Drowning is one of the most common causes accidental death worldwide, but its diagnosis remains a challenging task in forensic pathology. Several authors have suggested that diatom analysis be conducted via an enzymatic digestion method that uses proteinase K to provide objective evidence for drowning; we employed this method in our study because of its superior applicability as compared to the conventional disorganization methods. The purpose of this study was to examine the reclaiming ratio of diatoms from experimentally drowned animal organs, which could be influenced by diatom morphology. The authors injected 3 diatoms species (Cyclotella striata, Navicula incerta, and Pleurosigma angulatum) into a rat's airway and compared the detection rate to investigate the factors that influence the sensitivity of diatom analysis. The results are as follows: (1) Average reclaiming ratio in the lungs was 81.07 for Navicula incerta, 48.26 for Cyclotella striata, and 5.35 for Pleurosigma angulatum. (2) The detection rates from the closed organs in 15 experimental animals were highest in the kidney (73%, 11/15), followed by the heart (67%, 10/15), brain (60%, 9/15), and liver (53%, 8/15). (3) Two Cyclotella striata was detected in the kidney of postmortem control group which suggest the possibility of contamination during laboratory procedure. In conclusion, the authors propose that diatom size could be a significant influencing factor for diatom extraction from the organs of drowned bodies; therefore, the results of diatom analysis must be interpreted after considering the diatom population of the drowning medium at the scene and the possibility of contamination during the laboratory procedure.
Animal Structures ; Animals ; Brain ; Diatoms ; Digestion ; Drowning ; Endopeptidase K ; Forensic Pathology ; Heart ; Kidney ; Liver ; Lung

Death by drowning is a major cause of unnatural death worldwide. It is therefore important to conduct forensic examination of immersed bodies following drowning, in order to determine the diagnosis of drowning, because no specific methods have been established thus far. Therefore, we performed a series of rat experiments to compare autopsy findings between seawater and fresh water drowning cases, which included the presence of pleural effusion and histologic findings of the lung. The results showed that the volume of pleural effusion increased in the seawater drowning group compared to the fresh water drowning group, and the total weight of lung was affected by the type of drowning medium and postmortem interval. However, histologic findings of the lung showed no significant difference between the 2 types of drowning mediums.
Animals ; Autopsy ; Drowning ; Fresh Water ; Lung ; Pleural Effusion ; Rats ; Seawater

Drowning is a leading cause of accidental deaths worldwide, but its pathological diagnosis remains a challenge for forensic pathologists owing to a lack of pathognomonic findings in drowning deaths and inconclusive autopsy findings caused by postmortem changes. The aim of the present study was to investigate the pathway taken by inhaled drowning medium through the airway after death in a variety of experimental conditions, including underwater pressurization. We used methylene blue dye to monitor the spread of drowning medium to the lungs. Results of theses experiments demonstrated that it is possible for a significant amount of downing medium to enter the airway during immersion after death. Our results suggest that autopsies of immersed bodies and interpretation of these findings should be performed with special care.
Animal Experimentation* ; Animals* ; Autopsy ; Diagnosis ; Drowning* ; Immersion ; Inhalation* ; Lung ; Methylene Blue* ; Postmortem Changes

PURPOSE: The growth hormone receptor(GHR) is essential for the actions of growth hormone on postnatal growth and metabolism. GHR transcripts are characterized by the presence of disparate 5'untranslated exons. In contrast to L1 transcript, factors regulating the expression of the GC rich L2 transcript have remained unidentified. The purpose of this study is in order to characterize the mechanisms regulating expression of the L2 transcript in the murine GHR gene METHODS: Transient transfection experiments including deletional analysis and co-transfection assay were performed to find a region containing promoter activity in the L2 5'flanking sequence using BNCL2(mouse liver) cells, CV-1(African green monkey kidney) cells, HRP.1 trophoblasts and Drosophila Schneider(SL2) cells. Sequencing analysis was performed to find the region contained consensus binding sites for transcription factors. Standard gel shift(Electrophoretic mobility shift assay, EMSA) and supershift analysis using liver nuclear extracts was performed to establish proteins(transcription factors) bound this regulatory element. RESULTS: The 5'flanking region of the L2 untranslated region(UTR) exhibited promoter activity in BNCL2(mouse liver), CV-1(monkey kidney) cells and HRP.1 trophoblasts. Deletional analyses indicated the presence of a Sp binding site important for transcription of the L2 UTR and localized the major regulatory region within 75 bp of the 5'transcription start site. Sequencing analyses revealed the region contained consensus binding sites for the Sp family of transcription factors. EMSA and supershift EMSA revealed that in mouse liver nuclear extracts that Spl and Sp3 bound to this cis-element. Functional studies in Drosophila SL2 cells and BNCL2(mouse liver) cells established the ability of Sp3 and Sp1 to stimulate transcriptional activity via this cis-element. Functional studies in Drosophila SL2 cells demonstrated a functional interaction between Sp3 and Sp1 at this DNA-binding site. CONCLUSION: Sp family transcription factors play a role in regulation of L2 transcript gene expression in the 5'flanking region of the murine GHR gene.
Animals ; Binding Sites ; Cercopithecus aethiops ; Consensus ; Drosophila ; Electrophoretic Mobility Shift Assay ; Exons ; Gene Expression ; Growth Hormone* ; Humans ; Liver ; Metabolism ; Mice ; Receptors, Somatotropin* ; Regulatory Sequences, Nucleic Acid ; Transcription Factors* ; Transfection ; Trophoblasts

