Orthodontic positioning of an impacted supernumerary tooth: report of a case.
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Adult↗
Biomedical subjects
M Lieberman
Publications and source records attributed to M Lieberman.
[Orthodontic repositioning of an impacted supernumerary tooth].
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Adult↗
Interaction of (Na + K + 2 Cl) cotransport and the Na/K pump in cultured chick cardiac myocytes.
We have recently reported the presence of an electroneutral (Na + K + 2 Cl) cotransport mechanism that is bumetanide-sensitive and maintains Cli above its electrochemical equilibrium in cultured chick heart cells. In steady state, (Na + K + 2 Cl) cotransport is inwardly directed and so contributes to the Na influx that must be counterbalanced by the activity of the Na/K pump to maintain Nai homeostasis. We now show that manipulating (Na + K + 2 Cl) cotransport by restoring Clo to a Cl-free solution indirectly influences Na/K pump activity because the bumetanide-sensitive recovery of aiNa to its control level and the accompanying hyperpolarization could be blocked by 10(-4)M ouabain. In another protocol, when the Na/K pump was reactivated by restoring Ko (from 0.5 mM to 5.4 mM) and removing ouabain, the recovery of aNa was attenuated by 10(-4)M bumetanide. The relatively slow rate of ouabain dissociation coupled with the activation of Na influx by (Na + K + 2 Cl) cotransport clearly establishes the interaction of these transport mechanisms in regulating Nai. Although (Na + K + 2 Cl) cotransport is electroneutral, secondary consequences of its activity can indirectly affect the electrophysiological properties of cardiac cells.
Animals↗
The scid-hu mouse: current status and potential applications.
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Animals↗
Visual field defects detected in patients with Gilles de la Tourette syndrome: preliminary report.
The presence of visual field anomalies was measured using Goldmann kinetic perimetry in twelve patients, age 7 to 39 with Gilles de la Tourette syndrome. Refraction to the cupola was carefully controlled. The visual acuity of the group was good to excellent. Visual field alterations were prechiasmal, generally non-symmetric, and best described as arcuate defects, steps, baring of the blind spot and enlargement of the blind spot. Central fields were most commonly affected, i.e., I/2e to I/1B isopters. There was no evidence of glaucoma in any of the patients although two patients exhibited keratoconus and another one manifested moderate to high astigmatism. Visual involvement other than ocular and lid tics have not been reported in Tourette syndrome. This research represents clear evidence of additional physical components in this condition. Automated visual field measurements are not recommended in this population because of the presence of non-predictable tic and vocal behavior (both may result in head/eye movements). Suppression of tic behavior can be very fatiguing. (Eight of twelve of the patients reported exhibited signs of marked fatigue during testing.)
Adolescent↗
Monitoring cytosolic free magnesium in cultured chicken heart cells by use of the fluorescent indicator Furaptra.
Cytosolic free magnesium concentration [Mg2+]i and its regulation were studied in cultured embryonic chicken heart cells by use of the fluorescent indicator 2-[2-(5-carboxy)oxazole]-5-hydroxy-6-aminobenzofuran-N,N,O-triacet ic acid (Furaptra). The intracellular location of Furaptra was confirmed by its complete release from cells upon addition of saponin. The basal [Mg2+]i, which averaged 0.48 +/- 0.03 mM (n = 31), increased 3-fold on perfusion with sodium-free solution. This increase could not simply be attributed to intracellular sodium-extracellular magnesium exchange because a similar increase in [Mg2+]i occurred with magnesium-free, sodium-free perfusion. Furthermore, the increase in [Mg2+]i was largely attenuated when calcium was removed from the sodium-free perfusate. Thus, a substantial part of the increase in [Mg2+]i that occurs upon sodium-free perfusion is dependent on an increase in cytosolic free calcium (intracellular sodium-extracellular calcium exchange). The data suggest that [Mg2+]i is altered by calcium, most likely due to a competition for intracellular binding sites.
Animals↗
Intraosseous drug administration: successful resuscitation from asystole.
The case of a seven-month-old infant presenting in full cardiac arrest and resuscitated utilizing a right tibial intraosseous access line is presented. The child who presented in asystole appears to be the first reported case of the successful use of the intraosseous route as the sole source of drug administration. Flow time from tibia to clinical cardiac response was noted to be less than three minutes, similar to those in animal arrest models.
