Obesity is a risk factor for various diseases, including cardiovascular disease, diabetes, renal disease, hypertension, cancer, and neural disease. Adipose tissue in animals is important for the mobilization of lipids, milk production, deposition of fat in different depots, and muscle and meat production. Understanding the genetic and physiological causes of metabolic disease is a priority in biomedical genome research. In this study, we examined several variables in mice fed a high-fat diet, including serum composition, body weight, total calorie intake, and differentially expressed genes. Body weight and blood glucose levels were not significantly different between animals fed high-fat and normal diets. However, high-fat diet groups showed reduced calorie and food intakes. Levels of sodium, ionized calcium, glucose, hematocrit, hemoglobin, pH, PCO2, PO2, TCO2 +, HCO3 +, base excess, and SO2 in the blood were not significantly different between mice fed high-fat and normal diets. Serum potassium concentration, however, was lower in mice a high-fat diet. Differentially expressed genes were also compared between the two groups. The purpose of this study was to discover new genes as a result of annealing control primer (ACP) PCR using 20 random primers. Five down regulated genes were identified and three of others were upregulated by high-fat diet. Known genes were excluded from this result. In addition, the relationships among candidate genes and high-fat diet should be investigated according to potassium concentration in the blood. In conclusion, mice fed normal and high-fat diets showed no significant difference in body weight, whereas high-fat diet led to changes in blood composition and differential expression of several genes. These findings may provide a better understanding of the mechanisms underlying the association between obesity and metabolic diseases.
Adipose Tissue ; Animals ; Blood Glucose ; Body Composition ; Body Weight ; Calcium ; Cardiovascular Diseases ; Diet ; Diet, High-Fat* ; Gene Expression* ; Genome ; Glucose ; Hematocrit ; Hydrogen-Ion Concentration ; Hypertension ; Meat Products ; Metabolic Diseases ; Mice* ; Milk ; Obesity ; Polymerase Chain Reaction ; Potassium* ; Risk Factors ; Sodium

Successful hematopoietic stem cell transplantation (HSCT) involves the restoration of hematopoietic function after engraftment, arising from the differentiation and proliferation of hematopoietic stem cells. Several factors could influence the course of allogeneic-HSCT (allo-HSCT). Therefore, knowledge of serum proteome changes during the allo-HSCT period might increase the efficacy of diagnosis and disease prevention efforts. This study conducted proteomic analyses to find proteins that were significantly altered in response to allo-HSCT. Sera from five representative patients who underwent allo-HSCT were analyzed by 2-dimensional gel electrophoresis and liquid chromatography tandem mass spectrometry, and were measured on a weekly basis before and after allo-HSCT in additional 78 patients. Fourteen protein spots showing changes in expression were further examined, and most proteins were identified as acute phase proteins (APPs). Studies of 78 additional patients confirmed that C-reactive protein (CRP) and haptoglobin undergo expression changes during allo-HSCT and thus may have the potential to serve as representative markers of clinical events after allo-HSCT. Maximal CRP level affected the development of major transplant-related complications (MTCs) and other problems such as fever of unknown origin. Particularly, an increase in CRP level 21 days after allo-HSCT was found to be an independent risk factor for MTC. Maximal haptoglobin and haptoglobin level 14 days after allo-HSCT were predictive of relapses in underlying hematologic disease. Our results indicated that CRP and haptoglobin were significantly expressed during allo-HSCT, and suggest that their level can be monitored after allo-HSCT to assess the risks of early transplant-related complications and relapse.
Adolescent ; Adult ; Biological Markers ; C-Reactive Protein/*metabolism ; Female ; Haptoglobins/*metabolism ; Hematopoietic Stem Cell Transplantation/*adverse effects ; Humans ; Male ; Middle Aged ; Proteome/*metabolism ; Proteomics ; Transplantation Conditioning ; Transplantation, Homologous ; Young Adult

