polymorphisms that alter OAS activity are also associated with viral infection, diabetes and cancer. Thus detection of OAS enzyme activity with a simple spectrophotometric method in cells will be important in clinical research
ID4 as a tumor suppressor: mechanism of action of ID4 in prostate cancer, 2013
No full textId proteins are members of basic helix-loop-helix family. However, Id proteins lack the basic binding domain, which prevents DNA binding, and thereby regulates transcription. There are four members in the Id protein family termed Idl-4. In prostate cancer the expression of Idl and Id3 is high, whereas member Id4 expression is low. Decreased expression of Id4 is due to promoter hypermethylation in prostate cancer as well as many other cancers. This observation led us to hypothesize that Id4 acts as a tumor suppressor in prostate cancer. Furthermore, evidence suggests ectopic Id4 expression in metastatic prostate cancer cell line DU145 induced cell cycle arrest, apoptosis, and senescence. In this study, we expanded on these earlier studies to demonstrate that gain of Id4 attenuates cancer phenotype whereas loss of Id4 promotes cancer phenotype in prostate cancer cell lines DU145 and LNCaP, respectively. Upon over-expression of Id4 in DU145 cells (DU145+W4), there was an increase in apoptosis, due to decreased mitochondrial membrane potential (MMP) and increased expression of pro-apoptotic markers (PUMA, BAX, and p21). Inversely, silencing of Id4 in LNCaP cells (LNCaP-Id4) led to decreased apoptosis due to an intact mitochondrial membrane and decrease in the expression of pro-apoptotic markers (PUMA, BAX, and p21). Since BAX, PUMA, and p21 are direct transcriptional targets of p53, these results therefore prompted us to investigate the effect of Id4 on expression and activity of p53. LNCaP cells express wild-type p53. DU145 cells harbor mutant p53 (P223L and V274F), which lies within the DNA binding domain and abrogates p53 transcriptional activity. DU145 cells also express high levels of p53, due extended half-life. Surprisingly, there was decreased expression of p53 in DU145+Id4 cells associated with nuclear localization indicating enhanced transcriptional activity. We investigated p53 DNA binding and transcriptional activity. We determined that mutant p53 in DU145+Id4 cells was transcriptionally active evident by increased luciferase activity and binding of p53 to the promoters of its targets. In LNCaP-Id4, p53 expression was decreased which resulted in decreased p53 transcriptional activity and decreased DNA binding ability. The data suggested that Id4 can restore mutant p53 activity, which is a significant observation. Our results also suggest that Id4 promotes the assembly of a macromolecular complex involving CBP/p300 that results in acetylation of p53 at K373, a critical post-translational modification required for its biological activity. Loss of Id4 in LNCaP cells also abrogated wild type p53 DNA binding and transcriptional activity with concomitant loss of CBP/p300 requirement and decreased acetylation. In conclusion, we demonstrated that loss of Id4 promotes cancer phenotype in LNCaP cells. We also demonstrated that the tumor suppressor activity of Id4 is in part through regulation of CBP/p300 dependent acetylation and function of p53
ID4 acts as a tumor suppressor via P53: mechanistic insight, 2016
No full textOverexpression of tumor-derived mutant p53 is a common event in tumorigenesis, suggesting an advantageous selective pressure in cancer initiation and progression. Given that p53 is found to be mutated in 50% of all human cancers, restoration of mutant p53 to its wild type biological function has been a widely sought after avenue for cancer therapy. Most research efforts have largely focused on restoration of mutant p53 by artificial means given that p53 has some degree of conformational flexibility allowing for introduction of short peptides and artificial compounds. Recently, theoretical modeling and studies focused on restoration of mutant p53 by physiological means has raised the question of whether there are effective therapies worth exploring that focus on global physiological mechanisms of restoration of p53. Herein, we provide computational analysis of the thermodynamic stabilities of both wild-type and mutant p53 core domains by studying their respective minimum potential energies. Also, it is widely accepted that wild type p53 is modulated by various acetyl transferases as well as deactylases, but whether this mechanism of p53 modulation can be exploited for physiological restoration of mutant p53 remains under intense investigation. Using prostate cancer cell lines representative of varying stages of aggressiveness as a model, we show that ID4 dependent acetylation promotes mutant p53 DNA-binding capabilities to its wild type consensus sequence, thus regulating p53-dependent target genes leading to subsequent cell cycle arrest and apoptosis. Specifically, we identify that ID4 promotes acetylation of K373 and to a lesser extent K320, in turn regulating p53-dependent biological activities. Together, our data provides computational analysis of the core domain of certain mutant forms of p53 and a molecular understanding of ID4 dependent acetylation that suggests a strategy of enhancing p53 acetylation at sites K373 and K320, critical sites of post translational modification of p53, that may serve as a viable mechanism of physiological restoration of mutant p53 to its wild type biological function. KEY TERMS: ID4, p53, tumor suppressor, bhlh, prostate cancer, molecular dynamics, acetylation, Biology, Biophysics, Cancer Biology, Cell Biology, Life Sciences, Molecular Biolog
- …