Arrhythmias, Cardiac↗
Cytosolic free magnesium concentration in cultured chick heart cells.
Cytosolic free magnesium (Mgi) was measured in embryonic chick heart cells loaded with one of two newly developed 19F nuclear magnetic reasonance (NMR)-sensitive magnesium chelators, 4-methyl,5-fluoro-2-aminophenol-N,N,O-triacetate (MF-APTRA) and 5-fluoro-2-aminophenol-N,N,O-triacetate (5F-APTRA). The cells, embedded in strands of collagen, were superfused at a rate that allowed for solution changes in 2 min. In this preparation 19F- and 31P-NMR spectra were stable for at least 3.5 h. Because Na-coupled Mg countertransport may be a possible mechanism of Mg transport, in some experiments extracellular Na was reduced to 1 mM (choline substituted). This manipulation caused a 2.5-fold increase in Mgi from the basal level of 0.56 mM. A significant proportion of this increase in Mgi could be secondary to an increase in Cai that occurs with low extracellular Na (Nao) perfusion (Nai-Cao exchange). Perfusing cells with nominally Ca-free, 1 mM Na salt solution substantially attenuated the increase in Mgi that occurred with Ca present (1.25 mM) in the low Na (1 mM) solution. Furthermore, perfusion with 1 mM Na, Mg-free salt solution caused a 1.5-fold increase in Mgi, which cannot be attributable to Nai-Mgo exchange. Therefore attempts to describe the regulation of Mgi in heart cells must differentiate between the effects of Nai-Mgo exchange and competition for binding sites that are secondary to stimulation of ion gradient-coupled mechanisms.
Aminophenols↗
Infection of the SCID-hu mouse by HIV-1.
SCID-hu mice with human fetal thymic or lymph node implants were inoculated with the cloned human immunodeficiency virus-1 isolate, HIV-1JR-CSF. In a time- and dose-dependent fashion, viral replication spread within the human lymphoid organs. Combination immunohistochemistry and in situ hybridization revealed only viral RNA transcripts in most infected cells, but some cells had both detectable viral transcripts and viral protein. Infected cells were always more apparent in the medulla than in the cortex of the thymus. These studies demonstrate that an acute infection of human lymphoid organs with HIV-1 can be followed in the SCID-hu mouse.
Acquired Immunodeficiency Syndrome↗
The SCID-hu mouse: murine model for the analysis of human hematolymphoid differentiation and function.
The study of human hematopoietic cells and the human immune system is hampered by the lack of a suitable experimental model. Experimental data are presented showing that human fetal liver hematopoietic cells, human fetal thymus, and human fetal lymph node support the differentiation of mature human T cells and B cells after engraftment into mice with genetically determined severe combined immunodeficiency. The resultant SCID-hu mice are found to have a transient wave of human CD4+ and CD8+ T cells and human IgG (immunoglobulin G) in the peripheral circulation. The functional status of the human immune system within this mouse model is not yet known.
Animals↗
Endoproteolytic cleavage of gp160 is required for the activation of human immunodeficiency virus.
The envelope protein of human immunodeficiency virus (HIV) is synthesized as a polyprotein (gp160) and cleaved intracellularly to a gp120-gp41 heterodimer. In this study, the tryptic-like endoproteolytic cleavage site was removed by site-directed mutagenesis and replaced with a chymotryptic-like site. The resultant mutant, RIP7/mut10, was found to be indistinguishable from wild-type HIV when analyzed at the level of proviral replication, RNA processing, protein expression, and viral assembly. However, the gp160 polyprotein was not cleaved and the mutated virions were biologically inactive, until and unless they were exposed to limiting concentrations of chymotrypsin. As is the case for other enveloped mammalian viruses, endoproteolytic cleavage of the HIV envelope protein and release of a unique hydrophobic domain appear to be necessary for the full expression of viral infectivity.
Amino Acid Sequence↗
Quantitative microchemical imaging of calcium in Na-K pump inhibited heart cells.
