BACKGROUND: The wound healing process is impaired or delayed in aged patients. The development of a new wound healing model is needed. Nerve growth factor (NGF) plays a special role in wound healing because NGF is expressed only in proliferating tissues such as wounds. OBJECTIVE: The aim of our study was to develop a wound healing model using a 3-dimensional culture system, raft culture, by comparing the level of NGF expression according to the wound stage after an artificial wound was made to the raft samples. We tried to specifically localize the site of NGF expression both in mRNA and protein level. METHODS: Raft culture using normal human keratinocytes was done and a 2 mm slit wound was made in the center of the raft samples. Raft samples of no wound, 4 d, 7 d, and 9 d after wounding were prepared. In situ RT-PCR and immunohistochemistry were performed to detect and localize NGF expression after making wounds and the addition of substance P (SP). RESULTS: We failed to localize NGF mRNA expression in raft samples by in situ RT-PCR. Immunohistochemistry showed NGF staining throughout the epidermis although a little more dense staining was found in the basal layer. NGF(+) cells tended to increase until 7 d after wounding, but there were no significant differences according to the wounding days. There was `a tendency that the SP(+) group showed more NGF(+) cells than the SP(-) group, but there were no statistical differences. CONCLUSION: We think that our in vitro raft wound model using NGF expression could be used, at least in part, as an objective indicator for wound healing. In our raft model lacking nerve, NGF may not be suitable for representing wound healing process because this model can not reflect the interaction between the skin and the nervous system. Expression of growth factors or cytokines other than NGF need to be applied to our raft culture system.
Cytokines ; Epidermis ; Humans ; Immunohistochemistry ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Nerve Growth Factor ; Nervous System ; RNA, Messenger ; Skin ; Substance P ; Wound Healing* ; Wounds and Injuries*

Chronic mucocutaneous randidiasis is a clinical syndrome characte ized by chronic and reccurent superficial candidal infection of the skin, mucous membranes, and nails. This syndrome is frequently associated with immune deficiency or endocrinopathy, especially hypopar; thyroidism. We report a case of chrcinic mucocutaneous candidiasis associated with hypoparathyroidism in a 8- year-old girl.
Candidiasis ; Candidiasis, Chronic Mucocutaneous* ; Female ; Humans ; Hypoparathyroidism* ; Mucous Membrane ; Skin ; Thyroid Gland

BACKGROUND: Incretin hormone levels as a predictor of type 2 diabetes mellitus have not been fully investigated. Therefore, we measured incretin hormone levels to examine the relationship between circulating incretin hormones, diabetes, and future diabetes development in this study. METHODS: A nested case-control study was conducted in a Korean cohort. The study included the following two groups: the control group (n=149), the incident diabetes group (n=65). Fasting total glucagon-like peptide-1 (GLP-1) and total glucose-dependent insulinotropic peptide (GIP) levels were measured and compared between these groups. RESULTS: Fasting total GIP levels were higher in the incident diabetes group than in the control group (32.64±22.68 pmol/L vs. 25.54±18.37 pmol/L, P=0.034). There was no statistically significant difference in fasting total GLP-1 levels between groups (1.14±1.43 pmol/L vs. 1.39±2.13 pmol/L, P=0.199). In multivariate analysis, fasting total GIP levels were associated with an increased risk of diabetes (odds ratio, 1.005; P=0.012) independent of other risk factors. CONCLUSION: Fasting total GIP levels may be a risk factor for the development of type 2 diabetes mellitus. This association persisted even after adjusting for other metabolic parameters such as elevated fasting glucose, hemoglobin A1c, and obesity in the pre-diabetic period.
Case-Control Studies ; Cohort Studies ; Diabetes Mellitus, Type 2* ; Fasting ; Gastric Inhibitory Polypeptide* ; Glucagon-Like Peptide 1 ; Glucose ; Incretins ; Multivariate Analysis ; Obesity ; Risk Factors

