665 research outputs found
Clustering of farms based on slaughterhouse health aberration data
Large amounts of data from meat inspections can be used as a tool to support interventions for improvement of herd health. We applied time-series analyses on 3.5 years of meat inspection data of two pig slaughterhouses to identify differences in health aberration patterns over time at farm-level. A negligibly evidence of seasonality and a substantial trend pattern in percentage aberrations over time were identified. Differences exist in percentage health aberrations between the farms and months. This distinction is more elaborate than just grouping farms on basis of aberration incidence
Diagnostic markers based on a computational model of lipoprotein metabolism
Abstract Background: Dyslipidemia is an important risk factor for cardiovascular disease and type II diabetes. Lipoprotein diagnostics, such as LDL cholesterol and HDL cholesterol, help to diagnose these diseases. Lipoprotein profile measurements could improve lipoprotein diagnostics, but interpretational complexity has limited their clinical application to date. We have previously developed a computational model called Particle Profiler to interpret lipoprotein profiles. In the current study we further developed and calibrated Particle Profiler using subjects with specific genetic conditions. We subsequently performed technical validation and worked at an initial indication of clinical usefulness starting from available data on lipoprotein concentrations and metabolic fluxes. Since the model outcomes cannot be measured directly, the only available technical validation was corroboration. For an initial indication of clinical usefulness, pooled lipoprotein metabolic flux data was available from subjects with various types of dyslipidemia. Therefore we investigated how well lipoprotein metabolic ratios derived from Particle Profiler distinguished reported dyslipidemic from normolipidemic subjects. Results: We found that the model could fit a range of normolipidemic and dyslipidemic subjects from fifteen out of sixteen studies equally well, with an average 8.8% ± 5.0% fit error; only one study showed a larger fit error. As initial indication of clinical usefulness, we showed that one diagnostic marker based on VLDL metabolic ratios better distinguished dyslipidemic from normolipidemic subjects than triglycerides, HDL cholesterol, or LDL cholesterol. The VLDL metabolic ratios outperformed each of the classical diagnostics separately; they also added power of distinction when included in a multivariate logistic regression model on top of the classical diagnostics. Conclusions: In this study we further developed, calibrated, and corroborated the Particle Profiler computational model using pooled lipoprotein metabolic flux data. From pooled lipoprotein metabolic flux data on dyslipidemic patients, we derived VLDL metabolic ratios that better distinguished normolipidemic from dyslipidemic subjects than standard diagnostics, including HDL cholesterol, triglycerides and LDL cholesterol. Since dyslipidemias are closely linked to cardiovascular disease and diabetes type II development, lipoprotein metabolic ratios are candidate risk markers for these diseases. These ratios can in principle be obtained by applying Particle Profiler to a single lipoprotein profile measurement, which makes clinical application feasible
The consistency between planned and actually given nursing care in long-terminstitutional care
Continuous information exchange between healthcare professionals is facilitated by individualized care plans. Compliance with the planned care as documented in care plans is important to provide person-centered care which contributes to the continuity of care and quality of care outcomes. Using the Nursing Interventions Classification, this study examined the consistency between documented and actually provided interventions by type of nursing staff with 150 residents in long-term institutional care. The consistency was especially high for basic (93%) and complex (79%) physiological care. To a lesser extent for interventions in the behavioral domain (66%). Except for the safety domain, the probability that documented interventions were provided was high for all domains (≥ 91%, p > 0.05). NAs generally provided the interventions as documented. Findings suggest that HCAs worked beyond there scope of practice. The results may have implications for the deployment of nursing staff and are of importance to managers
