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Biomedical subjects

C Landis

Publications and source records attributed to C Landis.

11 recordsLinked to original sources
PubMed2005

Subjective and objective sleep indices in women with irritable bowel syndrome.

Patients with irritable bowel syndrome (IBS) commonly report sleep disturbances. This study examined self-report (Pittsburgh Sleep Quality Inventory) sleep quality and polysomnography (PSG) sleep variables in 18 women with mild-to-moderate IBS, 18 with severe IBS and 38 with age- and gender-matched controls. All women were studied on two consecutive nights in a sleep research laboratory where PSG data were collected. Retrospective and daily measures were obtained of self-reported sleep quality, psychological distress and gastrointestinal symptoms across one menstrual cycle. Self-report measures of psychological distress and sleep quality were significantly worse in the IBS-severe (IBS-S) group compared with controls. Rapid eye movement (REM) latency was higher in the two IBS groups on Night 1 than the control group (P = 0.06). Percentage time in REM was highest in the IBS-S on Night 2. All groups demonstrated greater sleep disruption on Night 1 (adaptation) when compared with Night 2. These results highlight the importance of considering the 'first-night effect' in those with IBS and the lack of concordance between self-report and objective indices of sleep in women with IBS.

Adult↗
PubMed2000

Three-dimensional reconstruction of thin filaments containing mutant tropomyosin.

Interactions of the components of reconstituted thin filaments were investigated using a tropomyosin internal deletion mutant, D234, in which actin-binding pseudo-repeats 2, 3, and 4 are missing. D234 retains regions of tropomyosin that bind troponin and form end-to-end tropomyosin bonds, but has a length to span only four instead of seven actin monomers. It inhibits acto-myosin subfragment 1 ATPase (acto-S-1 ATPase) and filament sliding in vitro in both the presence and absence of Ca(2+) (, J. Biol. Chem. 272:14051-14056) and lowers the affinity of S-1.ADP for actin while increasing its cooperative binding. Electron microscopy and three-dimensional reconstruction of reconstituted thin filaments containing actin, troponin, and wild-type or D234 tropomyosin were carried out to determine if Ca(2+)-induced movement of D234 occurred in the filaments. In the presence and absence of Ca(2+), the D234 position was indistinguishable from that of the wild-type tropomyosin, demonstrating that the mutation did not affect normal tropomyosin movement induced by Ca(2+) and troponin. These results suggested that, in the presence of Ca(2+) and troponin, D234 tropomyosin was trapped on filaments in the Ca(2+)-induced position and was unable to undergo a transition to a completely activated position. By adding small amounts of rigor-bonded N-ethyl-maleimide-treated S-1 to mutant thin filaments, thus mimicking the myosin-induced "open" state, inhibition could be overcome and full activation restored. This myosin requirement for full activation provides support for the existence of three functionally distinct thin filament states (off, Ca(2+)-induced, myosin-induced; cf.;, J. Mol. Biol. 266:8-14). We propose a further refinement of the three-state model in which the binding of myosin to actin causes allosteric changes in actin that promote the binding of tropomyosin in an otherwise energetically unfavorable "open" state.

Actin Cytoskeleton↗
PubMed1999

Effects of tropomyosin internal deletions on thin filament function.

Striated muscle tropomyosin spans seven actin monomers and contains seven quasi-repeating regions with loose sequence similarity. Each region contains a hypothesized actin binding motif. To examine the functions of these regions, full-length tropomyosin was compared with tropomyosin internal deletion mutants spanning either five or four actins. Actin-troponin-tropomyosin filaments lacking tropomyosin regions 2-3 exhibited calcium-sensitive regulation in in vitro motility and myosin S1 ATP hydrolysis experiments, similar to filaments with full-length tropomyosin. In contrast, filaments lacking tropomyosin regions 3-4 were inhibitory to these myosin functions. Deletion of regions 2-4, 3-5, or 4-6 had little effect on tropomyosin binding to actin in the presence of troponin or troponin-Ca(2+), or in the absence of troponin. However, all of these mutants inhibited myosin cycling. Deletion of the quasi-repeating regions diminished the prominent effect of myosin S1 on tropomyosin-actin binding. Interruption of this cooperative, myosin-tropomyosin interaction was least severe for the mutant lacking regions 2-3 and therefore correlated with inhibition of myosin cycling. Regions 3, 4, and 5 each contributed about 1.5 kcal/mol to this process, whereas regions 2 and 6 contributed much less. We suggest that a myosin-induced conformational change in actin facilitates the azimuthal repositioning of tropomyosin which is an essential part of regulation.

