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Biomedical subjects

V Prasad

Publications and source records attributed to V Prasad.

At least 109 records · Page 6Linked to original sources
PubMed1982

beta 2-Tubulin, a form of chordate brain tubulin with lesser reactivity toward an assembly-inhibiting sulfhydryl-directed cross-linking reagent.

Beta 1 and beta 2 are the designations given to two forms of beta-tubulin that have different electrophoretic mobilities on discontinuous polyacrylamide gels in the presence of sodium dodecyl sulfate [Little, M. (1979) FEBS Lett. 108, 283-286]. Beta 1 and beta 2 constitute respectively 75% and 25% of the total beta-tubulin in bovine brain. Although beta 1 appears to be ubiquitous in animals, beta 2 has so far only been found in the brains of cows, pigs, deer, rats, chicks, and dogfish but not in squid brain. Beta 2 is not found in bovine kidneys, in porcine lungs, or in any nonchordate tubulin that has been examined. When tubulin is reacted with the sulfhydryl-directed reagent N,-N'-ethylenebis(iodoacetamide) (EBI), beta 1, but not beta 2, is converted to a faster moving form, beta. The yield of beta 2 in this reaction is not altered by the presence of drugs. When [14C]EBI is used as a probe, most of the label is incorporated into beta 1 rather than beta 2. Tubulin molecules that have reacted with EBI to form beta are much less likely to polymerize into microtubules than are molecules that have not formed beta. In view of the observation that only beta 1, and not beta 2, can form beta, it is possible that beta 1 represents a form of tubulin whose assembly may be regulated by a mechanism involving sulfhydryls. In contrast, beta 2 may represent a form of tubulin whose assembly is regulated by some other mechanism.

Animals↗
PubMed1982

Effect of lithium upon desipramine enhanced shock-elicited fighting in rats.

Rats were tested for changes in shock-elicited fighting (SEF) following the chronic administration of saline (IP); lithium (Li+) (20 mEq./l tap water) + saline (IP); desipramine (DMI) (15 mg/kg, IP); and DMI + Li+ for 14 days. The repeated test trials indicated a significant decrease in SEF in Li+-saline group (p less than 0.05), a significant increase (p less than p.05) in the DMI group, but no difference in the DMI + Li+ group in comparison to saline controls. Combined treatment with DMI + Li+ significantly reduced (p less than 0.05) SEF in comprison to the DMI group. These results suggest that enhanced aggressivity resulting from chronic DMI administration and measured by SEF can be a useful behavioral model to study the action of lithium.

Aggression↗
PubMed1981

The effect of cyproterone acetate on shock elicited aggression in rats.

The aggressive behavior of male rats treated chronically with cyproterone acetate was measured following electric footshock. Shock elicited fighting behavior and body weight was recorded once every week for 4 weeks. The level of plasma testosterone, brain 5-HT and 5-HIAA and weight of testes were measured 24 hours after the last injection. No significant change was observed in the level of testosterone or brain 5-HT and 5-HIAA. A trend towards an increase in plasma testosterone and shock elicited fighting in rats treated with a higher dose of CA (10 mg/kg) may be indicative of some androgenic property of CA. On the other hand a slower gain in the body weight and a significant reduction in the testes weight of CA treated rats corroborate the well known antiandrogen property of this steroid. The balance of these androgenic and antiandrogenic properties of CA may account for the absence of significant changes in behavioral and biochemical measures.

Aggression↗
PubMedDate not supplied

Long-term amelioration of bilirubin glucuronidation defect in Gunn rats by transplanting genetically modified immortalized autologous hepatocytes.

