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Biomedical subjects

F Yin

Publications and source records attributed to F Yin.

25 records · Page 2Linked to original sources

Hair chromium levels in patients with vascular diseases.

The chromium levels in the hair of patients with hyperlipemia and coronary heart disease were found to be similar to those of healthy controls (p greater than 0.2). In patients with cerebral hemorrhage and cerebral thrombosis, significantly higher hair chromium values were observed than in healthy subjects (p less than 0.001). The possible significance of these findings is discussed.

Chromium↗

An improved video-based computer tracking system for soft biomaterials testing.

We present an improved video-based computer system for on-line tracking of small markers moving in a plane. The system consists of a CCD camera, a video monitor, a dedicated 80386/20 microcomputer, a video frame grabber, and custom software. Up to four markers can be tracked at the 30-Hz video frame rate using a two-step, correlation-based search procedure. We discuss the requisite hardware and software requirements and illustrate how this tracking system can be used to collect strain data during biaxial stretching tests on planar soft tissues. Operating at 30 Hz, this system is an improvement over those previously reported, which are either slower or yield less information.

Algorithms↗

N-nitrosodimethylamine in domestic beer in China.

Samples of domestic (Chinese) beer were analysed for N-nitrosamines using gas chromatography--high resolution mass spectrometry with a peak-matching technique. Of 26 samples tested, 20 (77%) were found to be contaminated with N-nitrosodimethylamine (NDMA)L. The mean content of these samples was 2.7 micrograms/litre, without correction for recovery of NDMA from beer (74% with a coefficient of variance of 18%). The remaining six samples contained less than 0.5 micrograms/litre, the lower limit of detection.

Beer↗

Determinants and clinical significance of jugular venous valve competence.

We studied the function of right internal jugular vein valves during cardiac catheterization in 32 patients and external jugular vein valves in vitro from 13 dogs. Patients with normal central venous pressure had competent valves during cough-induced transvalvular pressure gradients of 52.4 +/- 8.6 mm Hg. Ten of 15 patients with elevated central venous pressure had either incompetent or absent internal jugular valves, the latter occurring only in patients with long-standing, severe tricuspid regurgitation. During coughing, competent valves were also demonstrated in the left internal jugular and in the right and left subclavian veins. The excised canine valves were competent at a static transvalvular pressure of 81.8 +/- 3.7 mm Hg. Five of six excised valves remained competent during pulsatile transvalvular pressure of 64.8 +/- 1.9 mm Hg. Thus, thoracic inlet venous valves are usually competent during sudden increases in intrathoracic pressure. These valves may play an important role in establishing the extrathoracic arteriovenous pressure gradient necessary for forward blood flow during cardiopulmonary resuscitation and other states with high intrathoracic pressure.

Adult↗

Reduced inspiratory effort during intermittent mandatory ventilation with PEEP.

The use of intermittent mandatory ventilation (IMV) and positive and expiratory pressure (PEEP) may demand the patient mount an inspiratory pressure equivalent to the pressure level of the PEEP for spontaneous breathing. During respiratory failure, ineffective inspiratory muscles may be unable to consistently meet such demands, especially if high levels of PEEP are used. A technique which reduces the required inspiratory effort was devised for use in patients being treated with IMV and PEEP. Using this technique, isovolume inspiratory time was dramatically reduced and less inspiratory effort was required. This maneuver may assist spontaneous breathing in patients with respiratory failure on high levels of PEEP.

Humans↗

Signal pathways involved in apigenin inhibition of growth and induction of apoptosis of human anaplastic thyroid cancer cells (ARO).

Recently we demonstrated that several flavonoids can inhibit the proliferation of certain human thyroid cancer cell lines. Among the flavonoids tested, apigenin and luteolin are the most effective inhibitors of these tumor cell lines. In the present study, we investigated the signal transduction mechanism associated with the growth inhibitory effect of apigenin, using a human anaplastic thyroid carcinoma cell line, ARO (UCLA RO-81-A-1). Using Western blot method, it was shown that the inhibitory effect of apigenin on ARO cell proliferation is associated with an inhibition of both EGFR tyrosine autophosphorylation and phosphorylation of its downstream effector mitogen activated protein (MAP) kinase. Protein levels of these signaling molecules were not affected. The inhibitor of phosphorylation by apigenin occurred within 30 min and continued for 4 h. A dose-dependent inhibition was demonstrable ranging from 12.5 microM to 50 microM. The level of phosphorylated c-Myc, a nuclear substrate for MAPK, was depressed from 16-48 h after apigenin treatment, finally leading to a programmed cell death involving DNA fragmentation. Furthermore, treatment with apigenin resulted in the inhibition of both anchorage-dependent and anchorage-independent thyroid cancer cell growth. In summary, apigenin is a promising inhibitor of signal transduction pathways that regulate the growth (anchorage-dependent and independent) and survival of human anaplastic thyroid cancer cells. Apigenin may provide a new approach for the treatment of human anaplastic thyroid carcinoma for which no effective therapy is presently available.

Apigenin↗

Apigenin inhibits growth and induces G2/M arrest by modulating cyclin-CDK regulators and ERK MAP kinase activation in breast carcinoma cells.

We have previously reported that apigenin inhibits the growth of thyroid cancer cells by attenuating epidermal growth factor receptor (EGF-R) tyrosine phosphorylation and phosphorylation of ERK mitogen-activated protein (MAP) kinase. In this study, we assessed the growth inhibitory effect of apigenin on MCF-7 breast carcinoma cells that express two key cell cycle regulators, wild-type p53 and the retinoblastoma tumor suppressor protein (Rb), and MDA-MB-468 breast carcinoma cells that are mutant for p53 and Rb negative. We found that apigenin potently inhibited growth of both MCF-7 and MDA-MB-468 breast carcinoma cells. The approximate IC50 values determined after 3 days incubation, were 7.8 micrograms/ml for MCF-7 cells, and 8.9 micrograms/ml for MDA-MB-468 cells, respectively. Because the cell cycle studies using FACS showed that both MCF-7 and MDA-MB-468 cells were arrested in G2/M phase after apigenin treatment, we studied the effects of apigenin on cell cycle regulatory molecules. We observed that G2/M arrest by apigenin involved a significant decrease in cyclin B1 and CDK1 protein levels, resulting in a marked inhibition of CDK1 kinase activity. Apigenin reduced the protein levels of CDK4, cyclins D1 and A, but did not affect cyclin E, CDK2 and CDK6 protein expression. In MCF-7 cells, apigenin markedly reduced Rb phosphorylation after 12 h. We also found that apigenin treatment resulted in a dose- and time-dependent inhibition of ERK MAP kinase phosphorylation and activation in MDA-MB-468 cells. These results suggest that apigenin is a promising antibreast cancer agent and its growth inhibitory effects are mediated by targeting different signal transduction pathways in MCF-7 and MDA-MB-468 breast carcinoma cells.

Antineoplastic Agents↗