• Journal of Korean Neurosurgical Society
• /
• v.59 no.5
• /
• pp.492-497
• /
• 2016

Objective : Decompressive craniectomy is an effective therapy to relieve high intracranial pressure after acute brain damage. However, the optimal timing for cranioplasty after decompression is still controversial. Many authors reported that early cranioplasty may contribute to improve the cerebral blood flow and brain metabolism. However, despite all the advantages, there always remains a concern that early cranioplasty may increase the chance of infection. The purpose of this retrospective study is to investigate whether the early cranioplasty increase the infection rate. We also evaluated the risk factors of infection following cranioplasty. Methods : We retrospectively examined the results of 131 patients who underwent cranioplasty in our institution between January 2008 and June 2015. We divided them into early (${\leq}90days$) and late (>90 days after craniectomy) groups. We examined the risk factors of infection after cranioplasty. We analyzed the infection rate between two groups. Results : There were more male patients (62%) than female (38%). The mean age was 49 years. Infection occurred in 17 patients (13%) after cranioplasty. The infection rate of early cranioplasty was lower than that of late cranioplasty (7% vs. 20%; p=0.02). Early cranioplasty, non-metal allograft materials, re-operation before cranioplasty and younger age were the significant factors in the infection rate after cranioplasty (p<0.05). Especially allograft was a significant risk factor of infection (odds ratio, 12.4; 95% confidence interval, 3.24-47.33; p<0.01). Younger age was also a significant risk factor of infection after cranioplasty by multivariable analysis (odds ratio, 0.96; 95% confidence interval, 0.96-0.99; p=0.02). Conclusion : Early cranioplasty did not increase the infection rate in this study. The use of non-metal allograft materials influenced a more important role in infection in cranioplasty. Actually, timing itself was not a significant risk factor in multivariate analysis. So the early cranioplasty may bring better outcomes in cognitive functions or wound without raising the infection rate.

• The Korean Journal of Nuclear Medicine
• /
• v.30 no.4
• /
• pp.570-575
• /
• 1996

For brain perfusion SPECT imaging, $^{99m}Tc$-HMPAO and $^{99m}Tc$-ECD are commonly used. Although these two tracers usually show similar distribution, it is well known that discrepant finding might be noted between $^{99m}Tc$-HMPAO and $^{99m}Tc$-ECD imaging in some conditions. Luxury perfusion(perfusion/metabolism mismatch) is one of the examples and could be observed in subacute cerebral infarction. We report a case of subacute cerebral infarction that revealed luxury perfusion. Increased perfusion was found in $^{99m}Tc$-HMPAO SPECT and perfusion defect was found in $^{99m}Tc$-ECD SPECT. We found large area of mismatch with a consecutive acquisition-subtraction method. Crossed cerebellar diaschisis was observed in both SPECT images.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.22 no.6
• /
• pp.692-701
• /
• 1993

This study was designed to examine effects of the various levels of sardine and safflower oil mix on lipid contents of serveral tissues in dietary hyperlipidemic rats. Experimental oils were 16% butter(control group), 8% butter+8% olive oil(group 2), 8% butter+8% sardine oil(group 3), 8% butter+6% sardine oil+2% safflower oil(group 4), 8% butter+4% sardine oil+4% safflower oil(group 5), 8% butter+2% sardine oil+6% safflower oil(group 6) and 8% butter+8% safflower oil(group 7). The diet administered to the male rats of Sprague-Dawley were fed for 4 weeks. In the fatty aicd composition of brain phospholipid, n-3 EPA and DHA contents were increased, and DHA content was remarkably high in the phosphatidylethanolamine(PE) component. Arachidonic acid content were high in the cardiolipin component. In the fatty acid composition of heart phospholipid, PUFA contents were highest in the group 5 and DHA content was higher in the groups 4 and 5, particularly. Fatty acid composition of spleen lipid showed that n-3 EPA and DHA contents were higher in the group 3 than in the other groups.

• Journal of Life Science
• /
• v.17 no.3 s.83
• /
• pp.305-311
• /
• 2007

Glucocorticoids (GCs) alter metabolism, synaptogenesis, apoptosis, neurogenesis, and dendritic morphology in the hippocampus. To better understand how glucocorticoids regulate these aspects of hippocampal biology, we studied gene expression patterns in the CA3 (Hippocampal pyramidal cell field CA3) and dentate gyrus (DG). Litter-matched Lewis inbred rats treated for 20 days with either 9.5 mg per day sustained-release corticosterone or placebo pellets were compared with high-density oligonucleotide microarray analysis (Rat Neurobiology U34 Arrays, Affymetrix). In placebo-treated rats, 32 genes were expressed at greater levels in CA3 than DG, whereas 3 genes were expressed at great levels in DC than CA3. Regional differences were also apparent in corticosterone-induced changes in the hippocampal transcriptome. Six genes in CA3 and 41 genes in DC were differentially regulated by corticosterone. As per the glucocorticoid effects on gene transcription in the brain, forty three of these genes were upregulated, and 4 genes were downregulated. Genes differentially expressed in hippocampus included those for 13 neurotransmitter proteins, 5 ion channel related proteins, 4 transcription factors, 3 neurotrophic factors, 1 cytokine, 1 apoptosis related protein, and 5 genes involved in synaptogenesis. Interestingly, GCs can have suppressive effects on brain BDNF mRNA transcription, one of the neurotrophic factors. These results indicate the diversity of targets affected by chronic exposure to corticosterone and highlight important regional differences in hippocampal neurobiology.

