Effect of yogic training on serum LDH levels

LDH is a glycolytic enzyme utilised during exercise to provide energy to contracting muscles. Chronic submaximal exercise for a longer duration shows about two-fold increase in LDH levels. Yogic practises might be bringing similar effects. The present work was designed to study effect of yogic training on LDH levels. Fourteen female and six male students of average age or 18 years were subjected to yogic training for six weeks. Serum LDH levels were found before and after the training course by spectrophotometric method of Henry et al. The serum LDH levels were within normal limits and showed significant increase both in females and males after yogic training. It indicates that Yoga has similar effect on LDH levels like endurance training.     

Variability in cardiovascular and plasma norepinephrine responses to head-up tilt in healthy human subjects.

Eight healthy, young adult males underwent three separate, 10-min 70 degrees head-up tilts (HUT) over a period of nine days, in order to assess the intra- and inter-individual variability of cardiovascular and plasma norepinephrine (NE) responses to the manoeuvre. Cardiovascular parameters and plasma NE were measured in the basal state and at 2-min intervals during the HUT. The results indicate that: (1) the intra-individual variability is a smaller component of the total variability of both cardiovascular and plasma NE responses to HUT; (2) the variability in cardiovascular parameters is smaller than that in plasma NE levels, both basal and in response to postural stress; (3) there does not appear to be any difference in variability when expressed either as the maximal or the mean response to HUT; and (4) there does not appear to be an increase in the variability of the measured parameters over the duration of the HUT.     

Clinical significance of serum and cerebro spinal fluid bilirubin indices in neonatal jaundice

To assess the value of unbound bilirubin (UB) and saturation index (SI) in serum and CSF as indicators of Kernicterus, we studied 50 icteric neonates (serum indirect bilibrubin (IB) greater than or equal to 7 mg/dl) and 20 controls (IB less than 7 mg/dl) during the first week of life. Serum and CSF were obtained simultaneously in all neonates. Of 36 neonates with IB greater than 12 mg/dl 19 had evidence of kernicterus. UB was estimated by Sephadex gel filtration and SI by salicylate displacement technique. Positive correlation (r = +0.85) was obtained between serum and CSF UB levels. There was a significant difference (p less than 0.05) between mean serum and CSF UB levels in kernicterus and non-kernicterus neonates (kernicterus serum UB = 0.71 +/- 0.22) mg/dl, CSF UB = 0.16 +/- 0.06 mg/dl: non-kernicteric serum UB = 0.40 +/- 0.10 mg/dl, CSF UB = 0.10 +/- 0.03 mg/dl). A critical serum UB level 0.5 mg/dl and a danger zone of CSF UB (0.1 to 0.15 mg/dl) was observed in presence of kernicterus. Neonates with kernicterus and 30% non-kernicteric had serum SI greater than or equal to 8. Mean values of serum and CSF SI were comparable in all neonates. The serum and CSF UB and SI, and the mean percentage cross over of UB from serum to CSF when statistically compared were not significantly influenced by risk factors.     

Serial doxycycline and metronidazole in prevention of recurrent periodontitis in high-risk patients.

The efficacy of metronidazole and doxycycline in preventing recurrent periodontitis was studied in 23 patients. After treatment in the previous 7 months with either bimonthly scaling and 3 weeks of systemic doxycycline (11 subjects) or scaling and placebo (12 subjects), patients were monitored for recurrent periodontitis and were scaled every 2 months. When either a periodontal abscess or greater than 2 mm loss of gingival attachment was observed, metronidazole was administered (250 mg every 8 hours) for 10 days. In the placebo plus metronidazole group, 5 patients (42%) exhibited recurrent periodontitis after the metronidazole regimen compared with only one (9%) in the doxycycline plus metronidazole group (P less than 0.096). Subgingival plaque samples at study and healthy control sites were screened for the presence of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Eikenella corrodens, and Fusobacterium nucleatum by immunofluorescence and for spirochetes using Ryu's stain. Presence/absence analysis of the sum of scores of the 6 individual pathogens demonstrated large reductions (P less than 0.005) in the frequency of detection of pathogens in the former doxycycline compared with the placebo plus metronidazole group at both study and control sites before and one month after metronidazole. By 7 months after metronidazole, there was no detectable difference between groups. These results indicate that prevention of recurrent periodontitis with metronidazole may be enhanced by previous treatment with doxycycline.     

