A method of analyzing improvisations in music therapy.
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Acquired Immunodeficiency Syndrome↗
Biomedical subjects
C Lee
Publications and source records attributed to C Lee.
Selective requirement for Cdc25C protein synthesis during meiotic progression in porcine oocytes.
Fundamental differences between meiosis and mitosis suggest that the shared central cell cycle machinery may be regulated differently during the two division cycles. This paper focuses on unique features of Cdc25C protein function during meiotic progression. We report on the existence of oocyte-specific CDC25C transcripts that differ from their somatic counterparts in the 3' untranslated region. While CDC25C mRNA levels remain constant in fully-grown oocytes, corresponding protein levels increase progressively during maturation to a maximum at metaphase II. Elevation of Cdc25C protein levels in G2-oocytes by mRNA injection failed to increase MPF-kinase levels or to induce premature entry into M-phase. Likewise, antisense-induced arrest of translation (translational arrest) had no effect on chromosome condensation, nucleolar disassembly, or nuclear membrane contraction. By contrast, translational arrest inhibited subsequent events including membrane disassembly and spindle formation. Neither up- nor down-regulation of Cdc25C synthesis after metaphase I plate formation influenced progression to metaphase II. However, translational arrest during metaphase resulted in incomplete chromosome decondensation and abnormal pronuclear membrane assembly after activation. We conclude that Cdc25 protein, translated from unique transcripts, is preferentially located in the oocyte nucleus and is essential for progress through late diakinesis. Subsequently, new synthesis of Cdc25C protein is required for the orderly transition from meiotic to mitotic cell division.
Animals↗
Hsp72 induction: a potential molecular mediator of the delay phenomenon.
The molecular basis of enhanced ischemic tissue survival in flaps preconditioned by surgical delay is poorly understood. Because elevated expression of so-called heat shock or stress proteins has been shown to protect tissues/organs against ischemic injury, the authors examined whether the levels of the most highly induced stress protein-hsp72-were elevated in delayed muscle flaps using a rat muscle flap model. Bilateral latissimus dorsi muscle flaps based on the thoracodorsal vessels were elevated in 16 male Sprague-Dawley rats. For each animal, one side was selected randomly to undergo preconditioning by surgical delay for a 7-day period prior to elevation. Delay was accomplished by preserving the thoracodorsal pedicle and a single large distal intercostal perforating vessel. After bilateral flap elevation, latissimus dorsi tissue was harvested from proximal, central, and distal flap segments 0, 1, 3, and 7 days postoperatively (N = 4 for each group), and was analyzed for the expression of hsp72 via Western blot analysis. At the time of harvest, flap viability was assessed by staining with nitroblue tetrazolium. Flap perfusion was measured prior to muscle elevation and harvest using laser Doppler flowmetry. The results demonstrate that delayed muscle flaps had significantly greater total perfusion (p < 0.05) and survival (p < 0.03) 1, 3, and 7 days after elevation compared with the acutely elevated control tissue. Western blot analysis revealed that tissues harvested from the delayed flaps expressed substantially higher levels of hsp72 compared with the acutely elevated control samples. Segmental analysis also revealed a proximal > middle > distal expression of hsp72 in the delayed flaps (p < 0.05). Flap preconditioning by surgical delay increases the expression of hsp72. Moreover, regional differences in hsp72 gene expression are associated with differences in perfusion and survival of delayed muscle flaps. These results indicate that hsp72 may play a substantial role in mediating the delay phenomenon.
Analysis of Variance↗
Cranial nerve VII region of the traumatized facial skeleton: optimizing fracture repair with the endoscope.
