Four soluble factors—putrescine, glucosamine, nicotinamide, and signal transducer and activator of transcription 3 (STAT3) inhibitor BP-1-102—were shown to differentiate bone marrow mononucleated cells (BMNCs) into functional insulin-producing cells (IPCs) in vitro. Transplantation of these IPCs improved hyperglycemia in diabetic mice. However, the role of endogenous BMNC regeneration in this effect was unclear. This study aimed to evaluate the effect of these factors on in vivo BMNC differentiation into IPCs in diabetic mice. Mice were orally administered the factors for 5 days, twice at 2-week intervals, and monitored for 45–55 days. Glucose tolerance, glucose-stimulated insulin secretion, and pancreatic insulin content were measured. Chimeric mice harboring BMNCs from insulin promoter luciferase/green fluorescent protein (GFP) transgenic mice were used to track endogenous BMNC fate. These factors lowered blood glucose levels, improved glucose tolerance, and enhanced insulin secretion. Immunostaining confirmed IPCs in the pancreas, showing the potential of these factors to induce β-cell regeneration and improve diabetes treatment.

Four soluble factors—putrescine, glucosamine, nicotinamide, and signal transducer and activator of transcription 3 (STAT3) inhibitor BP-1-102—were shown to differentiate bone marrow mononucleated cells (BMNCs) into functional insulin-producing cells (IPCs) in vitro. Transplantation of these IPCs improved hyperglycemia in diabetic mice. However, the role of endogenous BMNC regeneration in this effect was unclear. This study aimed to evaluate the effect of these factors on in vivo BMNC differentiation into IPCs in diabetic mice. Mice were orally administered the factors for 5 days, twice at 2-week intervals, and monitored for 45–55 days. Glucose tolerance, glucose-stimulated insulin secretion, and pancreatic insulin content were measured. Chimeric mice harboring BMNCs from insulin promoter luciferase/green fluorescent protein (GFP) transgenic mice were used to track endogenous BMNC fate. These factors lowered blood glucose levels, improved glucose tolerance, and enhanced insulin secretion. Immunostaining confirmed IPCs in the pancreas, showing the potential of these factors to induce β-cell regeneration and improve diabetes treatment.

Four soluble factors—putrescine, glucosamine, nicotinamide, and signal transducer and activator of transcription 3 (STAT3) inhibitor BP-1-102—were shown to differentiate bone marrow mononucleated cells (BMNCs) into functional insulin-producing cells (IPCs) in vitro. Transplantation of these IPCs improved hyperglycemia in diabetic mice. However, the role of endogenous BMNC regeneration in this effect was unclear. This study aimed to evaluate the effect of these factors on in vivo BMNC differentiation into IPCs in diabetic mice. Mice were orally administered the factors for 5 days, twice at 2-week intervals, and monitored for 45–55 days. Glucose tolerance, glucose-stimulated insulin secretion, and pancreatic insulin content were measured. Chimeric mice harboring BMNCs from insulin promoter luciferase/green fluorescent protein (GFP) transgenic mice were used to track endogenous BMNC fate. These factors lowered blood glucose levels, improved glucose tolerance, and enhanced insulin secretion. Immunostaining confirmed IPCs in the pancreas, showing the potential of these factors to induce β-cell regeneration and improve diabetes treatment.

Four soluble factors—putrescine, glucosamine, nicotinamide, and signal transducer and activator of transcription 3 (STAT3) inhibitor BP-1-102—were shown to differentiate bone marrow mononucleated cells (BMNCs) into functional insulin-producing cells (IPCs) in vitro. Transplantation of these IPCs improved hyperglycemia in diabetic mice. However, the role of endogenous BMNC regeneration in this effect was unclear. This study aimed to evaluate the effect of these factors on in vivo BMNC differentiation into IPCs in diabetic mice. Mice were orally administered the factors for 5 days, twice at 2-week intervals, and monitored for 45–55 days. Glucose tolerance, glucose-stimulated insulin secretion, and pancreatic insulin content were measured. Chimeric mice harboring BMNCs from insulin promoter luciferase/green fluorescent protein (GFP) transgenic mice were used to track endogenous BMNC fate. These factors lowered blood glucose levels, improved glucose tolerance, and enhanced insulin secretion. Immunostaining confirmed IPCs in the pancreas, showing the potential of these factors to induce β-cell regeneration and improve diabetes treatment.

