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At least 1,423 records · Page 79Linked to original sources
PubMed2002

Interplay among energy metabolism, organ mass and digestive enzyme activity in the mouse-opossum Thylamys elegans: the role of thermal acclimation.

The potential for thermal acclimation in marsupials is controversial. Initial studies suggest that the thermoregulatory maximum metabolic rate (MMR) in metatherians cannot be changed by thermal acclimation. Nevertheless, recent studies reported conspicuous seasonality in both MMR and in basal metabolic rate (BMR). We studied the role of thermal acclimation in the Chilean mouse-opossum, Thylamys elegans, by measuring MMR and BMR before and after acclimation to cold or warm conditions. Following acclimation we also measured the mass of metabolically active organs, and the activity of a key digestive enzyme, aminopeptidase-N. No significant effect of thermal acclimation (i.e. between cold- and warm-acclimated animals) was observed for body mass, MMR, body temperature or factorial aerobic scope. However, the BMR of cold-acclimated animals was 30 % higher than for warm-acclimated individuals. For organ mass, acclimation had a significant effect on the dry mass of caecum, liver and kidneys only. Stepwise multiple regression using pooled data showed that 71 % of the variation in BMR is explained by the digestive organs. Overall, these results suggest that MMR is a rather rigid variable, while BMR shows plasticity. It seems that T. elegans cannot respond to thermal acclimation by adjusting its processes of energy expenditure (i.e. thermogenic capacity and mass of metabolically active organs). The lack of any significant difference in aminopeptidase-N specific activity between warm- and cold-acclimated animals suggests that this response is mainly quantitative (i.e. cell proliferation) rather than qualitative (i.e. differential enzyme expression). Finally, as far as we know, this study is the first to report the effects of thermal acclimation on energy metabolism, organ mass and digestive enzyme activity in a marsupial.

Acclimatization↗
PubMed2026

Evaluating a Genome-Wide Polygenic Score for Handgrip Strength and Its Interplay with Leisure-Time Physical Activity Across the IGEMS Twin Cohorts.

PURPOSE: Polygenic scores (PGSs) may help assess genetic predisposition to multifactorial traits. We examined whether age, sex, and leisure-time physical activity (LTPA) modify the association between a PGS for handgrip strength (HGS) and measured HGS in older adults. METHODS: PGS for HGS (PGS hgs) , based on Pan-UK Biobank genome-wide association study data, was calculated for 5103 participants (aged 40-96; 44% women) from eight twin cohorts in Denmark, Sweden, Australia, the United States, and Finland within the IGEMS consortium. Sex-standardized HGS and self-reported LTPA were assessed cross-sectionally. Linear mixed models estimated associations between PGS hgs and HGS, including interactions with age, country, and LTPA, as well as an association between PGS hgs and LTPA. Fixed-effect within-pair models were conducted to assess environmental contributions. RESULTS: Higher PGS hgs was associated with greater HGS (&#x3b2; = 2.14, SE = 0.15, P < 0.001), explaining 4.6% of HGS variance overall, with modest variation across countries. In sex-stratified models, PGS hgs explained 5.2% of the variance in females and 4.3% in males. No statistically significant interaction with age was found. A significant PGS hgs &#xd7; LTPA interaction (&#x3b2; = -0.034, P = 0.013) indicated that the association between LTPA and HGS was more pronounced among individuals with lower PGS hgs . The within-pair models offered limited support for the independent environmental impact of LTPA. CONCLUSIONS: The PGS hgs was associated with measured HGS in the meta-analysis, highlighting the potential of PGSs to capture individual differences in strength-related traits across populations. The association of PGS hgs with HGS was moderated by LTPA, such that the beneficial impact of LTPA on HGS was greater among individuals with a lower genetic propensity for HGS.

Humans↗
PubMed2006

Social inclusion: an interplay of the determinants of health - new insights into elder abuse.