Phenobarbital is a long-acting barbiturate causing generalized depression of neuronal activity in the brain. Its effect is primarily achieved through enhanced GABA-mediated synaptic inhibition. Its use as an antiepileptic agent was first described in 1912. Before the introduction of phenytoin, phenobarbital is used as sedative-hypnotics. It is used for the treatment of epilepsy and status epilepticus. All barbiturates, including phenobarbital, have a high potential far abuse. They were frequently used for suicide attempts in the past, but they have in large part been replaced by benzodiazepines. the onset of symptoms depends on the drug and the route of administration. Mild to moderate barbiturate intoxication resembles ethanol inebriation with slurred speech, ataxia, and lethargy. Severe acute barbiturate intoxication is life threatening. Early deaths are generally cardiovascular-related. Hypotension, shock, pulmonary edema, and cardiac arrest that occurs with large doses are caused by depression of central sympathetic tone and as well as by direct depression of cardiac contractility. The potentially fatal oral dose of phenobarbital is 6-l0g. We describe an 23-year-old woman with pulmonary edema and cardiac arrest after ingestion of 18 grams of phenobarbital. She was completely recovered by successful cardiopulmonary resuscitation and hemoperfusion. We report a case with literature review.
Ataxia ; Barbiturates ; Benzodiazepines ; Brain ; Cardiopulmonary Resuscitation ; Depression ; Eating ; Epilepsy ; Ethanol ; Female ; Heart Arrest* ; Hemoperfusion ; Humans ; Hypotension ; Lethargy ; Neurons ; Phenobarbital* ; Phenytoin ; Pulmonary Edema* ; Shock ; Status Epilepticus ; Suicide ; Young Adult

BACKGROUND: Metabolic syndrome (MetS) is a condition characterized by a cluster of metabolic disorders and is associated with increased risk of cardiovascular disease (CVD). This study analyzed data from the Korean Health and Genome Study to examine the impact of MetS on CVD. METHODS: A total of 8,898 subjects (4,241 males and 4,657 females), 40 to 69 years of age, were enrolled and evaluated for the development of new onset CVD from 2001 to 2012 (median 8.1 years of follow-up). RESULTS: The prevalence of MetS at baseline was 22.0% (932/4,241) and 29.7% (1,383/4,657) in males and females, respectively. MetS was associated with increased risk of coronary heart disease (CHD; hazard ratio [HR], 1.818; 95% confidence interval [CI], 1.312 to 2.520 in males; HR, 1.789; 95% CI, 1.332 to 2.404 in females) and CVD (HR, 1.689; 95% CI, 1.295 to 2.204 in males; HR, 1.686; 95% CI, 1.007 to 2.192 in females). Specifically, MetS was associated with risk of future stroke in females only (HR, 1.486; 95% CI, 1.007 to 2.192). Among MetS components, abdominal obesity and hypertension were independent predictors of both CHD and CVD. In addition, a higher number of MetS components correlated with higher CVD risk. CONCLUSION: MetS is a significant risk factor for the development of CVD although its impact varies between sexes.
Cardiovascular Diseases* ; Coronary Disease ; Female ; Genome ; Humans ; Hypertension ; Male ; Obesity, Abdominal ; Prevalence ; Risk Factors ; Sex Factors* ; Stroke

