As degenerative spinal disease among spinal diseases causing lumbar and cervical spinal pain is the endless repetition of "the biological healing of mechanical damage" occurring over a lifetime, spinal pain by degenerative spinal disease occurs as a series of successive changes through the repetitive damage-healing process of various spinal structures including the intervertebral disc rather than a temporary phenomenon of any given pathophysiologic change in one moment. Degenerative spinal disease generally begins with degeneration of the intervertebral disc. Then herniation of the intervertebral disc resulting in subsequent radicular pain occurs when the nucleus pulposus with degeneration located in the intervertebral disc tears and penetrates the annulus fibrosus. Subsequently, disc space narrowing occurs and alters the spinal biomechanics, followed by degenerative changes to the vertebral endplate, vertebra itself, and facet joint. Finally, these changes lead to spinal stenosis, which is the final destination of degenerative spine disease. Although the exact pathogenesis of spinal pain could be still unclear because of some inconsistencies between the degenerative changes in the spine and the clinical manifestations of spinal pain, an accurate understanding of the pathophysiology and future predictions for further mechanical injury as well as thorough history taking and careful attention to the long-term clinical courses and other associated risk factors including daily life posture and work posture are needed for successful treatment of spinal pain.
Intervertebral Disc ; Low Back Pain ; Neck Pain ; Posture ; Risk Factors ; Spinal Diseases* ; Spinal Stenosis ; Spine ; Zygapophyseal Joint

Trichosporon pullulans has recently been recognized as a human pathogen. Given its rarity, however, few reports describe infection attributable to this fungal pathogen. In immunocompromised hosts, T. pullulans infection is associated with significant mortality. For the first time in Korea, we report a case of T. pullulans infection in a non.neutropenic patient. A 70.year.old woman was diagnosed with metastatic colon cancer. She did not undergo chemotherapy and received only supportive care and intravenous nutrition via the subclavian vein. Sixteen days after admission, a fever developed. Three sets of blood culture and a catheter tip culture were carried out and T. pullulans grew in all cultures. Although she was treated with amphotericin B deoxycholate and catheter removal, she died on hospital day 40 due to persistent fungemia.
Amphotericin B ; Catheters ; Colonic Neoplasms ; Deoxycholic Acid ; Drug Combinations ; Female ; Fever ; Fungemia ; Humans ; Immunocompromised Host ; Korea ; Subclavian Vein ; Trichosporon

Amiodarone is a potent antiarrhythmic agent and can cause potentially life-threatening pulmonary fibrosis. Of the numerous side effects associated with amiodarone therapy, lugn toxicity is one of the most serious adverse reactions. Recently, we experienced a case of amiodarone-induced pulmonary toxicity (APT), which induced severe dyspnea and productive coughing, confirmed by cytologic and electron microscopic examination of the bronchoalveolar lavage (BAL). The symptoms and abnormalities in the chest X-ray were improved after the withdrawal of amiodarone. Cytologic examination of the BAL revealed numerous foam cells with cytoplasmic vacuoles or small particles. Ultrastructurally, the foam cells demonstrated characteristic lysosomal inclusions, which were electron-dense multilamellated bodies, crystalloid bodies, and mixed forms with small lipid vacuoles. It is strongly suggested that only cytologic and electron microscopic examination of the BAL without open lung biopsy is enough for diagnosis of APT, when APT is clinically suspected in a patient who has a history or ingestation of amiodarone.
Amiodarone ; Biopsy ; Bronchoalveolar Lavage* ; Cough ; Cytoplasm ; Diagnosis ; Dyspnea ; Foam Cells ; Humans ; Lung ; Microscopy, Electron ; Pulmonary Fibrosis ; Thorax ; Vacuoles

