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In balanced solution, the partial substitution of chloride by acetate might have a potential harmful effect with nitric oxide release, reduction of cardiac output and hypotension.
This is particularly true for the A1 receptor subtype, which is coupled with inhibition of cAMP synthesis and with the activation of potassium conductance, with consequent inhibition of neuronal firing and neurotransmitter release, reduction of heart rate, and other inhibitory effects.
Exenatide reproduces many of the action of GLP-1, such as enhancement of glucose-induced insulin secretion, inhibition of glucagon release, reduction of fasting and postprandial glucose concentrations, delay of gastric emptying, inhibition of appetite and induction of weight loss [ 94- 97].
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Ethanol has been known to suppress reproductive activity in laboratory animals and humans through the inhibition of luteinizing hormone (LH) release by reduction of gonadotropin-releasing hormone (GnRH) secretion from the hypothalamus.
Based on previous research, since the advantages of these systems are to achieve the therapeutic concentration, the desired drug release rate prolonged drug release and reduction of the repeating dosage.
In a NOx storage and reduction (NSR) catalyst, the release and reduction of NOx occurs over a very short period.
A release force reduction of about 40% was observed with the modified polymer mr-I 7000R compared to the unmodified original.
Results over the analysed loading rates have shown an interlaminar fracture energy release rate reduction of 19% for woven reinforcement, and 31% for unidirectional.
The model adequately describes the NO breakthrough profile during 100 min lean exposure as well as the subsequent release and reduction of the stored NO.
In addition, hypermagnesemia can block the peripheral and autonomic nervous systems via anatomization of calcium effects, suppression of acetylcholine release, and reduction of postsynaptic membrane responsiveness and depress the conduction system of the heart and sympathetic ganglia [11].
Besides the correlation between base deficit and duration of resuscitation efforts, metabolic acidosis may be associated with mortality by its hemodynamic effects, as depression of ventricular function, catecholamine release and reduction of ventricular responsiveness to catecholamines [4].
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