BACKGROUND: Verrucous carcinoma (VC) accounts for 1–10% of cases of squamous cell carcinoma (SCC) in the oral cavity, and 75% of VC occur in the oral cavity. Only 3% of primary intraosseous squamous cell carcinomas (PIOSCC), which means SCC occurring primarily in the bone, are VC. Verrucous carcinoma arising from odontogenic cysts (OC) is very rare, with only seven cases reported to date. CASE PRESENTATION: This study reported a case of a patient who underwent partial maxillectomy and neck dissection for VC that occurred in the right anterior maxilla. The patient was admitted to the emergency department at our institution 8 years ago and showed cystic lesions in the anterior maxilla on facial computed tomography (CT) images. Treatment through other departments including assessment of laceration in the mental region and only suture was performed. This report highlights a very rare case of VC in the right anterior maxilla arising from a previous cystic lesion. CONCLUSIONS: Since PIOSCC can arise from OC, appropriate treatment of intraosseous cysts and regular radiologic evaluation are necesssary. Surgical exicision of the primary lesion without neck dissection can lead to good prognosis for patients with primary intraosseous verrucous carcinoma.
Carcinoma, Squamous Cell ; Carcinoma, Verrucous ; Emergency Service, Hospital ; Humans ; Lacerations ; Maxilla ; Mouth ; Neck Dissection ; Odontogenic Cysts ; Prognosis ; Sutures

The differentiation of mass-forming autoimmune pancreatitis (AIP) from pancreatic cancer is critical because AIP can be successfully treated with steroid therapy and unnecessary surgery avoided. We herein report a case of 69-year-old male with a prior history of recurrent AIP who developed a pancreatic body mass with upstream duct dilatation. Laboratory findings were nonspecific for AIP or pancreatic cancer, although an endoscopic ultrasonography-guided biopsy revealed chronic inflammation. To differentiate mass-forming AIP from pancreatic cancer, we administered oral steroids for 2 weeks. After steroid therapy, a computed tomography scan revealed a decrease in the pancreatic mass size and improvement in dilatation of the upstream duct. So we could differentiate mass-forming AIP from pancreatic cancer; thereafter resolution of pancreatic lesion could be achieved with further steroid therapy. In conclusion, a 2-week steroid trial followed by radiologic imaging was helpful to differentiate mass-forming AIP from pancreatic cancer.
Aged ; Biopsy ; Dilatation ; Humans ; Inflammation ; Male ; Pancreatic Neoplasms* ; Pancreatitis* ; Steroids ; Unnecessary Procedures

Purpose: Breast cancer is known to be influenced by genetic and environmental factors, and several susceptibility genes have been discovered. Still, the majority of genetic contributors remain unknown. We aimed to analyze the plasma proteome of breast cancer patients in comparison to healthy individuals to identify differences in protein expression profiles and discover novel biomarkers. Methods: This pilot study was conducted using bioresources from Seoul National University Bundang Hospital’s Human Bioresource Center. Serum samples from 10 breast cancer patients and 10 healthy controls were obtained. Liquid chromatography-mass spectrometry analysis was performed to identify differentially expressed proteins. Results: We identified 891 proteins; 805 were expressed in the breast cancer group and 882 in the control group. Gene set enrichment and differential expression analysis identified 30 upregulated and 100 downregulated proteins in breast cancer. Among these, 10 proteins were selected as potential biomarkers. Three proteins were upregulated in breast cancer patients, including cluster of differentiation 44, eukaryotic translation initiation factor 2-α kinase 3, and fibronectin 1. Seven proteins downregulated in breast cancer patients were also selected: glyceraldehyde-3-phosphate dehydrogenase, α-enolase, heat shock protein member 8, integrin‑linked kinase, tissue inhibitor of metalloproteinases-1, vasodilatorstimulated phosphoprotein, and 14-3-3 protein gamma. All proteins had been previously reported to be related to tumor development and progression. Conclusion The findings suggest that plasma proteome profiling can reveal potential diagnostic biomarkers for breast cancer and may contribute to early detection and personalized treatment strategies. A further validation study with a larger sample cohort of breast cancer patients is planned.

