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Biomedical subjects

S Tan

Publications and source records attributed to S Tan.

At least 217 records · Page 12Linked to original sources
PubMed1987

[Behavior of left ventricular filling after left ventricular aneurysmectomy: evaluation by pulsed Doppler echocardiography].

The pattern of diastolic flow velocity was studied using pulsed Doppler echocardiography to evaluate postoperative left ventricular (LV) diastolic function in patients who underwent left ventricular aneurysmectomy. This study involved 16 patients who experienced ischemic heart disease from January 1985 to April 1986. The patients were categorized in two groups; the aneurysm group comprised by seven patients undergoing aneurysmectomy, and the bypass group which included nine patients undergoing only coronary artery bypass grafting. Pulsed Doppler studies were performed five to 22 days before, and at an average of 12 days after surgery. Preoperative cardiac catheterization and cineangiography were performed and, myocardial infarct size was estimated by the Wagner's method. Using pulsed Doppler echocardiography, LV filling dynamics were assessed by the peak velocity in the rapid filling phase (R), the peak velocity in the atrial contraction phase (A), and the ratio of A to R (A/R ratio) of the mitral flow velocity pattern. All data were average in five consecutive beats. 1. The estimated myocardial infarct size (%MI) in both groups before surgery was 38.5% in the aneurysm group and 32.5% in the bypass group, and there was no significant difference between these groups. 2. The preoperative cardiac index (2.9 in the aneurysm group vs 2.8 1/min/m2 in the bypass group), left ventricular end-diastolic pressure (16.1 vs 17.3 mmHg), and left ventricular ejection fraction (0.43 vs 0.36) were not significantly different between the two groups. 3. The preoperative A/R ratio was 1.5 in the aneurysm group and this was significantly higher than that of the bypass group (1.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Epitopic mapping of structural and nonstructural Aleutian disease virus proteins.

Common antigenic properties for p85 and p75 but a different antigenic character for p71 Aleutian disease virus (ADV) proteins were demonstrated by Western blot analysis with monoclonal antibodies. It was shown that four hybridomas (ADV-Hy 47, 66, 77 and 84) with specific reactivity for structural proteins p85 and p75 also recognized p25 but not the p71, nonstructural, protein. In turn, the monoclonal antibody ADV-Hy 2 recognized the p71 protein only. For further studies of their antigenic properties, the ADV proteins were subjected to enzymatic or chemical cleavage. The derived peptide fragments were analyzed by epitopic mapping. Depending on the cleavage reagent and monoclonal antibody applied, specific peptide maps were revealed. The maps of p85 and p75 were very similar, indicating that both proteins shared an extensive antigenic relationship. After cleavage with alpha-chymotrypsin and N-chlorosuccinimide and by using the ADV-Hy 84 monoclonal antibody, unique peptide fragments were identified with p85 which had no counterparts in p75 fragments.

Aleutian Mink Disease Virus↗
PubMed1986

Effects of high-calcium and/or high-sodium diet on basal and angiotensin II-stimulated blood pressure in the spontaneously hypertensive rat.

Direct conscious blood pressure (BP) was measured via indwelling femoral cannula to evaluate the effects of chronic diet supplements with Na, Ca or both, offered to 3-week-old weanling spontaneously hypertensive rats (SHR). Despite similar food intakes, body weights were reduced within 1-2 weeks on high-Ca diets. Blood pressure was unchanged by 5.5 weeks of diet treatments. However, irrespective of concomitant Na supplement, more prolonged treatment with the high-Ca diet completely abolished the further increase in BP between the 9th and 12th weeks of age, which was noted in the rats fed the normal or high-Na diets. Angiotensin-stimulated BP was attenuated by high-Ca diets regardless of diet Na, similar to basal readings. These weight and pressure effects of Ca were not reproduced by high-Na diet alone. For all four groups, BP was directly and significantly correlated with body weight, both at 9 and 12 weeks of age. These studies demonstrate the potential role of growth retardation in the antihypertensive action of oral Ca loading in young rats.

Angiotensin II↗
PubMed1986

[A case-control study of diet and colo-rectal cancer in Japan].

A case-control study of cancer of the colon and rectum was conducted in Kyoto, Japan. A total 62 cases of cancer of the colon and 52 cases of cancer of the rectum were individually matched by age at interview (+/- 5 years) and sex to same number of hospital controls. Cooking with oil and confectionery were significantly increased risk factors for cancer of the rectum. Margarine was a significantly increased risk factor for cancer of the colon. These results suggests that dietary fat plays an etiologic role in carcinogenesis of the large intestine. Factors already demonstrated or thought to affect the development of colo-rectal cancer were also reviewed.

