Congenital nasal pyriform aperture stenosis: a diagnostic clue to solitary maxillary central incisor prior to eruption in three infants.
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Biomedical subjects
Publications and source records attributed to L S Chen.
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In this study, we put dead pigs indoors, outdoors and underground respectively, and kept a detailed record of the natural decay process, especially the tension of the pig's abdomen produced by corruptive gas. The result showed that the decay speed was closely related to temperature, humidity, rainfall, position of corpses on the ground, insect parasitism. The obtained data could provide an important referential basis for inferring time after death.
BACKGROUND: The renin-angiotensin system has been known to regulate blood pressure and body fluid homeostasis. Several lines of evidence have shown that renin gene expression and release are up-regulated by beta-adrenergic stimulation, sodium depletion, and angiotensin converting enzyme inhibition, but down-regulated by cytokines. To further characterize the human renin gene (hREN) promoter structure, its regulation, and to identify an appropriate cell system for study, we examined five cell lines and investigated drug effects on the hREN promoter expression. METHODS: Using the hREN-luciferase reporter gene constructs in the DNA transfection assays, approximately 5 kb of the hREN 5' flanking region was assessed for promoter activity in five different cell lines. Regulation of the hREN promoter activity was investigated using Y-1 adrenal cells that were transfected with the hREN-luciferase DNA and were treated with forskolin, calcium ionophore A23187, phorbol ester, angiotensin II (Ang II), or cytokines. RESULTS: Transient transfection analysis showed that the 5 kb hREN 5' flanking DNA alone was able to confer significant promoter activity in Y-1 adrenal cells. In transfected Y-1 cells, luciferase reporter expression was induced by forskolin, suppressed by the calcium ionophore A23187, and phorbol ester in a dose-dependent manner, but was unaffected by angiotensin II (Ang II). However, when Y-1 reporter cells were transfected with human angiotensin II receptor type 1 (AT1) cDNA, hREN promoter activity was dose-dependently down-regulated by Ang II, which was blockable by losartan, an AT1-selective antagonist. Further studies also showed that hREN promoter activity in Y-1 cells was selectively down-regulated by TNF alpha. Deletion of the hREN promoter sequences between position -3916 and -2822 not only enhanced hREN promoter activity by approximately tenfold, but also caused a failure of down-regulation by TNF alpha. In contrast, neither interleukin (IL)-1 alpha, IL-1 beta, IL-2, nor IL-6 exerted any significant effect. CONCLUSIONS: Together the results suggest that TNF alpha is a negative regulator of the hREN expression in the adrenal cells, and that the TNF alpha responsiveness may be controlled by elements located between the positions -3916 and -2822 of the hREN promoter. Moreover, the Y-1 cell line may provide a valuable model system for studying renin gene regulation.
Enamel crystallites form in a protein matrix located proximal to the ameloblast cell layer. This unique organic extracellular matrix is constructed from structural protein components biosynthesized and secreted by ameloblasts. To date, three distinct classes of enamel matrix proteins have been cloned. These are the amelogenins, tuftelin, and ameloblastin, with recent data implicating ameloblastin gene expression during cementogenesis. The organic enamel extracellular matrix undergoes assembly to provide a three-dimensional array of protein domains that carry out the physiologic function of guiding enamel hydroxyapatite crystallite formation. Using the yeast two-hybrid system, we have surveyed these three known enamel gene products for their ability to direct self-assembly. We measured the capacity of the enamel gene products to direct protein-to-protein interactions, a characteristic of enamel proteins predicated to be required for self-assembly. We provide additional evidence for the self-assembly nature of amelogenin and tuftelin. Ameloblastin self-assembly could not be demonstrated, nor were protein-to-protein interactions observed between ameloblastin and either amelogenin or tuftelin. Within the limits of the yeast two-hybrid assay, these findings constrain the emerging model of enamel matrix assembly by helping to define the limits of enamel matrix protein-protein interactions that are believed to guide enamel mineral crystallite formation.
BACKGROUND: The objective is to estimate parameters of the natural history of panic disorder, including its prodrome, incidence, recovery and recurrence. METHOD: In 1981 the Baltimore Epidemiologic Catchment Area Study interviewed 3481 individuals probabilistically selected from the household population. During 1993-1996, 1920 of these individuals (73% of survivors) were interviewed again. Baseline and follow-up interviews included the National Institute of Mental Health Diagnostic Interview Schedule. During the follow-up, a subsample was assessed by psychiatrists using the World Health Organization Schedules for Clinical Assessment in Neuropsychiatry (SCAN). RESULTS: There were 35 new cases of panic disorder in 24,475 person years of exposure, yielding an annual incidence of 1.43 per 1000 per year. Data from the SCAN assessments suggest the incidence estimate is conservative. Incidence is greater in females and declines with age. About one-third of the new cases arise without agoraphobia, but about half have anxiety of some sort present for many years prior to meeting criteria for diagnosis. People with agoraphobia have less intense onsets but slower recoveries than those without agoraphobia. CONCLUSIONS: Panic is heterogeneous in its pattern of onset and recovery. Some of the heterogeneity is associated with the presence of other anxiety over a long period of the life.
