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At least 1,531 records · Page 85Linked to original sources
PubMed2001

Canes, crutches and home care services: the interplay of human and technological assistance.

This brief reports the results of a study investigating the efficacy of canes, crutches, walkers, and wheelchairs for people who need assistance with everyday activities and asks the question, does low assistive technology replace human help for people with disabilities? Study results show that canes and crutches are low cost, versatile aids that can partially substitute for human assistance by reducing the overall number of hours of care required. They can also reduce out-of-pocket expenses for supportive services. Walkers and wheelchairs, on the other hand, appear to supplement, rather than substitute for, human assistance. The brief concludes by recommending that greater use of canes and crutches be actively encouraged to increase the independence of people who need help with daily activities.

Activities of Daily Living↗
PubMed2003

Interplay of portal pressure, portal perfusion and hepatic arterial inflow in modulating expression of hepatic encephalopathy in patients with spontaneous or artificially created portosystemic shunts.

The major theme of this discussion is how portal pressure after portosystemic shunt procedures may modulate the expression of hepatic encephalopathy. Decades of emphasis on the paramount importance of maintaining portal venous perfusion after shunt procedures is now being re-examined. In countries where non-cirrhotic portal hypertension is common, physicians have long recognized that hepatic encephalopathy is rare even with total portosystemic shunting. However, once decompressive shunts are created, hepatic encephalopathy becomes a clinical problem. Why this occurs needs to be better understood. In the meantime, there has been virtual abandonment of surgical shunts in favor of endoscopic variceal ablation treatment. This is despite the fact that surgical shunts that only partially decompress the portal hypertension are associated with excellent long-term control of variceal bleeding and low rates of hepatic encephalopathy. The time has come to once again examine the key relationship between portal pressure, portal perfusion with hepatic arterial inflow in inducing hepatic encephalopathy after creation of portosystemic shunts.

Hepatic Encephalopathy↗
PubMed2004

Evidence of oxytocin/oxytocin receptor interplay in human prostate gland and carcinomas.

Data on the presence of oxytocin receptors (OTR) within the prostate are still controversial and variable among different species. In the present study, OTR expression and localization has been investigated in human hyperplastic and neoplastic prostate at mRNA and protein levels using in situ hybridization (ISH) and immunohistochemistry (ICC) techniques, respectively. In all the cases studied, epithelial cells expressed OTR mRNA and protein. Interestingly, this expression was more intense in neoplastic epithelial cells compared to the hyperplastic ones. In order to determine whether OTR might mediate a biological effect of oxytocin (OT) in prostate cancer cells, OTR expression was studied by RT-PCR and immunofluorescence technique in the human androgen-independent prostate cancer cell line DU145. In addition, a possible heterotopic production of OT by DU145 cells was studied using RT-PCR. The data obtained showed that DU145 cells expressed OTR, whereas no OT mRNA was detected. When DU145 cells were treated with OT (100 nM) a significant inhibition of cell proliferation was observed, while co-incubation with the OT antagonist OTA (100 nm) abolished such an effect. The involvement of apoptosis in the OT effect contrasting cell proliferation was excluded by ISEL technique, which revealed a similar pattern of DNA fragmentation in either untreated or OT-treated cells. Altogether, the data indicate that the OT/OTR system could be involved in the control of prostate neoplastic pathology.

Cell Division↗
PubMed2004

The interplay between behavior and neurodegeneration in rat models of Parkinson's disease and stroke.

The effects of extreme disuse or overuse of the limbs in rat models of Parkinson's disease and stroke are discussed. In unilaterally lesioned rats, immobilizing one forelimb in a cast forces complete disuse of this limb and extreme overuse of the uncasted limb. This procedure has diverse effects on histological and behavioral outcomes in these models, depending upon how and when it is applied relative to the lesion. Effects on behavioral outcome, post-lesion plasticity events, and expression of trophic factors are discussed. The effects of forced disuse or overuse vary among lesion types and can include neuroprotection, changes in synaptogenesis, or even exaggeration of tissue loss. The diversity of behavior-driven structural changes in the brain underscores the potential importance of carefully tailoring physical restorative therapy to specific neurological problems in order to optimize outcomes. In addition, we stress the need to recognize the reciprocal influence that behavior and the brain can have upon each other.

Animals↗
PubMedDate not supplied

Prolonged activation of tumor necrosis factor (TNF)-alpha and its soluble receptors in chronic heart failure patients both in the compensated and decompensated state. Interplay between their levels and metalloproteinase-3.

