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Tibial intramedullary canal axis and its influence on the intramedullary alignment system entry point in Koreans.

Dai Soon KWAK ; Chang Whan HAN ; Seung Ho HAN

Anatomy & Cell Biology.2010;43(3):260-267. doi:10.5115/acb.2010.43.3.260

Using computerized tomographic data and three dimensional model, we studied the influence of tibial intramedullary canal axis and other morphologic factors of the tibia on the entry point for tibial intramedullary alignment guides. Various anatomical parameters including tibial anteroposterior dimensions (AP), mediolateral dimensions (ML), aspect ratio (ML/AP), bowing and the intramedullary canal axis were studied. In addition, the entry point for the intramedullary alignment guide for primary and revision total knee arthroplasty were studied. The averaged entry point at the level of the tibial plateau was 5.7+/-2.2 mm anterior and 4.3+/-2.0 mm lateral to the classical entry point (P<.001). Furthermore, this entry point was more anterolateral in females when compared to males (P<.001). At a depth 10 mm below the tibial plateau, the entry point was on average 8.8+/-1.9 mm anterior and 2.9+/-1.9 mm lateral to the center of the cut surface. With increasing tibial varus the entry point tended to shift laterally at both levels (r=0.49) (P<.001). In Korean, the entry point for tibial intramedullary alignment systems is anterolateral to the classically described entry point. Moreover, the increment of tibial varus necessitates more lateral placement of the entry point. Intraoperatively, the entry point can be localized during primary knee arthroplasty to a point 15.9+/-2.8 mm anterior to and 1.2+/-2.8 mm lateral to the lateral tibial spine. For revision knee arthroplasty the point is on average 8.8+/-1.9 mm anterior and 2.9+/-1.9 mm lateral to the center of the cut surface of the tibia at a depth of 10 mm from the articular surface.
Arthroplasty ; Axis, Cervical Vertebra ; Female ; Humans ; Knee ; Male ; Spine ; Tibia

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Resected femoral anthropometry for design of the femoral component of the total knee prosthesis in a Korean population.

Dai Soon KWAK ; Suhyoun HAN ; Chang Whan HAN ; Seung Ho HAN

Anatomy & Cell Biology.2010;43(3):252-259. doi:10.5115/acb.2010.43.3.252

We measured the mediolateral (ML) and anteroposterior (AP) length, height and widths of the anterior, posterior and inferior section of the resected distal femurs using three dimensional computer tomographic measurements in 200 knees from 100 cadavers. We also calculated the aspect ratio (ML/AP) and compared the measured parameters with that of six conventionally used total knee femoral prostheses. We found that the average ML (70.2+/-5.5 mm) and AP (53.9+/-3.8 mm) dimensions from our study were lower than those reported from Western populations. The aspect ratio showed a progressive decline with an increasing antero-posterior dimension. All of the compared designs showed undersizing for the mediolateral dimension distally and for the widths of the resected medial and lateral posterior femoral condyles. But some of the compared designs showed oversizing for the height of the resected medial and lateral posterior femoral condyles. This study provides guidelines for designing a suitable femoral component for total knee prostheses that fit Asian populations.
Anthropometry ; Asian Continental Ancestry Group ; Cadaver ; Femur ; Humans ; Knee ; Knee Prosthesis ; Prostheses and Implants

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Migratory defect of mesencephalic dopaminergic neurons in developing reeler mice.

Woo Young KANG ; Sung Soo KIM ; Sung Kuk CHO ; Soyeon KIM ; Haeyoung SUH-KIM ; Young Don LEE

Anatomy & Cell Biology.2010;43(3):241-251. doi:10.5115/acb.2010.43.3.241

Reelin, an extracellular glycoprotein has an important role in the proper migration and positioning of neurons during brain development. Lack of reelin causes not only disorganized lamination of the cerebral and cerebellar cortex but also malpositioning of mesencephalic dopaminergic (mDA) neurons. However, the accurate role of reelin in the migration and positioning of mDA neurons is not fully elucidated. In this study, reelin-deficient reeler mice exhibited a significant loss of mDA neurons in the substantia nigra pars compacta (SNc) and a severe alteration of cell distribution in the retrorubal field (RRF). This abnormality was also found in Dab1-deficinet, yotari mice. Stereological analysis revealed that total number of mDA neurons was not changed compared to wild type, suggesting that the loss of mDA neurons in reeler may not be due to the neurogenesis of mDA neurons. We also found that formation of PSA-NCAM-positive tangential nerve fibers rather than radial glial fibers was greatly reduced in the early developmental stage (E14.5) of reeler. These findings provide direct evidence that the alteration in distribution pattern of mDA neurons in the reeler mesencephalon mainly results from the defect of the lateral migration using tangential fibers as a scaffold.
Animals ; Brain ; Cerebellar Cortex ; Dopaminergic Neurons ; Glycoproteins ; Mesencephalon ; Mice ; Mice, Neurologic Mutants ; Nerve Fibers ; Neurogenesis ; Neurons ; Substantia Nigra

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Regulation of endothelial nitric oxide synthase by agmatine after transient global cerebral ischemia in rat brain.