OBJECTIVE: Cranial nerve VII (CN VII) is anatomically positioned adjacent to the condylar neck of the mandible and arch of the midface. Fracture treatment of this region of the facial skeleton remains controversial because of difficult surgical access. Conservative management rarely achieves anatomic fracture repair and can result in irreversible structural deformity and dysfunction. Traditional operative methods require access through very visible facial incisions and risk injury to the facial nerve. We report endoscopic methods of facial fracture repair in the region of CN VII that achieve excellent fracture reduction and stabilization, with minimal risk of facial nerve injury by using hidden incisions. METHODS: A consecutive series of 65 endoscopically assisted facial fracture repairs were analyzed. Endoscopic repairs of the condylar neck (n = 40) of the mandible were performed through an intraoral incision. Endoscopic arch repairs (n = 25) of the midface were performed through a preauricular incision. Outcomes were evaluated by postoperative fracture reduction on radiographs, occlusion, interincisal jaw opening, and facial nerve function. RESULTS: Thirty-seven of 40 condylar neck mandible fractures went on to anatomic bone union, whereas 3 of 40 had either incomplete fracture reduction or re-fracture through the plate. There was one temporary palsy of CN VII that completely resolved spontaneously. Jaw opening exceeded 40 mm by the 8th postoperative week. Computed tomographic images demonstrated anatomic arch repair in all 25 endoscopically repaired cases. Six of seven endoscopically repaired Le Fort III facial fractures went on to restoration of their premorbid occlusion. One of seven had an excellent restoration of the occlusal interface but a cant to the occlusal plane. Two of seven had improved but incomplete restoration of the malar prominence and enopthalmos ipsilateral to the side of endoscopic arch repair. Eight of 25 endoscopic arch repairs developed temporary paralysis of the frontal branch of CN VII that recovered completely by the 10th postoperative week. CONCLUSION: We have developed novel endoscopically assisted techniques to facilitate repair of facial fractures in the region of CN VII. These techniques have been successfully applied to accurately restore the facial skeleton to its preinjury anatomic position in the region of CN VII with minimal risk of facial paralysis by using limited and well-hidden incisions.
Adolescent↗
Calcaneal fillet of sole flap: durable coverage of the traumatic amputation stump.
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Amputation, Surgical↗
Tracking participants: lessons from the Women's Health Australia Project.
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Adult↗
Inhibition of c-myc expression in cells by targeting an RNA-protein interaction using antisense oligonucleotides.
Antisense oligodeoxynucleotides (ODNs) are designed to bind to and inhibit a target mRNA. We used a novel approach for the design of ODNs to the c-myc mRNA using protein binding sites as targets for ODN action. Our strategy was to identify ODNs that could interfere with the coding region determinant-binding protein (CRD-BP), a protein that binds to the CRD region of the c-myc mRNA. Using an in vitro gel shift assay, we show that ODN molecules can occlude the CRD-BP from the mRNA. The best ODN, CRD-ODN4, was able to inhibit RNA binding of the CRD-BP by 75%. This effect was sequence-specific and concentration dependent. K562 cells treated with a 2'-O-methyl derivative of CRD-ODN4 showed a concentration-dependent decrease in both c-myc mRNA and protein levels, with a maximal 65% inhibition of protein expression at 200 nM CRD-ODN4. In contrast, a 2'-O-methyl ODN derivative targeting the translation initiation codon (antimyc-aug) reduced c-myc protein but actually increased mRNA levels, an effect resulting at least partly from stabilization of the c-myc mRNA. CRD-ODN4 treatment did not alter the c-myc mRNA half-life. CRD-ODN4 was more effective in inhibiting K562 cell growth than antimyc-aug, reducing cell number by approximately 70% after 48 h of exposure to 750 nM. The correlation between ODN effects on RNA-protein interactions in vitro and those observed in cells supports the hypothesis that CRD-ODN4 inhibits the interaction between the CRD-BP and the c-myc mRNA and that disrupting this RNA-protein interaction reduces c-myc expression in cells.
Binding, Competitive↗
Development and evaluation of a molecular viability assay for Pneumocystis carinii.
Despite recent declines in incidence, Pneumocystis carinii pneumonia (PCP) remains the most commonly occurring opportunistic illness among persons with AIDS in the United States. While P. carinii DNA has been detected in patient respiratory specimens and in air samples collected from various indoor environments housing PCP patients, the viability of these organisms is unknown. For this reason, we have developed and evaluated a molecular viability assay for P. carinii. This method is based upon the detection of P. carinii mRNA by a reverse transcription-PCR that employs specific primers from a member of the heat shock protein 70 family. Under optimal assay conditions, these primers were capable of detecting as few as 100 viable trophozoites as determined by ethidium bromide staining, while no signal was obtained from 10(6) trophozoites killed by heat, desiccation, or UV radiation. This assay was also capable of distinguishing P. carinii from other common fungi present in the air. Therefore, this molecular viability assay may be useful in conjunction with standard bioaerosol collection devices and procedures for the detection of viable P. carinii collected from various indoor environments. It may also be useful in confirming the presence of viable trophozoites in respiratory specimens collected by noninvasive techniques from putatively infected individuals.
