The latest medical research on Microbiology
The research magnet gathers the latest research from around the web, based on your specialty area. Below you will find a sample of some of the most recent articles from reputable medical journals about microbiology gathered by our medical AI research bot.
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Heparin dosage, level, and resistance in SARS-CoV2 infected patients in intensive care unit.Biochemistry
Patients with COVID-19 frequently exhibit a hypercoagulable state with high thrombotic risk, particularly those admitted to intensive care units (ICU). Thromboprophylaxis is mandatory in these patients; nevertheless, thrombosis still occurs in many cases. Thus, the problem of assessing an adequate level of anticoagulation in ICU patients becomes evident during the COVID-19 pandemic. The aim of this study was to evaluate the heparin resistance and the efficacy of heparin monitoring using an anti-Xa activity assay.
Thirty-seven heparin-treated patients admitted to ICU for SARS-CoV-2 pneumonia were retrospectively studied for antifactor Xa activity (anti-Xa), activated partial thromboplastin time (APTT), Antithrombin, Fibrinogen, D-Dimer, Factor VIII, von Willebrand Factor, and the total daily amount of heparin administered. The correlation between APTT and anti-Xa was evaluated for unfractionated heparins (UFH). The correlations between the daily dose of UFH or the dosage expressed as IU/kg b.w. for low molecular weight heparin (LMWH) and anti-Xa were also evaluated.
Twenty-one patients received calcium heparin, 8 sodium heparin, and 8 LMWH. A moderate correlation was found between APTT and anti-Xa for UFH. APTT did not correlate with coagulation parameters. 62% of UFH and 75% of LMWH treated patients were under the therapeutic range. About 75% of patients could be considered resistant to heparin.
SARS-COV2 pneumonia patients in ICU have frequently heparin resistance. Anti-Xa seems a more reliable method to monitor heparin treatment than APTT in acute patients, also because the assay is insensitive to the increased levels of fibrinogen, FVIII, and LAC that are common during the COVID-19 inflammatory state.
Evaluation of a commercial set of frozen plasmas for instrument-to-instrument comparability.Biochemistry
To perform comparability of instruments, the laboratory can select patient samples spanning the reportable range or can use plasma sets from commercial suppliers. We evaluated ExpertCor Routine (ECR) plasma set (Stago), a set of frozen plasmas enabling to verify the agreement between different coagulation analysers. Additionally, we evaluated whether the concept of transference of the reference range is acceptable between instruments, once comparability between the instruments is approved.
Patient samples and the ECR plasma set were evaluated for method comparison for prothrombin time, activated partial thromboplastin time and fibrinogen on five instruments. Results of one instrument were compared to the mean of all analysers by Passing-Bablok regression and Bland-Altman analysis. Reference ranges were checked on all instruments.
The %mean difference was ≤5% and ≤3.7% for all analyser/parameter combinations, for ECR and patient sample data sets, respectively. All predefined criteria to fulfil good comparability between instruments were met. The between-instrument comparison with the ECR plasma set and the patient samples was equal for PT, INR and fibrinogen. After demonstrating comparability between instruments by either of the two plasma sample sets, reference ranges can be used interchangeably between identical instruments.
Instrument-to-instrument reproducibility showed comparable results using a data set obtained with patient samples or a commercial plasma set. Once comparability between instruments is confirmed, defined reference ranges can be transferred from one instrument to the other instrument without additional testing. The ECR plasma set is a good alternative to the use of local patient samples to evaluate instrument comparability.
Functionalizing biomaterials to promote neurovascular regeneration following skeletal muscle injury.Cellular Physiology
During embryogenesis, blood vessels and nerves develop with similar branching structure in response to shared signaling pathways guiding network gr...
Engineering Fiber Anisotropy within Natural Collagen Hydrogels.Cellular Physiology
It is well-known that biophysical properties of the extracellular matrix (ECM) in- including, stiffness, porosity, composition, and fiber alignment...
Infantile leukemia-What factors determine its distinct biological nature? Clinicopathological study of 78 cases.Biochemistry
Infantile leukemia encompasses a heterogeneous group which needs stratifying for treatment selection.