Understanding the cellular and molecular events that regulate the formation of enamel is a major driving force in efforts to characterize critical events during amelogenesis. It is anticipated that through such an understanding, improvements in prevention, diagnosis and treatment-intervention into heritable and acquired diseases of enamel could be achieved. While knowledge of the precise role of an enamel-specific protein in directing the formation of inorganic crystallites remains refractory, progress has been made with other aspects of amelogenesis that can be brought to bear on the subject. One such area of progress has been with the identification of an ameloblast-lineage specific amelogenin gene promoter. This promoter can be used to direct the expression of enamel-specific proteins, as well as the expression of proteins foreign to amelogenesis, into the enamel extracellular matrix where their effect on biomineralization can be ascertained in a prospective manner. The resulting enamel from such animals can be examined by morphologic and biochemical modalities in order to identify the effect of the transgene protein on enamel crystallite formation and subsequent biomineralization. This manuscript outlines such a strategy with the potential for enhancing our understanding of amelogenesis.
Previous reports have demonstrated that the phospholemman (PLM), a 72-residue plasma-membrane protein enriched in skeletal muscle and heart, is a major substrate phosphorylated in response to insulin and adrenergic stimulation. Here we describe the isolation and characterization of human and rat PLM cDNA from the heart. Both PLM proteins share significant nucleotide and amino acid sequence and structural similarities with the previously published canine PLM and, to a lesser degree, with Na+/K(+)-ATPase gamma subunit, Mat-8 protein, and CHIF protein. Despite the functional diversity, all these proteins are quite small and possess a single transmembrane domain. Human PLM appears to be a unique gene localized on chromosome 19q13.1. The PLM mRNA is widely distributed in human tissues, with the highest expression in skeletal muscle and heart, suggesting a functional role in muscle contraction. Like canine PLM, both human and rat PLM induce a hyperpolarization-activated chloride current when expressed in Xenopus oocytes. The high degree of sequence and functional conservation among the mammalian PLM proteins indicates that this gene is conserved throughout evolution.
Human cDNAs for methionine synthase (5-methyltetrahydrofolate:L-homocysteine S-transmethylase; EC 2.1.1. 13) have been isolated from fetal and adult liver and HepG2 libraries. The cDNAs span 7.2 kilobases (kb) and consist of a 394-base pair upstream untranslated region, a 3795-base pair open reading frame encoding a 1265-residue 140.3-kDa protein, and about 3 kb of 3' region. The deduced protein sequence shares 53 and 63% identity with the Escherichia coli and the presumptive Caenorhabditis elegans proteins, respectively, and contains all residues implicated in B12 binding to the E. coli protein. Several potential polymorphisms and a cryptic splice deletion were detected in the coding region of the cDNAs. A polymorphism that results in a D919G modification in the protein is fairly common in human DNA samples. Northern analyses of poly(A) mRNA indicated two major species of about 8 and 10 kb in human tissues and some minor, partially spliced species. mRNA levels were highest in the pancreas, skeletal muscle, and heart of the adult and in the kidney in the fetus and were low in adult liver. Genomic clones were isolated and the 5' region was analyzed. Exon 1 is preceded by a number of potential promoter sites, including an E box, CAAT boxes, and a GC box, but this region lacks a TATA element. The human methionine synthase gene was localized to chromosome region 1q42.3-43 by in situ hybridization.
BACKGROUND: Natural history can be characterized by incidence, recurrence, and duration of episodes. Research on the incidence of major depression is rare; studies of recurrence and duration are limited to clinical samples. METHODS: The Baltimore, Md, site of the Epidemiologic Catchment Area Program followed up its 1981 baseline cohort of 3481 respondents with an additional assessment in 1993 to 1996. Interviews were obtained from 1920 respondents (73% of the survivors). The Diagnostic Interview Schedule and the same survey procedures as in 1981 were used, augmented with a Life Chart Interview for dating the onset and duration of syndromes. RESULTS: There were 71 new cases of Diagnostic interview Schedule/DSM-IV major depression and 23,698 person-years of exposure, generating an estimated incidence of 3.0 per 1000 per year. Incidence peaked while subjects were in their 30s, with a smaller peak when they were in their 50s. Prodromal symptoms often occurred many years before the full criteria for diagnosis were met. Women were at higher risk for becoming new cases but had neither higher risk for recurrence nor longer episodes than men. Episodes of depression lasted for 12 weeks. The duration of an episode, and time to an episode-free year, was longer in the first episode than in recurrent episodes. CONCLUSIONS: The incidence estimated in this study is consistent with that found in the few other similar studies performed. The bimodality of onset suggests the value of further exploring the heterogeneity of depression via its natural history. Reported differences in prevalence between men and women seem to be due to differences in incidence, not chronicity.