Sphenoid sinus mucocele with the intracranial extension is a rare disease but should be included in the differential diagnosis of destructive changes of the sella turcica, since a seemingly harmful intracranial procedure may be attempted. With the use of CT scan and MRI, it can be diagnosed preoperatively with a much better accuracy. Three histologically-verified cases of sphenoid mucocele with intracranial extension developing headache, visual disturbance and/or amenorrhea are described with a review of the literatures. All cases were successfully operated upon by the intranasal procedure.
Amenorrhea ; Diagnosis, Differential ; Female ; Headache ; Magnetic Resonance Imaging ; Mucocele* ; Rare Diseases ; Sella Turcica ; Sphenoid Sinus* ; Tomography, X-Ray Computed

Atrial Fibrillation (AF) is thought be caused by oxidative stress. Oxidative stress at the cellular level results from many factors, including exposure to alcohol, medications, cold, toxins or radiation. In this study we investigated gene transcriptional profiles on the human myocardial tissues from AF and oxidative stress conditions. Right atrial appendages were obtained from AF patients (n = 26) undergoing the Maze procedure, and from control patients (n = 26) who were in normal sinus rhythm and undergoing coronary artery bypass graft operation. To examine the effects of oxidative stress on AF, we used radioactive complementary DNA (cDNA) microarrays to evaluate changes in the expression of 1,152 known genes. This technology, which monitors thousands of genes simultaneously, gives us a better picture of the interactions between AF and oxidative stress. Total RNAs prepared from the retrieved tissues were used to synthesize(33)P-labeled cDNAs by reverse transcription and hybridized to cDNA microarrays. Gene expression profiles showed that 30 genes were upregulated and 25 were downregulated in AF patients compared with control patients. Moreover, comparison rank analysis revealed that the expression of five genes related to reactive oxygen species (ROS)-including flavin containing monooxygenase 1, monoamine oxidase B, ubiquitin specific protease 8, tyrosinase-related protein 1, and tyrosine 3-monooxygenase-increased by more than 2.0 of the Z-ratio, and two genes related to anti-oxidants including glutathione peroxidase 1, and heme oxygenase 2-decreased to the Z-ratio levels of <= -2.0. Apparently, a balanced regulation of pro- and anti-oxidation can be shifted toward pro-oxidation and can result in serious damage similar to that of human AF. Western blotting analysis confirmed the upregulation of tyrosinase-related protein 1 and tyrosine 3-monooxygenase and the downregulation of heme oxygenase 2. These results suggested that the gene expression pattern of myocardial tissues in AF patients can be associated with oxidative stress, resulting in a significant increase in ROS. Thus, the cDNA microarray technique was useful for investigating transcription profiles in AF. It showed that the intracellular mechanism of oxidative stress plays a pivotal role in the pathologic progression of AF and offers novel insight into potential treatment with antioxidants.
Atrial Appendage/metabolism ; Atrial Fibrillation/*genetics/*metabolism ; Blotting, Western ; DNA, Complementary/genetics ; *Gene Expression Profiling ; Gene Expression Regulation ; Human ; Myocardium/metabolism ; Oligonucleotide Array Sequence Analysis ; Oxidative Stress/*genetics ; Reactive Oxygen Species/metabolism ; Support, Non-U.S. Gov't

BACKGROUND: During the fetal stage, the epidermis and adnexal epithelium might express different types of cytokeratin (CK) by developmental stages. The objective of this study is to observe the expressions of CK1, CK10 and CK14 in the skin of human fetuses. METHODS: Immunohistochemical stains were applied to the skin of 42 fetuses ranging from 10 to 36 gestation weeks. Three different portions of the body (i.e., scalp, chest and sole) were sampled. Immunohistochemical staining with monoclonal antibodies against CK1, 10, 14 were done. RESULTS: We found that CK14 was expressed in the basal layer of the epidermis and adnexae of fetuses beween 10 to 36 gestation weeks. However, stronger expression in the middle than the basal layer was noted in the soles of 15-week fetuses followed by exclusive basal expression. The sebaceous gland, the outer root sheath of the hair follicle and the eccrine duct epithelium also showed CK14 expressions, while CK14 was negative in hair germ and acini. Both CK1 and CK10 were expressed in the epidermis of fetuses ranging between 10 to 36 gestation weeks at the suprabasal layer of the scalp, chest and sole; while they were negative in the basal layer and skin adnexae including sebaceous, hair and eccrine gland. CONCLUSIONS: Expression of cytokeratins in the fetal skin were noted at 10 weeks throughout the entire gestation period and were similar in the three different sites, except in the early stage of the sole. The main expression sites of K14 were the basal layer of the epidermis, the eccrine ducts and the outer root sheath cells of hair, suggesting the same origin, while those of K1 and K10 were in the suprabasal layer of epidermis.
Antibodies, Monoclonal ; Coloring Agents ; Eccrine Glands ; Epidermis ; Epithelium ; Fetus ; Hair ; Hair Follicle ; Humans ; Keratins* ; Pregnancy ; Scalp ; Sebaceous Glands ; Skin* ; Thorax

