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Pre-eclampsia (PE) is a pregnancy-associated condition initiated by placental factors. We have demonstrated that placental extracellular vesicles (pcEVs) cause hypertension and proteinuria in pregnant and non-pregnant mice.
An observational study with both case-control and longitudinal designs.
A single centre at the Department of Obstetrics and Gynaecology, Tianjin Medical University.
We collected blood samples and clinical information from 54 PE patients, 33 normally pregnant women at 30-36 gestational weeks and on postpartum days 1 and 4 for the cross-sectional study, and at 22-31, 32-35 and 36-40weeks for the longitudinal study. Non-pregnant women were also recruited.
Blood samples were analysed using flow cytometry, coagulation tests and ELISA.
The primary outcome was plasma pcEV and other extracellular vesicles (EVs), and their expressions of anionic phospholipids and von Willebrand factor (VWF). Secondary variables included coagulation, ADAMTS-13 and the anionic phospholipid-binding proteins.
Plasma pcEVs progressively increased from pregnant women during non-menstrual period (NW) to PE patients (interquartile range [IQR] for NW 206/microlitre [116-255], normal pregnancy [NP] 1108/microlitre [789-1969] and PE 8487/microlitre [4991-16752]) and predicted PE. EVs from endothelial cells, platelets and erythrocytes accounted for <10% of pcEVs. VWF became hyper-adhesive in PE patients and contributed to the pregnancy-associated hypercoagulability.
Placental, platelet- and endothelial cell-derived EVs were significantly elevated in PE patients, but only pcEVs predicted PE. These EVs played a causal role in the pregnancy-induced hypercoagulability.
Placenta-derived extracellular vesicles predict pre-eclampsia and the associated hypercoagulability.
Placenta-derived extracellular vesicles predict pre-eclampsia and the associated hypercoagulability.
Diagnosis of acute exacerbation (AE) of cystic fibrosis (CF) must be precise because both under- and over-prescription of antibiotics may be detrimental. How lung function tests contribute to diagnose AE is unclear. We aimed to describe variation of spirometry and oscillometry measurements, at Stable state and at AE in adults with CF.
Patients were included in a retrospective single-centre study when both spirometry (FEV1, FVC) and oscillometry (X5, R5, R5-R20 and AX) data were available for at least one Stable and one AE visit between December 2016 and July 2019. For each visit, we calculated variation (Δ) in spirometry and oscillometry indices in comparison with personal best values. Measurements were expressed as % of predicted values and Z-scores when applicable. Areas under ROC curves (AUC) were computed.
Forty-two patients (28±9years, FEV1 64±21%) were included; 80 AE and 104 Stable visits were analysed. FEV1 (L, %pred and Z-score) and FVC (%pred and Z-score) varied significantly between AE and Stable visits (p<.05), although differences were small (80ml/2.7%pred for FEV1). Among oscillometry indices, X5 (kPa.s.L
), R5-R20 (kPa.s.L
) and AX (kPa/L) varied significantly. The AUCs for the variation in spirometry indices ranged from 0.601 (ΔFVC L) to 0.635 (ΔFEV1%pred). They were not significantly different from the AUCs for ΔX5 (0.589), ΔR5-R20 (0.649) and ΔAX (0.598).
Performance of both spirometry and oscillometry to discriminate AE from Stable state was poor. selleck chemical Variation of oscillometry indices (X5, R5-R20, AX) may be helpful when spirometry is unreliable or uncomfortable.
Performance of both spirometry and oscillometry to discriminate AE from Stable state was poor. Variation of oscillometry indices (X5, R5-R20, AX) may be helpful when spirometry is unreliable or uncomfortable.
This study aimed to isolate actinomycetes from marine environments and examine their antifungal activity against Talaromyces marneffei both in vitro and in vivo.
Nineteen out of 101 actinomycete extracts were active and further determined for their minimum inhibitory concentrations (MIC). Three extracts of AMA50 that isolated from sediment showed strong antifungal activity against T. marneffei yeast (MICs ≤0·03-0·25µgml
) and mould (MICs 0·5-16µgml
) forms. The hexane extract from the cells of AMA50 (AMA50CH) exhibited the best activity against both the forms (MIC≤1µgml
). Three extracts from AMA50 killed the melanized yeast cells at 0·5µgml
. The AMA50CH was further tested for protective effects in Caenorhabditis elegans model. At concentrations of 1-8µgml
, the AMA50CH prolonged survival of T. marneffei-infected C. elegans with a 60-70% survival rate. The composition of AMA50CH was determined by gas chromatography-mass spectrometry. The major components were n-hexadecanoic acid, tetradecanoic acid and pentadecanoic acid. Sequencing analysis revealed that isolate AMA50 belonged to the genus Streptomyces.
The AMA50CH from Streptomyces sp. AMA50 was the most effective extract against T. marneffei.
Talaromyces marneffei is one of the most important thermally dimorphic pathogenic fungi. These results indicated the potency of marine-derived actinomycete extracts against T. marneffei both in vitro and in vivo.
Talaromyces marneffei is one of the most important thermally dimorphic pathogenic fungi. These results indicated the potency of marine-derived actinomycete extracts against T. marneffei both in vitro and in vivo.
We present a patient with paraplegia secondary to anterior spinal cord infarct below T6, with subsequent development of chronic low-back and bilateral lower-extremity neuropathic pain with an atrophic cord. In this patient with reduced spinal cord mass and modified neuroanatomy, spinal cord stimulation was surprisingly very effective.
The primary objective of this report is to describe a case in which a patient benefited from spinal cord stimulator therapy in a way that is not explained by the traditionally accepted mechanism of action.
A spinal cord stimulator was implanted with two 16-contact leads placed in series starting at the top of T6.
He reported complete resolution of low-back pain and about 50% resolution of bilateral lower-extremity pain.
Traditionally accepted mechanisms of action of dorsal column stimulation and suppression of wide-dynamic-range neurons are unlikely to explain the relief obtained in our patient with an atrophic spinal cord. No single consensus has been reached on the primary mechanism through which spinal cord stimulation renders its therapeutic effects.
Read More: https://www.selleckchem.com/products/taurochenodeoxycholic-acid.html
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