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Biomedical subjects

Y Z Chang

Publications and source records attributed to Y Z Chang.

10 recordsLinked to original sources
PubMed2001

Sheathless capillary electrophoresis/electrospray mass spectrometry using a carbon-coated tapered fused-silica capillary with a beveled edge.

A tapered capillary tip containing a beveled edge was developed for use in sheathless capillary electrophoresis/electrospray mass spectrometry (CE/ESI-MS). The optimal flow rate of a 75-microm-i.d., 90-microm-o.d. beveled tapered capillary tip was similar to a conventional flat tapered tip with a 25-microm orifice. Using a mixture of coptisine, berberine, and palmatine chloride, the sheathless CE/ ESI-MS sensitivity of a beveled 75 microm tapered tip capillary was found to be similar to a 25 microm flat tip. Although both tips offer similar CE/ESI-MS sensitivity, the beveled tapered capillary tip is more rugged and durable than a conventional 25-microm tapered capillary because of the larger outside diameter and inside diameter. To make electrical contact, the capillary tip was smeared with paint marker followed by the application of a carbon coating using a graphite pencil. Using this refined carbon-coating procedure, the capillary tip can be operated with aprotic solvents.

Carbon↗
PubMed2001

Beta-endorphin- and GABA-mediated depressor effect of specific electroacupuncture surpasses pressor response of emotional circuit.

It has been proved that input of specific electroacupuncture (EA) can activate beta-endorphin(beta-EP)ergic and noradrenergic neurons projecting to the rostral ventrolateral medulla (RVL), the latter acting upon the RVL-GABAergic interneurons, thereby produce depressor effect. The present study further shows that: (1) The EA depressor effect is strong enough to surpass the pressor response of the AC (nucleus amygdaloideus centralis)-emotional circuit, (2) both beta-endorphin (beta-EP) and GABA in the RVL mediate the EA antagonistic effect, (3) the EA effect does not take place in the AC and paraventricular nucleus (two key nuclei besides the RVL, which also have beta-EPergic input) in the emotional circuit.

Acupuncture Points↗
PubMed1999

Mechanisms underlying pressor response of subfornical organ to angiotensin II.

In urethane-anesthetized rats, microinjection of angiotensin II (AII) into either the subfornical organ (SFO), nucleus paraventricularis (NPV), or rostral ventrolateral medulla (RVL), respectively, all induced pressor responses, but the heart rate remained unchanged. Preinjection of [Sar1, Thr8]-angiotensin II (ST-AII, an AII antagonist) into bilateral NPV blocked the SFO-pressor response to AII. Bilateral RVL pretreated with ST-All markedly attenuated the pressor response of the SFO or NPV to AII. Hexamethonium or methyl atropine (IV) also reduced the SFO-pressor response. The results show that All can activate the SFO, NPV, and RVL successively, thereby inducing the pressor response; both excitation of sympathetic nerves and inhibition of the cardiac vagus are involved in this response.

Angiotensin II↗
PubMed1999

[Role of brain angiotensin II system in subfornical organ-pressor responses].

We studied the role of brain angiotensin II in subfornical organ-pressor responses using urethane-anesthetized, tubocurarine-immobilized rats, and the present work obtained the following findings: (1) angiotensin II (A II) induced pressor responses by injection into several brain regions: either subfornical organ (SFO),nucleus paraventricularis (NPV) or its projection areas, including rostral ventrolateral medulla (RVLM),periaqueductal gray matter (PAG) and locus coeruleus (LC); (2) SFO pressor responses were markedly attenuated by preinjection of [Sar(1),Thr(8)]-A II (ST-A II, an A II antagonist) into bilateral NPV or RVLM,while NPV pressor responses were suppressed by ST-A II injection into the RVLM; (3) both SFO- and NPV-pressor responses were decreased by ST-A II preinjection into bilateral PAGL; and (4) ST-A II preinjection into bilateral LC could only attenuate NPV pressor responses without affecting SFO pressor responses. Taken together with our previous findings that the RVLM mediates the pressor responses of the PAG and LC, the present results indicate that A II activates A II ergic neurons in the SFO may evoke pressor responses by acting upon RVLM through NPV and NPV- PAG -RVLM system. Whereas NPV- LC- RVLM system was not involved in the SFO pressor responses.