Benzo[a]pyrene (B[a]P) is a polycyclic aromatic hydrocarbon and ubiquitous environmental toxin with known harmful effects to human health. Abnormal phenotypes of keratinocytes are closely associated with their exposure to B[a]P. Resorcinol is a component of argan oil with reported anticancer activities, but its mechanism of action and potential effect on B[a]P damage to the skin is unknown. In this study, we investigated the effects of resorcinol on B[a]P-induced abnormal keratinocyte biology and its mechanisms of action in human epidermal keratinocyte cell line HaCaT. Resorcinol suppressed aryl hydrocarbon receptor (AhR) activity as evidenced by the inhibition of B[a]P-induced xenobiotic response element (XRE)-reporter activation and cytochrome P450 1A1 (CYP1A1) expression. In addition, resorcinol attenuated B[a]P-induced nuclear translocation of AhR, and production of ROS and pro-inflammatory cytokines. We also found that resorcinol increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activity. Antioxidant response element (ARE)-reporter activity and expression of ARE-dependent genes NAD(P)H dehydrogenase [quinone] 1 (NQO1), heme oxygenase-1 (HO-1) were increased by resorcinol. Consistently, resorcinol treatment induced nuclear localization of Nrf2 as seen by Western analysis. Knockdown of Nrf2 attenuated the resorcinol effects on ARE signaling, but knockdown of AhR did not affect resorcinol activation of Nrf2. This suggests that activation of antioxidant activity by resorcinol is not mediated by AhR. These results indicate that resorcinol is protective against effects of B[a]P exposure. The mechanism of action of resorcinol is inhibition of AhR and activation of Nrf2-mediated antioxidant signaling. Our findings suggest that resorcinol may have potential as a protective agent against B[a]P-containing pollutants.

Among the possible venous thromboembolic events in nephrotic syndrome, renal vein thrombosis and pulmonary embolism are common, while portal vein thrombosis (PVT) is rare. This report describes a 26-year-old man with histologically proven minimal change disease (MCD) complicated by PVT. The patient presented with epigastric pain and edema. He had been diagnosed with MCD five months earlier and achieved complete remission with corticosteroids, which were discontinued one month before the visit. Full-blown relapsing nephrotic syndrome was evident on laboratory and clinical findings, and an abdominal computed tomography revealed PVT. He immediately received immunosuppressants and anticoagulation therapy. An eight-week treatment resulted in complete remission, and a follow-up abdominal ultrasonography showed disappearance of PVT. In conclusion, PVT is rare and may not be easily diagnosed in patients with nephrotic syndrome suffering from abdominal pain. Early recognition of this rare complication and prompt immunosuppression and anticoagulation therapy are encouraged to avoid a fatal outcome.
Abdominal Pain ; Adrenal Cortex Hormones ; Adult ; Anticoagulants ; Edema ; Fatal Outcome ; Follow-Up Studies ; Humans ; Immunosuppression ; Immunosuppressive Agents ; Nephrosis, Lipoid* ; Nephrotic Syndrome ; Proteinuria ; Pulmonary Embolism ; Renal Veins ; Thrombosis ; Ultrasonography ; Venous Thrombosis*

Acute esophageal necrosis is a rare clinical entity characterized by the endoscopic finding of extensive black discoloration of the esophageal mucosa. Acute esophageal necrosis in a patient with diabetic ketoacidosis has rarely been reported. We report a case of acute esophageal necrosis in a patient with diabetic ketoacidosis. The patient had coffee ground emesis and, after an esophagogastroduodenoscopy with mucosal biopsy, acute esophageal necrosis was diagnosed. The patient was treated conservatively with an intravenous proton pump inhibitor and oral sucralfate without any complications.
Biopsy ; Coffee ; Diabetes Mellitus ; Diabetic Ketoacidosis ; Endoscopy, Digestive System ; Esophagus ; Humans ; Mucous Membrane ; Necrosis ; Proton Pumps ; Sucralfate ; Vomiting