Actins↗
PubMed1999

Functional consequences of troponin T mutations found in hypertrophic cardiomyopathy.

Missense mutations in the cardiac thin filament protein troponin T (TnT) are a cause of familial hypertrophic cardiomyopathy (FHC). To understand how these mutations produce dysfunction, five TnTs were produced and purified containing FHC mutations found in several regions of TnT. Functional defects were diverse. Mutations F110I, E244D, and COOH-terminal truncation weakened the affinity of troponin for the thin filament. Mutation DeltaE160 resulted in thin filaments with increased calcium affinity at the regulatory site of troponin C. Mutations R92Q and F110I resulted in impaired troponin solubility, suggesting abnormal protein folding. Depending upon the mutation, the in vitro unloaded actin-myosin sliding speed showed small increases, showed small decreases, or was unchanged. COOH-terminal truncation mutation resulted in a decreased thin filament-myosin subfragment 1 MgATPase rate. The results indicate that the mutations cause diverse immediate effects, despite similarities in disease manifestations. Separable but repeatedly observed abnormalities resulting from FHC TnT mutations include increased unloaded sliding speed, increased or decreased Ca(2+) affinity, impairment of folding or sarcomeric integrity, and decreased force. Enhancement as well as impairment of contractile protein function is observed, suggesting that TnT, including the troponin tail region, modulates the regulation of cardiac contraction.

Amino Acid Sequence↗
PubMed1998

Guidelines for prescribing melatonin.

Although compelling logic suggests that melatonin may be effective for a variety of disorders, there are few empirical clinical studies. The optimal dose of melatonin is not clear; most studies have used doses that produce supraphysiological blood levels. The timing of melatonin administration is important. Melatonin has few immediate side-effects except drowsiness, but the effects of chronic administration are unclear. Melatonin may be effective in reducing jet lag. In elderly patients with poor sleep and documented low melatonin production, melatonin may be helpful. In several studies, melatonin has been shown to shorten sleep latency. Further studies are needed to clarify the efficacy and safety of melatonin.

Aged↗
PubMed1995

Effects of continuous environmental illumination on the albino rat hypothalamo-neurohypophysial system.

Continuous environmental illumination or constant light (LL) exposure causes a suppression of daily water intake, and long-term exposure of greater than 19 days produces a hypertrophy of magnocellular neuroendocrine cells (MNCs) in the hypothalamus. These findings led Glantz to hypothesize that LL increases the secretion of vasopressin (VP). We wanted to determine whether LL could trigger morphological changes within the hypothalamo-neurohypophysial system (HNS) seen with other manipulations that result in enhanced hormone release. The posterior pituitary of male albino rats that were exposed to LL for 24 or 48 h were examined ultrastructurally for evidence of enhanced hormone release. In addition, water intake, plasma VP levels, and MNC size within the supraoptic nucleus (SON) were measured. After LL exposure, the posterior pituitary morphology was different, suggesting enhanced hormone release. LL exposure did not affect plasma VP or the size of SON MNCs, but did suppress drinking behavior. These data show that posterior pituitary morphology is affected rapidly by LL exposure. The HNS response to LL exposure may consist of changes within the first 24 h of LL found within the posterior pituitary followed later by hypertrophy of the SON MNCs.

Animals↗
PubMed1994

Constitutively active stimulatory G-protein alpha s in beta-cells of transgenic mice causes counterregulation of the increased adenosine 3',5'-monophosphate and insulin secretion.