Air Pollution, Indoor↗
Targeted disruption of the mPer3 gene: subtle effects on circadian clock function.
Neurons in the mammalian suprachiasmatic nucleus (SCN) contain a cell-autonomous circadian clock that is based on a transcriptional-translational feedback loop. The basic helix-loop-helix-PAS proteins CLOCK and BMAL1 are positive regulators and drive the expression of the negative regulators CRY1 and CRY2, as well as PER1, PER2, and PER3. To assess the role of mouse PER3 (mPER3) in the circadian timing system, we generated mice with a targeted disruption of the mPer3 gene. Western blot analysis confirmed the absence of mPER3-immunoreactive proteins in mice homozygous for the targeted allele. mPer1, mPer2, mCry1, and Bmal1 RNA rhythms in the SCN did not differ between mPER3-deficient and wild-type mice. Rhythmic expression of mPer1 and mPer2 RNAs in skeletal muscle also did not differ between mPER3-deficient and wild-type mice. mPer3 transcripts were rhythmically expressed in the SCN and skeletal muscle of mice homozygous for the targeted allele, but the level of expression of the mutant transcript was lower than that in wild-type controls. Locomotor activity rhythms in mPER3-deficient mice were grossly normal, but the circadian cycle length was significantly (0.5 h) shorter than that in controls. The results demonstrate that mPer3 is not necessary for circadian rhythms in mice.
ARNTL Transcription Factors↗
Saccades from torsional offset positions back to listing's plane.
Rapid eye movements include saccades and quick phases of nystagmus and may have components around all three axes of ocular rotation: horizontal, vertical, and torsional. In this study, we recorded horizontal, vertical, and torsional eye movements in normal subjects with their heads upright and stationary. We asked how the eyes are brought back to Listing's plane after they are displaced from it. We found that torsional offsets, induced with a rotating optokinetic disk oriented perpendicular to the subject's straight ahead, were corrected during both horizontal and vertical voluntary saccades. Thus three-dimensional errors are synchronously reduced during saccades. The speed of the torsional correction was much faster than could be accounted for by passive mechanical forces. During vertical saccades, the peak torsional velocity decreased and the time of peak torsional velocity was delayed, as the amplitude of vertical saccades increased. In contrast, there was no consistent reduction of torsional velocity or change in time of peak torsional velocity with an increase in the amplitude of horizontal saccades. These findings suggest that 1) the correction of stimulus-induced torsion is neurally commanded and 2) there is cross-coupling between the torsional and vertical but not between the torsional and horizontal saccade generating systems. This latter dichotomy may reflect the fact that vertical and torsional rapid eye movements are generated by common premotor circuits located in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). When horizontal or vertical saccade duration was relatively short, the torsional offset was not completely corrected during the primary saccade, indicating that although the saccade itself is three-dimensional, saccade duration is determined by the error in the horizontal or the vertical, but not by the error in the torsional component.
Adult↗
Direct visualization of the genomic distribution and organization of two cervid centromeric satellite DNA families.
Several repetitive DNA fragments were generated from PCR amplifications of caribou DNA using primer sequences derived from the white-tailed deer satellite II DNA clone OvDII. Two fragments, designated Rt-0.5 and Rt-0.7, were sequenced and found to have 96% sequence similarity. These caribou clones also had 85% sequence similarity with OvDII. Multiple-colored fluorescence in situ hybridization (FISH) studies with satellite I and satellite II DNA probes to caribou metaphase chromosomes and extended chromatin fibers provided direct visualization of the genomic organization of these two satellite DNA families, with the following findings: (1) Cervid satellite I DNA is confined to the centromeric regions of the acrocentric autosomes, whereas satellite II DNA is found at the centromeric regions of all chromosomes except for the Y. (2) For most acrocentric chromosomes, the satellite I signal appeared to be medially located at the primary constriction, in contrast to that of satellite II, which appeared to be oriented toward the lateral sides as two separate fluorescent dots. (3) The satellite II clone Rt-0.7 appeared to be enriched in the centromeric region of the caribou X chromosome, a pair of biarmed autosomes, and a number of other acrocentric autosomes. (4) Fiber-FISH demonstrated that the satellite I and satellite II arrays were juxtaposed. On highly extended chromatin fibers, the total length of the hybridization signals for the two satellite DNA arrays often reached 300-400 microm. The length of a given satellite II array usually reached 200 microm, corresponding to 2 x 10(3) kb of DNA in a given centromere.
