Background: We first determined the efficacy of lesional injection of tonsil-derived MSCs (mesenchymal stem cells) for the treatment of 5-fluorouracil induced oral mucositis. Methods: Oral mucositis was induced in hamsters by administration of 5-fluorouracil (day 0, 2, 4) followed by mechanical trauma (day 1, 2, 4). The experimental groups included MT (mechanical trauma only), 5-FU + MT (mechanical trauma with 5-fluorouracil administration), TMSC (mechanical trauma with 5-fluorouracil administration, tonsil-derived mesenchymal stem cells injection), DEXA (mechanical trauma with 5-fluorouracil administration, dexamethasone injection), and saline (mechanical trauma with 5-fluorouracil administration, saline injection). Results: On day 10, gross and histologic analyses showed that nearly complete healing and epithelialization of the cheek mucosa of the TMSC group, whereas the other groups showed definite ulcerative lesions. Compared with the MT and DEXA groups, CD31 expression was greater in the TMSC group on days 10 and 14. Tendency towards a decrease in MMP2 expression with the time in the TMSC group was observed. In addition, the TMSC group showed higher expression of TGF-β, and NOX4 on day 10 compared with the other groups. Scratch assay demonstrated that the conditioned media harvested from tonsil-derived MSCs significantly increased migratory efficacy of NIH3T3 cells. Transwell assay showed that the preferential migration of tonsil-derived MSCs to the wound area. Conclusion Intralesional administration of tonsil-derived MSCs may accelerate wound healing of 5-fluorouracil induced oral mucositis by upregulating neovascularization and effective wound contraction. In addition, tonsil-derived MSCs might contribute to oral ulcer regeneration via the stimulation of fibroblast proliferation and migration.

Background: We first determined the efficacy of lesional injection of tonsil-derived MSCs (mesenchymal stem cells) for the treatment of 5-fluorouracil induced oral mucositis. Methods: Oral mucositis was induced in hamsters by administration of 5-fluorouracil (day 0, 2, 4) followed by mechanical trauma (day 1, 2, 4). The experimental groups included MT (mechanical trauma only), 5-FU + MT (mechanical trauma with 5-fluorouracil administration), TMSC (mechanical trauma with 5-fluorouracil administration, tonsil-derived mesenchymal stem cells injection), DEXA (mechanical trauma with 5-fluorouracil administration, dexamethasone injection), and saline (mechanical trauma with 5-fluorouracil administration, saline injection). Results: On day 10, gross and histologic analyses showed that nearly complete healing and epithelialization of the cheek mucosa of the TMSC group, whereas the other groups showed definite ulcerative lesions. Compared with the MT and DEXA groups, CD31 expression was greater in the TMSC group on days 10 and 14. Tendency towards a decrease in MMP2 expression with the time in the TMSC group was observed. In addition, the TMSC group showed higher expression of TGF-β, and NOX4 on day 10 compared with the other groups. Scratch assay demonstrated that the conditioned media harvested from tonsil-derived MSCs significantly increased migratory efficacy of NIH3T3 cells. Transwell assay showed that the preferential migration of tonsil-derived MSCs to the wound area. Conclusion Intralesional administration of tonsil-derived MSCs may accelerate wound healing of 5-fluorouracil induced oral mucositis by upregulating neovascularization and effective wound contraction. In addition, tonsil-derived MSCs might contribute to oral ulcer regeneration via the stimulation of fibroblast proliferation and migration.