Synthesis and antimicrobial activity of new substituted 10-methyl-1,2-dihydro-1-oxo-1,2,4-triazino(4,5-a)indoles

Ten new 4,8-disubstituted 10-methyl-1,2-dihydro-1-oxo-1,2,4-triazino(4,5-a)indoles (5 and 6) were prepared by refluxing various 5-substituted indole-2-carbohydrazides (4) with triethylorthoformate or triethylorthoacetate in dimethylformamide. These derivatives were evaluated for their antimicrobial activity. Some of the title compounds possess fairly potent antimicrobial activity.     

1.5 tesla magnetic resonance imaging of acute spinal trauma

Fifty patients with spinal injury above L2 were studied with MRI; forty-two had initial and followup studies permitting correlation of MRI abnormalities with neurologic improvement. Two discrete patterns of MRI abnormality were identified, presumably representing cord hemorrhage and edema respectively. A third pattern appeared to represent a mixed type of injury. The correlation between the MRI patterns of cord injury and neurologic recovery was excellent. The ability of MRI to demonstrate and characterize acute cord injury appears to exceed that of other diagnostic techniques.     

Modulation of MK-801 response by dopaminergic agents in mice

Various doses of the non-competitive N-methyl-d-aspartate (NMDA) receptor antagonists, MK-801 (0.1–0.5 mg/kg) and ketamine (2.5–10 mg/kg), produced a dose-dependent increase in stereotypic behaviour in naive mice. MK-801 (0.1 mg/kg) and ketamine (2.5 mg/kg) potentiated the stereotypic response of apomorphine (0.1–0.5 mg/kg) in mice pretreated with reserpine (5 mg/kg, 24 h prior) and alpha-methyl-p-tyrosine (150 mg/kg, 1 h prior) but not in naive mice. SKF 38393, a D₁ dopamine agonist, enhanced whereas B-HT 920, a D₂ dopamine agonist, reduced the stereotypic response of MK-801 in naive mice. The response of MK-801 was blocked by pretreatment with haloperidol (0.5 mg/kg), molindone (2.5 mg/kg), clozapine (7.5 mg/kg) and SCH 23390 (0.1 mg/kg). The present data suggest involvement of endogenous DA transmission in the stimulant action of non-competitive NMDA antagonists in mice. Dopamine D₁ and D₂ receptor stimulation, respectively, exert opposing effects on the behavioural expression of MK-801 in mice.     

Glucose-deprivation-induced [3H]D-aspartate release from isolated bovine and human retinae.

The glucose deprivation-induced release of [3H]D-aspartate was studied in bovine and human retinas in a superfusion apparatus. [3H]D-aspartate release was significantly increased upon omitting glucose in the superfusion buffer. This effect was dependent on external Ca2+ because L- and N-type Ca2+-channel blockers, such as diltiazem (1 microM), nitrendipine (1 microM), and omega-conotoxin (100 nM), significantly reduced the effect of glucose-deprivation induced release of [3H]D-aspartate. Furthermore, while glutamate receptor agonists (L-glutamate, N-methyl-D-aspartate, but not kainate) potentiated the effects of glucose deprivation, antagonists (MK-801, MCPG, ifenprodil, and L-AP3) at these receptors blocked the glucose deprivation-induced release process. Taken together, these studies have demonstrated that under conditions of glucose deprivation, as may happen during ischemic events in vivo, the retinal glutamatergic nerve endings and/or glial cells promote the efflux of [3H]D-aspartate into the extracellular environment. This process appears to be receptor-mediated and dependent on extracellular Ca2+ and is similar to previous reports pertaining to brain tissues.