Social and economic exclusion and inclusion are receiving growing attention and study in North America for their usefulness as a conceptual framework that addresses the many dimensions of poverty and inequality in our society. A discussion of social and economic exclusion/ inclusion flows naturally out of the population health field in which the social determinants of health have become well-established over the last twenty years or more. The determinants of health provide a broad and inclusive outline within which to situate prevention, early detection and effective intervention of the abuse of older persons. A Social Inclusion Lens offers exciting possibilities for addressing the issue of elder abuse and neglect.

Aged↗
PubMed1999

Interaction between impaired and unimpaired speakers: inter-subjectivity and the interplay of culturally shared and situation specific knowledge.

The part played by culturally shared knowledge in interaction is generally recognised. However, the details of how it may be manifested in interaction are largely undocumented. This study explores this issue in the context of interactions between impaired and unimpaired speakers, using a conversation analytic approach in combination with a communication task commonly employed in experimental social psychology. Three exemplary cases are analysed. Results show that when the task interaction is co-constructed, the interaction is collaboratively enacted, participants' actions are in alignment, and the task outcome is relatively accurate. When the unimpaired speaker proceeds on the basis of culturally shared knowledge, and thereby 'unilaterally' manages the interaction, two courses of action are available to the impaired speaker. The impaired speaker may make attempts to provide situation specific details. In this case, because each participant is drawing on different resources to construct the interaction, their actions are out of alignment, and the task outcome is less accurate. Alternatively, the impaired speaker may concur with the culturally shared knowledge drawn on by the unimpaired speaker, in which case the participants' actions are in alignment, but the task outcome is highly inaccurate. The authors conclude that by combining a conversation analytic approach with a communication task which reflects participants' everyday experiences, orientations to different interaction resources can be drawn out. This can have relevance for, and help to elicit, practices in everyday interaction.

Adult↗
PubMed2025

Comparative virulence analysis of seven diverse strains of Orientia tsutsugamushi reveals a multifaceted and complex interplay of virulence factors responsible for disease.

Orientia tsutsugamushi is an obligate intracellular bacterium found in Leptotrombidium mites that causes the human disease scrub typhus. A distinguishing feature of O. tsutsugamushi is its extensive strain diversity, yet differences in virulence between strains are not well defined nor well understood. We sought to determine the bacterial drivers of pathogenicity by comparing seven strains using murine infections combined with epidemiological human data to rank each strain in terms of relative virulence. Murine cytokine expression data revealed that the two most virulent strains, Ikeda and Kato, induced higher levels of IL-6, IL-10, IFN-&#x3b3; and MCP-1 than other strains, consistent with increased levels of these cytokines in patients with severe scrub typhus. We sought to identify the mechanistic basis of the observed differential virulence between strains by comparing their genomes, in vitro growth properties and cytokine/chemokine induction in host cells. We found that there was no single gene or gene group that correlated with virulence, and no clear pattern of in vitro growth rate that predicted disease. However, microscopy-based analysis of the intracellular infection cycle revealed that the only fully avirulent strain in our study, TA686, differed from all the virulent strains in its subcellular localisation and expression of its surface protein ScaC. This leads us to a model whereby drivers of pathogenicity in Orientia tsutsugamushi are distributed throughout the genome, likely in the large and varying arsenal of effector proteins encoded by different strains, and that these interact in complex ways to induce differing immune responses and thus differing disease outcomes in mammalian hosts.

Orientia tsutsugamushi↗
PubMed2006

Interplay between the p53 tumor suppressor protein family and Cdk5: novel therapeutic approaches for the treatment of neurodegenerative diseases using selective Cdk inhibitors.