Colonic Neoplasms↗
PubMed1985

Prostaglandins, alpha-adrenergic receptors and lipolysis in hamster fat cells.

In hamster fat cells, PGE2, PGI1 and clonidine (alpha 2-adrenoceptor agonist) were shown to inhibit markedly lipolysis stimulated by methylisobutylxanthine (MIX) (2 X 10(-4) M) and slightly that provoked by isoprenaline (5 X 10(-7) M). The similar inhibitory actions of the alpha 2-adrenoceptor agonist clonidine and PGE2 on lipolysis stimulated by MIX led us to examine possible reversal of the antilipolytic effect of PGE2 by yohimbine (alpha 2-adrenoceptor antagonist). However, the absence of an effect of yohimbine on PGE2, antilipolytic action indicated that the PGE2 receptor was different from the alpha 2-adrenoceptor of hamster fat cells. In these studies, PGE2 was shown to be a more potent antilipolytic agent that PGI2 (IC50 values 2 X 10(-9) and greater than 10(-4) M respectively).

1-Methyl-3-isobutylxanthine↗
PubMed1985

Comparative studies of prostaglandin E2, phenylisopropyladenosine, clonidine and propranolol on lipolysis stimulated by methylisobutylxanthine and isoprenaline in hamster fat cells.

The antilipolytic effects of prostaglandin E2 (PGE2), phenylisopropyladenosine (PIA), clonidine (alpha-2 adrenoceptor agonist) and propranolol (beta- adrenoceptor antagonist) on lipolysis stimulated by methylisobutylxanthine (MIX) (2 x 10(-4)M) and isoprenaline (5 x 10(-7)M) were compared in hamster fat cells. PGE2, PIA and clonidine inhibited markedly lipolysis stimulated by MIX, and slightly that stimulated by isoprenaline. Whilst propranolol inhibited markedly lipolysis stimulated by isoprenaline and slightly that stimulated by MIX. These results indicate that the inhibitory activity of PGE2, adenosine and alpha-2-adrenergic receptor stimulation depends upon the presence of MIX, whereas that of the beta-adrenoceptor blockade does not.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Anti-lipolytic action of prazosin in hamster fat cells.

Using isolated white fat cells of the hamster, we studied the possible inhibitory effects on lipolysis of the preferentially selective alpha-1-adrenoceptor blocking and anti-hypertensive agent prazosin. Parallel studies were undertaken with the preferentially alpha-2-adrenoceptor blocking agent yohimbine. Neither of the compounds had any significant effects on basal (non-stimulated) lipolysis. When lipolysis was stimulated by noradrenaline or isoprenaline, however, prazosin showed significant anti-lipolytic effects from a concentration of 10(-6) M. Lipolysis stimulated by methylisobutylxanthine was antagonized by prazosin only at a concentration of 10(-4) M, and dibutyrylcyclic adenosine 3'5' monophosphate-stimulated lipolysis was not inhibited at all. It is suggested that prazosin inhibits lipolysis by preventing adenyl cyclase activation by an indirect mechanism not identifiable with an alpha-2-adrenergic function but associated possibly with the formation of a local inhibitory mediator. These observations are compatible with a reduction of the outflow of free fatty acids from adipose stores in patients undergoing prazosin therapy and thus a breaking of the "vicious circle" leading to elevated plasma lipoproteins and may explain, in part at least, the reduction in plasma lipid levels observed during prazosin treatment in man.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Comparative effects of RX 781094, mianserin, yohimbine, rauwolscine and prazosin in reversing clonidine inhibition of MIX-stimulated lipolysis in hamster isolated white fat cells.

Different alpha-adrenergic receptor antagonists: RX 781094, yohimbine and rauwolscine (selective alpha 2-adrenergic antagonists); mianserin (tetracyclic anti-depressant, antagonist at alpha 2-presynaptic autoreceptors) and prazosin (selective alpha 1-adrenergic antagonist) were used at concentrations ranging from 10(-7) to 10(-4) M, to reverse clonidine inhibition of MIX-stimulated lipolysis in the hamster fat cell. In this adipose tissue (like human but unlike rat) there co-exist prolipolytic beta-adrenoceptors and antilipolytic alpha-adrenoceptors. Although no effects were observed with prazosin, RX 781094 was ten times more potent than yohimbine or its isomer rauwolscine in reversing clonidine inhibition of the MIX-stimulated lipolysis. Mianserin was an effective blocker only from a concentration of 10(-4) M, consistent with its relative lack of specificity for alpha 2-adrenoceptors cited elsewhere. Overall these results confirm the utility of this model for testing compounds presumed to act at alpha 2-adrenoceptors.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Application of agents active at the alpha 2-adrenoceptor of fat cells to the treatment of obesity--a critical appraisal.

