Coronary artery dissection presenting to the ED as an acute myocardial infarction.
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Adult↗
Biomedical subjects
C C Lee
Publications and source records attributed to C C Lee.
A current concept of trauma-induced multiorgan failure.
Trauma deaths continue to show a trimodal distribution: immediately at the scene, within the first 24 hours during initial resuscitation, and in the next 3 to 4 weeks as a result of multiple organ failure.(1) Failure to resuscitate adequately in the emergency department can lead to acidosis, hypothermia, and coagulopathy, which can result in multiple organ failure and cause death in these patients. Our current understanding of the initial response to shock and trauma and the development of the systemic inflammatory response syndrome and progressive organ failure is one of a continuum initiated and perpetuated by inflammation and inflammatory mediators. The pathophysiologic character, diagnosis, prevention, and treatment of traumatic injury-induced multiple organ failure are discussed.
Emergency Medicine↗
Identification of mutations including de novo mutations in Korean patients with hypokalaemic periodic paralysis.
BACKGROUND: Hypokalaemic periodic paralysis (hypoPP) is an autosomal dominant disorder involving the abnormal function of ion channels and it is characterized by paralysis attacks of varying severity, accompanied by a fall in blood potassium levels. Linkage analysis showed that the candidate locus responsible for hypoPP was localized to chromosome 1q31-32, and this locus encoded the muscle dihydropyridine-sensitive calcium channel alpha(1)-subunit (CACNA1S). So far, three different mutations in CACNA1S gene have been identified in patients with hypoPP: Arg528His, Arg1239His and Arg1239Gly in Caucasian patients. However, there are few reports about the mutations of CACNA1S gene in other races. METHODS: In this study, four Korean families with five hypoPP patients were screened for mutations of CACNA1S gene with polymerase chain reaction-based restriction analysis and single-strand conformation polymorphism analysis. To determine the mode of inheritance, haplotype analysis was done with three microsatellite markers (D1S1726, CACNL1A3, and D1S1723). RESULTS: Arg528His mutation was detected in three families, and one family had no known mutations. Moreover, for the first time, we detected de novo Arg528His mutations in two out of three families with hypoPP. Haplotype analysis using three microsatellite markers (D1S1726, CACNL1A3, and D1S1723) suggested the occurrence of de novo Arg528His mutations in two of the three families with Arg528His mutation. CONCLUSIONS: Arg528His mutations of CACNA1S, including de novo Arg528His mutations, were found in Korean patients with hypoPP. These results imply that de novo mutation, in addition to non-penetrance, is one of the genetic mechanisms that can explain the previous clinical observation that hypoPP occurs sporadically without family history.
Adolescent↗
The role of technetium-99m sestamibi myocardial perfusion single-photon emission computed tomography (SPECT) in the detection of cardiovascular involvement in systemic lupus erythematosus patients with non-specific chest complaints.
OBJECTIVES: Systemic lupus erythematosus (SLE) can affect multiple organs. Coronary artery disease has received increasing recognition as a major cause of morbidity and mortality in SLE in recent years. The purpose of this study was to evaluate the utility of technetium-99m sestamibi single-photon emission computed tomography ((99m)Tc-sestamibi SPECT) in the detection of cardiovascular involvement in SLE patients with non-specific clinical chest symptoms such as chest discomfort and/or dyspnoea and/or occasional palpitation. METHODS: Thirty-three SLE female patients (age range: 22-45 yr) with non-specific complaints such as chest discomfort and/or dyspnoea and/or occasional palpitation were investigated using a (99m)Tc-sestamibi myocardial perfusion SPECT scan at rest and after dipyridamole infusion in a stress study. The age- and sex-matched healthy group (24 cases) and SLE patients without any cardiovascular symptoms/signs (28 cases) were also included as controls in this study. The results of the uptake pattern of (99m)Tc-sestamibi were classified into four types including normal, persistent perfusion defect, reversible perfusion defect and reverse redistribution. RESULTS: Perfusion abnormalities were detected in 27 cases (seven patients had persistent perfusion defects, 15 patients had reversible perfusion defects, one patient had both persistent and reversible perfusion defects, two patients showed a reverse redistribution pattern and two patients had both reversible perfusion defects and a reverse redistribution pattern). The results of the SPECT in the healthy group were all normal. However, perfusion abnormalities were detected in 12 cases in the group of asymptomatic SLE patients. CONCLUSIONS: (99m)Tc-sestamibi myocardial perfusion SPECT is a useful non-invasive imaging modality to detect cardiovascular involvement in SLE patients with non-specific clinical complaints of heart disease.