INTRODUCTION: Recent clinical and experimental studies indicate that upregulation of the TNF system can contribute to the progression of cardiac remodeling and heart failure decompensation, by promoting alterations in cardiomyocyte biology and extracellular matrix metabolism. Extracellular matrix turnover is regulated by the matrix metalloproteinases (MMPs), which are endogenous enzymes responsible for extracellular collagen degradation. The present study investigates the fluctuation of serum levels of TNF-alpha, soluble TNF receptor-1 (sTNFR1) and -2 (sTNFR2), in patients with chronic heart failure both during acute decompensation and the stable state of the syndrome. The second goal of this study was to determine if a relationship exists between serum MMPs profiles (MMP-1, MMP-2, MMP-3) and circulating TNF-alpha or its soluble receptors. METHODS: Our patient group consisted of 52 patients with chronic heart failure (NYHA III-IV; mean age: 65 +/- 4 years; hypertensive cardiomyopathy: 20, ischemic cardiomyopathy: 17, dilated cardiomyopathy: 10, valvular disease: 5), who were hospitalized for acute decompensation of the syndrome. Our control group consisted of 30 healthy subjects (mean age: 57 +/- 6 years). Serum levels of TNF-alpha, sTNFR1, sTNFR2 and MMP-1,-2,-3 were measured in heart failure patients by ELISA at admission and after one month as follow-up. Values are expressed as medians and interquartile ranges. RESULTS: In our patient group, we observed a statistically significant increase in the levels of sTNFR1 and sTNFR2 at admission (sTNFR1: 5.15 ng\mL, 4.49-8.90 ng\mL, P < 0.001, sTNFR2: 13.40 ng\mL, 6.10-21.50 ng\mL, P < 0.001), and at one-month follow-up (sTNFR1: 5.30 ng\mL, 4.61-6.90 ng\mL, P < 0.001, sTNFR2: 21.80 ng\mL, 11.50-25.20 ng\mL, P < 0.001), compared to the control group (sTNFR1: 3.83 ng\mL, 3.70-3.95 ng\mL, sTNFR2: 4.00 ng\mL, 3.40-5.40 ng\mL). There was a statistically significant difference in the levels of sTNFR2 between admission and follow-up (P < 0.05). Significant correlations between serum MMP-3 and sTNFR2 levels both at admission and follow up (r -/+ 0.460, P -/+ 0.005 and r -/+ 0.338, P -/+ 0.044, respectively) were also found. CONCLUSIONS: Soluble TNF receptors are elevated in heart failure patients both in acute decompensation and stable phase. We have detected higher levels of soluble TNFR2 during the compensated phase of heart failure, suggesting that TNFR2 receptors appear to stabilize the cytokine and thereby prolong its half-life and biological functions. Finally, TNF system-mediated cardiac remodeling may exist through the activation of MMP-3 signaling pathways.

Aged↗
PubMed2004

Polyomaviruses and cancer--interplay between viral proteins and signal transduction pathways.

Polyomaviruses are highly suspected to be involved in the development of cancer. A strong correlation has been established between the activity of an early viral genome and the development of a transformed phenotype. Polyomavirus transforming antigens (T-antigens) are the major suspects in the process of deregulating cellular equilibrium. Multiple interactions between T-antigens and cellular regulatory proteins have been detected at different regulatory levels including signal transduction, gene expression, cell cycle progression, and possible DNA repair. In this context, we are reviewing the most recent experimental evidence which, in combination with more than thirty years of studies of polyomaviruses, could help us understand whether and how viral infection contributes to the development of malignant transformation.

Animals↗
PubMedDate not supplied

HIV-1 integration: an interplay between HIV-1 integrase, cellular and viral proteins.

To achieve a productive infection, the reverse transcribed cDNA of the human immunodeficiency virus type 1 (HIV-1) has to be inserted in the host cell genome. The main protein required to accomplish this reaction is the virally encoded integrase. In vitro, the recombinant integrase is capable of catalyzing the two subsequent reactions of the integration process, namely the 3' processing followed by the strand transfer, without other viral and/or cellular proteins. However, a number of studies indicate that the in vivo integration process also involves cellular proteins, assisting the virus to integrate in the cellular genome. These cellular proteins can play a role during different steps of the integration process, including nuclear import, integrase catalysis, integration site selection and DNA gap repair. In this review we summarize the candidate cellular proteins involved in the HIV-1 integration process identified so far and discuss their potential roles during HIV-1 replication.

Apoptosis↗
PubMed2005

[The interplay of magnesium and vitamin K2 on bone mineralization].

Magnesium (Mg) is most likely restored in bone matrix, implicating a pivotal role in bone mineralization. Mg-insufficient bone reveals fragility to mechanical loading despite normal or higher levels of bone mineral content, permitting stimulated osteoclastic bone resorption. In contrast, vitamin K(2) (MK-4:menatetrenone) inhibited osteoclastic bone resorption stimulated by the Mg-insufficiency, thereby normalizing bone remodeling. The Mg-insufficiency caused an increased concentration of calcium, which resulted in an extremely-high purity of hydroxyapatite (HA) crystal [Ca(10)(PO(4))(6)(OH)(2)] and accelerated mineralization in bone. In contrast, MK-4 did not affect the calcium-concentration nor HA-purity, but repressed mineralization accelerated by Mg-insufficiency. Thus, MK-4 appears to recover the "bone quality" lessened by the Mg-insufficiency by two mechanisms:controlling bone turnover and mineralization.

Animals↗
PubMed2005

Genomic profiling. Interplay between clinical epidemiology, bioinformatics and biostatistics.

OBJECTIVES: The current literature on the use of microarrays to generate prognostic profiles is still a methodological wasteland. Many valid questions, such as how profiling studies should be evaluated and what conclusions can be drawn, remain unanswered. Or how can flaws in the collection, analysis and interpretation of data be detected? Undiscovered imperfections can lead to a waste of valuable resources as well as be a latent source of false conclusions. METHODS: Three seminal papers on the prognosis of breast cancer using genomic profiling will be discussed. Six principles of good experimental design will be used for methodological guidance: defining relevant endpoints, avoiding systematic bias, generalizability of results, appropriately sized samples to achieve sufficient power, simple design to improve interpretability, and avoiding artificial assumptions. RESULTS: Severe violations of at least one of the six principles of good experimental design can be found in each of the three papers. A strategy is presented to assess whether a study has achieved a high level of methodological quality. This strategy also helps to establish a suitable protocol for future profiling projects. CONCLUSIONS: Determining the design of a study in a protocol is a first step to avoid impending pitfalls. The protocol should deal with the problem of understanding the complex reality behind genomic profiling. There are basic guiding principles which can help handle the complex task of designing prognostic studies to find genomic signatures.

Biometry↗