High fructose intake induces hyperglycemia and hypertension. However, the mechanism by which fructose induces metabolic syndrome is largely unknown. We hypothesized that high fructose intake induces activation of the renin-angiotensin system (RAS), resulting in hypertension and metabolic syndrome. We provided 11-week-old Sprague–Dawley rats with drinking water, with or without 20% fructose, for two weeks. We measured serum renin, angiotensin II (Ang II), and aldosterone (Aldo) using ELISA kits. The expression of RAS genes was determined by quantitative reverse transcription polymerase chain reaction. High fructose intake increased body weight and water retention, regardless of food intake or urine volume. After two weeks, fructose intake induced glucose intolerance and hypertension. High fructose intake increased serum renin, Ang II, triglyceride, and cholesterol levels, but not Aldo levels. High fructose intake increased the expression of angiotensinogen in the liver; angiotensin-converting enzyme in the lungs; and renin, angiotensin II type 1a receptor (AT1aR), and angiotensin II type 1b receptor (AT1bR) in the kidneys. However, expression of AT1aR and AT1bR in the adrenal glands did not increase in rats given fructose. Taken together, these results indicate that high fructose intake induces activation of RAS, resulting in hypertension and metabolic syndrome.

High fructose intake induces hyperglycemia and hypertension. However, the mechanism by which fructose induces metabolic syndrome is largely unknown. We hypothesized that high fructose intake induces activation of the renin-angiotensin system (RAS), resulting in hypertension and metabolic syndrome. We provided 11-week-old Sprague–Dawley rats with drinking water, with or without 20% fructose, for two weeks. We measured serum renin, angiotensin II (Ang II), and aldosterone (Aldo) using ELISA kits. The expression of RAS genes was determined by quantitative reverse transcription polymerase chain reaction. High fructose intake increased body weight and water retention, regardless of food intake or urine volume. After two weeks, fructose intake induced glucose intolerance and hypertension. High fructose intake increased serum renin, Ang II, triglyceride, and cholesterol levels, but not Aldo levels. High fructose intake increased the expression of angiotensinogen in the liver; angiotensin-converting enzyme in the lungs; and renin, angiotensin II type 1a receptor (AT1aR), and angiotensin II type 1b receptor (AT1bR) in the kidneys. However, expression of AT1aR and AT1bR in the adrenal glands did not increase in rats given fructose. Taken together, these results indicate that high fructose intake induces activation of RAS, resulting in hypertension and metabolic syndrome.

BACKGROUND: Menstrual irregularity is a common major complaint in women of reproductive age. It is also a known marker for underlying insulin resistance. We investigated the association between menstrual irregularity and metabolic syndrome in the general population of middle-aged women in Korea. METHODS: This cross-sectional study used data from the Korea National Health and Nutrition Examination Survey 2010-2012. A total of 2,742 subjects were included in the analysis. Participants were divided into two categories based on their menstrual cycle regularity and the relationship between metabolic syndrome and its variables was investigated by multiple logistic regression analysis. RESULTS: Adjusted analyses revealed significantly higher odds ratios for metabolic syndrome, high waist circumference, high triglyceride levels, and low high density lipoprotein cholesterol levels with the presence of menstrual irregularity. CONCLUSION: Metabolic syndrome and its components (high waist circumference, high triglyceride levels, and low high density lipoprotein cholesterol levels) were significantly associated with menstrual irregularity in women of reproductive age.
Cholesterol, HDL ; Cross-Sectional Studies ; Female ; Humans ; Insulin Resistance ; Korea ; Logistic Models ; Menstrual Cycle ; Nutrition Surveys ; Obesity ; Odds Ratio ; Polycystic Ovary Syndrome ; Triglycerides ; Waist Circumference

Nitrobenzene is a poisonous agent, not commonly encountered in clinical practice, which belongs to the aniline dyes. Ingestion of nitrobenzene may cause methemoglobinemia, a condition in which the iron in hemoglobin is oxidized from the ferrous state to the ferric state, resulting in the inability to transport oxygen. A 41-year-old man presented with the clinical features of methemoglobinemia after drinking nitrobenzene. The patient was treated conservatively with intravenous methylene blue. We report a case of acute methemoglobinemia due to ingestion of nitrobenzene.
Aniline Compounds ; Coloring Agents ; Drinking ; Eating ; Hemoglobins ; Humans ; Iron ; Methemoglobinemia ; Methylene Blue ; Nitrobenzenes ; Oxygen

