Some technical aspects of MLC inhibition by sera obtained from multiparous women were studied. The variability of the MLC response was very high. The serum source used in the cultures was probably to a large extent responsible for this variability. Aspecific inhibition, which was observed with some test sera, could be removed by dialysis against PBS. To make the evaluation of inhibition by immune sera objective, a scoring system was introduced for the degree of inhibition. Test sera were usually added to the cultures. Alternatively, stimulator and responder cells were preincubated with the test serum. Preincubation of the stimulator cells did not show a difference in inhibition pattern when this was compared with serum addition. Preincubation of the responder cells showed a completely different inhibition pattern. The MLC inhibition test compared very well with an indirect immunofluorescence test and a cytotoxicity test using B-cell enriched cell suspensions.
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http://dx.doi.org/10.1111/j.1399-0039.1977.tb01114.x | DOI Listing |
Phys Rev Lett
December 2024
University of Strathclyde, Institute of Photonics, SUPA Dept of Physics, Glasgow, United Kingdom.
We report a spiking flip-flop memory mechanism that allows controllably switching between neural-like excitable spike-firing and quiescent dynamics in a resonant tunneling diode (RTD) neuron under low-amplitude (<150 mV pulses) and high-speed (ns rate) inputs pulses. We also show that the timing of the set-reset input pulses is critical to elicit switching responses between spiking and quiescent regimes in the system. The demonstrated flip-flop spiking memory, in which spiking regimes can be controllably excited, stored, and inhibited in RTD neurons via specific low-amplitude, high-speed signals (delivered at proper time instants) offers high promise for RTD-based spiking neural networks, with the potential to be extended further to optoelectronic implementations where RTD neurons and RTD memory elements are deployed alongside for fast and efficient photonic-electronic neuromorphic computing and artificial intelligence hardware.
View Article and Find Full Text PDFJ Vis Exp
January 2025
Department of Cardiac Surgery, the First Affiliated Hospital of Xinjiang Medical University;
The objective of this study was to investigate the cardioprotective effects of Munziq on abnormal body fluid myocardial ischemia-reperfusion injury (MIRI) and its underlying mechanism.Normal rats and rats with abnormal body fluid (ABF) were pre-treated with Munziq for 21 days. Following this, MIRI models were established.
View Article and Find Full Text PDFHum Cell
January 2025
Department of Tumor Pathology, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuoka-Shimoaizuki, Eiheiji, Fukui, 910-1193, Japan.
Only a few human ovarian endometrioid carcinoma cell lines are currently available, partly due to the difficulty of establishing cell lines from low-grade cancers. Here, using a cell immortalization strategy consisting of i) inactivation of the p16-pRb pathway by constitutive expression of mutant cyclin-dependent kinase 4 (R24C) (CDK4) and cyclin D1, and ii) acquisition of telomerase reverse transcriptase (TERT) activity, we established a human ovarian endometrioid carcinoma cell line from a 46-year-old Japanese woman. That line, designated JFE-21, has proliferated continuously for over 6 months with a doubling time of ~ 55 h.
View Article and Find Full Text PDFGraefes Arch Clin Exp Ophthalmol
January 2025
National Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, 270 Xueyuan West Road, Wenzhou, 325027, Zhejiang, China.
Purpose: To investigate whether in diabetic cataract (DC), FoxO1 regulates high glucose (HG)-induced activation of NLRC4/IL-6 inflammatory mediators in human lens epithelial cells (SRA01/04) via the JAK1/STAT1 pathway, leading to cataract formation.
Methods: Expression levels of FoxO1, inflammatory factor IL-6 and inflammatory vesicle NLRC4 were examined in SRA01/04 under high glucose (HG) stress at 25-150 mM. Rat lenses were also cultured using HG medium with or without the addition of the FoxO1 inhibitor AS1842856 and the JAK1 agonist RO8191.
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