A prospective study was conducted to see whether emergent esophagogastroduodenoscopy (EGD) in patients with active upper gastrointestinal (GI) bleeding is associated with more oxygen desaturation than nonemergent EGD. Emergent EGD was performed in the study patients with active upper GI bleeding. Nonemergent EGD was performed in the control patients. Determination of oxygen saturation (Sao2) was measured by pulse oximeter. A decrease in Sao2 of > 4% was more frequent in the study patients (26%, 13 of 50) than in controls (6%, 3 of 50) (P < .01). During EGD, mean oxygen saturation decreased significantly in both groups of patients. After EGD, mean oxygen saturation did not recover toward the pre-endoscopy insertion level in the study group (P < .01). A linear association was found that oxygen desaturation = 5.46 + 0.15 (status) -0.06 (baseline oxygen saturation). Emergent EGD for active upper GI bleeding in the emergency department tends to be associated with more frequent significant oxygen desaturation than nonemergent EGD. Continuous oxygen supplementation and oxygen saturation monitoring may be used during emergent nonsedated EGD in the emergency department.
A prothrombotic state caused by a deficiency of protein C or protein S, each an inhibitor of coagulation cascade, increases the risk of ischemic cerebrovascular accident (ICVA) in young adults. This retrospective review studies the relationship of protein C or S deficiency with childhood ICVA. From 1989 to 1995, 37 children were diagnosed by neuroimaging with ICVA unrelated to any known preexisting diagnosis. Protein C deficiency or protein S deficiency was the only identified risk factor for 5.4% (2 patients) and 13.5% (5 patients), respectively, of these 37 children. The data suggest that protein C or protein S deficiency is an important risk factor of ICVA in children.
A population-based case-control study was conducted in Washington County, Maryland (United States) to explore the association between incident bladder cancer and exposure to drinking water from chlorinated surface sources. Cancer cases were White residents, enumerated in a 1975 county census and reported to the Washington County Cancer Registry (n = 294) between 1975 and 1992. White controls, frequency matched by age (+/- 5 years) and gender, were selected randomly from the census (n = 2,326). Households receiving municipal water, which generally derived from chlorinated surface waters, were treated as having 'high exposure' and all others, as 'low exposure.' Duration of exposure to type of drinking water was based on length of residence in the census household prior to 1975. Odds ratios (OR) were calculated using logistic regression methods, adjusting for age, gender, tobacco use, and urbanicity. Bladder cancer risk was associated weakly in the general population with duration of exposure to municipal water. The association was limited to those who had smoked cigarettes. In ever-smokers compared with never-smokers with low exposure, the adjusted ORs for bladder cancer risk with increasing exposure were 1.3, 1.4, 1.4, 1.7, 2.2, 2.8, respectively, for 0, 1-10, 11-20, 21-30, 31-40, > 40 years' exposure duration. The ORs in smokers were not diminished after adjusting for smoking history and intensity.
A simple spectrophotometric assay has been developed for determining concentrations of the new cardioprotective agent, GP531, in human plasma. The method is adapted from the Bratton-Marshall assay (BMA) for the detection of primary aromatic amines. The assay can be used to measure plasma concentrations of the drug during i.v. infusion administration to patients. The limit of quantitation of the assay is 1 microgram/ml using a 0.8 ml sample ultrafiltrate of plasma. The colorimetric assay correlates well with a previously described high performance liquid chromatographic (HPLC) procedure.
Information regarding the genetic factors and environmental conditions that influence presenilin-1 (PS-1) gene expression is essential for the elucidation of its pathophysiological role in Alzheimer's disease (AD). Previous in situ hybridization studies have demonstrated that neurons are the predominant cell type expressing PS-1 in the mammalian central nervous system (CNS) under physiological conditions. In this study, we examined the consequences of an experimentally induced focal injury on PS-1 gene expression in the mouse CNS. Physical lesions to white matter regions produced a robust increase in PS-1 gene expression in non-neuronal cells immediately surrounding the site of injury. These findings underscore the epidemiological evidence that implicate head injury as a risk factor for AD and suggest a possible role for PS-1 in this capacity.