Angiotensin II↗
PubMed1994

Role of regulatory peptide in pathogenesis of shock.

The present study evaluated the pathogenetic roles of three kinds of regulatory peptide. The results showed that (i) plasma endothelin (ET) level elevated significantly in septic shock rats, persistent intravenous drip of low doses ET caused development of shock state in normal rats and the irreversible outcome of light hemorrhagic shock. Furthermore, i. v. administration of specific ET-antiserum was significantly effective to septic shock rats. (ii) Plasma calcitonin gene-related peptide (CGRP) increased by 260% in septic shock rats, i. v. drip of low doses CGRP both in early and late sepsis were effective to shock rats. (iii) Angiotensin-II (ANG-II) contents of heart and aorta increased dramatically both in early and late septic shock, and inhibiting its increase with Captopril in late sepsis significantly improved the shock state, but results were inverse in early sepsis. It could be concluded that ET was one of the most important factors participating in the pathogenesis of shock, CGRP had a compensatory regulatory role in shock and the role of tissue ANG-II was different during different periods of shock.

Angiotensin II↗
PubMed1993

[Roles of vagal projection areas afferents on vagal input-evoked depressor response].

Vagal afferents project directly or indirectly to several brain areas. In urethane-anesthetized and bilaterally vagotomized rats, either procaine injection into the nucleus tractus solitarii (NTS) or beta-endorphin antiserum injection into the rostral ventrolateral medulla (RVL) markedly decreased the depressor (DpV) and bradycardia response to stimulation of cervical vagal afferents, while propranolol (or beta-endorphin antiserum) injection into the nucleus paraventricularis and procaine injection into the area postrema had no significant effect. In left vagotomized rats, the DpV remained unchanged after methyl atropine (i.v), but the bradycardia response during the DpV was attenuated. Since our previous study has shown the NTS can induce a depressor response via its beta-endorphinergic projections to RVL, the above results suggest that the inhibitory effect of vagal afferents on the RVL-sympathoexcitatory neurons via NTS beta-endorphinergic neurons represents one aspect of the mechanism underlying DpV.

Afferent Pathways↗
PubMed1992

[Pressor response to glutamate-injection into hypothalamic paraventricular nucleus and its relation to pressor response of locus coeruleus and depressor response of A1].

In urethane-anesthetized, tubocurarine-immobilized and artificially ventilated rats, microinjection of L-glutamate (Glu) into hypothalamic paraventricular nucleus (NPV) or locus coeruleus (LC) induced a pressor response. The LC-pressor response could be attenuated by preinjection of phentolamine or propranolol into bilateral NPV; Preinjection of phentolamine or bicuculline into bilateral NPV could also attenuate the depressor effect of A1-excitation by Glu, but preinjection of propranolol had no such effect; suggesting that the LC-pressor or A1-depressor effect is mediated partly by NPV, and GABAergic inhibitory interneurons in NPV may be involved in A1-depressor response.

Animals↗
PubMed1991

Factors affecting local or regional recurrence in breast cancer.

Between 1975 and 1989, 535 patients with infiltrating ductal carcinoma of the breast in various clinical stages were treated by modified radical mastectomy and axillary node clearance, followed by chemotherapy, endocrine therapy or radiotherapy. Median follow-up was 3 years (5 months to 15 years). Fifty-eight local or regional recurrences occurred. The 5-year and 10-year actuarial risks of breast recurrences were 14% +/- 2% and 23% +/- 4%, respectively. Using multivariate analysis with the Cox regression model, the most important multivariate-adjusted independent contributing factors to local or regional breast recurrences were age less than or equal to 40 (p less than 10(-4), relative risk = 2.94), positive lymph nodes greater than 3 (p less than 10(-3), relative risk = 2.57), and multicentricity (p = 0.044, relative risk = 2.73). The overall 5-year survival rate of recurrent patients was 64 +/- 7%, and was significantly worse when breast recurrence occurred in the first 18 months after operation. The multivariate-adjusted relative risk of death for early recurrence was 4.35 (p = 0.04). The unadjusted 5-year survival rate for early recurrence was 58% +/- 1%, and 85% +/- 8% for late recurrence. This study confirms the relationship between young age and low breast control rates. It emphasizes the adverse prognosis of early breast recurrences as compared to the relatively favorable outcome of late recurrences.

Adult↗