• Clinical and Experimental Pediatrics
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• v.46 no.12
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• pp.1217-1223
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• 2003

Purpose : This study was conducted to assess clinical practices related to the evaluation and treatment of patients with acute gastrointestinal infection(AGI) in infants and children. This survey also evaluated the current opinion regarding the use of rotavirus vaccine. Methods : This survey was conducted using a self-administered questionnaire provided to 82 pediatricians in private clinics of Jeonbuk province. From April to June, 2002, 63 of 82 pediatricians(76.8 %) responded to the survey. Results : The annual proportion of patients with AGI was 13%. The highest proportion of patients with diarrhea were reported for the months of October through December. For the treatment of diarrhea, pediatricians preferred to prescribe lactobacillus products, oral rehydration solution, enzyme products, anti-emetics, anti-diarrheal formula, nothing by mouth(NPO) and bowel movement inhibitors in descending order of frequency. Most pediatricians(79.4%) prescribed antibiotics in less than 20% of patients with AGI. Amoxicillin was the most commonly prescribed antibiotics followed by trimethoprim/sulfamethoxazole(TMP/SMX) and amoxicillin/clavulanate. Clinical manifestations that pediatricians considered as important factors in prescribing antibiotics were bloody diarrhea, mucoid diarrhea, high fever, persisting disease and abdominal pain. Diagnostic procedures that pediatricians preferred for AGI patients were stool examination(rotavirus antigen, RBC, WBC), abdominal X-ray, and serum electrolytes. Pediatricians had a strong interest in rotavirus vaccine(71.4%). Conclusion : Acute gastrointestinal illness remains a common problem, especially during the winter months in Korea. AGI manifesting as watery diarrhea is appropriately treated with commonly available agents but pediatricians appear ready to consider additional approaches to decrease the sizable disease burden of AGI among children in Korea.

• Journal of Korean Neurosurgical Society
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• v.30 no.3
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• pp.263-271
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• 2001

Objective : Glioblastomas, the most common type of primary brain tumors, are highly invasive and cause massive tissue destruction at both the tumor invading edges and in areas that are not in direct contact with glioma cells. As a result, patients with high-grade gliomas are faced with a poor prognosis. Such grim statistics emphasize the need to better understand the mechanisms that underlie glioma invasion, as these may lead to the identification of novel targets in the therapy of high grade gliomas. Protein kinase C(PKC) is a family of serine/threonine kinases and an important signal transduction enzyme that conveys signals generated by ligand-receptor interaction at the cell surface to the nucleus. PKC appears to be critical in regulating many aspects of glioma biology. The purpose of this study was to assess accurately the role of PKC in the invasion regulation of human gliomas based on hypothesis that protein kinase C(PKC) is functional in the process of glial tumor cell invasion. Method : To test this hypothesis, U-87 malignant glioma cell line intracellular PKC levels were up and down regulated and their invasiveness was tested. Intracellular PKC level was characterized using PKC activity assays. Invasion assays including barrier migration and spheroid confrontation were used to study the relationship between PKC concentration and invasiveness. Result : The cell line which were treated by PKC inhibitor tamoxifen and hypericin exhibited decreased PKC activity and decreased invasive abilities dose dependently both in matrigel invasion assay and tumor spheroid fetal rat brain aggregates(FRBA) confrontation assay. However, the cell line that was treated by PKC activator 12-O-tetradecanylphorbol-13acetate(TPA) did not exhibit increases in either PKC activity or invasive ability. Conclusion : These studies suggest that PKC may be a useful molecular target for the chemotherapy of glioblastoma and other malignancies and that a therapeutic approach based on the ability of PKC inhibitors may be helpful in preventing invasion.

• Tuberculosis and Respiratory Diseases
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• v.47 no.2
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• pp.172-183
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• 1999