Animals↗
Loss of TGF-beta signaling contributes to autoimmune pancreatitis.
Recent observations suggest that immune response is involved in the development of pancreatitis. However, the exact pathogenesis underlying this immune-mediated response is still under debate. TGF-beta has been known to be an important regulating factor in maintaining immune homeostasis. To determine the role of TGF-beta in the initiation or progression of pancreatitis, TGF-beta signaling was inactivated in mouse pancreata by overexpressing a dominant-negative mutant form of TGF-beta type II receptor in the pancreas, under control of the pS2 mouse trefoil peptide promoter. Transgenic mice showed marked increases in MHC class II molecules and matrix metalloproteinase expression in pancreatic acinar cells. These mice also showed increased susceptibility to cerulein-induced pancreatitis. This pancreatitis was characterized by severe pancreatic edema, inflammatory cell infiltration, T- and B-cell hyperactivation, IgG-type autoantibodies against pancreatic acinar cells, and IgM-type autoantibodies against pancreatic ductal epithelial cells. Therefore, TGF-beta signaling seems to be essential either in maintaining the normal immune homeostasis and suppressing autoimmunity or in preserving the integrity of pancreatic acinar cells.
Animals↗
Controlled human exposure to methyl tertiary butyl ether in gasoline: symptoms, psychophysiologic and neurobehavioral responses of self-reported sensitive persons.
The 1990 Clean Air Act mandated oxygenation of gasoline in regions where carbon monoxide standards were not met. To achieve this standard, methyl tertiary butyl ether (MTBE) was increased to 15% by volume during winter months in many locations. Subsequent to the increase of MTBE in gasoline, commuters reported increases in symptoms such as headache, nausea, and eye, nose, and throat irritation. The present study compared 12 individuals selected based on self-report of symptoms (self-reported sensitives; SRSs) associated with MTBE to 19 controls without self-reported sensitivities. In a double-blind, repeated measures, controlled exposure, subjects were exposed for 15 min to clean air, gasoline, gasoline with 11% MTBE, and gasoline with 15% MTBE. Symptoms, odor ratings, neurobehavioral performance on a task of driving simulation, and psychophysiologic responses (heart and respiration rate, end-tidal CO(2), finger pulse volume, electromyograph, finger temperature) were measured before, during, and immediately after exposure. Relative to controls, SRSs reported significantly more total symptoms when exposed to gasoline with 15% MTBE than when exposed to gasoline with 11% MTBE or to clean air. However, these differences in symptoms were not accompanied by significant differences in neurobehavioral performance or psychophysiologic responses. No significant differences in symptoms or neurobehavioral or psychophysiologic responses were observed when exposure to gasoline with 11% MTBE was compared to clean air or to gasoline. Thus, the present study, although showing increased total symptoms among SRSs when exposed to gasoline with 15% MTBE, did not support a dose-response relationship for MTBE exposure nor the symptom specificity associated with MTBE in epidemiologic studies.
Adult↗
Epidemiology of diabetes mellitus in children in Hong Kong: the Hong Kong childhood diabetes register.