Adult↗
Acute failure of oxygen delivery.
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Adult↗
Hair removal by long-pulse alexandrite laser in oriental patients.
The laser depilation system, cleared by the Food and Drug Administration since 1995, is evolving rapidly. However, the parameters in the hair removal function of these devices emphasize use for white people with fair skin (Fitzpatrick types I, II, or III). The characteristics of oriental skin and hair are black, coarse hairs in darker skin (Fitzpatrick types IV or V). As seen, the higher the skin melanin content, the more difficult to remove hair by laser. The authors report 146 oriental patients (156 body sites) who underwent treatment with the long-pulse alexandrite laser (wavelength, 755 nm) depilation system since November 1997. Percentage of hair removal (clearance rate) was assessed, and the histological change from laser pulse damage was observed. After two treatments, the clearance rates in the axillae and the leg were 61% and 62% respectively in the 15 to 20-J group (N = 47), and were 66% and 67% respectively in 21 to 25-J group (N = 64). After five treatments, 59 patients (37 axillae and 22 legs, all of which received 21-25 J per square centimeter of laser energy treatment during the course) had an average clearance rate of 91% (axillae) and 86% (leg), and the clearance rates have been maintained near 90% after long-term follow-up (average follow-up, 17 months). Minimal and transient complications are noted. In conclusion, using a combination of longer wavelength (but still in the optimal window of 630-870 nm), long pulse duration (10-40 msec), high fluence (but limited up to 25 J per square centimeter), multiple treatments, and concomitant direct cooling applied to the skin of oriental patients (Fitzpatrick types IV and V) with black, moderately coarse hair shafts achieves satisfying long-term hair removal results.
Axilla↗
Time course of cerebral infarction in the middle cerebral arterial territory: deep watershed versus territorial subtypes on diffusion-weighted MR images.
PURPOSE: To examine possible differences between the evolution of cerebral watershed infarction (WI) and that of territorial thromboembolic infarction (TI) by using diffusion-weighted (DW) and T2-weighted magnetic resonance (MR) images and apparent diffusion coefficient (ADC) maps. MATERIALS AND METHODS: Fourteen patients with TI and nine with WI underwent MR imaging from the acute to chronic infarction stages. ADC maps were derived from DW images. Lesion-to-normal tissue signal intensity ratios on ADC maps (rADC), echo-planar T2-weighted images, and DW images were calculated. Lesion volumes at acute or early subacute infarction stages were measured on DW images, and final lesion volumes were estimated on fluid-attenuated inversion-recovery images. RESULTS: Analysis of variance revealed a significant difference in temporal evolution patterns of rADC between WI and TI (P <.001). rADC pseudonormalization following TI began about 10 days after symptom onset, but that following WI did not occur until about 1 month after symptom onset. The Pearson correlation coefficient between final and initial infarct volumes was 0.9899 for both infarction subtypes, indicating that the initial ischemic injury volume measured at the acute or early subacute stage predicted the final lesion volume fairly well. CONCLUSION: The evolution time of ADC is faster for TI than for WI. This difference, which likely originates from the different pathophysiologic and hemodynamic features of the two infarction types, might account for the relatively large range of ADC values reported for the time course of ischemic strokes.
Acute Disease↗
MPer1 and mper2 are essential for normal resetting of the circadian clock.
Mammalian Per1 and Per2 genes are involved in the mechanism of the circadian clock and are inducible by light. A light pulse can evoke a change in the onset of wheel-running activity in mice by shifting the onset of activity to earlier times (phase advance) or later times (phase delays) thereby advancing or delaying the clock (clock resetting). To assess the role of mouse Per (mPer) genes in circadian clock resetting, mice carrying mutant mPer1 or mPer2 genes were tested for responses to a light pulse at ZT 14 and ZT 22, respectively. The authors found that mPer1 mutants did not advance and mPer2 mutants did not delay the clock. They conclude that the mammalian Per genes are not only light-responsive components of the circadian oscillator but also are involved in resetting of the circadian clock.
