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Biomedical subjects

F Ito

Publications and source records attributed to F Ito.

At least 235 records · Page 13Linked to original sources
PubMed1984

[Studies on serum CEA levels measured by enzyme immunoassay using monoclonal CEA-antibodies].

A double determinant enzyme immunoassay (EIA) using two monoclonal antibodies against CEA was established in the Abott laboratory. Serum CEA levels from patients with various cancers and benign diseases were measured using this EIA in comparison with the results obtained by radioimmunoassay (RIA) using polyclonal antibody against CEA. A significant correlation was noted between the values measured by the two methods. When serum CEA levels were more than 100 ng/ml, the values for EIA were found to be higher than those for RIA. However, this EIA was judged to be useful for monitoring cancer patients.

Antibodies, Monoclonal↗
PubMed1983

The spindle potential in the frog muscle spindle does not require external Na+.

Spindle potential recorded from the sensory nerve terminal of isolated frog muscle spindles disappeared within 20-30 min after the spindle receptor was perfused with Na+-free (Li, Tris or choline) Ringer's solution, whereas the amplitude of spindle potential was not attenuated for periods up to 60 min when the spindles were perfused in a Na+-free Ringer's solution containing both 10 mM TEA and 0.1 mM 4-aminopyridine after being washed with a normal Ringer's solution containing both the K+-channel blockers. It is concluded that the time-dependent decrease in the amplitude of spindle potential during the application of Na+-free solution is not ascribable to a decrease in the inward current carried by Na+, but is due to an increase in an outward current carried by K+.

Animals↗
PubMed1983

Effects of ruthenium ions on the sensory terminal discharges of the frog muscle spindle.

The presence of a mixed Na+-Ca2+ spike along the sensory terminal of the frog muscle spindle was verified. When the terminal was perfused with Ringer's solution containing 0.1-0.5 mM ruthenium red (RuR), the amplitude and duration of the spike were increased, occurring as a prolonged or a long-lasting depolarization of up to 20-30 s duration following individual afferent spikes evoked spontaneously or antidromically by electrical stimulation. In an isotonic TEA solution, the amplitude and duration of the afferent spikes were increased; however, no prolonged depolarization occurred. Adding 0.2 mM RuR to the TEA solution produced the prolonged and long-lasting depolarization. All responses disappeared in the presence of 3 microM TTX or Na+-free Ringer's solution. An impedance decrease along the terminal was observed during the prolonged or long-lasting depolarization. The prolonged depolarization was blocked by the addition of Ca2+-blockers; the afferent spikes remained. In preparations preincubated with 0.1 mM RuR, increasing CaCl2 in Ringer's solution from 0.2 mM, resulted in shortening of the duration of individual spikes with prolonged depolarization and in increase in the maximum rate of rise (MRR) of the spikes. Preincubation with higher concentrations of RuR produced higher sensitivities in the modifications of the duration and MRR to the change in [Ca2+]O. The responses were retained by adding RuR or RuCl3 to Ca2+-free Ringer's solution containing 0.1-5 mM EGTA, although all responses disappeared in Ca2+-free EGTA Ringer's solution. It is concluded that the RuR-induced prolonged response is produced by an influx of Na+.

Action Potentials↗
PubMed1983

Electrical threshold of the sensory nerve terminal of the frog muscle spindle: a role of spindle potential for generating afferent impulses.

The threshold at the terminal node in the capsule of frog muscle spindle, where afferent impulses are initiated, was calculated to be 2 nA on average, from data of intracellularly recorded threshold depolarization of the node against antidromic stimulation and of a mean attenuation ratio of the stimulation current from the stimulation site to the recording site. Using a similar procedure, the absolute value of orthodromically generating current at the node during static stretch of the spindle from the in situ length was calculated to be approximately 0.9 nA. It thus is supposed that at the terminal node the afferent impulses may be triggered by abortive spikes of 1.1 nA or more in amplitude, which are generated along non-myelinated filaments, being superimposed on the generating current.

Afferent Pathways↗
PubMed1983

Biosynthesis and processing of placental alkaline phosphatase.

Polypeptides of 61,500 and 64,500 apparent molecular weights were the precursor and fully processed forms of placental alkaline phosphatase monomer synthesized by choriocarcinoma cells in vivo. [3H] Mannose was incorporated into both polypeptides whereas [3H] glucosamine was incorporated mainly into the 64,500-dalton polypeptide, suggesting processing by the addition of glucosamine moieties. In the absence of microsomal membranes, choriocarcinoma mRNA directed the cell-free synthesis of the preprotein form of alkaline phosphatase monomer of apparent Mr = 60,000. The unglycosylated monomer had an apparent Mr = 58,000. In the presence of microsomal membranes, the 60,000-dalton polypeptide was processed to a polypeptide of apparent Mr = 61,500, comigrating with the precursor form of alkaline phosphatase monomer.

Alkaline Phosphatase↗
PubMed1983

Arrest of 3T3 cells in G1 phase by low density lipoprotein.

Low density lipoprotein (LDL) and high density lipoprotein (HDL) were purified from normal human serum by KBr density gradient centrifugation and gel filtration through Sepharose 4B. LDL reversibly inhibited proliferation of Swiss/3T3 cells, whereas HDL had no inhibitory effect on cell growth. The LDL-induced inhibition was LDL-dose dependent and was reversed by the addition of mevalonate, a product of the reaction of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (mevalonate: NADP+ oxidoreductase (CoA-acylating), EC 1.1.1.34). These data suggest that a specific reduction in the activity of HMG-CoA reductase produced by the addition of LDL is the main cause of the inhibition of cell proliferation. Studies of the effect of LDL on the cell cycle showed that it inhibited the entry of cells arrested in G0/G1 into the S phase but that it did not affect the transition of cells at the G1/S boundary into the M phase. The cell cycle of 3T3 is arrested solely in G1 by LDL.

Cells, Cultured↗
PubMed1983

Inhibition of thymidine transport by low density lipoprotein and its lipid components.

We previously showed that low density lipoprotein (LDL) induces an early decrease in the thymidine-transport rate and subsequently inhibits cell proliferation. We now have demonstrated that a dose-dependent decrease in the rate of thymidine transport was found in all the cell lines examined irrespective of their sensitivity to the inhibitory effect of LDL on cell growth. Thus, inhibition of both transport and cell growth by LDL are not necessarily coupled. In contrast, 3-O-methyl-D-glucose transport was not affected by an addition of LDL. The specific inhibition of transport was not suppressed by an addition of chloroquine. Thus, degradation of LDL within the lysosome was not required for LDL to inhibit thymidine transport. A mixture of lipids extracted from LDL was as inhibitory as LDL in the various types of cells examined. Calf serum also prevented the inhibitory effect of both LDL and its lipid constituents equally. Phosphatidylcholine produced no decrease in thymidine transport, but cholesterol inhibited it. We concluded that LDL-associated lipids, particularly cholesterol, play an essential role in the LDL-induced decrease of transport.

3-O-Methylglucose↗