We collected 78 cases of infantile leukemia and retrospectively analyzed their clinicopathological data.
Infantile leukemia featured a ratio of acute myeloid leukemia (AML) to B-lymphoblastic leukemia (B-ALL) of 1:2, with a better survival for AML than B-ALL (median survival 36 vs 24 months). When stratified by age, "early" infantile B-ALL (2-6 months) showed a high rate of KMT2A rearrangement (100%), similar to the rate seen in congenital B-ALL (1 month) (100%) and higher than seen in "late" infantile B-ALL (≥7 months) (68%). The three categories of infantile B-ALL exhibited an age-dependent increase in survival (median survival 8.5, 24, and >24 months, respectively). The age-dependent survival benefit remained after excluding the cases negative for KMT2A rearrangement. Conversely, infantile AML lacked an age-dependent pattern of survival.
The clinical outcome of infantile leukemia depends on the type of leukemia. Given the age-dependent survival, infantile B-ALL can be divided into three subcategories.
Prognostic evidence of LEF1 isoforms in childhood acute lymphoblastic leukemia.Biochemistry
The lymphoid enhancer factor 1 (LEF1) is a DNA-binding transcription factor that functions in the Wnt signaling pathway. Increased LEF1 activity is associated with progression of several types of cancer including leukemia. Here, we investigated LEF1 isoform expression and genomic variations in acute lymphoblastic leukemia (ALL).
LEF1 isoform expression was evaluated by quantitative real-time PCR in 87 newly diagnosed childhood ALL patients and controls. Moreover, Western blot analysis was performed for detection of LEF1 expression and the hotspot region of LEF1 was screened by deep sequencing.
The LEF1 mRNA expression of B cell ALL patients was higher than the controls (LEF1-total P = .011, LEF1-long P = .026). Moreover, B-ALL samples showing higher total LEF1 expression had significantly shorter relapse-free survival (P = .008) and overall survival (P = .011). Although full-length LEF1 expression was similar to the controls in T-ALL, 50% (n = 15) of the ALL patients had increased full-length LEF1 protein expression. Imbalance between short- and full-length LEF1 isoforms may lead to cell survival in ALL. Beside the LEF1 activation, LEF1 gene variations were rarely observed in our cohort.
The results indicate that the Wnt pathway may have a pathogenic function in a group of ALL patients and high LEF1-total expression might be a marker for shorter relapse-free survival time in B cell ALL.
Leukemic stem cells shall be searched in the bone marrow before "tyrosine kinase inhibitor-discontinuation" in chronic myeloid leukemia.Biochemistry
Leukemic stem cells (LSCs) of chronic myeloid leukemia (CML), persisting in the bone marrow (BM) niche, could be responsible for the relapses within the patients of whom the treatment-free remission (TFR) had been attempted. We assessed the presence of the CML LSCs in the peripheral blood (PB) and concurrently in the BM in the patients with chronic-phase CML (CP CML).
Thirty-eight patients with CP CML were included into the study. CD45+ /CD34+ /CD38- cells with positive CD26 expression were considered as CML LSCs (CD26+ LSC) by using multiparameter flow cytometry (FCM).
Mean BCR-ABL, PB LSC, and BM LSC were 58.528 IS (37.405-83.414 IS), 237.5 LSC/μL (16-737.5 LSC/μL), and 805 LSC/106 WBCs (134.6-2470 LSC/106 WBCs), respectively, in newly diagnosed CML patients. In the patients with BCR-ABL positive hematopoiesis, mean BCR-ABL, PB LSCs, and BM LSCs were 30.09 IS (0.024-147.690 IS), 13.5 LSC/μL (0-248.7 LSC/μL) and 143.5 LSC/106 WBCs (9-455.2 LSC/106 WBCs), respectively. No CML LSCs were detected in PB of patients who achieved deep molecular response (DMR). BM LSCs of the patients who were in DMR were 281.1 LSC/106 WBCs (3.1-613.7 LSC/106 WBCs). The amount of PB LSCs was highest in patients with newly diagnosed CML (P < .001).