Animals↗
Polymorphic DNA haplotypes at the human low-density lipoprotein receptor gene locus in Koreans.
Many low-density lipoprotein (LDL) receptor mutations have been identified and characterized, demonstrating a high degree of allelic heterogeneity at this locus. The ability to identify mutant LDL-receptor genes for prenatal diagnosis of familial hypercholesterolemia (FH) or to study the role of the LDL-receptor gene in polygenic hypercholesterolemia requires the use of closely linked restriction fragment lenghth polymorphisms (RFLPs). In the present study nine different RFLPs (TaqI, StuI, HincII, BstEII, AvaII, PvuII, MspIA, MspIB, and NcoI) and a sequence variation at Arg450 were used to clarify the characteristics of the LDL-receptor gene in Koreans. A total of 978 LDL-receptor alleles from 244 members of 43 different pedigrees (15 normal and 28 FH pedigrees) and 245 individuals (187 normal and 58 FH) were analyzed. Frequencies of these polymorphisms did not differ significantly between controls and FH patients. Individually, seven sites--TaqI, BstEII, AvaII, MspIA, MspIB, NcoI and Arg450--had heterozygosity indices ranging from 0.3610 to 0.4601, whereas the PvuII site displayed low levels of polymorphism and StuI was monomorphic. Haplotypes were constructed for 215 individuals of 13 normal and 24 FH pedigrees using the nine polymorphisms. Of 512 (= 2(9)) possible combinations for the nine polymorphic sites, 39 unique haplotypes were detected. The frequency distribution of individual haplotypes ranged from 1/155 (0.65%) to 40/155 (25.8%). The four most common haplotypes accounted for 59.4% of those sampled. Statistical analysis of the haplotypes indicated marked linkage disequilibrium for these 10 sites and throughout the region containing the LDL-receptor gene. Owing to the high degree of linkage disequilibrium over the entire locus, not all RFLPs were informative. We rank each RFLP according to its informativeness and present a strategy for the optimal selection of RFLPs for pedigree analysis.
Genetics, Population↗
Comparison of photosensitizer (AIPcS2) quantification techniques: in situ fluorescence microsampling versus tissue chemical extraction.
A noninvasive in situ fluorescence-based method for the quantification of the photosensitizer chloroaluminum disulfonated phthalocyanine was compared to the highly accurate but nonreal time ex vivo spectrofluorometry method. Our in vivo fluorescence technique is designed to allow real-time assessment of photosensitizer in tumor and normal tissues and therefore temporally optimal light delivery. Laser-induced fluorescence was used to measure photosensitizer concentration from multiple microscopic regions of tissue. Ex vivo chemical extraction was used to quantify photosensitizer concentration in the same volume of tissue. The amount of photosensitizer in the vascular and/or parenchymal compartments of skeletal muscle and liver was determined by quantifying fluorescent signal in vivo, ex vivo and after blood removal. Confocal microscopy was used to spatially document photosensitizer localization 30 min and 24 h after delivery. While a linear correlation can exist between the fluorescence intensity measured by our fiber-optic bundle system and actual tissue concentration, temporal changes to this calibration line exist as the photosensitizer changes its partitioning fraction between the blood (vasculature) and the tissue parenchyma. In situ photosensitizer fluorescence microsampling (dosimetry) systems can be performed in real time and linearly correlated to actual tissue concentration with minimal intertissue variance. Tissue-specific differences may require temporal alterations in the calibration.
Animals↗
The combination of zidovudine and interferon alpha-2B in the treatment of adult T-cell leukemia/lymphoma.