In anesthetized cats the effects of lactate-activated muscle spindle upon the group Ia muscular afferent fibers were studied. Laminectomy was done from L5 to Sl spinal cord level. Extracellular recording was done at dorsal root to record the impulse discharge from group Ia muscular afferent fibers. 1) Muscle spindle of Gastrocnemius-Soleus muscle were activated by lactate injection and exhibited increased impulse discharge through group Ia muscular afferent fibers. 2) There was latency of 7-12 seconds before muscle spindle is activated by lactate injection. But the whole response was not dose related. 3) The response pattern after lactate injection was divided into three groups which were excitation, inhibition and inhibition with preceding excitation. 4) Some responses were similar to those of bradykinin, sympathetic stimulation (adrenaline injection) and succinylcholine injection. 5) It was suggested that muscle spindle has characteristics of polymodal receptor which has responses to not only mechanical stimulation but also chemical stimulation.
Animals ; Bradykinin ; Cats ; Lactic Acid ; Laminectomy ; Muscle Spindles ; Spinal Cord ; Spinal Nerve Roots ; Stimulation, Chemical ; Succinylcholine

OBJECTIVE: To evaluate the basophil histamine releasability in response to IgE- and non- IgE-mediated stimuli in children with atopic asthma. Met: Basophil histamine releasability was measured in Dermatophagoides farinae (D. farinae)-sensitive atopic asthmatics, D.farinae-sensitive healthy atopics, non-atopic asthmatics, and healthy non-atopics. Basophils were stimulated with D.farinae, goat antihuman IgE antibody, formyl-Met-Leu-Phe(fMLP), and Calcium ionophore A23187. Histamine was measured by automated fluorometric technique. RESULTS: Sponianeous histamine release was higher in atopic asthmatics compared to healthy non-atopics. Histamine release by D.farinae and by anti-IgE antibody was higher in atopic asthmatics compared to the other groups. There was no difference in histamine release by fMLP among all groups. Histamine release by Calcium ionophore was higher in healthy atopics and non-atopic asthmatics compared to healthy non-atopics. The atopics showed correlation between histamine release by D.farinae, by anti-IgE antibody and total serum IgE levels. CONCLUSIONS: Spontaneous and IgE-mediated histamine release were related to the presence of both atopy and asthma, whereas non-IgE mediated histamine release was different depending on the stimuli.
Asthma* ; Basophils* ; Calcimycin ; Calcium ; Child* ; Dermatophagoides farinae ; Goats ; Histamine Release ; Histamine* ; Humans ; Immunoglobulin E

