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Intracellular Application of Macromolecules Through Patch Pipettes in Brain Slices
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Meenakshi Alreja, George K. Aghajanian
The macromolecule of interest is added to the patch-pipette solution at the desired concentration. The pH of the pipette solution should be readjusted after addition of the macromolecule as some substances can alter the pH of the solution (e.g., the catalytic subunit of cAMP-dependent protein kinase). It is also important to adjust the composition of the patch-pipette solution for various ions or chemicals that may have been added to the vial containing the macromolecules. Again, an example is the protein kinase A which usually comes as a lyophilized powder containing K salts and sucrose, which makes it essential to adjust the concentration of the potassium gluconate and sucrose in the patch-pipette solution in which it will be diluted.
Cochlear mechanisms and processes
Published in Stanley A. Gelfand, Hearing, 2017
In addition to the fast electromotile response, slower motile responses are also produced when OHCs are exposed to chemical agents, the efferent neurotransmitter acetylcholine, and electrical stimulation (e.g., Brownell et al., 1985; Zenner et al., 1985; Flock et al., 1986; Kachar et al., 1986; Ashmore, 1987; Ulfendahl, 1987; Slepecky et al., 1988a,b; Zajic and Schacht, 1991; Holley, 1996). A vivid illustration is provided by Figure 4.35, which shows the reactions of a guinea pig OHC that was removed from the cochlea and exposed to potassium gluconate (Slepecky et al., 1988b).
Hyperosmolar Potassium Inhibits Corneal Myofibroblast Transformation and Prevent Corneal Scar
Published in Current Eye Research, 2023
Kai Liao, Zekai Cui, Zhijie Wang, Yu Peng, Shibo Tang, Jiansu Chen
A previous study that demonstrated the effectiveness of potassium gluconate treatment on skin wound healing suggested that it could be an efficient treatment to prevent scar formation.14 Consistently, we found that KCl could inhibit corneal myofibroblast transformation, and the antifibrotic effect of KCl was dose-dependent. However, no changes were observed in the NaCl treatment group, suggesting that potassium is an effective critical component of the antifibrotic effect. Besides, our results showed that KCl eye drops could prevent corneal scarring. KCl is a metal ion that can easily penetrate the corneal epithelial barrier. Therefore, the application of KCl eye drops was selected instead of subconjunctival injections. In addition, the effect of medication of our eye drops in other days is worth further study.
Endocytosis of ATB0,+(SLC6A14)-targeted liposomes for drug delivery and its therapeutic application for pancreatic cancer
Published in Expert Opinion on Drug Delivery, 2020
Longfa Kou, Huirong Huang, Xinlu Lin, Xinyu Jiang, Yi Wang, Qiuhua Luo, Jin Sun, Qing Yao, Vadivel Ganapathy, Ruijie Chen
As ATB0,+ is a Na+/Cl− -coupled concentrative amino acid transporter, the influence of Na+ and Cl− on the uptake of LYS-LPs was examined to verify the involvement of ATB0,+ in the uptake process. This was done by replacing NaCl in the uptake buffer iso-osmotically with N-methyl-D-glucamine chloride (Na+-free buffer), and replacing NaCl, KCl, and CaCl2 iso-osmotically with sodium gluconate, potassium gluconate, and calcium gluconate (Cl− -free buffer), respectively. In addition, α-methyl-D,L-tryptophan (α-MT), a selective blocker of SLC6A14, was used to test its effect on the uptake of LYS-LPs after blocking ATB0,+. Lysine (1 mM), glycine (1 mM), and arginine (1 mM) were used to compete with lysine-conjugated liposomes for ATB0,+ interaction, and glutamate (1 mM), not a substrate for ATB0,+, was used as a negative control.
Flucloxacillin-induced hypokalaemia: a case report
Published in Acta Clinica Belgica, 2018
The patient was under chronic treatment with lisinopril 20 mg and hydrochlorothiazide 12.5 mg for treating essential hypertension. She had no obvious gastro-intestinal losses and had a normal diet. The patient did not receive insulin. After hypokalaemia was noted, treatment with oral potassium gluconate 4 × 10 ml was started and later intravenous potassium supplementation (1 L NaCl 0.9% with 30 meQ potassium, later gradually increased to 60 meQ, infusion over 24 h) was associated. Because of persistent severe hypokalaemia, hydrochlorothiazide was discontinued. However, serum potassium remained low (with serum potassium values as low as 2.3 mmol/l seven days after stopping hydrochlorothiazide 12.5 mg). Furthermore, spironolactone 25 mg was started and gradually increased to 100 mg because of persistent hypertension in the presence of hypokalaemia. Subsequently, an extended laboratory evaluation showed a normal serum sodium (143 mmol/l), normal serum magnesium (0.71 mmol/l), normal serum bicarbonate (29 mmol/l), normal creatinine (0.9 mg/dl), low aldosterone (30 pg/ml) and mildly elevated cortisol (26,22 μg/dl). Urine analysis showed a urinary sodium of 75 mmol/l, urinary potassium of 47 mmol/l and a urinary chloride of 84 mmol/l. A 24-h urinary cortisol excretion was normal (67 μg/24 h). Serum potassium levels normalised after treatment with flucloxacillin was discontinued. Figure 1 shows the evolution of serum potassium.