Adult T-cell leukemia/lymphoma (ATL) is frequently a very aggressive malignancy with a poor survival despite aggressive multiagent chemotherapy. The combination of the antiretroviral drug zidovudine (AZT) and interferon alpha (IFNalpha) has been reported to induce remissions in patients with ATL. The purpose of this study was to evaluate the clinical response and toxicity following administration of a combination of IFNalpha-2b and AZT in patients with human T-cell lymphotropic virus type I (HTLV-I)-associated ATL. Eighteen patients with ATL (chronic. crisis, acute or lymphoma type) were treated with the combination of AZT (50 - 200 mg orally 5 times a day) and IFNalpha-2b (2.5 - 10 million units subcutaneously daily). Three patients had objective responses lasting more than one month. One patient had a clinical complete remission, lasting 21.6 months and two patients had partial remissions lasting 3.7 and 26.5 months. Six patients were not considered evaluable for response due to short and/or interrupted periods of treatment. Seventeen patients have died with a median survival time after initiation of therapy of 6 months. Neutropenia and thrombocytopenia were the dose limiting toxicities. In conclusion, the response rate in this study was lower than noted in the two previous published series. This may be due to the amount and type of prior treatment our patients had received.
Adult↗
A challenge for reform in South Korea.
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Health Care Reform↗
Delineation of CTG repeats and clinical features in a Taiwanese myotonic dystrophy family.
Myotonic dystrophy (DM) is an inherited, autosomal dominant muscular disease which is primarily caused by a CTG trinucleotide expansion mutation on chromosome 19q13.3. The size of this trinucleotide repeat is related both to the age of onset and to the severity of the clinical manifestation. This disease is very rare in Taiwan, and clinical and genetic study on DM has not yet been documented in this area. Here, we present both clinical features and degrees of CTG expansion for a Taiwanese DM family. All of the DM patients examined in this family showed obvious clinical manifestations by age 30, which included facial and limb muscle weakness with atrophy, myotonia, and ptosis. In addition, individual DM members also exhibited variable phenotypes, which may reflect the complexity of the pathogenic mechanism. Because the collection of blood specimens was considered to be an invasive procedure, a genetic study on this DM family was performed using buccal cells. Our results confirmed that four members showing classic symptoms of DM had CTG repeat expansion in the DMI locus, and that one member with ptosis and minor muscle weakness in the right foot was a normal homozygote for CTG repeat. These data demonstrate that buccal cells can provide clear and reliable results, and thus, are suitable for a family study of DM.
Alleles↗
Prenatal diagnosis of oculocutaneous albinism two mutations located at the same allele.
A pregnant woman accepted amniocentesis on account of the previous birth of type 1 oculocutaneous albinism (OCA1). PCR revealed that the fetus had two mutations (862delTT, Arg 299His). The father had one missense mutation (Arg 299Ser) and the mother had the same mutations as the fetus. Two mutations of the fetus located at the same allele were suspected. Postpartal follow-up confirmed his carrier status. For recessive disorders, faced with a fetus with two mutations, the importance of performing segregation analysis of mutation on both parents is emphasized. This could exclude two mutations located at the same allele and prevent the unnecessary termination of a fetus with carrier status.
Adult↗
Endotracheal tube fires during carbon dioxide laser surgery on the larynx--a case report.
Endotracheal tube (ETT) fire is a catastrophic disaster that may occur during laser surgery of the upper airway. Several means are available for protection of polyvinyl chloride (PVC) tube from fire, but they are not perfect in prevention of fires caused by laser beam. The PVC tube is hazardous for carbon dioxide (CO2) laser surgery if it is not well wrapped with metallized foil tape. We report a case that a PVC ETT wrapped with aluminum foil ignited during CO2 laser surgery of the larynx. In this report, we emphasize the shaft of the PVC tube must be completely wrapped with aluminum foil to prevent exposure of any surface if it is used in CO2 laser surgery of the upper aero digestive tract.
Aged↗
Treatment of intractable generalized dystonia by bilateral posteroventral pallidotomy--one-year results.
