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Biomedical subjects

M Nath

Publications and source records attributed to M Nath.

27 records · Page 2Linked to original sources
PubMed1984

Ascorbic acid in thyroidectomized rats. II) Ascorbic acid status of the storage tissues and hepatic biosynthesis of glucuronic acid.

Depletion of ascorbic acid from adrenals, brain and epididymis along with loss in weight were noticed in the state of thyroidectomy. This decrease appears to be due to an effect of thyroidectomy on the membrane integrity since the membrane bound sialic acid was found to be significantly lowered in these tissues as a consequence of the elevated activity of sialidase. Thyroidectomy was also found to cause an adverse effect on the activities of hepatic UDP-glucuronyl transferase and beta-glucuronidase with no alteration in UDP-glucose dehydrogenase.

Adrenal Glands↗
PubMed1979

Ulnar compression neuropathy: an uncommon complication in surgical repair of pressure ulcers.

Four patients with paraplegia at levels T3 or below were required to remain in the prone position for periods of 3 to 5 weeks following plastic surgical repair of their pressure ulcers. Serial nerve conduction studies permitted early identification of compromise of ulnar nerve function prior to onset of symptoms. These objective findings are helpful in encouraging patients to protect the nerve, thus preventing palsy.

Adult↗
PubMedDate not supplied

Metabolic studies in congenital vitamin D deficiency rickets.

Congenital rickets in 3 newborns of mothers with advanced nutritional osteomalacia, healed with maternal breast milk feeding when mothers alone were given calcium supplements and 7.5 mg of intravenous D2 and the mother baby pair protected from sunlight. Maternal plasma biochemistry indicated more severe vitamin D deficiency compared to their newborns (intrauterine foetal priority). The first dose of 7.5 mg of vitamin D3 and calcium supplements to mother healed osteomalacia but did not appear to heal the rickets of their breast fed infants (extrauterine maternal priority for vitamin D). A second dose given at 3 months interval healed the rickets in their infants and the biochemistry of the mother and baby returned towards normal. Congenital rickets developed when maternal bone mineral and vitamin D stores had been completely exhausted. Raised IPTH levels in the newborn suggested that foetal parathyroids were responsive to hypocalcaemic stimulus.

Adult↗