• Journal of The Korean Society of Inherited Metabolic disease
• /
• v.20 no.2
• /
• pp.37-43
• /
• 2020

Phenylketonuria is the most prevalent disorder caused by an inborn error in aminoacid metabolism. It results from mutations in the phenylalanine hydroxylase (PAH) gene. If untreated or late treated, results in profound and irreversible mental disability. Newborn screening test identify patients with phenylketouria. The early initiation of a phenylalanine restricted diet very soon prevents most of the neuropsychiatric complications. However, the diet therapy is difficult to maintain and compliance is poor, especially in adolescents and adulthood. Since 2015, American Medical College of Medical Genetics and Genomics (ACMG) recommended more strong restrictive diet therapy for target blood level of phenylalanine (<360 umol/L). For over four decades the only treatment was a very restrictive low phenylalanine diet. This changed in 2007 with the approval of cofactor therapy (Tetrahydrobiopterin, BH4) which is effective in up to 30% of patients. Data from controlled clinical trials with sapropterin dihydrochloride indicate a similar occurrence of all-cause adverse events with this treatment and placebo. Large neutral aminoacids (LNAA) competes with phenylalanine for transport across the blood-brain-barrier and have a beneficial effect on executive functioning. A new therapy has just been approved that can be effective in most patients with PAH deficiency regardless of their degree of enzyme deficiency or the severity of their phenotype. Phenylalanine ammonia lyase (PAL-PEG) was approved in the USA by FDA in May of 2018 for adult patients with uncontrolled blood phenylalanine concentrations on current treatment. Nucleic acid therapy (therapeutic mRNA or gene therapy) is likely to provide longer term solutions with few side effects.

• Korean Journal of Radiology
• /
• v.20 no.4
• /
• pp.662-670
• /
• 2019

Objective: A developmental venous anomaly (DVA) is a vascular malformation of ambiguous clinical significance. We aimed to quantify the susceptibility of draining veins (χ_vein) in DVA and determine its significance with respect to oxygen metabolism using quantitative susceptibility mapping (QSM). Materials and Methods: Brain magnetic resonance imaging of 27 consecutive patients with incidentally detected DVAs were retrospectively reviewed. Based on the presence of abnormal hyperintensity on T2-weighted images (T2WI) in the brain parenchyma adjacent to DVA, the patients were grouped into edema (E+, n = 9) and non-edema (E-, n = 18) groups. A 3T MR scanner was used to obtain fully flow-compensated gradient echo images for susceptibility-weighted imaging with source images used for QSM processing. The χ_vein was measured semi-automatically using QSM. The normalized χ_vein was also estimated. Clinical and MR measurements were compared between the E+ and E- groups using Student's t-test or Mann-Whitney U test. Correlations between the χ_vein and area of hyperintensity on T2WI and between χ_vein and diameter of the collecting veins were assessed. The correlation coefficient was also calculated using normalized veins. Results: The DVAs of the E+ group had significantly higher χ_vein (196.5 ± 27.9 vs. 167.7 ± 33.6, p = 0.036) and larger diameter of the draining veins (p = 0.006), and patients were older (p = 0.006) than those in the E- group. The χ_vein was also linearly correlated with the hyperintense area on T2WI (r = 0.633, 95% confidence interval 0.333-0.817, p < 0.001). Conclusion: DVAs with abnormal hyperintensity on T2WI have higher susceptibility values for draining veins, indicating an increased oxygen extraction fraction that might be associated with venous congestion.

• Asian-Australasian Journal of Animal Sciences
• /
• v.18 no.11
• /
• pp.1552-1556
• /
• 2005

The UCPs are members of the mitochondrial inner membrane transporter family, present in the mitochondrial inner membrane. Their main function is increasing the energy expenditure via diminishing the resulting production of ATP from mitochondrial oxidative phosphorylation instead of yielding dissipative heat. They are associated with the metabolism of fat and regulation of energy expenditure. The UCP gene can be viewed as the candidate gene for chicken fatness. In the present study, RT-PCR and Northern Blot methods were developed to investigate the expression of the UCP gene in ten tissues including heart, liver, spleen, lung, kidney, gizzard, intestine, brain, breast muscle and abdominal fat of chicken. The results of both RT-PCR and Northern Blot methods showed that the UCP gene expressed specific in breast muscle. The expression levels of UCP gene in breast muscles from egg-type and meat-type chickens of hatching, 2, 4, 6 and 8 wk of age were detected by RT-PCR assay and results showed that the expression levels of UCP gene were related to breeds. Expression level of UCP gene in layers was higher than that in broilers at various weeks of age except at 6 wk. The UCP gene's expression was higher at 6 wk and had no significant difference among other weeks of age in broilers; in layers the expression level of UCP gene had no significant difference among weeks of age. The experiment results also showed that insulin could increase the expression level of UCP gene by 40% compared with control group.