BACKGROUND: Recent study has revealed that bilateral posteroventral pallidotomy (PVP) significantly improve dystonic movements and improve motor function of those patients with generalized dystonia (GD). However, there is only a limited number of patients who have been reported so far. METHODS: This study was conducted to evaluate the clinical efficacy of surgical treatment with bilateral PVP on patients with intractable GD. All the studied patients were regularly rated with standardized scales (Burke-Fahn-Marsden Evaluation Scale for Dystonia) for dystonic movement and living disability before and after surgery. RESULTS: There were 18 patients, 8 males and 10 females with an average age of 24.8 years, included in the study. Postoperatively, there were slow, partial, but steady improvements of the dystonic movement and daily living function. Maximal effects were noted at the sixth month and the clinical benefits were sustained one year after the surgical treatment when there were statistically significant improvements in 13% of total dystonia movement score and 9% of the total disability score (p < 0.05). Upon further analysis, improvements of dystonic movements were statistically significant in the regions of mouth (50%), speech/swallowing (19%) and neck (43%), and daily living functions in speech (14%) and eating/swallowing (29%). CONCLUSIONS: Bilateral posteroventral pallidotomy was only partially effective for the treatment of GD, and it produced clinical improvement in the dystonic movement limited to the craniocervical region. We therefore suggest that patients with GD should be carefully selected for the treatment of bilateral posteroventral pallidotomy, despite the surgery having a partially beneficial effect on this kind of movement.
Adolescent↗
GL331 induces down-regulation of cyclin D1 expression via enhanced proteolysis and repressed transcription.
GL331 is a novel podophyllotoxin-derived compound. In this study, GL331 induced human lung adenocarcinoma cell line CL1-5 growth arrest before death during the initial 24-h incubation period. We found that GL331 had no inhibitory effect on the expression of cyclins E, A, B1, CDK 4, and CDK 2; instead, its cell growth-inhibitory effect was partly attributable to an early down-regulation of cyclin D1 expression and in turn the reduction of retinoblastoma protein phosphorylation. GL331 enhanced the proteolysis of cyclin D1, and a proteasome inhibitor was able to block GL331-caused cyclin D1 reduction, suggesting that GL331-stimulated cyclin D1 degradation was through proteasomal processes. Additionally, GL331 reduced cellular cyclin D1 mRNA level down to 45% of control in 4 h and further to around 20% in 12 h. However, GL331 did not accelerate the disappearance of cyclin D1 mRNA under the condition of transcription blockage induced by actinomycin D. It was reported that a certain region in the 3'-untranslated region (UTR) of cyclin D1 mRNA mediated the mRNA degradation upon extracellular stresses. Herein, transient transfection studies demonstrated that the 3'-UTR insertion did not confer the susceptibility of luciferase reporter gene to the GL331 treatment. Together, these data suggested that GL331 did not decrease the stability of cyclin D1 mRNA. On the other hand, we found that GL331 specifically inhibited the cyclin D1 promoter-driven luciferase reporter activity. Western blot analyses showed that GL331 decreased the level of phosphorylated extracellular signal-regulated kinase (Erk), with no effect on p38 or c-Jun NH(2)-terminal kinase. Furthermore, GL331's inhibition of cyclin D1 promoter was attenuated by ectopic Erk-2 overexpression. These data suggested that GL331 inhibited cyclin D1 gene transcription via the Erk signaling pathway. In summary, we report that GL331 induced an early decline of cyclin D1 expression by dual mechanisms: 1) enhancement of protein turnover and 2) repression of Erk-mediated gene transcription.
Antineoplastic Agents, Phytogenic↗
Mutation analysis of a family with hereditary hemorrhagic telangiectasia associated with hepatic arteriovenous malformation.
Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disorder characterized by multisystemic vascular dysplasia. Two related genes, endoglin and activin receptor-like kinase (ALK-1), have been mapped to chromosomes 9q34 and 12q13, respectively. We describe a Taiwanese HHT family with hepatic arteriovenous malformation. Clinical and molecular evaluations were performed in eight members of this family, and HHT symptoms were found in three adults. Short tandem repeat markers were used to perform linkage analysis, and this family was classified as HHT type 2 (ALK-1 gene). The exons of ALK-1 were amplified using the polymerase chain reaction and subjected to direct DNA sequencing. The mutation causing the disease was located at ALK-1 codon 411, causing an arginine to glutamine substitution. Five members of this family carried the mutated ALK-1 gene. This investigation successfully used linkage and sequencing techniques to perform molecular diagnosis of HHT.
Activin Receptors, Type I↗