Quantitative electron probe X-ray imaging techniques have been utilized to determine simultaneously the element content within a single cultured embryonic chick heart cell and its intracellular compartments as well as the average elemental content of several heart cells within a population. These features of microchemical imaging have permitted establishment of data regarding: (1) the heterogeneity of calcium accumulation in mitochondrial, cytoplasmic and nuclear compartments under conditions which elevate total cell calcium without producing irreversible cell injury; and (2) the variability of calcium accumulation from cell to cell within the population sampled. The results indicate that during Na-K pump inhibition (K-free HT-BSS, 10(-4) M ouabain, 60 min) elevation of mitochondrial calcium, measured in situ by electron probe X-ray microanalysis, to levels more than 100 times greater than in the basal state, may not cause irreversible mitochondrial uncoupling and cell death.
Calcium↗
Forced eruption combined with gingival fiberotomy. A technique for clinical crown lengthening.
A new approach to clinical crown lengthening has been developed and described. The technique combines controlled eruptive tooth movement and incision of the supracrestal gingival attachment. The procedure was performed in patients with severe destruction of a tooth crown and in whom clinical crown lengthening procedures were essential before the teeth could be properly restored. Controlled eruptive forces were activated by simple orthodontic appliances. During the active phase of forced eruption, repeated intrasulcular incisions through the junctional epithelium and the supracrestal connective tissue attachment were performed. The technique prevented coronal displacement of the gingiva and the attachment apparatus during the orthodontic extrusion, thus overcoming the need for corrective osseous surgery.
Adolescent↗
Indirect induction of radiation lymphomas in mice. Evidence for a novel, transmissible leukemogen.
The transmission of a lymphomagenic agent(s) from the bone marrow of irradiated mice to thymic target cells has been demonstrated by: (a) the induction of T cell lymphomas in nonirradiated thymic grafts implanted in irradiated, Thy-l-congenic mice, (b) the induction of T cell lymphomas of host origin in mice infused with bone marrow from irradiated, Thy-l-congenic donors. The latter procedure also yields an appreciable number of pre-B cell lymphomas of uncertain origin. The results confirm Kaplan's theory that radiation induces thymic lymphomas in mice by an indirect mechanism. However, the previously described radiation leukemia virus is clearly not involved in the majority of transferred lymphomas. We propose that the mediating agent in radiation lymphomagenesis is a novel, transmissible agent induced in the bone marrow, but exerting its transforming activity on cells in the thymus. The nature and mode of action of the agent are under investigation.
Animals↗
The stomatognathic system in myotonic dystrophy.
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Adolescent↗
Effects of sodium-potassium pump inhibition and low sodium on membrane potential in cultured embryonic chick heart cells.
1. When the Na+-K+ pump of cultured embryonic chick heart cells was inhibited by addition of ouabain with or without removal of external K+, the membrane potential rapidly depolarized to -40 mV and the Na+ content approximately doubled within 3 min. 2. After this, exposure to an [Na+]o of 27 mM caused a fall in Na+ content, a gain in Ca2+ content and a hyperpolarization. The hyperpolarization was approximately 25 mV in a [K+]o of 0 or 5.4 mM after 3 min of pump inhibition. After approximately 10 min of pump inhibition, the same hyperpolarization was observed in a [K+]o of 5.4 mM but in K+-free solution the hyperpolarization increased to approximately 44 mV. 3. Varying [K+]o during the 10 min period of Na+-K+ pump inhibition showed that the increase in hyperpolarization was associated with the period of exposure to K+-free solution rather than the [K+]o at the time of lowering [Na+]o. 4. Changes in Na+ and Ca2+ content induced by exposure to an [Na+]o of 27 mM in K+-free solution were similar at 3 and 10 min. This and the above observations suggest that the increased hyperpolarization was due to an increased membrane resistance. 5. 10 mM-Cs+ reduced the low-[Na+]o hyperpolarization by 26% but did not significantly affect the movements of Na+ and Ca2+. 1 mM-La3+ reduced the low-[Na+]o hyperpolarization by 15%: it also totally blocked the rise in Ca2+ content and partially blocked the fall in Na+ content. 1 mM-Ba2+ reduced the low-[Na+]o hyperpolarization by 20%. 6. Raising [Ca2+]o from 2.7 to 13.5 mM produced similar but smaller hyperpolarizations (approximately 6 mV after 3 min pump inhibition). High [Ca2+]o caused a rise in Ca2+ content but no significant drop in Na+ content. The hyperpolarization in high [Ca2+]o was insensitive to verapamil (20 microM) and 10 mM-Cs+. 7. We conclude from the disparities between the magnitudes of the hyperpolarizations and the changes in ion contents that Na+-Ca2+ exchange cannot be unequivocally identified as electrogenic solely from the low-[Na+]o hyperpolarizations.