STUDY DESIGN: Infectious spondylitis patients were classified according to their cause in pyogenic and tuberculous and compared by each. SUMMARY OF LITERATURE REVIEW: Tuberculous spondylitis shows chronic clinical course and disc space sparing with much pus formation in radiologic finding compared to pyogenic spondylits. PURPOSE: To compare pyogenic and tuberculous spondylitis in clinical, radiological, pathological difference for appropriate management of infectious spondylitis. MATERIALS AND METHODS: We reviewed sixty two cases of infectious spondylitis confirmed by culture and pathologic findings of specimens which obtained by surgical method at the orthopaedic department of the Dong-A university hospital between June 1990 and November 1998. RESULTS: There were 18 cases of pyogenic and 44 cases of tuberculous spondylitis, and combined infection case was absent. Average period between beginning of symptom and diagnosis was 6.4 months in pyogenic spondylitis(4-11 months), 3.9 months in tuberculous spondylitis(3-39 months). The average number of affected vertebra was 2.3 in pyogenic spondylitis and 3.9 in tuberculous spondylitis. 6 cases of pyogenic spondylitis(33%) showed high fever(above 38degree C) which not presented in tuberculous spondylitis. We could not find considerable difference in leukocyte count, ESR, CRP level and simple radiologic finding, MRI finding between pyogenic and tuberculous spondylitis. CONCLUSIONS: In our study, most pyogenic spondylitis shows chronic and inactive feature, so clinical, radiological, laboratory findings are not appropriate guide to differentiate between pyogenic and tuberculous spondylitis. Culture growth of infecting agent and histologic examination are reliable and essential diagnostic method for pyogenic and tuberculous spondylitis.
Diagnosis ; Humans ; Leukocyte Count ; Magnetic Resonance Imaging ; Spine ; Spondylitis* ; Suppuration

Hepatocyte growth factor (HGF) is a potent mitogen and promoter of proliferation of insulin producing beta cells of pancreatic islets. To study the role of HGF, an adenoviral vector carrying the human HGF (Ad.hHGF) gene was transfected into the streptozotocin-induced diabetic mice and evaluated the effect on the blood glucose metabolism and the insulin-secreting beta cells of pancreatic islets. Ad.hHGF gene transfection resulted in amelioration of hyperglycemia and prolongation of survival period in the diabetic mice. Concomitantly adenoviral- mediated hHGF gene therapy slightly increased serum insulin concentration and the expression of insulin in the pancreatic islet. Although the proliferation of beta-cell mass was not noticeable, the beneficial effect of HGF is significant to an almost deteriorated pancreatic islets. Taken together, these data suggest that the Ad.hHGF gene therapy into diabetic mice may prevent the further destruction and present as a beneficial remedy for type 1 diabetic patients.
Adenoviridae/*genetics/physiology ; Animals ; Blood Glucose/analysis ; Body Weight ; Diabetes Mellitus, Experimental/blood/genetics/*metabolism/*therapy ; *Gene Therapy ; Hepatocyte Growth Factor/genetics/*metabolism ; Humans ; Hyperglycemia/blood/complications/genetics/*therapy ; Insulin/blood ; Islets of Langerhans/metabolism/*pathology ; Male ; Mice ; Mice, Inbred BALB C ; Recombinant Proteins/genetics/metabolism ; Survival Rate

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for their anti-inflammatory and analgesic effects; however, their prolonged use significantly contributes to peptic ulcer disease (PUD) and its complications, such as bleeding and perforation. The pathogenesis primarily involves cyclooxygenase (COX) enzyme inhibition and direct mucosal injury, leading to impaired gastrointestinal defense mechanisms. Multiple risk factors, including advanced age, a history of ulcers, and the concurrent use of anticoagulants or corticosteroids, significantly increase the risk of ulcers and related complications. Global epidemiological studies demonstrate considerable geographical variation in prevalence rates. Despite higher NSAID usage, high-income countries exhibit relatively lower rates, primarily due to well-established preventive strategies. Prevention should be based on careful risk stratification that accounts for both gastrointestinal and cardiovascular factors. Proton pump inhibitors have demonstrated superior efficacy in both prevention and treatment, while selective COX-2 inhibitors offer an alternative strategy, though they require careful cardiovascular risk assessment. The synergistic interaction between NSAID use and Helicobacter pylori infection necessitates testing and eradication, particularly in high-risk patients. NSAID discontinuation remains the primary therapeutic strategy when feasible, with studies showing significantly improved healing rates compared with continued use. Recent advances include the emergence of potassium-competitive acid blockers, which provide rapid and sustained acid suppression, offering promising alternatives for both prevention and treatment. Continued research aimed at optimizing preventive strategies and developing novel therapeutic approaches remains essential for improving clinical outcomes in NSAID-induced PUD.