OBJECTIVES: To establish a registry for Chinese children with onset of type 1 (insulin dependent) diabetes mellitus before 15 years of age and to determine the incidence of childhood onset type 1 diabetes mellitus in Chinese children in Hong Kong. RESEARCH DESIGN AND METHODS: A registry was established in 1997 to collect childhood diabetes cases retrospectively from all districts in Hong Kong. The study included all newly diagnosed cases of diabetes with onset < 15 yr of age from 1st January 1984 to 31 December 1996. Primary ascertainment was based on review of medical records at all regional public hospitals in Hong Kong and survey of all the registered practitioners in Hong Kong. The secondary source of validation was made impractical, if not impossible, because of the recent implementation of the Personal Data Privacy Ordinance in Hong Kong. RESULTS: A total of 255 diabetic cases were identified, 227 type 1 diabetes mellitus (218 were Chinese), 18 type 2 diabetes mellitus and 11 secondary diabetes. 246 patients were Chinese and 9 non-Chinese. The age-standardized incidence of type 1 and type 2 diabetes mellitus in southern Chinese children in Hong Kong was 1.4/100,000/yr and 0.1/100,000/yr respectively for children < 15 yr of age during the study period. The incidence rates for type 1 diabetes were 0.9, 1.5 and 1.7 per 100,000/yr for 0-4 years, 5 to 9 years and 10 to 14 years age-groups respectively. The incidence for males was 1.2/100,000/yr and for females 1.7/100,000/yr. A significant increase in the incidence was demonstrated during the study period by simple linear regression (slope 0.14/100,000/year, r2 = 0.73, p = 0.0002) CONCLUSIONS: A diabetic registry is established in Hong Kong. This study documents a very low incidence rate of childhood type 1 diabetes mellitus in southern Chinese children in Hong Kong and we have seen an increasing incidence of the disease in the past 13 years.
Adolescent↗
Effect of exercise training on erythrocyte insulin-like growth factor-I receptor binding in adolescent males.
Exercise training leads to tissue anabolism by acting through the growth hormone (GH)-insulin-like growth factor-I (IGF-I) axis, but the role of tissue IGF-I receptors in this process is not known. Erythrocyte IGF-I receptor binding is known to be affected by circulating levels of IGF-I. We hypothesized that training would lead to alterations in erythrocyte IGF-I binding. Thirty-eight adolescent males (mean age 16+/-0.7 yr) were randomized to a control (n=18) or endurance training intervention lasting 5 weeks. Erythrocyte IGF-I binding was measured by standard techniques. Quantity of receptor binding sites (R), binding affinity constant (Kaff), and nonspecific binding (NS) were calculated. Training led to increases (p<0.05) in 1) Kaff x R - an index of overall binding capacity (control, 7.3 +/-8.0%; trained, 60+/-21%); and 2) NS (control, 1.5+/-6.6%; trained 23.2+/-7.5%). Kaff, R, and R/erythrocyte increased in trained subjects, but not significantly so. These results suggest a training-associated upregulation of IGF-I binding. Finally, the unexpected increase in NS may reflect IGF binding protein activity, rather than changes in the erythrocyte IGF-I receptors themselves.
Adolescent↗
Economic impact of febrile morbidity and use of permethrin-impregnated bed-nets in a malarious area I. Study of demographics, morbidity, and household expenditures associated with febrile morbidity in the Republic of Benin.
In preparation for a study on the effect of bed net use on malaria, this article describes febrile morbidity and malaria expenditures in a sub-Saharan area (Benin) of hyperendemic malaria. The 325 randomly selected households were visited weekly between April 1994 and March 1995 to determine febrile morbidity and household expenditures for prevention and treatment. The results indicate that rural children had two febrile episodes annually compared with 0.3 episodes among children living in the city. There was no difference in mean annual febrile episodes between adults and children (adults = 1.5, children = 1.5; P = 0.48) and in the expenditures per febrile episode (adults = US$1.85, children = US$1.62; P = 0.45). Annual prevention expenditures were higher for adults than for children (US$1.73 and US$1.28, respectively; P < 0.001), although there was no significant difference in expenditures for annual treatment for adults and children (US$2.15 and US$2.34, respectively). These and other findings are analyzed further and discussed.
Adult↗
Economic impact of febrile morbidity and use of permethrin-impregnated bed nets in a malarious area II. Determinants of febrile episodes and the cost of their treatment and malaria prevention.
The objective of this study is to determine the effect of permethrin insecticide-treated bed net (PITN) use on the incidence of febrile episodes and on household malaria expenses in Benin. Over the course of one year, 208 randomly selected PITN user and non-user households were visited weekly to determine expenditures on febrile morbidity and its treatment, and to monitor spending on malaria prevention. Multivariate analyses were performed to distinguish the effects of PITN use from other important determinants of morbidity, such as malaria-related beliefs and practices, income, and other socio-economic variables. Results from the logistic regression analysis show that the use of PITNs decreases the risk of febrile episodes by 34% in children living in the rural zone. Multiple regression analysis reveals that PITN use does not reduce prevention and treatment expenses. These expenses are significantly associated with women's income. This report also discusses other factors associated with febrile morbidity and malaria-related expenditures.
Adult↗