The L-gulono-gamma-lactone oxidase gene (Gulo) encodes an essential enzyme in the synthesis of ascorbic acid from glucose. On the basis of previous findings of bone abnormalities in Gulo-/- mice under conditions of ascorbic acid insufficiency, we investigated the effect of ascorbic acid insufficiency on factors related to bone metabolism in Gulo-/- mice. Four groups of mice were raised for 4 weeks under differing conditions of ascorbic acid insufficiency, namely, wild type; ascorbic acid-sufficient Gulo-/- mice, 3-week ascorbic acid-insufficient Gulo-/- mice, and 4-week ascorbic acid-insufficient Gulo-/- mice. Four weeks of ascorbic acid insufficiency resulted in significant weight loss in Gulo-/- mice. Interestingly, average plasma osteocalcin levels were significantly decreased in Gulo-/- mice after 3 weeks of ascorbic acid insufficiency. In addition, the tibia weight in ascorbic acid-sufficient Gulo-/- mice was significantly higher than that in the other three groups. Moreover, significant decreases in trabecular bone volume near to the growth plate, as well as in trabecular bone attachment to the growth plate, were evident in 3- or 4-week ascorbic acid-insufficient Gulo-/-. In summary, ascorbic acid insufficiency in Gulo-/- mice results in severe defects in normal bone formation, which are closely related to a decrease in plasma osteocalcin levels.
Animals ; Ascorbic Acid* ; Down-Regulation* ; Glucose ; Growth Plate ; L-Gulonolactone Oxidase ; Metabolism ; Mice ; Osteocalcin* ; Osteogenesis* ; Plasma ; Tibia ; Weight Loss