Diffuse alveolar damage (DAD) is a histological change in lung tissue, and is generally caused by an acute lung injury, which is characterized by bilateral and widespread damages. Localized DAD occurs very rarely. The causes for DAD are numerous, but the chief cause is acute interstitial pneumonia or acute exacerbation of idiopathic interstitial pneumonia, in cases of idiopathic manifestation. The 82-year-old patient, in this case study, showed a DAD lesion in only 1 lobe. The patient was otherwise healthy, with no previous symptoms of DAD. He was admitted to our medical center owing to localized infiltration, observed on his chest radiograph. Laboratory studies showed no signs of infections. DAD was confirmed by a surgical lung biopsy. The patient received corticosteroid treatment and had gradually improved. We report the case of a patient with localized, idiopathic DAD that cannot be classified as acute interstitial pneumonia or acute exacerbation of idiopathic interstitial pneumonia.
Acute Lung Injury ; Aged, 80 and over ; Biopsy ; Humans ; Idiopathic Interstitial Pneumonias ; Idiopathic Pulmonary Fibrosis ; Lung ; Lung Diseases, Interstitial ; Lung Injury ; Thorax

Nontuberculous mycobacteria (NTM) are widely present in the environment, although they rarely cause infection in humans. However, infection by NTM has been increasingly recognized worldwide in the context of the human immunodeficiency virus (HIV) epidemic and therapeutic immunosuppression. Mycobacterium kansasii is a slow-growing photochromogenic mycobacterium, which mainly causes pulmonary infection in patients with predisposing lung diseases, and, occasionally, disseminated infection with poor outcomes in immunocompromised patients. We report on the first case of lymphadenitis caused by infection with M.kansasii in an HIV-infected patient in Korea. The patient showed significant improvement after receiving antituberculous therapy (isoniazid, rifabutin) in combination with surgical drainage and highly active antiretroviral therapy (abacavir, lamivudine, and lopinavir/ritonavir).
Antiretroviral Therapy, Highly Active ; Drainage ; HIV ; Humans ; Immunocompromised Host ; Immunosuppression ; Korea ; Lamivudine ; Lung Diseases ; Lymphadenitis ; Mycobacterium ; Mycobacterium kansasii ; Nontuberculous Mycobacteria

Sweet's syndrome is a reactive dermatosis characterized clinically by fever, leukocytosis, and multiple, erythematous, painful plaques. Histopathologic examination reveals a band-like dense dermal inflammatory infiltrate composed mainly of neutrophils with papillary dermal edema, and no features of vasculitis. We report a case of a 56-year-old female diagnosed with cervical cancer, who underwent surgery and concurrent chemoradiation therapy. Approximately 3 years after completing treatment, she presented with erythematous plaques, principally within the radiation field; the skin biopsy showed features consistent with Sweet's syndrome.
Biopsy ; Edema ; Female ; Fever ; Humans ; Leukocytosis ; Middle Aged ; Neutrophils ; Skin ; Skin Diseases ; Sweet Syndrome ; Uterine Cervical Neoplasms ; Vasculitis

OBJECTIVES: To evaluate the Community-Based Participatory Research (CBPR) professional periodontal care program model for patients with hypertension and diabetes. METHODS: This descriptive case study included 151 participants of the professional periodontal care program. The CBPR-based professional periodontal care program consists of 5-steps: ‘Issue identification and prioritization’ (Step 1), ‘Strategy development’ (Step 2), ‘Entry into community’ (Step 3), ‘Implementation’ (Step 4), and ‘Transition’ (Step 5). Quantitative data were analyzed using frequency analysis, and descriptive data with PASW 23.0 (SPSS Inc., Chicago, IL, USA). The results of the Focus group interview (FGI) were classified as ‘general opinions regarding the program planning and operation receptiveness’, ‘sustainability’, ‘potential spread of the program’, and ‘improvement of program’. The interviews were qualitative research involving seven people. RESULTS: 1. Participants increased their interest in health and oral health by managing their hypertension, diabetes, and periodontal disease using community resources. Through this, healthy practices and improved awareness helped to prevent complications and manage periodontal diseases. 2. Community organizations actively cooperated, resulting in positive changes in oral health practices (increased registration of patients in education centers for hypertension and diabetes, and increased number of patients visiting the local dental clinic). In the future, it was positive to participate in the program continuously. CONCLUSIONS: The most important step is ‘Entry into community’, which has led to active participation and cooperation of community organizations and participants. Therefore, community organizations and strategy development should be discussed, and the role of community leaders should be emphasized to build cooperative relationships. In addition, participation in and collaboration with health-based projects should be achieved through a search of various community organizations.
Chronic Disease ; Community-Based Participatory Research ; Consumer Participation ; Cooperative Behavior ; Education ; Focus Groups ; Humans ; Hypertension* ; Oral Health ; Periodontal Diseases ; Qualitative Research