To evaluate the effect of chronically elevated adenylyl cyclase, we targeted the expression of a constitutively active mutant alpha-subunit (alpha s+) of Gs to the insulin-producing pancreatic beta-cells of transgenic mice. As assessed by the polymerase chain reaction, expression of alpha s+ mRNA was restricted to the transgenic pancreas. Histological analysis by light microscopy and immunohistochemistry for insulin, glucagon, and somatostatin appeared normal in transgenic islets. Pancreatic insulin content was quantitatively the same for alpha s+ transgenic and control mice. Comparisons of glucose homeostasis, insulin secretion, and islet cAMP revealed the expected differences between alpha s+ transgenic and control mice; in every case, however, responses to glucose alone were normal, and the differences were observed only when measurements were performed in the presence of isobutylmethylxanthine (IBMX), an inhibitor of cAMP phosphodiesterase. 1) In vivo, ip glucose tolerance was normal in alpha s+ transgenics; when ip glucose was preceded by administration of IBMX, the rise in blood glucose was approximately 33% less in the transgenic than in the control mice. 2) Insulin secretion from the perfused pancreas stimulated sequentially with 11 and 22 mM glucose caused characteristic first and second phase insulin release that did not differ between transgenic and control pancreases. IBMX increased biphasic insulin release from all pancreases, but caused a 2-fold greater than normal release from the transgenics. 3) Similarly, batch-incubated alpha s+ and control islets secreted equivalent amounts of insulin in the presence of glucose (22 mM) alone, whereas the combination of glucose plus IBMX was twice as effective on alpha s+ islets. 4) Islet cAMP levels paralleled insulin secretion; in the presence of IBMX, but not glucose alone, cAMP was increased 2-fold more in alpha s+ vs. control islets. We conclude that expression of constitutively active alpha s mutant in pancreatic beta-cells of transgenic mice is functionally effective, causing the physiological phenotype of increased islet cAMP and insulin secretion. However, these changes are uncovered only in the presence of IBMX; without IBMX, glucose homeostasis and islet function appear normal. This normalization, or counterregulation, of cAMP synthesis presumably is accomplished by a compensatory increase in cAMP degradation, possibly via increased activity of cAMP phosphodiesterase.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Increased stimulatory G protein in neoplastic human thyroid tissues.

Prior studies in our laboratory have shown that thyroid neoplasms produce increased amounts of cyclic adenosine monophosphate (cAMP). Thyroid-stimulating hormone receptors act through the stimulatory G protein (Gs) to activate adenylate cyclase, the enzyme responsible for cAMP production. The purpose of this study is to measure the activity and amount of Gs in human normal and neoplastic thyroid tissue to see whether alterations in Gs are responsible for the increased cAMP production seen in thyroid neoplasms. Four tumors with a high TSH-stimulated cyclase activity of 497.6 +/- 71.9 pmol/mg/30 min versus 35.9 +/- 13.5 pmol/mg/30 min for normal tissue from the same patients were studied. In reconstitution studies measuring Gs activity, neoplastic thyroid tissue produced 637 +/- 106 pmol cAMP/mg S49/mg thyroid membrane min versus 363 +/- 133 pmol cAMP/mg 549/mg thyroid membrane/min produced by normal thyroid tissue. Qualitative assessments of the amount of Gs present with cholera toxin-mediated adenosine diphosphate ribosylation showed increased Gs in thyroid tumors. Western blotting with antibodies directed against Gs showed a 3.3 +/- 0.6-fold increase in the amount of Gs in these thyroid tumors. These experiments identify an increase in the amount of an otherwise normal Gs as the biochemical defect responsible for the increased cAMP production in this group of tumors.

Adenocarcinoma↗
PubMed1980

Dose-response relation of CSF sodium and renal sodium excretion, and its absence in homozygous Brattleboro rats.

Constant intraventricular infusion (3.3--6.6 microliters/min) of artificial cerebrospinal fluid with sodium concentrations of 100, 150, 200, 250, 300, and 350 mM produced a linear dose-related change in renal sodium excretion in conscious, unrestrained Sprague-Dawley rats. The periventricular receptors stimulated were able to evoke substantial changes in body sodium balance; the 350 mM Na CSF produced an estimated 14% deficit in the content of Na in the extracellular fluid over a 5-hour infusion period. This is the first demonstration of such a dose-response relation over a wide range of CSF Na concentration (above and below normal) in conscious animals. Both the dose-response relation, and the magnitude of the effects, suggests an important physiologic role for this control mechanism. The natriuresis in response to 300 mM sodium infusion was identical in Long-Evans Brattleboro rats heterozygous for diabetes insipidus (DI), and in Sprague-Dawley rats, but was completely absent in homozygous animals. Although the experimental methods (conscious unrestrained rats) precluded simultaneous evaluation of efferent pathways other than antidiuretic hormone (ADH), the evidence from the DI rats suggests that ADH may be the efferent pathway for the response.

Animals↗