Mitochondrial ATP-sensitive potassium (mitoKATP) channels play a role in early and late ischemic preconditioning. Nevertheless, the subunit composition of mitoKATP channels remains unclear. In this study, we investigated the subunit composition of mitoKATP channels in mitochondria isolated from rat cardiac myocytes. Mitochondria were visualized using the red fluorescence probe, Mitrotracker Red, while mitoKATP channels were visualized using the green fluorescence probe, glibenclamide-BODIPY. The immunofluorescence confocal microscopy revealed the presence of Kir6.1, Kir6.2 and SUR2 present in the cardiac mitochondria. Western blot analysis was carried to further investigate the nature of mitoKATP channels. For SUR proteins, a 140-kDa immunoreactive band that corresponded to SUR2, but no SUR1 was detected. For Kir6.2, three bands (~4, ~6, and ~0 kDa) were detected, and a specific ~6-kDa immunoreactive band corresponding to Kir6.1 was also observed. These observations suggest that the subunits of mitoKATP channels in rat myocytes include Kir6.1, Kir6.2, and a SUR2-related sulfonylurea-binding protein.
Animals ; Blotting, Western ; Fluorescence ; Fluorescent Antibody Technique ; Ischemic Preconditioning ; KATP Channels* ; Microscopy, Confocal ; Mitochondria ; Muscle Cells ; Myocytes, Cardiac* ; Potassium ; Rats*

Cardiac hypertrophy contributes an increased risk to major cerebrovascular events. However, the molecular mechanisms underlying cerebrovascular dysfunction during cardiac hypertrophy have not yet been characterized. In the present study, we examined the molecular mechanism of isoproterenol (ISO) -evoked activation of Ras/Raf/MAPK pathways as well as PKA activity in cerebral artery of rabbits, and we also studied whether the activations of these signaling pathways were altered in cerebral artery, during ISO-induced cardiac hypertrophy compared to heart itself. The results show that the mRNA level of c-fos (not c-jun and c-myc) in heart and these genes in cerebral artery were considerably increased during cardiac hypertrophy. These results that the PKA activity and activations of Ras/Raf/ERK cascade as well as c-fos expression in rabbit heart during cardiac hypertrophy were consistent with previous reports. Interestingly, however, we also showed a novel finding that the decreased PKA activity might have differential effects on Ras and Raf expression in cerebral artery during cardiac hypertrophy. In conclusion, there are differences in molecular mechanisms between heart and cerebral artery during cardiac hypertrophy when stimulated with beta2 adrenoreceptor (AR), suggesting a possible mechanism underlying cerebrovascular dysfunction during cardiac hypertrophy.
Cardiomegaly* ; Cerebral Arteries* ; Heart* ; Isoproterenol ; Rabbits ; RNA, Messenger

To characterize cytosolic Ca2+ fluctuations under metabolic inhibition, rat ventricular myocytes were exposed to 200microM 2, 4-dinitrophenol (DNP), and mitochondrial Ca2+, mitochondrial membrane potential (delta psi m), and cytosolic Ca2+ were measured, using Rhod-2 AM, TMRE, and Fluo-4 AM fluorescent dyes, respectively, by Laser Scanning Confocal Microscopy (LSCM). Furthermore, the role of sarcolemmal Na+/Ca2+ exchange (NCX) in cytosolic Ca2+ efflux was studied in KB-R7943 and Na+-free normal Tyrode's solution (143 mM LiCl ). When DNP was applied to cells loaded with Fluo-4 AM, Fluo-4 AM fluorescence intensity initially increased by 70+/-10% within 70+/-10 s, and later by 400+/-200% at 850+/-46 s. Fluorescence intensity of both Rhod-2 AM and TMRE were initially decreased by DNP, coincident with the initial increase of Fluo-4 AM fluorescence intensity. When sarcoplasmic reticulum (SR) Ca2+ was depleted by 1microM thapsigargin plus 10microM ryanodine, the initial increase of Fluo-4 AM fluorescence intensity was unaffected, however, the subsequent progressive increase was abolished. KB-R7943 delayed both the first and the second phases of cytosolic Ca2+ overload, while Na+-free solution accelerated the second. The above results suggest that: 1) the initial rise in cytosolic Ca2+ under DNP results from mitochondrial depolarization; 2) the secondary increase is caused by progressive Ca2+ release from SR; 3) NCX plays an important role in transient cytosolic Ca2+ shifts under metabolic inhibition with DNP.
Animals ; Caffeine ; Cytosol* ; Fluorescence ; Fluorescent Dyes ; Membrane Potential, Mitochondrial ; Microscopy, Confocal ; Mitochondria ; Muscle Cells* ; Rats* ; Ryanodine ; Sarcoplasmic Reticulum ; Thapsigargin