Cyclin-dependent kinases (Cdks) play a key role in orchestrating the coordination of cell cycle progression in proliferating cells. The escape from the proper control of the cell cycle by the upregulation of cyclins or aberrant activation of Cdks leads to malignant transformation. In quiescent cells and/or terminally differentiated cells, the expression pattern and activity of Cdks is altered. In postmitotic neurons, expression of mitotic kinases is downregulated, whereas Cdk5 expression becomes upregulated. Similarly to other Cdks, free Cdk5 displays no enzymatic activity and requires complex formation with a specific regulatory subunit. Two activators of Cdk5 have been identified. p35 and its isoform p39 bind to, and thereby activate, Cdk5. Unlike mitotic kinases, Cdk5 does not require activating phosphorylation within the T-loop. Because p35 is a short-lived protein, the p35/Cdk5 complexes are unstable. The stability of the p35 protein is regulated by its Cdk5-mediated phosphorylation of p35. Activated p35/Cdk5 kinase phosphorylates numerous physiological targets. The proper phosphorylation of the most important substrates, such as tau protein and neurofilament H, is essential for the correct regulation of the cytoskeletal organization, thereby regulating cell adhesion, motility, and synaptic plasticity. Moreover, Cdk5 regulates the activity of the p53 tumor suppressor via phosphorylation. p53 is upregulated in multiple neuronal death paradigms, including hypoxia, ischemia, and excitotoxicity, and plays a key role in the induction of apoptosis. On the other hand, an abnormally high expression and elevated activity of Cdk5 was observed in neurodegenerative diseases, suggesting the application of Cdk inhibitors for their therapy. Considering the action of some Cdk inhibitors on the expression and activity of the p53 protein, their therapeutic efficacy must be carefully evaluated.

Animals↗
PubMed2004

Interplay of Pax6 and SOX2 in lens development as a paradigm of genetic switch mechanisms for cell differentiation.

When the cloning era arrived, our first target for cloning was the delta1-crystallin gene of the chicken, the lens-specific gene expressed earliest following lens induction. We have investigated the regulation of this gene with the idea that the mechanism of its activation must reflect that of lens differentiation per se. We here summarize the investigation carried out in our group along this line over the past 20 years. The delta1-crystallin gene is regulated by an enhancer in the third intron, and the specificity of this regulation is governed by a DNA region (called DC5) of only 30 bp DNA bound by two transcription factors. These factors have been identified as SOX1/2/3 (Group B1 SOX proteins, SOX2 being the major player) and Pax6, and have been shown to bind cooperatively to DC5 and form a ternary complex having a robust potency for transcriptional activation. In the embryo, Pax6 is widely expressed in the head ectoderm before the lens is formed, and as the optic vesicle comes into contact with the ectoderm, SOX2/3 expression is induced in the contacted area of the ectoderm, thereby allowing Pax6 and SOX2/3 to meet in the same cell nucleus, where they can then activate a battery of genes for early lens development including delta1-crystallin. Thus, the cooperative action of Pax6 and SOX2 initiates lens differentiation. More broadly, SOX1/2/3 interact with various partner transcription factors, and participate in defining distinct cell states that depend on the partner factors: Pax6 for lens differentiation, Oct3/4 for establishing the epiblast/ES cell state, and Brn2 for the neural primordia. Thus, the regulation of SOX2 (and SOX1/3) and its partner factors, exemplified by Pax6, determines the spatio-temporal order of the occurrence of cell differentiation.

Animals↗
PubMed2006

Interplay between FGF10 and Notch signalling is required for the self-renewal of pancreatic progenitors.

Recent studies have shown that persistent expression of FGF10 in the developing pancreas of transgenic mice results in enhanced and prolonged proliferation of pancreatic progenitors, pancreatic hyperplasia and impaired pancreatic differentiation. These studies have also suggested that FGF10 prevents the differentiation of pancreatic progenitors by maintaining persistent Notch signalling. Here, we provide experimental evidence sustaining the capacity of FGF10 to induce the proliferation of pancreatic precursors, while preventing their differentiation. Using explant cultures of E10.5 isolated dorsal pancreatic epithelium, we found that FGF10 maintained Notch activation and induced the expansion of pancreatic precursors while blocking their differentiation. In addition, by using a gamma-secretase inhibitor, we were able to down-regulate the expression of Hes1, a target gene of the Notch pathway in explant cultures of pancreatic epithelium treated with FGF10. In such explants, the effect of FGF10 on the proliferation and maintenance of pancreatic progenitors was suppressed. These results demonstrate that activation of the Notch pathway is required as a downstream mediator of FGF10 signalling in pancreatic precursor cells.