The effects of estriol on oxygen uptake, glucose release, lactate and pyruvate production, beta-hydroxybutyrate and acetoacetate production in perfused rat liver as well as, carbon uptake in rat liver and intracellular calcium in isolated Kupffer cells were investigated. Basal oxygen consumption of perfused liver increased significantly in estriol or ethanol-treated rats. But these increased effects were blocked by gadolinium chloride pretreatment. In a metabolic study, pretreatment with estriol resulted in a decrease in glucose production and in glycolysis while an increase in ketogenesis. A more oxidized redox state of the mitochondria was indicated by increased ratios of perfusate [lactate]/[pyruvate] and decreased ratios of perfusate [beta-hydroxybutyrate]/[acetoacetate]. Carbon uptake of Kupffer-cell increased significantly in estriol-treated rats. But these increased uptake were not shown in rats pre-treated by gadolinium chloride blocking phagocytosis. In isolated Kupffer cells from estriol-treated rats, intracellular calcium was more significantly increased after addition of lipopolysaccharide (LPS) than in controls. These findings suggest that the metabolic effects of estriol (two mg per 100 mg body wt) can be summarized to be highly toxic in rat liver, and these findings suggest that oral administration of estrogens may induce hepatic dysfunctions and play a role in the development of liver disease.
3-Hydroxybutyric Acid/metabolism ; Acetoacetates/metabolism ; Animal ; Calcium/metabolism ; Carbohydrates/metabolism ; Carbon/metabolism ; Cells, Cultured ; Colloids/metabolism ; Estriol/pharmacology* ; Estriol/metabolism ; Ethanol/pharmacology ; Female ; Gadolinium/pharmacology ; Glucose/biosynthesis ; Intracellular Fluid/metabolism ; Kupffer Cells/metabolism ; Kupffer Cells/cytology ; Lactates/metabolism ; Lipids/metabolism ; Liver/metabolism ; Liver/drug effects* ; Oxygen Consumption ; Phagocytosis ; Pyruvic Acid/metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To evaluate at which pH level various local anesthetics precipitate, and to confirm which combination of corticosteroid and local anesthetic crystallizes. METHODS: Each of ropivacaine-HCl, bupivacaine-HCl, and lidocaine-HCl was mixed with 4 different concentrations of NaOH solutions. Also, each of the three local anesthetics was mixed with the same volume of 3 corticosteroid solutions (triamcinolone acetonide, dexamethasone sodium phosphate, and betamethasone sodium phosphate). Precipitation of the local anesthetics (or not) was observed, by the naked eye and by microscope. The pH of each solution and the size of the precipitated crystal were measured. RESULTS: Alkalinized with NaOH to a certain value of pH, local anesthetics precipitated (ropivacaine pH 6.9, bupivacaine pH 7.7, and lidocaine pH 12.9). Precipitation was observed as a cloudy appearance by the naked eye and as the aggregation of small particles (<10 µm) by microscope. The amount of particles and aggregation increased with increased pH. Mixed with betamethasone sodium phosphate, ropivacaine was precipitated in the form of numerous large crystals (>300 µm, pH 7.5). Ropivacaine with dexamethasone sodium phosphate also precipitated, but it was only observable by microscope (a few crystals of 10-100 µm, pH 7.0). Bupivacaine with betamethasone sodium phosphate formed precipitates of non-aggregated smaller particles (<10 µm, pH 7.7). Lidocaine mixed with corticosteroids did not precipitate. CONCLUSION: Ropivacaine and bupivacaine can precipitate by alkalinization at a physiological pH, and therefore also produce crystals at a physiological pH when they are mixed with betamethasone sodium phosphate. Thus, the potential risk should be noted for their use in interventions, such as epidural steroid injections.
Adrenal Cortex Hormones ; Anesthetics, Local* ; Betamethasone ; Bupivacaine ; Crystallization* ; Dexamethasone ; Hydrogen-Ion Concentration ; Lidocaine ; Sodium

Eradication of Helicobacter pylori using first-line therapy is becoming less effective. Subjects who had been treated for H. pylori infection were prospectively enrolled through an on-line database registry from October 2010 to December 2012. Demographic data, detection methods, treatment indication, regimens, durations, compliance, adverse events, and eradication results for H. pylori infection were collected. Data of 3,700 patients from 34 hospitals were analyzed. The overall eradication rate of the first-line therapy was 73.0%. Eradication failure was significantly associated with old age, concomitant medication, and comorbidity. Regional differences in eradication rates were observed. The most common first-line therapy was proton pump inhibitor-based triple therapy (standard triple therapy, STT) for 7 days (86.8%). The eradication rates varied with regimens, being 73% in STT, 81.8% in bismuth-based quadruple therapy, 100% in sequential therapy, and 90.3% in concomitant therapy. The eradication rate in treatment-naïve patients was higher than that in patients previously treated for H. pylori infection (73.8% vs. 58.5%, P < 0.001). The overall eradication rate for second-line therapy was 84.3%. There was no statistical difference in eradication rates among various regimens. H. pylori eradication rate using STT is decreasing in Korea and has become sub-optimal, suggesting the need for alternative regimens to improve the efficacy of first-line therapy for H. pylori infection.
Adult ; Age Factors ; Aged ; Anti-Bacterial Agents/*therapeutic use ; Databases, Factual ; Drug Therapy, Combination ; Female ; Helicobacter Infections/*drug therapy/microbiology ; Helicobacter pylori/isolation & purification ; Humans ; Internet ; Logistic Models ; Male ; Middle Aged ; Prospective Studies ; Proton Pump Inhibitors/*therapeutic use ; Registries ; Republic of Korea ; Treatment Outcome