Background: Nitric oxide is a short-lived effector molecule derived from L-arginine by the nitric oxide synthase(NOS). Nitric oxide plays a role in a number of physiologic and pathophysiologic functions including host defense, edema formation, and regulation of smooth muscle tone. Some kinds of cells including macrophage are known to produce large quantities of nitric oxide in response to inflammatory stimuli such as interleukin-$1\beta$(IL-$1\beta$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), interferon-$\gamma$(IFN-$\gamma$) and lipopolysaccharide(LPS). Reactive oxygen species are also known to be important in the pathogenesis of acute cell and tissue injury such as acute lung injury model Methods: Using the RA W264.7 cells, we have examined the ability of oxidant hydrogen peroxide($H_2O_2$) to stimulate nitric oxide production and inducible NOS mRNA expression. Also, we have examined the effects of NOS inhibitors and antioxidants on $H_2O_2$ induced nitric oxide production. Results: Stimulation of RAW264.7 cells with combinations of 100 ng/ml IL-$1\beta$, 100 ng/ml TNF-$\alpha$, and 100 U/ml IFN-$\gamma$ or 100 U/ml IFN-$\gamma$ and $1{\mu}g/ml$ LPS induced the synthesis of nitric oxide as measured by the oxidation products nitrite($NO_2^-$) and nitrate($NO_3^-$). Addition of $250 {\mu}M-2$ mM $H_2O_2$ to the cytokines significantly augmented the synthesis of $NO_2^-$ and $NO_3^-$(p<0.05). When cells were incubated with increasing concentrations of $H_2O_2$ in the presence of IL-$1\beta$, TNF-$\alpha$ and IFN-$\gamma$ at constant level, the synthesis of $NO_2^-$ and $NO_3^-$ was dose-dependently increased(p<0.05). $N^G$-nitro-L-arginine methyl ester(L-NAME), dose dependently, significantly inhibited the formation of $NO_2^-$ and $NO_3^-$ in cells stimulated with LPS, IFN-$\gamma$ and $H_2O_2$ at constant level(p<0.05). Catalase significantly inhibited the $H_2O_2$-induced augmentation of cytokine-induced $NO_2^-$ and $NO_3^-$ formation(p<0.05). But, boiled catalase did not produce a significant inhibition in comparison with the native enzyme. Another antioxidant 2-mercaptoethanol and orthophenanthroline dose-dependently suppressed $NO_2^-$ and $NO_3^-$ synthesis(p<0.05). Northern blotting demonstrated that H:02 synergistically stimulated the cytokine-induced iNOS mRNA expression in RA W264.7. Conclusion: These results suggest that $H_2O_2$ contributes to inflammatory process by augmenting the iNOS expression and nitric oxide synthesis induced by cytokines.

• Childhood Kidney Diseases
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• v.14 no.2
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• pp.154-165
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• 2010

Purpose : We know little about the natural course of IgA nephropathy (IgAN) in association with histologic changes especially in children. We investigated clinicopathologic features with long-term follow-up biopsy to clarify the outcomes and prognostic indicators for childhood IgAN. Methods : From our patients' medical records, we retrieved 20 patients with IgAN, to whom renal biopsies had been performed for the initial diagnosis and follow-up to find out any histologic changes. Initial and follow-up biopsies were classified by Haas classification. The changes of these parameters were compared with the evolution of clinical features. Results : Patients were treated with angiotensin-converting enzyme inhibitors in combination with angiotensin receptor blockers (in subclass II or above) and short-term cyclosporine A(in patients showing nephrotic syndrome). Histologic improvement in 7 cases and deterioration in 3 cases were observed. At the time of last biopsy, 10 cases (50%) showed clinical remission and the others showed improved clinical features. These clinical outcomes did not correlate with initial Haas classifications. Hypertension at onset observed in 5 cases (25%) revealed significant correlation with clinical outcome (P =0.01) and last Haas classification (P =0.007). None of the cases showed progression to CRF or ESRD. Conclusion : During a mean follow-up of $10.8{\pm}3.4$ years, childhood IgAN showed good clinicopathologic outcome. Hypertension at onset was only a strong predictor of clinicopathologic outcomes, but initial Haas classification cannot predict outcomes in children. Histologic change of IgAN in long term follow-up period cannot be completely predicted by clinical data and vice versa. Therefore, a renal biopsy should be considered as a part of follow-up plan.

• Journal of Acupuncture Research
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• v.22 no.3
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• pp.1-12
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• 2005

It was clarified that ethanol extract herb-acupuncture solution (EE-UD) and hydrotherapy herb-acupuncture solution (WE-UD) in Ulmus davidiana Planch (Ulmaceae), are the excellent inhibitors of cathepsin K and L. WE-UD inhibited cathepsin K when IC50 value was 5.32 ${\square}g$/ml, and suppressed cathepsin L when IC50 value was 6.34 ${\square}g$/ml. However, EE-UD indicated the activity of inhibiting cathepsin K and L in the level of 1.45 ${\square}g$/ml and 2.43 ${\square}g$/ml, thus it showed more significance than WE-UD. It could be observed that EE-VD is an excellent inhibitor to cathepsin K with Ki value of 0.8 ${\square}g$/ml. This activity is increased by 10-fold even in the analytical experiment when having operations like glutathione in pH 7.0. Also, this supports the mixture of GSH thiolate anion, thus it was thought that this increase in effectiveness is probably attributable to the enhanced chemical function in the combinations of herb-acupuncture solution towards a place of activity in enzyme. WE-UD showed the time-dependent inhibiting property, thus it allowed to know the disunion and the compounding speed in constant cathepsin K during the process of experiment. Finally, EE-UD was proved to suppress the absorbent bone ash in the experiment related to osteoclast in rats for test, and to the bone in rodent. It was proved that WE-UD has the effect of inhibiting the protease in cathepsin K and L, and in collagen of bone. These results strongly suggest that it is effective in preventing the progress of bone damage, which was induced due to cathepsin K. Also, it obtained the conclusion that it is effective to the reabsorption activity of bone in the bone marrow cells.