Chin Hee MUN ; Won Taek LEE ; Kyung Ah PARK ; Jong Eun LEE

Anatomy & Cell Biology.2010;43(3):230-240. doi:10.5115/acb.2010.43.3.230

Nitric oxide (NO) production by endothelial nitric oxide synthase (eNOS) plays a protective role in cerebral ischemia by maintaining vascular permeability, whereas NO derived from neuronal and inducible NOS is neurotoxic and can participate in neuronal damage occurring in ischemia. Matrix metalloproteinases (MMPs) are up-regulated by ischemic injury and degrade the basement membrane if brain vessels to promote cell death and tissue injury. We previously reported that agmatine, synthesized from L-arginine by arginine decarboxylase (ADC) which is expressed in endothelial cells, has shown a direct increased eNOS expression and decreased MMPs expression in bEnd3 cells. But, there are few reports about the regulation of eNOS by agmatine in ischemic animal model. In the present study, we examined the expression of eNOS and MMPs by agmatine treatment after transient global ischemia in vivo. Global ischemia was induced with four vessel occlusion (4-VO) and agmatine (100 mg/kg) was administered intraperitoneally at the onset of reperfusion. The animals were euthanized at 6 and 24 hours after global ischemia and prepared for other analysis. Global ischemia led severe neuronal damage in the rat hippocampus and cerebral cortex, but agmatine treatment protected neurons from ischemic injury. Moreover, the level and expression of eNOS was increased by agmatine treatment, whereas inducible NOS (iNOS) and MMP-9 protein expressions were decreased in the brain. These results suggest that agmatine protects microvessels in the brain by activation eNOS as well as reduces extracellular matrix degradation during the early phase of ischemic insult.
Agmatine ; Animals ; Arginine ; Basement Membrane ; Brain ; Brain Ischemia ; Capillary Permeability ; Carboxy-Lyases ; Cell Death ; Cerebral Cortex ; Endothelial Cells ; Extracellular Matrix ; Glycosaminoglycans ; Hippocampus ; Ischemia ; Matrix Metalloproteinases ; Microvessels ; Models, Animal ; Neurons ; Nitric Oxide ; Nitric Oxide Synthase Type III ; Rats ; Reperfusion

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Changes in transcript and protein levels of calbindin D28k, calretinin and parvalbumin, and numbers of neuronal populations expressing these proteins in an ischemia model of rat retina.

Shin Ae KIM ; Ji Hyun JEON ; Min Jeong SON ; Jiook CHA ; Myung Hoon CHUN ; In Beom KIM

Anatomy & Cell Biology.2010;43(3):218-229. doi:10.5115/acb.2010.43.3.218

Excessive calcium is thought to be a critical step in various neurodegenerative processes including ischemia. Calbindin D28k (CB), calretinin (CR), and parvalbumin (PV), members of the EF-hand calcium-binding protein family, are thought to play a neuroprotective role in various pathologic conditions by serving as a buffer against excessive calcium. The expression of CB, PV and CR in the ischemic rat retina induced by increasing intraocular pressure was investigated at the transcript and protein levels, by means of the quantitative real-time reverse transcription-polymerase chain reaction, western blot and immunohistochemistry. The transcript and protein levels of CB, which is strongly expressed in the horizontal cells in both normal and affected retinas, were not changed significantly and the number of CB-expressing horizontal cells remained unchanged throughout the experimental period 8 weeks after ischemia/reperfusion injury. At both the transcript and protein levels, however, CR, which is strongly expressed in several types of amacrine, ganglion, and displaced amacrine cells in both normal and affected retinas, was decreased. CR-expressing ganglion cell number was particularly decreased in ischemic retinas. Similar to the CR, PV transcript and protein levels, and PV-expressing AII amacrine cell number were decreased. Interestingly, in ischemic retinas PV was transiently expressed in putative cone bipolar cell types possibly those that connect with AII amacrine cells via gap junctions. These results suggest that these three calcium binding proteins may play different neuroprotective roles in ischemic insult by their ability to buffer calcium in the rat retina.
Amacrine Cells ; Animals ; Blotting, Western ; Calcium ; Calcium-Binding Protein, Vitamin D-Dependent ; Calcium-Binding Proteins ; Cell Count ; Ganglion Cysts ; Gap Junctions ; Humans ; Immunohistochemistry ; Intraocular Pressure ; Ischemia ; Neurons ; Proteins ; Rats ; Retina

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Differential regulation of Purkinje cell dendritic spines in rolling mouse Nagoya (tg(rol)/tg(rol)), P/Q type calcium channel (alpha1(A)/Ca(v)2.1) mutant.