Joints ; Mandible ; Maxilla ; Orthognathic Surgery ; Recurrence ; Skull

BACKGROUND: Through a genome-wide search using the genetic markers(RFLP genetic markers), the familial hypertrophic cardiomyopathy(FHCM) with an autosomal dominant mode of inheritance has been firstly detected to be genetically linked to chromosome 14q1. The subsequent studies have shown that the point mutations at the exons encoding for the head and head /rod junction of the cardiac beta myosin heavy chain(beta-MHC) are the most frequent type of mutation in the FHCM families genetically implicated with a linkage to beta-MHC, whereas the alpha/beta-MHC hybrid gene and a large deletion at the 3' region of beta-MHC gene were also rarely detected. With the other families genetically implicated with the chromosomes 1,11,15,16 and 18, FHCM also manifests locus heterogeneity, a phenomenon in which abnormalities at different genes are involved in different families. In addition, a korean FHCM family with 403Arg-->Gln mutation of beta-MHC gene has been previously found by an american research group. METHODS: For clinical diagnosis, echocardiography and electrocardiography were performed on the individual members of a korean FHCM family. The microsatellite markers(MYO-I,MYO-II) located in the beta-MHC gene region were amplified by PCR(polymerase chain reaction) and the polymorphism was analyzed for the possible linkage to the phenotypic expression of FHCM. Independently, the same PCR products of the exons 13 and 23 were digested with the specific restriction enzymes for the presence of the most frequently reported point mutations of beta-MHC gene (403 and 908 amino acid mutations). Single strand conformation polymorphism(SSCP) of the exon 13 and 23 of the beta-MHC gene was also analyzed of the mobility shift expected if any point mutation is present at these two exons. RESULTS: The inheritance pattern of HCM(hypertrophic cardiomyopathy) in the family is considered as autosomal dominant. In this family(KU 101), one of the microsatellite markers(MYO-II) indicated the possible cosegregation between the allele was also present in the 32-year-old brother of the proband, who reveals no clinical signs of the disease. The other microsatellite genetic marker(MYO-I) was uninformative, without giving the discriminating power to verify the linkage to beta-MHC gene. In the analysis for two common mutations of beta-MHC gene by PCR-RFLP and PCR-SSCP, no evidence was found for 403 and 908 amino acid mutations and any point mutation in the exons 13 and 23. CONCLUSIONS: Based on the linkage analysis using microsatellite genetic markers, there was a possibility that the disease could be linked to an abnormality in the beta-MHC gene of the chromosome 14q1.
Adult ; Alleles ; Cardiomyopathy, Hypertrophic, Familial* ; Diagnosis ; Echocardiography ; Electrocardiography ; Exons ; Genetic Markers ; Head ; Humans ; Inheritance Patterns ; Mass Screening* ; Microsatellite Repeats ; Point Mutation ; Polymerase Chain Reaction ; Population Characteristics ; Siblings ; Ventricular Myosins* ; Wills

BACKGROUND: Through a genome-wide search using the genetic markers(RFLP genetic markers), the familial hypertrophic cardiomyopathy(FHCM) with an autosomal dominant mode of inheritance has been firstly detected to be genetically linked to chromosome 14q1. The subsequent studies have shown that the point mutations at the exons encoding for the head and head /rod junction of the cardiac beta myosin heavy chain(beta-MHC) are the most frequent type of mutation in the FHCM families genetically implicated with a linkage to beta-MHC, whereas the alpha/beta-MHC hybrid gene and a large deletion at the 3' region of beta-MHC gene were also rarely detected. With the other families genetically implicated with the chromosomes 1,11,15,16 and 18, FHCM also manifests locus heterogeneity, a phenomenon in which abnormalities at different genes are involved in different families. In addition, a korean FHCM family with 403Arg-->Gln mutation of beta-MHC gene has been previously found by an american research group. METHODS: For clinical diagnosis, echocardiography and electrocardiography were performed on the individual members of a korean FHCM family. The microsatellite markers(MYO-I,MYO-II) located in the beta-MHC gene region were amplified by PCR(polymerase chain reaction) and the polymorphism was analyzed for the possible linkage to the phenotypic expression of FHCM. Independently, the same PCR products of the exons 13 and 23 were digested with the specific restriction enzymes for the presence of the most frequently reported point mutations of beta-MHC gene (403 and 908 amino acid mutations). Single strand conformation polymorphism(SSCP) of the exon 13 and 23 of the beta-MHC gene was also analyzed of the mobility shift expected if any point mutation is present at these two exons. RESULTS: The inheritance pattern of HCM(hypertrophic cardiomyopathy) in the family is considered as autosomal dominant. In this family(KU 101), one of the microsatellite markers(MYO-II) indicated the possible cosegregation between the allele was also present in the 32-year-old brother of the proband, who reveals no clinical signs of the disease. The other microsatellite genetic marker(MYO-I) was uninformative, without giving the discriminating power to verify the linkage to beta-MHC gene. In the analysis for two common mutations of beta-MHC gene by PCR-RFLP and PCR-SSCP, no evidence was found for 403 and 908 amino acid mutations and any point mutation in the exons 13 and 23. CONCLUSIONS: Based on the linkage analysis using microsatellite genetic markers, there was a possibility that the disease could be linked to an abnormality in the beta-MHC gene of the chromosome 14q1.
Adult ; Alleles ; Cardiomyopathy, Hypertrophic, Familial* ; Diagnosis ; Echocardiography ; Electrocardiography ; Exons ; Genetic Markers ; Head ; Humans ; Inheritance Patterns ; Mass Screening* ; Microsatellite Repeats ; Point Mutation ; Polymerase Chain Reaction ; Population Characteristics ; Siblings ; Ventricular Myosins* ; Wills