Tulane University

About: Tulane University is a education organization based out in New Orleans, Louisiana, United States. It is known for research contribution in the topics: Population & Blood pressure. The organization has 24478 authors who have published 47205 publications receiving 1944993 citations. The organization is also known as: University of Louisiana.

Value of Strong Ties to Disconnected Others: Examining Knowledge Creation in Biomedicine

Abstract: Knowledge creation requires the combination and exchange of diverse and overlapping knowledge inputs as individuals interact with exchange partners to create new knowledge. In this study, we examine knowledge creation among university research scientists as a function of their professional (ego) networks---those others with whom they collaborate for the purpose of creating new knowledge. We propose that knowledge creation relies, in part, on two attributes of a researcher's professional network structure---average tie strength and ego network density---and we provide insights into how these attributes jointly affect knowledge creation. Our study of over 7,300 scientific publications by 177 research scientists working with more than 14,000 others over an 11-year period provides evidence that the relationship between a research scientist's professional network and knowledge creation depends on both ego network density and average tie strength. Our evidence suggests that both attributes affect knowledge creation. Moreover, average tie strength interacts with density to affect knowledge creation such that researchers who maintain mostly strong ties with research collaborators who themselves comprise a sparse network have the highest levels of new knowledge creation.

Diverse Roles of Mitochondria in Immune Responses: Novel Insights Into Immuno-Metabolism.

Abstract: Lack of immune system cells or impairment in differentiation of immune cells is the basis for many chronic diseases Metabolic changes could be the root cause for this immune cell impairment These changes could be a result of altered transcription, cytokine production from surrounding cells, and changes in metabolic pathways Immunity and mitochondria are interlinked with each other An important feature of mitochondria is it can regulate activation, differentiation, and survival of immune cells In addition, it can also release signals such as mitochondrial DNA (mtDNA) and mitochondrial ROS (mtROS) to regulate transcription of immune cells From current literature, we found that mitochondria can regulate immunity in different ways First, alterations in metabolic pathways (TCA cycle, oxidative phosphorylation, and FAO) and mitochondria induced transcriptional changes can lead to entirely different outcomes in immune cells For example, M1 macrophages exhibit a broken TCA cycle and have a pro-inflammatory role By contrast, M2 macrophages undergo β-oxidation to produce anti-inflammatory responses In addition, amino acid metabolism, especially arginine, glutamine, serine, glycine, and tryptophan, is critical for T cell differentiation and macrophage polarization Second, mitochondria can activate the inflammatory response For instance, mitochondrial antiviral signaling and NLRP3 can be activated by mitochondria Third, mitochondrial mass and mobility can be influenced by fission and fusion Fission and fusion can influence immune functions Finally, mitochondria are placed near the endoplasmic reticulum (ER) in immune cells Therefore, mitochondria and ER junction signaling can also influence immune cell metabolism Mitochondrial machinery such as metabolic pathways, amino acid metabolism, antioxidant systems, mitochondrial dynamics, mtDNA, mitophagy, and mtROS are crucial for immune functions Here, we have demonstrated how mitochondria coordinate to alter immune responses and how changes in mitochondrial machinery contribute to alterations in immune responses A better understanding of the molecular components of mitochondria is necessary This can help in the development of safe and effective immune therapy or prevention of chronic diseases In this review, we have presented an updated prospective of the mitochondrial machinery that drives various immune responses

Cavernous neurotomy causes hypoxia and fibrosis in rat corpus cavernosum.

Abstract: The etiologies of erectile dysfunction (ED) after nerve-sparing radical prostatectomy have not been clearly elucidated. The aim of this study was to evaluate the effects of cavernous nerve injury on cavernous fibrosis, and to consider measures to prevent irreversible damage to the cavernous tissues. Twenty male Sprague-Dawley rats constituted the study population. The animals were divided into 2 groups; group 1 consisted of sham-operated rats (n = 10), and group 2 consisted of rats that underwent incision of both cavernous nerves (n = 10). Three months later, all rats underwent intracavernous papaverine injection (300 and 600 mg), and intracorporal pressures were recorded. Transforming growth factor-beta(1) (TGF-beta(1)) messenger RNA (mRNA) expression from rat penile tissue was measured using reverse transcriptase-polymerase chain reaction. Hypoxia-inducible factor-1alpha (HIF-1alpha), TGF-beta(1), and collagen I and III protein expressions were determined by Western blot analysis and immunohistochemical staining. Erectile function as studied with intracavernosal papaverine injection and histological analysis of penile cross-sections at 3 months was similar in both groups. TGF-beta(1) mRNA expression, HIF-1alpha, TGF-beta(1), and collagen I and III protein expressions were significantly greater in the neurotomy group. Immunohistochemical staining for TGF-beta(1), HIF-1alpha, and collagen III were qualitatively more positive in the neurotomy group, whereas collagen I staining was similar. This study demonstrates an increase in TGF-beta(1), HIF-1alpha, and collagen III synthesis in rat cavernosal smooth musculature after cavernous neurotomies. In theory, cavernous fibrosis may be reduced by employing various vasoactive agents or interventions that increase oxygenation to the corporal tissues during the postoperative period.

Comparison of bisulfite modification of 5-methyldeoxycytidine and deoxycytidine residues

Abstract: Sodium bisulfite is a mutagen which can specifically deaminate more than 96% of the cytosine residues in single-stranded DNA via formation of a 5,6-dihydrocytosine-6-sulfonate intermediate. Under the same reaction conditions, only 2-3% of the 5-methylcytosine (m5Cyt) residues in single-stranded XP-12 DNA, which has 34 mole% m5Cyt, was converted to thymine (Thy) residues. In contrast, at the deoxynucleoside and free base levels, the same treatment with bisulfite and then alkali converted 51% and > 95%, respectively, of the m5Cyt to the corresponding Thy derivatives. However, the rate of reaction of m5Cyt and its deoxyribonucleoside was much slower than that of the analogous quantitative conversion of cytosine or deoxycytidine to uracil or deoxyuridine, respectively. The much lower reactivity of m5Cyt and its derivatives compared to that of the unmethylated analogs is primarily due to a decrease in the rate of formation of the sulfonate adduct.