The extent of cyclic AMP (cAMP) mediated lipolysis in adipose tissue cells of man and several other animal species is regulated by the interplay of alpha- and beta-adrenoceptors modulating adenyl cyclase activity. Although the naturally-occurring catecholamines, and isoprenaline, are thought to act at the same pro-lipolytic beta-adrenoceptor antilipolytic agents, working through the alpha 2-adrenoceptor moiety of adenyl cyclase, appear to act at separate sites for: true alpha 2-agonists such as clonidine, for adenosine and for prostaglandins. Further, such antilipolytic agents are conspicuously more potent against lipolysis stimulated by methyl-isobutylxanthine (MIX) than against that stimulated by catecholamines. The nature of the dual character of adenyl cyclase remains to be elucidated. alpha 2 Adrenoceptor antagonists which promote lipolysis, and may possibly serve a therapeutic role in the treatment of obesity, may also provoke inappropriate insulin release which is contraindicated. Thus a problem in chemotherapy exists which may be resolved by new agents with differential tissue specificities. An example of this chemotherapeutic dilemma is possibly provided by the body weight accruing actions of tricyclic antidepressant compounds whose mechanism of action involves also (central) alpha 2-adrenoceptors.

Adenylyl Cyclases↗
PubMed1983

Regulation of adipose tissue metabolism via adrenergic mechanisms: actions of alpha-adrenoceptor agonists on lipolysis in hamster fat cells.

The effects of two alpha-1-adrenergic agonists (phenylephrine, cirazoline) and two alpha-2-adrenergic agonists (clonidine, guanabenz) were investigated on lipolysis stimulated by noradrenaline, isoprenaline, dibutyryl cyclic AMP (dbc AMP) or methylisobutylxanthine (MIX) in hamster adipose cells, in vitro. Phenylephrine enhanced basal lipolysis and that stimulated by dbc AMP and MIX, whereas cirazoline showed no measurable effects. Clonidine produced a slight but significant decrease of basal lipolysis. Both clonidine and guanabenz (from 10(-7) M) provoked a similar and clear inhibition (50-60 per cent) of MIX-stimulated lipolysis, compatible with the view that the alpha-adrenergic receptor of the hamster white fat cell is of the alpha-2 type. Noradrenaline-stimulated lipolysis was unaffect and isoprenaline-stimulated lipolysis moderately inhibited, by clonidine and guanabenz. Since the beta-adrenergic lipolytic effects of noradrenaline are known to be associated with a simultaneous alpha-adrenergic inhibitory stimulus, and one possible explanation of the but moderate inhibition of isoprenaline-induced lipolysis could be simultaneous beta-adrenergic stimulation (resulting in lipolysis), and alpha-adrenergic stimulation (inhibition of lipolysis), as with noradrenaline, the nature of isoprenaline as a pure beta-adrenergic agonist requires clarification.

Adipose Tissue↗
PubMed1983

Characterization of the beta-adrenoceptor of the adipose cell of the rat.

The dose-response curves of the beta-adrenergic agonists isoprenaline (mixed beta 1 and beta 2), prenalterol (beta 1-selective), noradrenaline (more beta 1 than beta 2) and salbutamol (beta 2-selective) were studied on adipose cells of the rat, in vitro. The observed lipolytic potencies were in the order: isoprenaline greater than noradrenaline greater than salbutamol greater than prenalterol. The effects of beta-adrenergic antagonists betaxolol (beta 1-selective) propranolol (non-selective) and ICI 118551 (beta 2-selective) on lipolysis stimulated by the various beta-adrenergic agonists showed that in each case propranolol was the most potent blocking agent. These observations are not compatible with the concept that regulation of lipolysis in adipose tissue is mediated exclusively either by adrenergic receptors of the classical beta 1 type, or of the classical beta 2 type. We propose therefore, that this beta-adrenergic receptor, because of its non-compliance with the current classification system, be termed a 'beta-3' or beta-hybrid' adrenoceptor. Thus cardio-selective beta-adrenergic blocking agents, like betaxolol, may offer a hitherto unrecognized clinical advantage in obese patients undergoing anti-hypertensive therapy by offering a reduced impediment to hormone-induced utilization of calorie stores in adipose tissue.

Adipose Tissue↗