Palm creases are helpful in revealing anthropologic characteristics and diagnosing chromosomal aberrations, and have been analyzed qualitatively and quantitatively. However, previous methods of analyzing palm creases were not objective so that reproducibility could not be guaranteed. In this study, a more objective morphologic analysis of palm creases was developed. The features of the improved methods include the strict definition of major and minor palm creases and the systematic classification of major palm creases based on their relationships, branches, and variants. Furthermore, based on the analysis of 3,216 Koreans, palm creases were anthropologically interpreted. There was a tendency for palm creases to be evenly distributed on the palm, which was acknowledged by the relationship between major and minor creases as well as by the incidences of major creases types. This tendency was consistent with the role of palm creases to facilitate folding of palm skin. The union of major palm creases was frequent in males and right palms to have powerful hand grip. The new method of analyzing palm creases is expected to be widely used for anthropologic investigation and chromosomal diagnosis.
Anthropology, Physical ; Chromosome Aberrations ; Dermatoglyphics ; Hand ; Hand Strength ; Humans ; Incidence ; Male ; Skin

The aim of this study was to delineate the shape of the popliteus muscle and determine the correct motor point site for treating spasticity. A total of 22 legs from 13 fresh Korean cadavers were evaluated. The x-axis was set as a transverse line across the lateral and medial epicondyle of the femur and the y-axis as a vertical line at the midpoint of the medial malleolus of the tibia and lateral malleolus of the fibula. The popliteus muscle is an obtuse triangle in shape. Superior, medial, and inferior angles were 27.2+/-4.3degrees, 114.8+/-19.8degrees, and 38.0+/-18.8degrees respectively. The lengths of the superior, medial, and lateral sides of the triangle were 7.6+/-1.0 cm, 6.2+/-1.0 cm, and 11.9+/-1.5 cm respectively. Nerve branches ran superficially on the periosteum of the tibia and entered the popliteus on its superficial surface. The diverging point of the nerve branch entered the popliteus from the tibial nerve located at the midline of the popliteal fossa and 17% of the leg length above the intercondylar line. Most nerve entry points (83.3%) were within a 2.0x3.0 cm rectangle with the center located at -1.0 cm (-7%) on the x-axis and -3.3 cm (-9%) on the y-axis.
Cadaver ; Denervation ; Femur ; Fibula ; Leg ; Muscle Spasticity ; Muscles ; Periosteum ; Tibia ; Tibial Nerve

Selective labeling of small populations of neurons of a given phenotype for conventional neuronal tracing is difficult because tracers can be taken up by all neurons at the injection site, resulting in nonspecific labeling of unrelated pathways. To overcome these problems, genetic approaches have been developed that introduce tracer proteins as transgenes under the control of cell-type-specific promoter elements for visualization of specific neuronal pathways. The aim of this study was to explore the use of tracer gene expression for neuroanatomical tracing to chart the complex interconnections of the central nervous system. Genetic tracing methods allow for expression of tracer molecules using cell-type-specific promoters to facilitate neuronal tracing. In this study, the rat tyrosine hydroxylase (TH) promoter and an adenoviral delivery system were used to express tracers specifically in dopaminergic and noradrenergic neurons. Region-specific expression of the transgenes was then analyzed. Initially, we characterized cell-type-specific expression of GFP or RFP in cultured cell lines. We then injected an adenovirus carrying the tracer transgene into several brain regions using a stereotaxic apparatus. Three days after injection, strong GFP expression was observed in the injected site of the brain. RFP and WGA were expressed in a cell-type-specific manner in the cerebellum, locus coeruleus, and ventral tegmental regions. Our results demonstrate that selective tracing of catecholaminergic neuronal circuits is possible in the rat brain using the TH promoter and adenoviral expression.
Adenoviridae ; Adrenergic Neurons ; Animals ; Brain ; Cells, Cultured ; Central Nervous System ; Cerebellum ; Gene Expression ; Lifting ; Locus Coeruleus ; Neurons ; Phenotype ; Proteins ; Rats ; Transgenes ; Tyrosine 3-Monooxygenase

Oxidative stress-induced cell death leads to phosphorylation of 14-3-3zeta at serine 58. 14-3-3zeta is detected at significant levels in cerebrospinal fluid after kainic acid (KA)-induced seizures. Here we examined temporal changes in 14-3-3zeta phosphorylation in the hippocampus and amygdala of mice after KA treatment. Mice were killed at 2, 6, 24, or 48 h after KA (30 mg/kg) injection. We observed an increase in TUNEL and Fluoro-Jade B (FJB)-stained neurons in the hippocampus and amygdala of KA-treated mice. Phospho (p)-14-3-3zeta and p-JNK expression was increased in the hippocampus 2 and 6 h after KA treatment, respectively. In immunohistochemical analysis, p-14-3-3zeta-positive cells were present in the CA3 region of the hippocampus and the central nucleus of amygdala (CeA) of KA-treated mice. Thus, phosphorylation of 14-3-3zeta at serine 58 may play an important role in KA-induced hippocampal and amygdaloid neuronal damage.
Amygdala ; Animals ; Cell Death ; Fluoresceins ; Hippocampus ; In Situ Nick-End Labeling ; Kainic Acid ; Mice ; Neurons ; Phosphorylation ; Seizures ; Serine

