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Biomedical subjects

N Jain

Publications and source records attributed to N Jain.

At least 91 records · Page 5Linked to original sources

The photoperiodic clock is blackheaded buntings (Emberiza melanocephala) is mediated by a self-sustaining circadian system.

Three experimental protocols were employed to clarify whether the circadian system is involved in photoperiodic time-measurement in the blackheaded bunting, Emberiza melanocephala. In a single-pulse paradigm, one 8-h light pulse was delivered at different times to groups of birds across three days of constant darkness (DD). Photoperiodic induction, as measured by a rise in plasma luteinizing hormone (LH), showed clear circadian rhythmicity. The second experiment examined the LH responses in birds exposed to lighting cycles using a Nanda-Hamner type of protocol and confirmed full photostimulation under 6L:30D. The third experiment measured the time of the first photoinduced rise in LH in birds subjected to 30 h of continuous light following entrainment under short days (6L:18D). This experiment aimed to identify the position of the photoinducible phase (phi i). LH first rose at hour 18 following dawn indicating that phi i lies in the middle of the day. Plasma concentrations of melatonin were also measured under 6L:18D and 6L:30D light cycles as another physiological marker of the circadian systems in buntings. The pattern of melatonin secretion with the driving oscillator being circadian in nature. It is concluded that the circadian pacemaker driving the photoinducible rhythm in blackheaded bunting is strongly self-sustaining and free-runs under constant conditions.

Animals↗

Radiobiological effects of low doses of tritiated water on developing mouse cerebellum from 17th day post-coitum.

Pregnant Swiss albino mice were maintain on tritiated drinking water of the activity of 111 and 11.1 kBq/ml after a priming injection of 74 and 7.4 kBq/ml body water respectively from 17th day of gestation till parturition. Animals were autopsied on 1, 2, 3, 4, 5 and 6 weeks postpartum and studied for cerebellar vulnerability. Cerebellum suffered from radiopathological changes in 1, 2 and 3 weeks age groups of mice in terms of degeneration and loss of Purkinje cells leading to formation of empty basquets, vacuolation in molecular layer and interfoliar connective tissue and pycnosis in granule cells of granular cell layer at 11.1 kBq dose level. Mice of 4, 5 and 6 weeks age groups, being relatively radioresistant, showed lesser changes in comparison with 1 to 3 week old mice. Though, the nature of the damage remained the same, it tended to intensify at 111 kBq dose thereby reflecting a dose dependent variation.

Animals↗

GAP-43 expression in the medulla of macaque monkeys: changes during postnatal development and the effects of early median nerve repair.

Expression of GAP-43, a neuronal specific growth associated phosphoprotein, has been highly correlated with the growth and remodeling of the nervous system during development and regeneration. As part of an effort to understand mechanisms of developmental plasticity in the somatosensory system, we determined how the expression of GAP-43 is affected by prenatal and early postnatal nerve cut and repair in macaque monkeys. We also observed normal developmental changes in the expression of GAP-43 during early postnatal life in macaque monkeys. The normal cuneate nucleus, as well as other nuclei of the ascending somatosensory pathways, had low levels of GAP-43 at birth that increased by 3 months and declined thereafter to reach adult levels between 8 and 15 months of age. Fiber tracts expressed low levels of GAP-43 at all postnatal ages, except the pyramidal tract which demonstrated high levels a birth that decreased over the first year. These observations suggest a gradual but differential synaptic maturation in lower brain stem nuclei as macaque monkeys mature. Greatly increased levels of GAP-43 were observed at the time of birth in the cuneate nucleus of two macaque monkeys with prenatal (E94 and El 14) nerve repair. Such an increase was not found after prenatal nerve repair with a postnatal survival time of 15 months, or after early postnatal nerve repair with short (80 days) or long (20 months) survivals. The results suggest that reorganization mechanisms at central terminals of peripheral nerves are very different following prenatal than postnatal nerve damage.

Animals↗

Anxiolytic activity of adenosine receptor activation in mice.

1. Purine analogues have been examined for anxiolytic- and anxiogenic-like activity in mice, by use of the elevated plus-maze. 2. The selective A1 receptor agonist, N6-cyclopentyladenosine (CPA) had marked anxiolytic-like activity at 10 and 50 microg kg(-1), with no effect on locomotor performance at these doses. 3. The A1 selective adenosine receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (CPX) had no significant effect on anxiety-related measures or locomotor behaviour, but blocked the anxiolytic-like activity of CPA. The hydrophilic xanthine, 8-(p-sulphophenyl) theophylline did not prevent anxiolysis by CPA. 4. Caffeine had anxiogenic-like activity at 30 mg kg(-1) which was prevented by CPA at 50 micro kg(-1). 5. The A2 receptor agonist, N6-[2-(3,5-dimethoxyphenyl)-2(2-methylphenyl)-ethyl]adenosine (DPMA) had no effect on anxiety behaviour but depressed locomotor activity at the highest dose tested of 1 mg kg(-1). The A2 receptor antagonist, 1,3-dimethyl-l-propargylxanthine (DMPX) had no effect on anxiety-related measures or locomotion and did not modify the anxiolytic-like activity of CPA. 6. Administration of DPMA in combination with anxiolytic doses of CPA prevented the anxiolytic-like activity of the latter. 7. The results suggest that the selective activation of central A1 adenosine receptors induces anxiolytic-like behaviour, while the activation of A2 sites causes locomotor depression and reduces the effects of A1 receptor activation. The absence of any effect of CPX alone suggests that the receptors involved in modulating behaviour in the elevated plus-maze in mice are not activated tonically by endogenous adenosine.