Ex vivo gene therapy, in which hepatocytes are harvested from mutants, retrovirally transduced with a normal gene and transplanted back into the donor, has been used for correction of inherited metabolic defects of liver. Major drawbacks of this method include limited availability of autologous hepatocytes, inefficient retroviral transduction of primary hepatocytes, and the limited number of hepatocytes that can be transplanted safely. To obviate these problems, we transduced primary hepatocytes derived from inbred bilirubin-UDP-glucuronosyl-transferase (BUGT)-deficient Gunn rats by infection with a recombinant retrovirus expressing temperature-sensitive mutant SV40 large T antigen (tsT). The immortalized cells were then transduced with a second recombinant retrovirus expressing human B-UGT, and a clone expressing high levels of the enzyme was expanded by culturing at permissive temperature (33 degrees C). At 37 degrees C, tsT antigen was degraded and the cells expressed UGT activity toward bilirubin at a level approximately twice that present in normal rat liver homogenates. For seeding the cells into the liver bed, 1 x 10(7) cells were injected into the spleens of syngeneic Gunn rats five times at 10-day intervals. Excretion of bilirubin glucuronides in bile was demonstrated by HPLC analysis and serum bilirubin levels were reduced by 27 to 52% in 40 days after the first transplantation and remained so throughout the duration of the study (120 days). None of the transplanted Gunn rats or SCID mice transplanted with the immortalized cells developed tumors.

Animals↗
PubMedDate not supplied

Propranolol-induced psychosis.

A 53-year-old black male with no history of neuropsychiatric behavioral problems was treated successfully with propranolol, furosemide, and minoxidil for previously uncontrolled hypertension. However, paranoid ideations, illusions, severe combativeness, and visual hallucinations developed shortly after initiation of the listed therapy. When atenolol was substituted for propranolol, all psychotic behavior resolved.

Haloperidol↗
PubMedDate not supplied

Decreased T3 and T4 levels following topical application of povidone-iodine in premature neonates.

Thyroid function and iodine levels of 30 preterm neonates were examined before and up to five days after topical exposure to 10% povidone-iodine application. Urinary iodine excretion significantly increased in the group closest to term (8.9 +/- 1.2 mg I/g creatinine x 10) vs controls (3.5 +/- 0.5 mg; p < 0.01). T3 levels significantly decreased at all sub-group gestational ages vs controls (p < 0.01-0.05). Similarly, both FT4 and TT4 levels were lower in the subgroups vs controls (p < 0.01-0.05). TSH levels however did not rise in any group. These data suggest partial failure of thyroid hormone synthesis, in a population of high-risk infants possibly already exhibiting features of the euthyroid-sick syndrome. Topical iodine-containing antiseptic solutions should be used with caution in this population since these antiseptics may modify serum thyroid hormone concentrations rapidly.

Administration, Topical↗
PubMedDate not supplied

Increase in bone density and plasma osteocalcin during growth hormone therapy in growth hormone deficient children.

UNLABELLED: Bone density in growth hormone (GH) deficient children is decreased more than expected for delayed skeletal maturation. Previous studies suggest GH enhances mineral retention and deposition in bone. Seven GH deficient prepubertal children were studied during 2 years of GH therapy to assess the effect on bone density and plasma osteocalcin. Bone density (radiographic photodensitometry) of the phalanges (cortical and trabecular bone) was expressed as the standard deviation score (SDS) of the mean for sex, bone age and chronological age. Relative osteopenia, less pronounced for bone density/bone age (BD/BA) than bone density/chronological age (BD/CA), improved significantly during GH therapy. After 12 months there was increase over pretreatment levels, significant for BD/CA (-1.65 +/- 0.46 vs -1.15 +/- 0.64; mean +/- SD: p = 0.002), but less pronounced for BD/BA. After 24 months increase in both measurements continued, reaching significance also for BD/BA (Pre: -1.02 +/- 0.55 vs -0.41 +/- 0.29; p = 0.011). Plasma osteocalcin levels were low before GH therapy (11.6 +/- 9.9 ng/ml; n = 7; vs control 24.4 +/- 12.5 ng/ml; n = 21; p < 0.05), rose significantly after one week (31.2 +/- 10.5 ng/ml; p < 0.001), with continued upward trend to plateau between 2-6 months, with elevated levels persisting during 2 years of GH therapy. CONCLUSION: The early and sustained rise in plasma osteocalcin and subsequent increase in bone density with continued gain over 24 months of the study suggests that GH therapy in GH deficient children has a significant prolonged effect on bone formation and mineralization in addition to stimulating linear growth.

Adolescent↗