Erythropoietin (EPO) has been demonstrated the ability of recombinant human erythropoietin (r-Hu-EPO), when administered intracerebro-ventricularly, to improve stroke outcome through the reduction of stroke damage. In a brain ischemic model, however, systemic administration of r-Hu-EPO has not been intensely investigated given that in general, large glycosylated molecules have been deemed incapable of crossing the blood-brain barrier. In this study, administration of r-Hu-EPO for 4 days, intraperitoneally after ischemia-reperfusion (I-R) increased the number of bromodeoxyuridine (BrdU)-positive cells in the penumbra (10.1+/-1.4, n=5, P<0.05) and in the subventricular zone (SVZ) of the lateral ventricle (LV) (25+/-2.7, n=5, P<0.05) as compared with those of I-R (penumbra: 2.5+/-0.7; SVZ of LV: 3.8+/-1.5). A significant increase of BrdU-positive cells in these areas was coincident with a strong immunoreactivity of oligodendrocyte progenitor cell marker (2', 3'-cyclic nucleotide 3'-phosphodiesterase). Furthermore, r-Hu-EPO administration increased the number of BrdU-positive cells in the choroid plexus (7.8+/-2.3, n=5, P<0.05) and in cerebral blood vessels (3.5+/-1.3, n=5, P<0.05) when compared with those of I-R (choroid plexus: 1.2+/-0.5; cerebral blood vessels: 0.6+/-0.1). These results suggest that, even when systemically administered, r-Hu-EPO may have therapeutic potential for stroke via the proliferation of oligodendroglial and endothelial progenitor cells.
Animals ; Blood Vessels ; Blood-Brain Barrier ; Brain ; Brain Ischemia ; Bromodeoxyuridine ; Choroid Plexus ; Erythropoietin ; Humans ; Lateral Ventricles ; Oligodendroglia ; Rats ; Stem Cells ; Stroke

Our previous research demonstrated that calponin-immunoreactivity was localized in myofibroblasts of the periglomerular region of human kidney specimens obtained at the time of transplantation from organ recipients. In the present study we examined calponin expression in two chronic nephropathy models, puromycin aminonucleoside (PAN) nephropathy and subtotal nephrectomy (SNx), to investigate the role of calponin in chronic renal injury. Male Sprague-Dawley rats were used, and both nephropathy models were established at 1, 2, 4, and 8 weeks after surgery. There were no periglomerular calponin-positive cells in sham, PAN 1 and 2 week, and SNx 1, 2, and 4 week groups. In SNx 8 week and PAN 4 and 8 week groups, only a few glomeruli with periglomerular calponin-reactivity, which covered half or a very small part of the periglomerular space, were observed. All glomeruli with periglomerular calponin-reactivity showed sclerotic changes, especially thickening of parietal epithelial cells (PECs). In conjunction with our previous report, this data represents the first documentation of the expression of calponin in renal myofibroblasts. We suggest that interactions between PECs and calponin-positive myofibroblasts may play a key role in the late stage of glomerulosclerosis.
Animals ; Calcium-Binding Proteins ; Epithelial Cells ; Humans ; Immunohistochemistry ; Kidney ; Kidney Failure, Chronic ; Male ; Microfilament Proteins ; Myofibroblasts ; Nephrectomy ; Puromycin Aminonucleoside ; Rats ; Rats, Sprague-Dawley ; Salicylamides ; Transplants

Nitric oxide is one of many proinflammatory mediators that are involved in temporomandibular joint (TMJ) inflammatory disorder and is synthesized by inducible nitric oxide synthase (iNOS). iNOS is transcriptionally regulated by nuclear factor-kappaB (NF-kappaB) in cases of inflammation, proliferation, and apoptosis. It has also been reported that nitric oxide is positively regulated by carrageenan and negatively regulated by hyaluronan in the knee joint. The aim of this study was to histologically evaluate how inflammation and cell proliferation of the synovial membrane are affected by the exogenous administration of carrageenan and hyaluronan in the rat TMJ by investigating iNOS, NF-kappaB, and anti proliferating cell nuclear antigen (PCNA) immunoreactivity. As results, immunoreactive cells to iNOS, NF-kappaB, and PCNA were normally localized only in the synovial membrane of wild type TMJs. The numbers of immunoreactive cells were extensively larger in the carrageenan-injected synovial membranes exhibiting excessive folding, and smaller in the hyaluronan-injected synovial membranes showing a few folds. These results indicate that a carrageenan injection induced inflammation and cell proliferation especially in the synovial membrane and that hyaluronan relieved the inflammation by decreasing inflammatory molecules in the synovial membrane.
Animals ; Apoptosis ; Carrageenan ; Cell Proliferation ; Hyaluronic Acid ; Inflammation ; Knee Joint ; NF-kappa B ; Nitric Oxide ; Nitric Oxide Synthase Type II ; Proliferating Cell Nuclear Antigen ; Rats ; Synovial Membrane ; Synovitis ; Temporomandibular Joint