• Journal of Life Science
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• v.21 no.1
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• pp.44-55
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• 2011

This study aimed to investigate the effects of water extract of Rubus coreanus (RCE) on the expression and activity of endothelial nitric oxide synthase (eNOS), as well as its signal transduction pathways in human umbilical vein endothelial cells (HUVECs). The specific inhibitors of NOS show RCE treatment increases NO production in HUVECs due to the up-regulation of eNOS rather than iNOS. The real-time expression level of eNOS mRNA was also increased upon RCE treatment in HUVECs. While a PKC-specific inhibitor, RO-317549, did not alter RCE-induced NO production in HUVECs, tamoxifen (estrogen receptor-specific inhibitor), PD98059 (ERK-specific inhibitor) and LY-294002 (PI3K/Akt-specific inhibitor) did have suppressive effects. Increased NO production by RCE seems to result from a higher level of active eNOS (pSer1177). Specifically, inhibition of ERK not only decreased the level of active eNOS, but also increased the inactive form of the enzyme (pThr495) in HUVECs. This study suggests that RCE treatment increases NO production in HUVECs due to the increased expression and activity of eNOS. It is also shown that RCE-induced eNOS activation occurs partly through the binding of RCE to the estrogen receptor, along with ERK and PI3K/Akt-dependent signal transduction pathways. In addition, the regulatory binding proteins of eNOS including Hsp90 and caveolin-1 were related to these effects of RCE on eNOS activity in HUVECs.

• Tuberculosis and Respiratory Diseases
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• v.84 no.4
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• pp.263-273
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• 2021

Cough is the most common respiratory symptom that can have various causes. It is a major clinical problem that can reduce a patient's quality of life. Thus, clinical guidelines for the treatment of cough were established in 2014 by the cough guideline committee under the Korean Academy of Tuberculosis and Respiratory Diseases. From October 2018 to July 2020, cough guidelines were revised by members of the committee based on the first guidelines. The purpose of these guidelines is to help clinicians efficiently diagnose and treat patients with cough. This article highlights the recommendations and summary of the revised Korean cough guidelines. It includes a revised algorithm for the evaluation of acute, subacute, and chronic cough. For a chronic cough, upper airway cough syndrome (UACS), cough variant asthma (CVA), and gastroesophageal reflux disease (GERD) should be considered in differential diagnoses. If UACS is suspected, first-generation antihistamines and nasal decongestants can be used empirically. In cases with CVA, inhaled corticosteroids are recommended to improve cough. In patients with suspected chronic cough due to symptomatic GERD, proton pump inhibitors are recommended. Chronic bronchitis, bronchiectasis, bronchiolitis, lung cancer, aspiration, intake of angiotensin-converting enzyme inhibitor, intake of dipeptidyl peptidase-4 inhibitor, habitual cough, psychogenic cough, interstitial lung disease, environmental and occupational factors, tuberculosis, obstructive sleep apnea, peritoneal dialysis, and unexplained cough can also be considered as causes of a chronic cough. Chronic cough due to laryngeal dysfunction syndrome has been newly added to the guidelines.

• Tuberculosis and Respiratory Diseases
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• v.46 no.2
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• pp.241-250
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• 1999

Background: Persistent nonproductive cough is a major adverse effect encountered with ACE inhibitor treatment and the most frequent reason for withdrawal of the drug. The mechanism of cough was postulated to be associated with accumulation of bronchial irritants which are substrates of ACE. It has been speculated that occurrence of this adverse effect is genetically predetermined ; in particular, variants of the genes encoding ACE. To investigate this relationship, we determined ACE gene Insertion/Deletion polymorphism in subjects with and without a history of ACE inhibitor-induced cough. Methods: Among the 339 patients with ACE inhibitor treatment, subjects who developed cough that resolved when not taking medication were designated to cough group and other subjects who did not complain cough were designated to non-cough group. Clinical characteristics of the patients were collected by review of medical records. ACE genotypes were determined by PCR amplification of DNA from peripheral blood and agarose gel electrophoresis. Results: 37 patients complained of dry cough(cough group) and 302 patients did not complained of cough(non-cough group). The incidence of ACE inhibitor induced dry cough was 10.9%. There was a preponderance of females in the cough group (M : F=24.3% : 75.7%) compared to the non-cough group (M : F=49.7% : 50.3%, p=0.004). There was no significant difference in mean age, underlying diseases, and kinds and frequencies of ACE inhibitors and their mean dosage between the both groups. ACE genotypic frequencies were I/I : I/D : D/D=16.2% : 18.9% : 64.9% in the cough group and 18.9% : 18.2% : 62.9% in the non-cough group which showed no significant difference between the both groups(p=0.926). Allelic frequencies were I : D = 25.7% : 74.3% and 28.0% : 72.0% in the cough and non-cough group respectively and the difference was not significant(p = 0.676). Conclusion: The incidence of ACE inhibitor-induced cough are 10.9%, and women are more susceptible to ACE inhibitor-induced cough. ACE inhibitor-induced dry cough is not associated with ACE gene Insertion/Deletion polymorphism.