Animals↗
Electrogenic sodium-calcium exchange in cultured embryonic chick heart cells.
1. The membrane potential (Em) of cultured chick embryonic heart cells depolarized to -36 mV after inhibition of the Na+-K+ pump by 0.1 mM-ouabain in a [K+]o of 24 mM: this was accompanied by a rise in Na+ content of approximately 65% in 3 min. Lowering [Na+]o to 27 mM then caused a fall in Na+ content, a rise in Ca2+ content and a small hyperpolarization of approximately 5 mV. The fall in Na+ content indicated a movement of Na+ which was in the opposite direction to the Na+ electrochemical gradient (a countergradient movement). 2. In the presence of 10 mM-Cs+ or 1 mM-Ba2+ the hyperpolarization was approximately 10 or approximately 30 mV, respectively. A 30 mV hyperpolarization took Em negative to the reversal potentials for K+, and Cl- as measured by ion-selective micro-electrodes. 3. The decay of the intracellular Na+ activity alpha iNa, in an [Na+]o of 27 mM followed a simple exponential time course (time constant, 36 s). The initial rate depended on the value to which [Na+]o was lowered in a manner suggesting a simple competitive inhibition of the exchange by external Na+. 4. The low-[Na+]o hyperpolarization was unaffected by amiloride (0.1 or 1 mM) or verapamil (20 microM). Both La3+ (1 mM) and Mn2+ (20 mM) blocked the hyperpolarization sufficiently to prevent Em hyperpolarizing negative to the reversal potentials for K+, Na+ and Cl-. 5. Re-establishing [Na+]o caused a rise in Na+ content and a countergradient drop in Ca2+ content. The effects of verapamil (20 microM), amiloride (0.1 and 1 mM), dichlorobenzamil (0.1 mM), quinidine (1 mM), Mn2+ (20 mM) and La3+ (1 mM) were tested on the movements of Na+ and Ca2+ both during exposure to an [Na+]o of 27 mM and on re-establishing [Na+]o. The only consistent and substantial effects were the attenuation by La3+ and Mn2+ and Ca2+ movements during exposure to an [Na+]o of 27 mM. However, neither La3+ nor Mn2+ affected the movements of Na+ and Ca2+ on re-establishing [Na+]o. 6. We conclude that cultured embryonic chick heart cells contain a Na+-Ca2+ exchange evidenced by the ability to cause movements of Na+ and Ca2+ which are counter to their respective electrochemical gradient and which are accompanied by downhill movements of the counter ion.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Activity of (+)-cyclaradine (Sch 31172) against herpes simplex virus in vitro and in vivo.
(+)-Cyclaradine (Sch 31172) is the carbocyclic derivative of adenosine arabinoside (9-beta-D-arabinofuranosyladenine). Because it is not deaminated by deaminase in serum, as is adenosine arabinoside, (+)-cyclaradine is about 2 to 5 times more active in vitro against herpes simplex virus. (+)-Cyclaradine has in vitro activity nearly equivalent to that of phosphonoformate but is significantly less active than acycloguanosine (acyclovir; ACV), trifluorothymidine, or 9-(1,3-dihydroxy-2-propoxymethyl)guanine. The absolute ratios of in vitro activities are difficult to determine because of variability among virus strains, inoculum size, and dependence on the tissue culture cell line in which the comparative test is carried out. (+)-Cyclaradine is active against TK-, ACV-resistant mutants. In the guinea pig model of vaginal herpes simplex virus infection, (+)-cyclaradine is only slightly less active than ACV when both molecules are nearly equivalently bioavailable; thus, the large difference in activity seen in vitro is not reflected in this in vivo model system.
Acyclovir↗