Short- and long-term effects of a physical activity counselling programme in COPD:A randomized controlled trial
SummaryBackgroundWe were interested in the effects of a physical activity (PA) counselling programme in three groups of COPD patients from general practice (primary care), outpatient clinic (secondary care) and pulmonary rehabilitation (PR).MethodsIn this randomized controlled trial 155 COPD patients, 102 males, median (IQR) age 62 (54–69) y, FEV1predicted 60 (40–75) % were assigned to a 12-weeks' physical activity counselling programme or usual care. Physical activity (pedometer (Yamax SW200) and metabolic equivalents), exercise capacity (6-min walking distance) and quality of life (Chronic Respiratory Questionnaire and Clinical COPD Questionnaire) were assessed at baseline, after three and 15 months.ResultsA significant difference between the counselling and usual care group in daily steps (803 steps, p = 0.001) and daily physical activity (2214 steps + equivalents, p = 0.001)) from 0 to 3 months was found in the total group, as well as in the outpatient (1816 steps, 2616 steps + equivalents, both p = 0.007) and PR (758 steps, 2151 steps + equivalents, both p = 0.03) subgroups. From 0 to 15 months no differences were found in physical activity. However, when patients with baseline physical activity>10,000 steps per day (n = 8), who are already sufficiently active, were excluded, a significant long-term effect of the counselling programme on daily physical activity existed in the total group (p = 0.02). Differences in exercise capacity and quality of life were found only from 0 to 3 months, in the outpatient subgroup.ConclusionOur PA counselling programme effectively enhances PA level in COPD patients after three months. Sedentary patients at baseline still benefit after 15 months.ClinicalTrials.gov: registration number NCT00614796
The TgsGP gene is essential for resistance to human serum in Trypanosoma brucei gambiense
Trypanosoma brucei gambiense causes 97% of all cases of African sleeping sickness, a fatal disease of sub-Saharan Africa. Most species of trypanosome, such as T. b. brucei, are unable to infect humans due to the trypanolytic serum protein apolipoprotein-L1 (APOL1) delivered via two trypanosome lytic factors (TLF-1 and TLF-2). Understanding how T. b. gambiense overcomes these factors and infects humans is of major importance in the fight against this disease. Previous work indicated that a failure to take up TLF-1 in T. b. gambiense contributes to resistance to TLF-1, although another mechanism is required to overcome TLF-2. Here, we have examined a T. b. gambiense specific gene, TgsGP, which had previously been suggested, but not shown, to be involved in serum resistance. We show that TgsGP is essential for resistance to lysis as deletion of TgsGP in T. b. gambiense renders the parasites sensitive to human serum and recombinant APOL1. Deletion of TgsGP in T. b. gambiense modified to uptake TLF-1 showed sensitivity to TLF-1, APOL1 and human serum. Reintroducing TgsGP into knockout parasite lines restored resistance. We conclude that TgsGP is essential for human serum resistance in T. b. gambiense
Differences between <i>Trypanosoma brucei gambiense</i> groups 1 and 2 in their resistance to killing by Trypanolytic factor 1
<p><b>Background:</b> The three sub-species of <i>Trypanosoma brucei</i> are important pathogens of sub-Saharan Africa. <i>T. b. brucei</i> is unable to infect humans due to sensitivity to trypanosome lytic factors (TLF) 1 and 2 found in human serum. <i>T. b. rhodesiense</i> and <i>T. b. gambiense</i> are able to resist lysis by TLF. There are two distinct sub-groups of <i>T. b. gambiense</i> that differ genetically and by human serum resistance phenotypes. Group 1 <i>T. b. gambiense</i> have an invariant phenotype whereas group 2 show variable resistance. Previous data indicated that group 1 <i>T. b. gambiense</i> are resistant to TLF-1 due in-part to reduced uptake of TLF-1 mediated by reduced expression of the TLF-1 receptor (the haptoglobin-hemoglobin receptor (<i>HpHbR</i>)) gene. Here we investigate if this is also true in group 2 parasites.</p>