Animals↗
PubMed2002

Tumour morphology--interplay between chromosome aberrations and founder cell differentiation.

Studies of haematological neoplasms have shown that alterations in structure and/or expression of transcription factor genes may play a crucial role for transforming stem cells or progenitor cells into malignant cells. These mutations typically arise through balanced translocations and appear to induce a block in cellular differentiation. The impact of the transforming mutation is highly dependent on the lineage of the founder cell and each specific translocation is limited to one or a few morphological subtypes. Originating from immature cells, these neoplasms have a high self-replicative capacity and are already before transformation protected from senescence by constitutive telomerase expression. Most solid tumours, on the other hand, probably originate from cells at higher levels of differentiation and require multiple mutations in oncogenes and tumour suppressor genes for neoplastic transformation. Absence of telomerase activity in the tumour-founding cell line predisposes to abnormal shortening of telomeric repeats in these cells during early clonal expansion. In turn, this triggers chromosomal breakage-fusion-bridge events through which the tumour genome is constantly reorganised, resulting in a complex and heterogeneous pattern of chromosome aberrations in the tumour cell population; the abnormal mitotic processes also give rise to cellular pleomorphism and nuclear atypia. Tumour morphology thus appears to be determined not only by the lineage of the transformed cell but also by its propensity for chromosomal instability.

Animals↗
PubMed2006

Interplay of human tissue kallikrein 4 (hK4) with the plasminogen activation system: hK4 regulates the structure and functions of the urokinase-type plasminogen activator receptor (uPAR).

The plasminogen activation system is involved in cancer progression and metastasis. Among other proteolytic factors, it includes the serine protease urokinase-type plasminogen activator (uPA) and its three-domain (D1D2D3) receptor uPAR (CD87), which focuses plasminogen activation to the cell surface. The function of uPAR is regulated in part through shedding of domain D1 by proteases, e.g., uPA itself or plasmin. Human tissue kallikrein 4 (hK4), which is highly expressed in prostate and ovarian tumor tissue, was previously shown to cleave and activate the pro-enzyme forms of prostate-specific antigen (PSA, tissue kallikrein hK3) and uPA. Here we demonstrate that uPAR is also a target for hK4, being cleaved in the D1-D2 linker sequence and, to a lesser extent, in its D3 juxtamembrane domain. hK4 may thus modulate the tumor-associated uPA/uPAR-system activity by either activating the pro-enzyme form of uPA or cleaving the cell surface-associated uPA receptor.

Dose-Response Relationship, Drug↗
PubMedDate not supplied

Pathogenetic interplay between osmotic and oxidative stress: the hepatic encephalopathy paradigm.

Hepatic encephalopathy (HE) defines a primary gliopathy associated with acute and chronic liver disease. Astrocyte swelling triggered by ammonia in synergism with different precipitating factors, including hyponatremia, tumor necrosis factor (TNF)-alpha, glutamate and ligands of the peripheral benzodiazepine receptor (PBR), is an early pathogenetic event in HE. On the other hand, reactive nitrogen and oxygen species (RNOS) including nitric oxide are considered to play a major role in HE. There is growing evidence that osmotic and oxidative stresses are closely interrelated. Astrocyte swelling produces RNOS and vice versa. Based on recent investigations, this review proposes a working model that integrates the pathogenetic action of osmotic and oxidative stresses in HE. Under participation of the N-methyl-D-aspartate (NMDA) receptor, Ca(2+), the PBR and organic osmolyte depletion, astrocyte swelling and RNOS production may constitute an autoamplificatory signaling loop that integrates at least some of the signals released by HE-precipitating factors.

