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Peanut is an important oilseed and food legume cultivated as a rain-fed crop in semi-arid tropics. Drought and high salinity are the major abiotic stresses limiting the peanut productivity in this region. Development of drought and salt tolerant peanut varieties with improved yield potential using biotechnological approach is highly desirable to improve the peanut productivity in marginal geographies. As abiotic stress tolerance and yield represent complex traits, engineering of regulatory genes to produce abiotic stress-resilient transgenic crops appears to be a viable approach. In the present study, we developed transgenic peanut plants expressing an Arabidopsis homeodomain-leucine zipper transcription factor (AtHDG11) under stress inducible rd29A promoter. A stress-inducible expression of AtHDG11 in three independent homozygous transgenic peanut lines resulted in improved drought and salt tolerance through up-regulation of known stress responsive genes (LEA, HSP70, Cu/Zn SOD, APX, P5CS, NCED1, RRS5, ERF1, NAC4, MIPS, Aquaporin, TIP, ELIP) in the stress gene network, antioxidative enzymes, free proline along with improved water use efficiency traits such as longer root system, reduced stomatal density, higher chlorophyll content, increased specific leaf area, improved photosynthetic rates, and increased intrinsic instantaneous WUE. Transgenic peanut plants displayed high yield compared to non-transgenic plants under both drought and salt stress conditions. Holistically, our study demonstrates the potentiality of stress-induced expression of AtHDG11 to improve the drought, salt tolerance in peanut.

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Lipid peroxidation in vitro homogenates of brain was examined as sequela of lead toxicity. The levels of malondialdehyde (MDA) in homogenates of rat brain (1 ml, 5% w/v) treated with lead (50 micrograms) alone or in combination with ascorbic acid (100 micrograms), alphatocopherol (100 micrograms) or hydroquinone (100 micrograms) were evaluated. The levels of MDA were consistently evoked by lead in a dose-related manner. The toxicity of lead was further advanced by the action of the pro-oxidant drug ascorbic acid on the brain. However, the anti-oxidant drugs alphatocopherol and hydroquinone decreased the toxic effect of lead on the brain. These results clearly show that the enhanced lipid peroxidation may provide a basis of lead-induced neurotoxicity.

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The effect of zinc (8 mg/kg body weight, intraperitoneally) administration daily for 7 consecutive days was studied on the levels of Zn++, Cu++ and Pb++ in the blood, spinal cord and different regions of the brain in rabbits. It was found that with increase in Zn++ concentration there was a decrease in copper levels and an increase in lead levels in almost all parts of the brain. In the blood, both copper and lead levels were significantly decreased. No definite mechanism for the changes can be postulated. The study suggests that changes of Zn++ concentration beyond physiological limits can affect the concentration of other essential and non-essential metal ions.

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The influence of haloperidol withdrawal on motor activity and circadian rhythm was observed in rats. Haloperidol was administered with the food at a concentration of 0.005%. Motor activity was recorded for 2 days on normal food, for 4 days on food with haloperidol addition and for another 5 days on normal food again in two groups of four rats each. Withdrawal of haloperidol raised the peak values during both phases impressively. The highest activity was observed on the day of haloperidol withdrawal but subsided again on the fifth day. The circadian rhythm remained unchanged.

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Dichlorvos (O,O-dimethyl-2:2-dichlorovinyl phosphate) was administered IP (3 mg/kg) daily for 10 days to a group of albino rats. Open field behavior was significantly depressed below the mean of the control group. On day 7, ambulation was reduced to 24% of the mean but recovered to 60% on day 10. Similarly, rearing response was decreased on day 7 and showed a fast recovery on day 10 but the preening response further declined on day 10. Defecation, on the contrary, was suppressed to 0% on day 7 and showed complete recovery on day 10. Motor activity showed a significant depression and fine movements were reduced more than gross movements in the second phase. Dopamine was significantly decreased on days 5 and 7 but showed a 13% recovery in the brain stem on day 10. Norepinephrine was significantly reduced in the cerebral hemisphere while serotonin was decreased both in cerebral hemisphere and brain stem. Neither of thse two amines showed significant recovery on day 10. Interesting concordance of the open field behavioral changes with the levels of dopamine, norepinephrine, and serotonin in the various regions of the rat brain was noticeable and has been discussed.

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1. In 18 Patients the plasma concentration of the neuroleptic drug thioridazine was measured twice a week by a fluorometric method during a period of treatment lasting for an average of 27 days. At the same time the psychopathological findings were recorded by means of the AMP system. 2. A significant correlation was found both between dosage per kg body weight and plasma level, and between age and plasma level. No connection with the sex of the patient could be demonstrated. 3. A curve-linear correlation appears to exist between plasma concentration and remission of symptoms. 4. In the course of the trial the plasma concentrations of thioridazine declined though the dosage was kept constant. This observation indicates an increased metabolism of the drug probably brought about by enzyme induction. In two cases where previous liver damage could be assumed, the plasma concentrations were found to be above the average level.

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The pattern of human growth hormone (HGH) release was studied in depressed patients during sleep under EEG control and employing high temperature exposure. The patients were free of drugs and were compared with corresponding control groups. In the sleep study (6 depressed patients), 2 patients showed no definite increase in HGH plasma concentration, and 3 patients showed an increase in HGH only in the second half of the night, independent of slow wave sleep (SWS). But sleep disturbances were present in all 5 patients. A correlation between SWS and HGH release was found in only 1 patient. One nondepressed control, without SWS, showed a delayed HGH response. Exposure to high temperature in normal subjects induced an acute HGH release. 8 of the 13 patients studied had a deficient HGH RESPONSE. All were depressive, with psycho motor retardation and marked vital and neurovegetative disturbances. These findings support the idea that, at least in a high percentage of depressed patients, there is a disturbance of the hypothalamic pituitary function.

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