Adenosine↗

Limits on plasticity in somatosensory cortex of adult rats: hindlimb cortex is not reactivated after dorsal column section.

1. To better understand the limits and extents of plasticity in sensory systems of adult mammals, we unilaterally sectioned the dorsal funiculus at thoracic levels in nine adult rats to deactivate ascending afferents from the hindpaw and lower body. After postsurgical recovery periods of 3 h to 3 mo, the region of primary somatosensory cortex (S1) representing the limbs and trunk was extensively mapped with microelectrodes. 2. Recording sites were later identified as being within the hindlimb representation and other parts of S1 by relating locations of microlesions to the cytochrome oxidase pattern in sections of cortex cut tangential to the pial surface. The extent and effectiveness of spinal cord lesions were evaluated by injecting cholera toxin B subunit conjugated with horseradish peroxidase (B-HRP) at various sites in the deafferented hindpaw. 3. In five animals with complete section of the dorsal funiculus, we failed to detect any response to cutaneous stimulation of any part of the body in the deafferented hindlimb cortex. In four other animals with incomplete lesions, neurons in some penetrations could be activated by hindlimb stimulation, but not by stimulating other body parts. In those cases without activation of hindlimb cortex, B-HRP was detected in the spinal cord only caudal to the lesion, and it was not transported to the nucleus gracilis. Limited transport past the lesion to nucleus gracilis was detected in cases with incomplete lesions. 4. The results indicate that forelimb inputs do not substitute for missing hindlimb inputs in primary somatosensory cortex in rats and that the potential for somatotopic reorganization is more limited than previously thought.

Afferent Pathways↗

Cell free ascitic fluid prevents loss of cell surface sialic acid from Zajdela Ascitic Hepatoma cells in culture.

In the Zajdela Ascitic Hepatoma (ZAH), a rat tumor, high levels of cell surface sialic acid residues are present which masked the immunogenicity of the cells. We have shown here that cell surface sialic acid level goes down rapidly when ZAH cells are put in culture. The reduction in surface sialic acid levels is due to a decrease in sialic acid residues on the major sialylated glycoprotein, gp 120, as well as a decrease in gp 120 polypeptide. The loss of sialic acid from the cultured cells is reduced if the cells are cultured in the presence of cell free ascitic fluid from ZAH tumor.

Animals↗

A ten years analysis of 500 intertrochantric fractures of the femur with impression to residual deformity and shortening.

A study of 500, cases with follow up period of 1 to 10 years were treated by conservative and operative means. The result of conservative treatment in type III and IV fractures were comparatively favourable with result of operative treatment in same grade of fractures. It can be concluded that if an anatomical reduction was achieved by proportioned vertical and horizontal traction forces and the reduction was monitored by periodic skiagram till sound clinical and reasonable radiological union, good functional end result could be obtained.

Aged↗

Interaction of procollagen I and other collagens with colligin.

Colligin is a collagen-binding glycoprotein of molecular mass 46000 Da localized to the endoplasmic reticulum (ER) of diverse kinds of cells that produce collagen I. In order to help define its role in collagen biosynthesis and to study the interaction of colligin with procollagen I in detail, the binding characteristics of colligin purified from L6 myoblasts have been studied. A total of 3 mol were found to bind/mol of procollagen I, with a Kd of about 25 nM. Both pure and separated pro alpha 1(I) and procollagen alpha 2 (I) chains were able to compete with procollagen I for binding to colligin. However, colligin binds to pro alpha 2 (I) with higher affinity than to pro alpha 1 (I). To find if the binding activity of colligin was altered during purification, an assay to measure colligin binding to procollagen in crude myoblast cell extracts was developed. This procedure gave the same binding parameters as did the highly purified colligin. Among different collagen types, colligin was found to bind to collagen I and collagen IV, but not to collagen III. In order to examine whether glycosylation or phosphorylation of colligin were required for the binding of colligin to procollagen I and to obtain enough colligin for further studies, recombinant protein was produced in Escherichia coli. An immunoaffinity purification scheme was used to get virtually pure protein in milligram yields. Comparison of the recombinant colligin with that isolated from L6 myoblasts showed that both types existed in solution as monomers and dimers. In addition, both types of colligins showed identical properties with regard to their binding to procollagen I and the isolated pro alpha 1(I) and pro alpha 2(I) chains. Post-translational modifications of colligin were thus not essential for binding to procollagen I.