Besides the conventional isomerase-mediated pathway, unsaturated fatty acids with old-numbered double bonds are also metabolized by reduction pathways with NADPH as cofactor. The relative contributions of these pathways were measured in intact rat-liver and rat-heart mitochondria with a novel stable isotope tracer technique. A mixture of equal amounts of unlabelled cis-5-enoyl-CoA and 13C4-labelled acyl-CoA of equal chain lengths was incubated with mitochondria. The isotope distribution of 3-hydroxy fatty acids produced from the first cycle of beta-oxidation was analysed with selected ion monitoring by gas chromatograph-mass spectrometer. 3-Hydroxy fatty acids produced from the reduction pathway of unsaturated fatty acids were unlabelled (m + 0) whereas those produced from saturated fatty acids were labelled (m + 4). The m + 0 content serves to indicate the extent of reduction pathway. Rotenone treatment was used to switch the pathway completely to reduction. The extent of m + 0 enrichment in untreated mitochondria normalized to the m + 0 enrichment of rotenone-treated mitochondria was the percentage of reduction pathway. With this technique, cis-4-decenoate was found to be metabolized completely by the reduction pathway in both liver and heart mitochondria. cis-5-Dodecenoate was metabolized essentially by the reduction pathway in liver mitochondria, but only to 75% in heart mitochondria. When the chain length was extended to cis-5-tetradecenoate, the reduction pathway in liver mitochondria decreased to 86% and that in heart mitochondria to 65%. The effects of carnitine, clofibrate and other conditions on the reduction pathway were also studied. Enrichments of the label on saturated fatty acids and 3-hydroxy fatty acids indicated that the major pathway of reduction was not by the direct reduction of the cis-5 double bond. Instead, it is most probably by a pathway that does not involve forming a reduced saturated fatty acid first.
Aberrant neural sprouting of mossy fiber terminals in the supragranular layer of dentate gyrus is consistently observed following seizures in an animal model of epilepsy. It is also observed in hippocampi taken from epileptic patients with hippocampal sclerosis. The aberrant neural sprouting with synaptic reorganization is one of the proposed cellular mechanisms underlying epileptogenesis. It is not known whether aberrant synaptogenesis can be induced in the cortex, as in hippocampus, by seizure activity. In this study, synaptic terminals in the cortex were measured after focal cortical seizures by a semiquantitative image analysis of synaptophysin immunoreactivity. Brief intracortical perfusion of kainic acid induced focal status epilepticus and destructive cortical lesions. Synaptophysin immunoreactivity was significantly increased in the area where kainic acid was perfused. The increase of synaptophysin immunoreactivity, indicating an increase of synaptogenesis, was observed at 2 and 4 weeks after focal cortical seizures. This result suggests that kainic acid-induced seizure activity is associated with long-lasting synaptogenesis in the cortex. Studies centering on the physiological consequences of aberrant synaptogenesis may lead to additional understanding of the mechanisms underlying cortical epileptogenesis.
Aminoimidazole-containing compounds have been found to be electroactive and can be detected by amperometric electrochemical detection (ECD) with a high degree of sensitivity. A liquid chromatography (LC) method using ECD was developed for measuring plasma concentrations of the aminoimidazole-containing drug GP531, a potent adenosine-regulating agent. Plasma samples were extracted with 2-propanol and analyzed by LC under isocratic conditions using a mobile phase of methanol-sodium phosphate (pH 6.3; 3.3 mM) (32:68, v/v). The potential of the glassy carbon working electrode was set at +800 mV. The limit of quantitation was 12.5 ng ml-1 of GP531 using 100 microliters of plasma. The method was used to define the pharmacokinetics of GP531 in monkey following i.v. administration.
We sought to analyze our experience with pediatric epilepsy surgery patients to determine the place of [18F]fluorodeoxyglucose (FDG) positron emission tomography (FDG-PET) in the preoperative evaluation of such children relative to chronic invasive intracranial monitoring. Fifty-six children who received an interictal FDG-PET as part of a phase 1 epilepsy surgery evaluation were compared with 44 children who did not have this study in a retrospective analysis of 100 patients accrued over a 4-year period. There was no significant difference between the two groups of children in terms of age or follow-up or was there a significant difference between the FDG-PET group and the no-FDG-PET group in regard to the numbers of children who had surgery, the type of procedure done, whether chronic invasive intracranial monitoring was performed, or outcome. The hypometabolic area demonstrated on interictal FDG-PET was concordant with that of the epileptogenic zone as mapped out with ictal recordings from subdural electrodes in 2 of 13 patients in whom a complete data set was available for comparison. In the other 11 children there was either poor agreement between interictal FDG-PET and ictal electrocorticographic data or the interictal FDG-PET was normal in the face of an epileptogenic focus which was successfully mapped by invasive electrophysiologic techniques and excised. We conclude that one cannot exclude a child with intractable partial seizures from surgical consideration because the interictal FDG-PET is normal; nor is there sufficient correlation between the interictal hypometabolic area on FDG-PET and the epileptogenic zone in terms of anatomic location and size to justify forgoing chronic invasive intracranial monitoring in children with intractable partial seizures being evaluated for epilepsy surgery unless there is absolute concordance between all neuroimaging, clinical, and video-electroencephalographic data.