In order to study the treatment of aneurysms, the technique of making experimental aneurysms in laboratory animals must be established. In our study, to examine the feasibility of making experimental aneurysm and selective angiography on the common carotid artery in rabbits and to determine the size of experimental aneurysm after surgery, saccular aneurysms were fashioned on the right common carotid artery in 17 rabbits using a vein pouch technique. Selective angiography of the common carotid artery was performed immediately after surgery, and at 1 week, 4 weeks, and 8 weeks after surgery. Also, histological changes in the aneurysms were observed. In 16 rabbits with established successful experimental aneurysm, no differences were found in diet intake and behavior before and after surgery. The patency of the carotid artery was confirmed by selective angiography. The average size of the aneurysm immediately after surgery was similar to that of 1 week postoperatively in selective angiography, however it increased with time at 4weeks and 8 weeks. Histologically, infiltration of inflammatory cells and hemorrhage were found at the junction of the carotid artery and the vein pouch at 1 week, which disappeared at 4 weeks and 8 weeks. This study suggests experimental saccular aneurysm using the vein pouch technique might form aneurysms similar to that of the human in its properties such as increment of size, and selective angiography might be suitable for assessment of experimental aneurysm. Therefore, this animal model may be suitable for investigating new treatment methodologies for human aneurysms.
Aneurysm ; Angiography ; Animals, Laboratory ; Carotid Arteries ; Carotid Artery, Common ; Diet ; Hemorrhage ; Humans ; Models, Animal ; Rabbits ; Veins

Intrahepatic cholangiocarcinoma is the second most common subtype of primary hepatobilliary cancer. Despite advances in surgical and medical therapy, its survival rate remains poor. Compared to hepatocellular carcinoma (HCC), the most common liver malignancy, the underlying mechanisms of cholangiocarcinoma carcinogenesis are poorly characterized. P-cadherin (CDH3) is a cadherin super family member. Although CDH3 is frequently over-expressed in cholangiocarcinoma tissues, its roles have never been characterized. To determine the roles of CDH3 in cholangiocarcinoma, we investigated CDH3 function in HuCCT1 cells using specific siRNA. Transfection with CDH3 siRNA did not affect proliferation of HuCCT1 cells. However, cell migration and invasion were significantly reduced when CDH3 was down-regulated. In addition, expressions of several biomarkers for epithelial-mesenchymal transition (EMT) were not changed by CDH3 down-regulation. These results suggest that CDH3 regulates cell migration independent of EMT in cholangiocarcinoma cells.
Biomarkers ; Cadherins ; Carcinoma, Hepatocellular ; Cell Movement ; Cholangiocarcinoma ; Down-Regulation ; Epithelial-Mesenchymal Transition ; Humans ; Liver ; Liver Neoplasms ; RNA, Small Interfering ; Survival Rate ; Transfection ; Cholangiocarcinoma

Mitochondria are subcellular organelles composed of two discrete membranes in the cytoplasm of eukaryotic cells. They have long been recognized as the generators of energy for the cell and also have been known to associate with several metabolic pathways that are crucial for cellular function. Mitochondria have their own genome, mitochondrial DNA (mtDNA), that is completely separated and independent from the much larger nuclear genome, and even have their own system for making proteins from the genes in this mtDNA genome. The human mtDNA is a small (~16.5 kb) circular DNA and defects in this genome can cause a wide range of inherited human diseases. Despite of the significant advances in discovering the mtDNA defects, however, there are currently no effective therapies for these clinically devastating diseases due to the lack of technology for introducing specific modifications into the mitochondrial genomes and for generating accurate mtDNA disease models. The ability to engineer the mitochondrial genomes would provide a powerful tool to create mutants with which many crucial experiments can be performed in the basic mammalian mitochondrial genetic studies as well as in the treatment of human mtDNA diseases. In this review we summarize the current approaches associated with the correction of mtDNA mutations in cells and describe our own efforts for introducing engineered mtDNA constructs into the mitochondria of living cells through bacterial conjugation.
Conjugation, Genetic ; Cytoplasm ; DNA ; DNA, Circular ; DNA, Mitochondrial ; Eukaryotic Cells ; Genome ; Genome, Mitochondrial ; Humans ; Membranes ; Metabolic Networks and Pathways ; Mitochondria ; Organelles ; Proteins