Animals↗

Inhibition of procollagen I degradation by colligin: a collagen-binding serpin.

Colligin is a collagen-binding glycoprotein localized to the endoplasmic reticulum (ER) and has been proposed to play a role in collagen biosynthesis. Its membership in the serpin family prompted us to examine its effect on procollagen degradation. We first showed that procollagen degradation can take place in the ER of L6 myoblasts by using brefeldin A to block transit from the ER. This degradation could be prevented by the serine protease inhibitors N-tosyl-L-lysine chloromethyl ketone (TLCK) and N-tosyl-L-phenylalanine chloromethyl ketone (TPCK). To examine procollagen degradation in vitro, isolated liver microsomes were incubated with procollagen. Intact microsomes were unable to degrade labeled procollagen I, fibronectin, or the cytoplasmic proteins, phosphorylase b and the RI subunit of the cAMP-dependent protein kinase. However, when the microsomes were permeabilized by treatment with detergent, they became capable of degrading procollagen and fibronectin, but not the cytoplasmic proteins. The degrading activity was not due to cross-contamination by lysosomal or cytoplasmic, multicatalytic proteases. The proteolysis of procollagen chains in the treated microsomes was partially inhibited by TPCK, TLCK, and leupeptin. The most effective inhibitor was, however, colligin. In its presence, the breakdown of procollagen I, but not of fibronectin, was specifically inhibited. Colligin itself was not degraded by the microsomal preparations. The protein degrading activity was localized to the microsomal membranes, and showed a pH optimum of about 8.0. From these studies it is inferred that one of the roles of colligin may be to protect the procollagen I chains in the ER from degradation prior to their transport to the cis-Golgi compartment.

Amino Acid Sequence↗

Evaluation of false positive blood cultures: guidelines for early detection of contaminated cultures in febrile children.

Young, febrile children are at risk for occult bacteremia. However, some positive blood cultures are contaminants. This study assesses the ability of preliminary blood culture results to distinguish between pathogens and contaminants. Positive blood cultures were obtained and evaluated from 210 otherwise well febrile children, at risk for occult bacteremia, three months to three years of age, who were without invasive bacterial disease. These children had entered a pediatric emergency department between 1983 and 1989 and were not admitted to the hospital. Blood cultures of true pathogens became positive more rapidly than contaminants, 13.8 +/- 7.0 hours versus 37.6 +/- 29.9 hours, respectively (P < 0.0001). Gram stain results were used as a diagnostic test for pathogenicity with a sensitivity of 98.1% and specificity of 54.5% for the entire population, and 100% and 77.3% respectively, for those cultures becoming positive after 24 hours. Time to positivity and initial gram stain results are valuable diagnostic tests in distinguishing between pathogens and contaminants for blood cultures obtained from children at risk for occult bacteremia.

Bacteremia↗

Immature thymocytes become sensitive to calcium-mediated apoptosis with the onset of CD8, CD4, and the T cell receptor expression: a role for bcl-2?

During intrathymic negative selection by clonal deletion, crosslinking of the T cell receptor (TCR) induces cell death by delivering an apoptotic signal(s) to the nucleus along a calcium-dependent pathway. We investigated the reactivity of early precursor-containing thymocytes to Ca(2+)-induced signals, and discovered a breakpoint in their sensitivity to calcium-mediated cell death (CMCD). CD25+CD8-4- TCR- (triple negative [TN]) thymocytes stimulated with a calcium ionophore maintain their viability and precursor activity. By contrast, their immediate progeny, CD25-CD8lo4loTCR alpha beta lo (triple low [TL]) cells react to calcium elevation by abrogation of precursor activity and apoptotic cell death. This developmental difference is specific for CMCD, since both CD25+TN and CD25-TL cells are susceptible to steroid-induced apoptosis. The presence of bcl-2 mRNA correlates directly to the resistance to CMCD-CD25+ TN cells express it and CD25-TL cells do not. These experiments show that thymocytes become sensitive to Ca(2+)-induced apoptosis as soon as they begin to express molecules that mediate thymic selection, and suggest that a concomitant downregulation of bcl-2 may mediate this phenomenon.

Animals↗

Regulation of expression of beta-galactoside alpha 2,6-sialyltransferase in a rat tumor, Zajdela ascitic hepatoma.

Tumor cell surface sialic acid levels determine a number of important properties governing cellular interactions and cell-cell communication. Towards understanding the mechanism of regulation of sialic acid levels upon cellular transformation, we have studied the regulation of expression of beta-galactoside alpha 2,6-sialyltransferase in a rat tumor, the Zajdela ascitic hepatoma. We demonstrate distinct differences in the regulation of expression of the enzyme in the tumor cells as compared to normal liver cells. The expression of sialyltransferase is regulated both at the transcriptional and post-transcriptional level in a tissue-specific manner.

Animals↗