BACKGROUND: BRCA1 mutated breast cancer cells exhibit the elevated cell proliferation and the higher metastatic potential. G protein-coupled receptor 30 (GPR30) has been shown to regulate growth of hormonally responsive cancers, such as ovarian and breast cancers, and high expression of GPR30 is found in estrogen receptor (ER)-negative breast cancer cells. ER-negative breast cancer patients often have a mutation in the tumor suppressor gene, BRCA1. This study explored antiproliferative effects of genistein, a chemopreventive isoflavone present in legumes, and underlying molecular mechanisms in triple negative breast cancer cells with or without functionally active BRCA1.METHODS: Expression of BRCA1, GPR30 and Nrf2 was measured by Western blot analysis. Reactive oxygen species (ROS) accumulation was monitored by using the fluorescence-generating probe, 2’,7’-dichlorofluorescein diacetate. The effects of genistein on breast cancer cell viability and proliferation were assessed by the MTT, migration and clonogenic assays.RESULTS: The expression of GPR30 was dramatically elevated at both transcriptional and translational levels in BRCA1 mutated breast cancer cells compared to cells with wild-type BRCA1. Notably, there was diminished Akt phosporylation in GPR30 silenced cells. Treatment of BRCA1 silenced breast cancer cells with genistein resulted in the down-regulation of GPR30 expression and the inhibition of Akt phosphorylation as well as the reduced cell viability, migration and colony formation. Genistein caused cell cycle arrest at the G₂/M phase in BRCA1-mutant cells through down-regulation of cyclin B1 expression. Furthermore, BRCA1-mutant breast cancer cells exhibited higher levels of intracellular ROS than those in the wild-type cells. Genistein treatment lowered the ROS levels through up-regulation of Nrf2 expression.CONCLUSIONS: Lack of functional BRCA1 activates GPR30 signaling, thereby stimulating Akt phosphorylation and cell proliferation. Genistein induces G2/M phase arrest by down-regulating cyclin B1 expression, which is attributable to its suppression of GPR30 activation and Akt phosphorylation in BRCA1 impaired breast cancer cells.
Blotting, Western ; Breast Neoplasms ; Breast ; Cell Cycle Checkpoints ; Cell Proliferation ; Cell Survival ; Cyclin B1 ; Down-Regulation ; Estrogens ; Fabaceae ; Genes, Tumor Suppressor ; Genistein ; Humans ; Phosphorylation ; Reactive Oxygen Species ; Triple Negative Breast Neoplasms ; Up-Regulation

Combination treatment with hypomethylating agents (HMAs) and venetoclax is being used increasingly in elderly patients with acute myeloid leukemia (AML).Venetoclax with HMAs has been reported to be associated with tumor lysis syndrome (TLS) in AML patients with high leukemic burden. We present a case of an elderly AML patient with low leukemic burden who developed TLS while receiving venetoclax and azacitidine (AZA). A 74-year-old man with newly diagnosed AML with NPM1 mutation received combination therapy with venetoclax and AZA in an outpatient clinic. Within 12 hours after starting venetoclax and AZA, the patient was admitted to the emergency room with fever, general weakness, and laboratory findings consistent with TLS. Based on our results, we recommend monitoring at the start of the treatment with venetoclax and HMAs to prevent and control TLS regardless of the leukemic burden and favorable genetic ris