Animals↗
PubMed2003

Homocysteine, methylenetetrahydrofolate reductase C677T polymorphism and the B-vitamins: a facet of nature-nurture interplay.

BACKGROUND: Methylenetetrahydrofolate reductase 677 (MTHFR 677) polymorphism may provoke hyperhomocysteinemia when folate status is low. The influence of MTHFR 677 mutation on homocysteine (HCY) levels in relation to vitamin B12 and folate status was investigated in the current study. SUBJECTS AND METHODS: 113 vegetarians, 123 omnivorous Germans, and 117 omnivorous Syrians were recruited. MTHFR 677 genotype, HCY, methylmalonic acid (MMA), total serum vitamin B12, serum folate, and vitamin B6 were determined using conventional methods. RESULTS: Omnivorous Germans displayed the lowest HCY levels compared with vegetarians and Syrians (median 8.0, 10.4, and 11.3 micromol/l, respectively). The highest serum folate and the highest MMA levels were found in vegetarians (median folate = 30.0; MMA = 355 nmol/l). Among vegetarians and Syrians, TT subjects had higher HCY levels than other genotypes which were, however, no longer significant in the highest folate tertiles. When the data were pooled, the odds ratio (OR, 95% CI) for HCY > 12 micromol/l was 3.81 (1.55-9.34) in TT compared with CC subjects. The OR increased to 28.85 (4.63-179.62) in TT subjects who had folate in the lowest tertile, and to 21.84 (4.81-99.1) in TT subjects who had MMA in the highest MMA tertile. CONCLUSION: MTHFR 677 TT individuals are more liable to hyperhomocysteinemia under vitamin B12 deficiency than the other two genotypes. In such a case, relative folate shortage may progressively increase HCY levels. TT individuals may have increased folate and vitamin B12 requirements compared to the other CC and CT genotypes.

Adolescent↗
PubMed2001

The riddle of femininity: the interplay of primary femininity and the castration complex in analytic listening.

This study elucidates the application of an analytic attitude to questions of gender and sexuality. The paper reports on a study group's exploration of the relative heuristic use of two important organising concepts in analytic work with female analysands: primary feminity and the phallic castration complex. A tendency to cling to one position over the other skews analytic listening. Two cases are presented of women struggling to consolidate positive feminine identifications and, to that end, working through conflicting feminine identifications and defences against a resolution of the awareness of gender differences. Analytic listening requires a view of each psychic construction as a layer to be understood in its own right yet as a cloak soon to reveal the next layer--a different construction. The study includes observations on perverse fantasies in women.

Adult↗
PubMed1999

The interplay between identifications and identity in the analysis of a violent young man: issues of technique.

In this paper, the author develops the distinction between 'identification' and 'identity'. Identification is a process that takes place in the unconscious and is the stuff of phantasies. Throughout his work, Freud postulated the fluidity of identificatory processes. 'Identity' in contrast, is an attempt that each individual makes to organise these conflicting identifications in order to achieve an illusion of unity, which allows an individual to make the statement 'I am this' (and not that). The author suggests that a fundamental characteristic present in some violent patients is an attempt by an individual, potentially overwhelmed by the extreme fluidity 'between masculine and feminine identificatory processes', to repudiate their feminine, passive identification, in order to establish a 'persona', an 'identity'. A technical challenge in the analysis of these patients is for the analyst to identify the 'shifts between the identificatory processes' and interpret them to the patients. She indicates that as the analyst is progressively more able to identify the patient's internal movement between different states and identificatory processes and interpret them, the patient is himself more able to tolerate the internal fluidity between identificatory processes.

Adolescent↗