Ultraviolet (UV) irradiation is an environmental factor that causes skin aging, and is also a major factor leading to cumulative alterations of skin structure, function and appearance. To investigate the effects of Selenium (Sel) on UV-induced skin aging, hairless mice were treated for 4 weeks with UV irradiation and topical application of Sel. Then, the effects of Sel were measured in the skin of these mice via histological analysis and Western blotting. According to the results of wrinkle formation analysis, the topical application of Sel induced a reduction in wrinkling formation in the damaged skin of the UV-irradiated mice. Additionally, our histological analysis demonstrated that the skin thickness in the Sel-treated group was less than in the UV-irradiated group. Furthermore, in an effort to investigate the mechanisms underlying the effects of Sel, the expression levels of matrix-metalloproteinase (MMP) and MAPK protein were assessed in both groups. The application of Sel induced a reduction in MMP-1 expression levels to the levels observed in the non-irradiated group. However, the expression level of MMP-9 was increased slightly in the Sel application group as compared with the vehicle application group. Additionally, the levels of ERK phosphorylation were increased by the application of Sel, but the levels of JNK and p38 were not altered by Sel treatment. These results suggest the possibility that Sel should be considered as a skin aging-protective and therapeutic drug candidate, which functions via the regulation of MMP expression levels.
Animals ; Blotting, Western ; Mice ; Mice, Hairless ; Phosphorylation ; Selenium ; Skin ; Skin Aging

Ischemic colitis is the most common form of ischemic injury to the gastrointestinal tract and this frequently occurs in the elderly. It manifests with sudden, left lower abdominal pain, diarrhea and hematochezia. Radiologic modalities such as barium enema may be helpful in delineating the degree and location of ischemic colitis, but colonoscopy is the procedure of choice for making the diagnosis. Ischemic colitis generally runs a benign course lasting a few days and it requires only supportive treatment in most cases. Complications of ischemic colitis and recurrence are rare. We report here on a case of colonic stricture that was caused by ischemic colitis, and we include a brief review of the relevant literature.
Abdominal Pain ; Aged ; Barium ; Colitis ; Colitis, Ischemic ; Colon ; Colonoscopy ; Constriction, Pathologic ; Diarrhea ; Enema ; Gastrointestinal Hemorrhage ; Gastrointestinal Tract ; Humans ; Recurrence

BACKGROUND: Fexofenadine (Allegra(R)) is a H1-receptor selective antihistamine which exhibits consistent efficacy and safety in the treatment of allergic diseases. We thought that fexofenadine may be useful in treatment of the pruritus associated with eczema. OBJECTIVE: The purpose of this study was to evaluate the efficacy and safety of fexofenadine in the treatment of pruritus associated with eczema. METHODS: In this study, patients with atopic and allergic contact dermatitis were divided into a group given fexofenadine 180 mg once daily with topical prednicarbate treatment group or a topical prednicarbate treatment only group, for 1 week. The primary efficacy parameter was the mean change from baseline in pruritus score, and the secondary parameters were the mean change in the incidence of scratching, the mean change in visual analogue scale (0~100 mm) of pruritus, and a comparison of patient satisfaction. RESULTS: 435 patients were included and the mean age was 32.9 years old. The mean pruritus score at baseline was 3.55 point in fexofenadine group and 3.51 point in the control group. Regarding the mean change in pruritus score, fexofenadine significantly decreased the severity of pruritus compared with the control group (p<0.05). There were no significant differences in the decrease in the incidence of scratching between the two groups. A decrease in pruritus levels utilizing visual analogue scale was significant in the fexofenadine group (p<0.05) and patient satisfaction was significantly higher in the fexofenadine group (p=0.0192). There was no significant difference in the incidence of adverse events between two groups (p=0.6237). CONCLUSION: Fexofenadine administered 180 mg once daily in combination with topical prednicarbate treatment was effective and well tolerated in this study.
Dermatitis, Allergic Contact ; Dermatitis, Atopic ; Eczema ; Humans ; Incidence ; Patient Satisfaction ; Prednisolone ; Pruritus ; Terfenadine