• Asian-Australasian Journal of Animal Sciences
• /
• v.22 no.5
• /
• pp.712-720
• /
• 2009

The goal of this study was to elucidate the expression and segmental distribution of the glomerular cationic amino acid metabolism transporter-2 (CAT-2) and thus to improve our understanding of porcine cationic amino acid transporters and amino acid absorption. Porcine CAT-2 was cloned, sequenced and characterized. The predicted amino acid sequence of porcine CAT-2 shared 86.1% and 92.1% identity with human and mouse CAT-2A, respectively. The tissue distribution patterns and ontogenic changes of CAT-2 mRNAs were determined by real-time Q-PCR. The results showed that porcine CAT-2 was highly expressed in the heart and intestinal tract (duodenum, ileum and jejunum). In addition, the mRNA of CAT-2 was found in liver, lung, kidney, brain and muscle. Within the intestinal tract, CAT-2 mRNA was most abundant in the ileum and rarely expressed in the duodenum. In the duodenum, the levels of CAT-2 mRNA reached their peak on day 7 (p<0.05) while in the jejunum, levels were low on day 1 and 7 and increased rapidly after day 26 before peaking on days 30 and 60 (p<0.05). The levels then dramatically decreased by day 90 (p<0.05). In the ileum, levels achieved their maximum on day 30 and then decreased significantly on day 60 (p<0.05).

• Molecules and Cells
• /
• v.20 no.1
• /
• pp.83-89
• /
• 2005

HtrA2/Omi is a mammalian mitochondrial serine protease homologous to the E. coli HtrA/DegP gene products. Recently, HtrA2/Omi was found to have a dual role in mammalian cells, acting as an apoptosis-inducing protein and being involved in maintenance of mitochondrial homeostasis. By screening a human brain cDNA library with $A{\beta}$ peptide as bait in a yeast two-hybrid system, we identified HtrA2/Omi as a binding partner of $A{\beta}$ peptide. The interaction between $A{\beta}$ peptide and HtrA2/Omi was confirmed by an immunoblot binding assay. The possible involvement of HtrA2/Omi in $A{\beta}$ peptide metabolism was investigated. In vitro peptide cleavage assays showed that HtrA2/Omi did not directly promote the production of $A{\beta}$ peptide at the ${\beta}/{\gamma}$-secretase level, or the degradation of $A{\beta}$ peptide. However, overexpression of HtrA2/Omi in K269 cells decreased the production of $A{\beta}40$ and $A{\beta}42$ by up to 30%. These results rule out the involvement of HtrA2/Omi in the etiology of Alzheimer's disease. However, the fact that overexpression of HtrA2/Omi reduces the generation of $A{\beta}40$ and $A{\beta}42$ suggests that it may play some positive role in mammalian cells.

• IMMUNE NETWORK
• /
• v.11 no.3
• /
• pp.135-154
• /
• 2011

The great discovery of microRNAs (miRNAs) has revolutionized current cell biology and medical science. miRNAs are small conserved non-coding RNA molecules that post-transcriptionally regulate gene expression by targeting the 3' untranslated region of specific messenger RNAs for degradation or translational repression. New members of the miRNA family are being discovered on a daily basis and emerging evidence has demonstrated that miRNAs play a major role in a wide range of developmental process including cell proliferation, cell cycle, cell differentiation, metabolism, apoptosis, developmental timing, neuronal cell fate, neuronal gene expression, brain morphogenesis, muscle differentiation and stem cell division. Moreover, a large number of studies have reported links between alterations of miRNA homeostasis and pathological conditions such as cancer, psychiatric and neurological diseases, cardiovascular disease, and autoimmune disease. Interestingly, in addition, miRNA deficiencies or excesses have been correlated with a number of clinically important diseases ranging from cancer to myocardial infarction. miRNAs can repress the gene translation of hundreds of their targets and are therefore well-positioned to target a multitude of cellular mechanisms. As a consequence of extensive participation in normal functions, it is quite logical to ask the question if abnormalities in miRNAs should have importance in human diseases. Great discoveries and rapid progress in the past few years on miRNAs provide the hope that miRNAs will in the near future have a great potential in the diagnosis and treatment of many diseases. Currently, an explosive literature has focussed on the role of miRNA in human cancer and cardiovascular disease. In this review, I briefly summarize the explosive current studies about involvement of miRNA in various human cancers and cardiovascular disease.