Sen Ich ODA ; Kea Joo LEE ; Tatsuo ARII ; Keiji IMOTO ; Byung Hwa HYUN ; In Sung PARK ; Hyun KIM ; Im Joo RHYU

Anatomy & Cell Biology.2010;43(3):211-217. doi:10.5115/acb.2010.43.3.211

Voltage dependent calcium channels (VDCC) participate in regulation of neuronal Ca2+. The Rolling mouse Nagoya (Cacna1a(tg-rol) ) is a spontaneous P/Q type VDCC mutant, which has been suggested as an animal model for some human neurological diseases such as autosomal dominant cerebellar ataxia (SCA6), familial hemiplegic migraine and episodic ataxia type-2. Morphology of Purkinje cell (PC) dendritic spine is suggested to be regulated by signal molecules such as Ca2+ and by interactions with afferent inputs. The amplitude of excitatory postsynaptic current was decreased in parallel fiber (PF) to PC synapses, whereas apparently increased in climbing fiber (CF) to PC synapses in rolling mice Nagoya. We have studied synaptic morphology changes in cerebella of this mutant strain. We previously found altered synapses between PF varicosity and PC dendritic spines. To study dendritic spine plasticity of PC in the condition of insufficient P/Q type VDCC function, we used high voltage electron microscopy (HVEM). We measured the density and length of PC dendritic spines at tertiary braches. We observed statistically a significant decrease in spine density as well as shorter spine length in rolling mice compared to wild type mice at tertiary dendritic braches. In proximal PC dendrites, however, there were more numerous dendritic spines in rolling mice Nagoya. The differential regulation of rolling PC spines at tertiary and proximal dendrites in rolling mice Nagoya suggests that two major excitatory afferent systems may be regulated reciprocally in the cerebellum of rolling mouse Nagoya.
Animals ; Ataxia ; Calcium ; Calcium Channels ; Cerebellar Ataxia ; Cerebellum ; Dendrites ; Dendritic Spines ; Excitatory Postsynaptic Potentials ; Humans ; Mice ; Microscopy, Electron ; Migraine with Aura ; Models, Animal ; Neurons ; Plastics ; Spine ; Sprains and Strains ; Synapses

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Combined actions of Na+/K+-ATPase, NCX1 and glutamate dependent NMDA receptors in ischemic rat brain penumbra.

Sungjin PARK ; Yongwook JUNG

Anatomy & Cell Biology.2010;43(3):201-210. doi:10.5115/acb.2010.43.3.201

Instrumental role of Na+ and Ca2+ influx via Na+/K+ adenosine triphosphatase (Na+/K+-ATPase) and Na+/Ca2+ exchanger 1 (NCX1) is examined in the N-Methyl-D-aspartate (NMDA) receptor-mediated pathogenesis of penumbra after focal cerebral ischemia. An experimental model of 3, 6, and 24 h focal cerebral ischemia by permanent occlusion of middle cerebral artery was developed in rats. The changes in protein expression of Na+/K+-ATPase and NCX1 as well as functional subunits of NMDA receptor 2A and 2B (NR2A and NR2B) in the penumbra were assessed using by quantitative immunoblottings. The most prominent changes of Na+/K+-ATPase (78+/-6%, n=4, *P<0.05) and NCX1 (144+/-2%, n=4, *P<0.05) in the penumbra were developed 24 h after focal cerebral ischemia. The expression of NR2A in the penumbra was significantly increased (153+/-9%, n=4, *P<0.05) whereas the expression of NR2B was significantly decreased (37+/-2%, n=4, *P<0.05) as compared with sham-operated controls 3 h after focal cerebral ischemia. However, the expression of NR2A and NR2B in the penumbra was reversed 24 h after focal cerebral ischemia (NR2A: 40+/-7%; NR2B: 120+/-16%, n=4, *P<0.05). Moreover, the decreased expression of neuronal nuclei (NeuN) in the penumbra was most prominent than that of glial fibrillary acidic protein (GFAP) 24 h after focal cerebral ischemia. These findings imply that intracellular Na+ accumulation via decreased Na+/K+-ATPase exacerbate the Ca2+ overload cooperated by the increased NCX1 and NR2B-containing NMDA receptor which may play an important role in the pathogenesis of the penumbra.
Adenosine Triphosphatases ; Animals ; Brain ; Brain Ischemia ; Glial Fibrillary Acidic Protein ; Glutamic Acid ; Immunoblotting ; Middle Cerebral Artery ; Models, Theoretical ; N-Methylaspartate ; Neurons ; Rats ; Receptors, N-Methyl-D-Aspartate

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Ethanol down regulates the expression of myelin proteolipid protein in the rat hippocampus.