<p><b>Methodology:</b> Isogenic resistant and sensitive group 2 <i>T. b. gambiense</i> were derived and compared to other T. brucei parasites. Both resistant and sensitive lines express the <i>HpHbR</i> gene at similar levels and internalized fluorescently labeled TLF-1 similar fashion to <i>T. b. brucei</i>. Both resistant and sensitive group 2, as well as group 1 <i>T. b. gambiense</i>, internalize recombinant APOL1, but only sensitive group 2 parasites are lysed.</p>
<p><b>Conclusions:</b> Our data indicate that, despite group 1 <i>T. b. gambiense</i> avoiding TLF-1, it is resistant to the main lytic component, APOL1. Similarly group 2 <i>T. b. gambiense</i> is innately resistant to APOL1, which could be based on the same mechanism. However, group 2 <i>T. b. gambiense</i> variably displays this phenotype and expression does not appear to correlate with a change in expression site or expression of <i>HpHbR</i>. Thus there are differences in the mechanism of human serum resistance between <i>T. b. gambiense</i> groups 1 and 2.</p>
DNA-based communication in populations of synthetic protocells
Developing molecular communication platforms based on orthogonal communication channels is a crucial step towards engineering artificial multicellular systems. Here, we present a general and scalable platform entitled ‘biomolecular implementation of protocellular communication’ (BIO-PC) to engineer distributed multichannel molecular communication between populations of non-lipid semipermeable microcapsules. Our method leverages the modularity and scalability of enzyme-free DNA strand-displacement circuits to develop protocellular consortia that can sense, process and respond to DNA-based messages. We engineer a rich variety of biochemical communication devices capable of cascaded amplification, bidirectional communication and distributed computational operations. Encapsulating DNA strand-displacement circuits further allows their use in concentrated serum where non-compartmentalized DNA circuits cannot operate. BIO-PC enables reliable execution of distributed DNA-based molecular programs in biologically relevant environments and opens new directions in DNA computing and minimal cell technology
Effect of priming with granulocyte colony-stimulating factor on the outcome of chemotherapy for acute myeloid leukemia
BACKGROUND: Sensitization of leukemic cells with hematopoietic growth
factors may enhance the cytotoxicity of chemotherapy in acute myeloid
leukemia (AML). METHODS: In a multicenter randomized trial, we assigned
patients (age range, 18 to 60 years) with newly diagnosed AML to receive
cytarabine plus idarubicin (cycle 1) and cytarabine plus amsacrin (cycle
2) with granulocyte colony-stimulating factor (G-CSF) (321 patients) or
without G-CSF (319). G-CSF was given concurrently with chemotherapy only.
Idarubicin and amsacrin were given at the end of a cycle to allow the
cell-cycle-dependent cytotoxicity of cytarabine in the context of G-CSF to
have a greater effect. The effect of G-CSF on disease-free survival was
assessed in all patients and in cytogenetically distinct prognostic
subgroups. RESULTS: After induction chemotherapy, the rates of response
were not significantly different in the two groups. After a median
follow-up of 55 months, patients in complete remission after induction
chemotherapy plus G-CSF had a higher rate of disease-free survival than
patients who did not receive G-CSF (42 percent vs. 33 percent at four
years, P=0.02), owing to a reduced probability of relapse (relative risk,
0.77; 95 percent confidence interval, 0.61 to 0.99; P=0.04). G-CSF did not
significantly improve overall survival (P=0.16). Although G-CSF did not
improve the outcome in the subgroup with an unfavorable prognosis, the 72
percent of patients with standard-risk AML benefited from G-CSF therapy
(overall survival at four years, 45 percent, as compared with 35 percent
in the group that did not receive G-CSF [relative risk of death, 0.75; 95
percent confidence interval, 0.59 to 0.95; P=0.02]; disease-free survival,
45 percent vs. 33 percent [relative risk, 0.70]; 95 percent confidence
interval, 0.55 to 0.90; P=0.006). CONCLUSIONS: Sensitization of leukemic
cells with growth factors is a clinically applicable means of enhancing
the efficacy of chemotherapy in patients with AML
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