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Biomedical subjects

J Shan

Publications and source records attributed to J Shan.

6 recordsLinked to original sources
PubMed1992

Parathyroid function in hypertension.

PHF, secreted by the PTG, induces hypertension by increasing vascular smooth muscle calcium uptake and thereby increasing intracellular calcium levels. PHF secretion is inhibited by dietary calcium and the effects of PHF are blocked by calcium channel antagonists. This explains the paradox whereby both calcium and calcium channel blockers may be effective antihypertensive agents. PHF may be secreted by a specific cell type in the parathyroid gland, numbers of which seem to correlate with PHF levels. Thus, the parathyroid gland does seem to play a role in some forms of hypertension, but this role is probably not due to its production of PTH, but may be related to the secretion of the new factor--PHF.

Animals↗
PubMed1990

Control of calcium channels in neuroblastoma cells (N1E-115).

Neuroblastoma cells (N1E-115) were used as models of transient (T) and long-lasting (L) Ca++ channels. The whole cell version of the patch clamp technique was used to measure inward Ca++ currents, and the fluorescent indicator, Fura-2, was used to measure changes in intracellular Ca++. Cells were cultured and selected during recording so that predominantly T or L channel currents were measured. T channel currents did not respond to dihydropyridine or parathyroid hormone, whereas L channel currents did. BAY-K-8644 increased and nifedipine decreased L channel currents. After a 15 mM KCl challenge, cells with predominantly T channels responded with a transient change in intracellular Ca++, while cells with predominantly L channels showed a sustained response. PTH inhibited the increase in intracellular Ca++ in cells with L channels, but not in those with T channels. PTH may be an example of an endogenous calcium channel blocker, at least in neuroblastoma cells.

Calcium Channel Blockers↗
PubMed1990

Specific inhibition of long-lasting, L-type calcium channels by synthetic parathyroid hormone.

The effect of an active synthetic N-terminal fragment of bovine parathyroid hormone (bPTH), bPTH-(1-34), on Ca2+ channels was studied in mouse neuroblastoma cells (N1E-115). With the whole-cell variation of the patch-clamp technique, T (transient) and L (long-lasting) types of Ca2+ currents were identified. Pharmacological characterization showed that the L current was amplified by the Ca2+ channel stimulator BAY K-8644, but the T current was unaffected. The administration of bPTH-(1-34) produced dose-related inhibition of the L current, which could be reversed by BAY K-8644. The peptide had no effect on the T current. In addition, use of the fluorescent indicator fura-2 showed that bPTH-(1-34) inhibited the KCl-stimulated increase in intracellular free Ca2+ in neuroblastoma cells with L channels but not in cells with T channels. An inactivated (oxidized) preparation of bPTH-(1-34) failed to affect the L current. High-affinity binding of labeled PTH analog to these neuroblastoma cells was also demonstrated. In addition, bPTH-(1-34) inhibited the L current in cultured vascular smooth muscle cells from rat tail artery. These data indicate that, in some tissues, PTH can act as an endogenous blocker of Ca2+ entry.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

[Induced labor for gravidae with low Bishop's scores (with report of 242 cases)].

In planned/selective delivery, gravidae with Bishop's score 5 or below 5 are deal with lower position water sac, the aim of which is to induce regular uterine contraction and complete physiological latent period of cervical dilation. From Oct 1986 to Dec 1988, 242 cases of primiparae by this method and the latent period in physiological limit. This is a great breakthrough in induced labour for gravidae with low Bishop's scores. We found that this method is simple, effective, safe, and economic. It not only alleviates pain of the gravidae, but also helps to prevent the rise of caesarean section rate.

Cervix Uteri↗