Dong Hoon LEE ; Jin Young JEONG ; Yoon Sook KIM ; Joon Soo KIM ; Yong Woon CHO ; Gu Seob ROH ; Hyun Joon KIM ; Sang Soo KANG ; Gyeong Jae CHO ; Wan Sung CHOI

Anatomy & Cell Biology.2010;43(3):194-200. doi:10.5115/acb.2010.43.3.194

It is well known that chronic ethanol treatment affects the synthesis of RNA and protein in the brain and the maintenance and function of nervous system. The changes in myelination-related genes are most prominent in human alcoholics. Previously, our cDNA microarray study showed altered Proteolipid protein (PLP), a major protein of central myelin. The present study aimed to gain more understanding of the expression of PLP after chronic ethanol treatment. Male Sprague-Dawley rats were daily treated with ethanol (15% in saline, 3 g/kg, i.p.) or saline for 14 days. Messenger RNAs from hippocampus of each group were subjected to cDNA expression array hybridization to determine the differential gene expressions. Among many ethanol responsive genes, PLP was negatively regulated by ethanol treatment, which is one of the most abundant proteins in the CNS and has an important role in the stabilization of myelin sheath. Using northern blot and immunohistochemical analysis, we showed the change in expression level of PLP mRNA and protein after ethanol treatment. PLP mRNA and protein were decreased in hippocampus of rat with chronic ethanol exposure, suggesting that ethanol may affect the stabilization of myelin sheath through the modulation of PLP expression and induce the pathophysiology of alcoholic brain.
Alcoholics ; Animals ; Blotting, Northern ; Brain ; Chimera ; DNA, Complementary ; Ethanol ; Gene Expression ; Hippocampus ; Humans ; Male ; Myelin Proteolipid Protein ; Myelin Sheath ; Nervous System ; Oligonucleotide Array Sequence Analysis ; Proteins ; Rats ; Rats, Sprague-Dawley ; RNA ; RNA, Messenger

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Effects of hypothyroidism on cell proliferation and neuroblasts in the hippocampal dentate gyrus in a rat model of type 2 diabetes.

Sun Shin YI ; In Koo HWANG ; Ji Won CHOI ; Moo Ho WON ; Je Kyung SEONG ; Yeo Sung YOON

Anatomy & Cell Biology.2010;43(3):185-193. doi:10.5115/acb.2010.43.3.185

We observed how the hypothyroid state affects diabetic states and modifies cell proliferation and neuroblast differentiation in the hippocampal dentate gyrus (DG). For this, 0.03% methimazole, an anti-thyroid drug, was administered to 7-week-old, pre-diabetic Zucker diabetic fatty (ZDF) rats by drinking water for 5 weeks, and the animals were sacrificed at 12 weeks of age. At this age, corticosterone levels were significantly increased in the ZDF rats compared to those in the control (Zucker lean control, ZLC) rats. Methimazole (methi) treatment in the ZDF rats (ZDF-methi rats) significantly decreased corticosterone levels and diabetes-induced hypertrophy of adrenal glands. In the DG, Ki67 (a marker for cell proliferation)- and doublecortin (DCX, a marker for neuronal progenitors)-immunoreactive cells were much lower in the ZDF rats than those in the ZLC rats. However, in ZDF-methi rats, numbers of Ki67- and DCX-immunoreactive cells were similar to those in the ZLC rats. These suggest that methi significantly reduces diabetes-induced hypertrophy of the adrenal gland and alleviates the diabetes-induced reduction of cell proliferation and neuronal progenitors in the DG.
Adrenal Glands ; Animals ; Cell Proliferation ; Corticosterone ; Dentate Gyrus ; Drinking Water ; Hypertrophy ; Hypothyroidism ; Methimazole ; Neurons ; Rats

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PINK1 and Parkin to control mitochondria remodeling.

Hyongjong KOH ; Jongkyeong CHUNG

Anatomy & Cell Biology.2010;43(3):179-184. doi:10.5115/acb.2010.43.3.179

Parkinson's disease (PD), one of the most common neurodegenerative diseases, is characterized by movement disorders and a loss of dopaminergic (DA) neurons. PD mainly occurs sporadically, but may also result from genetic mutations in several PD-linked genes. Recently, genetic studies with Drosophila mutants, parkin and PINK1, two common PD-associated genes, demonstrated that Parkin acts downstream of PINK1 in maintaining mitochondrial function and integrity. Further studies revealed that PINK1 translocates Parkin to mitochondria and regulates critical mitochondrial remodeling processes. These findings, which suggest that mitochondrial dysfunction is a prominent cause of PD pathogenesis, provide valuable insights which may aid in the development of effective treatments for PD.
Drosophila ; Mitochondria ; Movement Disorders ; Neurodegenerative Diseases ; Neurons ; Parkinson Disease

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