PubMed Health⌕ Search

Biomedical subjects

C Gopalan

Publications and source records attributed to C Gopalan.

13 recordsLinked to original sources
PubMed1992

The contribution of nutrition research to the control of undernutrition: the Indian experience.

Since diseases directly related to undernutrition are the major public health problems of India, nutrition research in the country has been largely directed towards elucidating their causes and identifying the most feasible methods for their prevention and control. This effort is an interdisciplinary exercise carried out in the laboratory, the clinic, and the field, with close interaction among biochemists, clinicians, and epidemiologists. Some of the identified solutions have found practical application; but, as in other areas of scientific endeavor, a gap exists between the acquisition of knowledge in the laboratories and its application in the field. Today, thanks to research efforts of the last few decades, we have the knowledge with which most diseases related to undernutrition can be prevented. Unfortunately, however, we do not always have the means of applying this knowledge under real-life conditions in the field. Even so, nutrition research during the last few decades has contributed significantly to the amelioration of undernutrition among poor communities in India.

Humans↗
PubMed1989

Effects of different opiates on hypothalamic monoamine turnover and on plasma LH levels in pro-oestrous rats.

Opiate inhibition of luteinizing hormone (LH) appears to involve changes in hypothalamic monoaminergic activity. Agonists of mu-, kappa- and sigma-opioid receptors and an opiate antagonist were administered at the onset of the preovulatory LH surge and their effects on hypothalamic monoamine turnover, and on plasma LH levels, investigated. The opiate antagonist, naloxone, significantly increased both noradrenaline (NA) turnover and plasma LH levels. Morphine (mu-agonist), significantly decreased NA concentration and plasma LH levels, but significantly increased dopamine (DA) and serotonin (5-HT) activity. Levorphanol (another mu-agonist) significantly decreased both NA and 5-HT concentrations and had no effect on circulating LH. Cyclazocine, ketocyclazocine and tifluadom (kappa-agonists) increased NA turnover but only tifluadom increased 5-HT turnover, also reducing LH levels significantly. N-Allylnormetazocine (SKF 10,047; sigma-agonist) increased 5-HT activity but did not alter LH levels. This study has confirmed the existence of a heterogenous group of opioid receptors within the hypothalamus which modulate monoamine neurotransmitters controlling LH release.

Animals↗
PubMed1987

The role of the hypothalamic beta-adrenergic system in controlling the LH rise in short-term castrated rats.

Intraventricular infusions of adrenaline and various pharmacological agents acting on beta-adrenergic receptor subtypes were carried out in rats orchidectomized 16 h previously. Infusions (10 microliter) of solutions containing the drugs were administered under anaesthesia induced with alphaxalone and alphadolone. Levels of LH were measured in plasma collected immediately before and at predetermined intervals after the infusion. The acute rise in LH levels after castration was increased still further by isoprenaline (a mixed beta 1- and beta 2-agonist), fenoterol (a beta 2-agonist) and atenolol (a beta 1-antagonist). In contrast, prenalterol (a beta 1-agonist) and (2RS,3RS)-3-isopropylamino-1-(7-methylindan-4-yloxy)++ +butan-2-ol (ICI 118,551) (a selective beta 2-antagonist) were inhibitory to LH release. Adrenaline itself, salbutamol (another selective beta 2-agonist), propranolol (a mixed beta-antagonist) and metoprolol (a beta 1-antagonist) did not significantly alter plasma LH concentrations at the doses administered. The stimulatory effect of isoprenaline on LH release was partially reduced when given together with ICI 118,551, but was not affected when administered simultaneously with atenolol. The inhibitory effect of ICI 118,551 was, however, prevented by concomitant administration with fenoterol, as was that of prenalterol when infused with atenolol. The results suggest that the hypothalamic mediation of the short-term changes in LH release in response to castration is exerted, at least in part, through the activation of a beta 2-stimulatory component and the suppression of a beta 1-inhibitory component.

Adrenergic beta-Agonists↗
PubMed1975

Famine oedema.

Explore the source record for details and available documents.

Adult↗