LSCs persisted in the BM of the patients with DMR, whereas there was no LSCs in the peripheral blood. The investigation of the CML LSCs in bone marrow before deciding TKI discontinuation could be justified to achieve and maintain stable TFR.
Assessment of positive iron balance in end-stage renal disease: Could hepcidin-25 be useful?Biochemistry
The aim of our study was to examine the relationship of hepcidin-25 with red blood cell and reticulocyte indices and to evaluate the diagnostic properties of hepcidin-25 in the assessment of positive iron balance in end-stage renal disease (ESRD) patients.
Eighty anemic ESRD patients (hemoglobin < 110 g/L) were classified as having iron deficiency (ID, N = 20), iron sufficiency (IS, N = 29), and positive iron balance (PB, N = 31) using the conventional biomarkers for iron status evaluation. Hepcidin-25 was determined by a chemiluminescent direct ELISA.
Hepcidin-25 was significantly negatively correlated with the proportion of hypochromic erythrocytes (%HYPO) (P = .034) and immature reticulocyte fraction (P = .010) in ID and with the absolute reticulocyte concentration in ID (P = .048) and PB (P = .040). In multivariate models, hepcidin-25 was independently negatively associated with the mean reticulocyte hemoglobin content (CHr; β = -0.493, P = .004) and red blood cell size factor (RSf) (β = -0.334, P = .036) only in the PB group. The best hepcidin-25 value to exclude PB was 66.13 µg/L, showing a sensitivity of 61.3%, a specificity of 75.5%, and an AUC of 0.808.
Our results suggest that hepcidin-25 levels are independently negatively associated with the iron demand for the most recent erythropoiesis only in PB. Hepcidin-25 performed acceptable in discriminating anemic ESRD patients with positive iron balance and may prove to be a useful additional tool in the evaluation of iron status.
Next-generation inward rectifier potassium channel modulators: Discovery and molecular pharmacology.Cellular Physiology
Inward rectifying potassium (Kir) channels play important roles in both excitable and non-excitable cells of various organ systems and could repres...
MicroRNA-129-5p Inhibited C2C12 Myogenesis and Repressed Slow Fiber Gene Expression in vitro.Cellular Physiology
The miR-129 family is widely reported as tumor repressors, while, their roles in skeletal muscle have not been fully investigated. Here, the functi...
CXCL2 benefits acute myeloid leukemia cells in hypoxia.Biochemistry
Drug resistance and relapse of acute myeloid leukemia (AML) is still an important problem in the treatment of leukemia. Leukemia outbreak causes severe hypoxia in bone marrow (BM), remolding BM microenvironment (niche), and transforming hematopoietic stem cell (HSC) niche into leukemia stem cell (LSC) niche. AML cells and the microenvironment usually conduct "cross-talk" through cytokines to anchor resistant AML cells into LSC niche, thus supporting their survival. Therefore, this study was aimed to investigate the role of CXCL2 in the hypoxic AML niche.
AML hypoxic niche was simulated by hypoxic culture of THP-1 and HL-60 cells in vitro, thus to study the effects of CXCL2 on the proliferation and migration of AML cells. The expression of hypoxia-inducible factor-1α (HIF-1α) and the activation of survival-related kinases such as PIM2 and mTOR under CoCl2 -simulated hypoxic conditions were detected. The correlation between CXCL2 and the prognosis of AML with big data was verified.
(a) CXCL2 promoted the proliferation and migration of AML cells. (b) CXCL2 up-regulated the expression of PIM2 by enhancing the transcriptional activity of HIF-1α. (c) CXCL2 activated mTOR in AML cells. (d) CXCL2 was associated with poor prognosis in AML.
CXCL2 promotes survival, migration, and drug resistance pathway of AML cells in hypoxia and is associated with poor prognosis in AML. Therefore, CXCL2 can be considered as an important factor in promoting the development of AML cells in hypoxia.
TRPV4 - Rho signaling drives cytoskeletal and focal adhesion remodeling in trabecular meshwork cells.Cellular Physiology
Intraocular pressure (IOP) is dynamically regulated by the trabecular meshwork (TM), a mechanosensitive tissue that protects the eye from injury th...