BACKGROUND/AIMS: Oxygen free radicals play an important role in acute pancreatitis. Pantoprazole as a proton pump inhibitor (PPI) has pancreatic anti-secretory effect and a pronounced inhibitory reactivity towards hydroxyl radicals. The objective of the study was to investigate the effect of pantoprazole on the course of acute pancreatitis. METHODS: We conducted a prospective randomized trial involving 40 patients with acute pancreatitis. Patients were divided into two groups. One group received PPI and the other group did not receive PPI. In the PPI group, patients received pantoprazole 40 mg intravenously twice a day for fasting time, and then 40 mg orally twice a day until discharge. RESULTS: There were no significant differences in baseline characteristics and laboratory markers between two groups. In the pantoprazole group, mean hospital stay was 7.4 days, time to start oral intake was 69.0 hours, and time to pain relief was 59.7 hours. Acute physiology and chronic health evaluation (APACHE) II score was 3.15 at admission day and 2.35 at discharge. On the other hand, in the non-pantoprazole group, mean hospital stay was 7.6 days, time taken to start oral intake was 71.4 hours, and time taken to pain relief was 61.8 hours. APACHE II score was 4.4 at admission and 2.85 at discharge. However, there were no significant differences between two groups. CONCLUSIONS: Treatment with pantoprazole did not have influence on the clinical course of acute pancreatitis. But, considering it was a pilot study, large scale prospective trials will be needed.
2-Pyridinylmethylsulfinylbenzimidazoles/therapeutic use ; APACHE ; Acute Disease ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Alcohol Drinking ; Eating ; Female ; Humans ; Length of Stay ; Male ; Middle Aged ; Pain Management ; Pancreatitis/*drug therapy/etiology ; Pilot Projects ; Prospective Studies ; Proton Pump Inhibitors/*therapeutic use ; Young Adult

Hypercalcemia commonly occurs because of primary hyperparathyroidism and metastatic malignancies, such as multiple myeloma, breast cancer and lung cancer; these causes account for 90% of cases. The other causes of hypercalcemia are numerous, and immobilization is an under-appreciated etiology. The mechanisms underlying immobilization-induced hypercalcemia are uncertain. However, an overall increased osteoclastic bone resorption and decreased osteoblastic bone formation can induce hypercalciuria and hypercalcemia. Additionally, hypercalcemia can induce and be associated with acute kidney injury, but it is rarely reported in immobilization hypercalcemia. We report here a 58-year-old man with suspected immobilization hypercalcemia associated with acute kidney injury and treated successfully with glucocorticoids.
Acute Kidney Injury ; Bone Resorption ; Breast Neoplasms ; Glucocorticoids ; Humans ; Hypercalcemia ; Hypercalciuria ; Hyperparathyroidism, Primary ; Immobilization ; Lung ; Middle Aged ; Multiple Myeloma ; Osteoblasts ; Osteoclasts ; Osteogenesis

Acute kidney injury associated with disseminated intravascular coagulation (DIC) and a coagulation factor defect may develop with infection, malignancy, severe trauma, or obstetric complications. However, a gynecological etiology, such as hysterectomy, in a patient with adenomyosis has rarely been reported. We describe a case of a 42-year-old women who presented with DIC and acute kidney injury after a total hysterectomy. We thought that the cause for the acute kidney injury might be small vascular thrombosis and acute tubulointerstital nephritis due to probable catastrophic antiphospholipid syndrome with DIC. The patient was successfully treated with steroid therapy.
Acute Kidney Injury ; Adenomyosis ; Adult ; Antiphospholipid Syndrome ; Blood Coagulation Factors ; Dacarbazine ; Disseminated Intravascular Coagulation ; Female ; Humans ; Hysterectomy ; Nephritis ; Thrombosis

Hypercalcemia commonly occurs because of primary hyperparathyroidism and metastatic malignancies, such as multiple myeloma, breast cancer and lung cancer; these causes account for 90% of cases. The other causes of hypercalcemia are numerous, and immobilization is an under-appreciated etiology. The mechanisms underlying immobilization-induced hypercalcemia are uncertain. However, an overall increased osteoclastic bone resorption and decreased osteoblastic bone formation can induce hypercalciuria and hypercalcemia. Additionally, hypercalcemia can induce and be associated with acute kidney injury, but it is rarely reported in immobilization hypercalcemia. We report here a 58-year-old man with suspected immobilization hypercalcemia associated with acute kidney injury and treated successfully with glucocorticoids.
Acute Kidney Injury ; Bone Resorption ; Breast Neoplasms ; Glucocorticoids ; Humans ; Hypercalcemia ; Hypercalciuria ; Hyperparathyroidism, Primary ; Immobilization ; Lung ; Middle Aged ; Multiple Myeloma ; Osteoblasts ; Osteoclasts ; Osteogenesis

Acute kidney injury associated with disseminated intravascular coagulation (DIC) and a coagulation factor defect may develop with infection, malignancy, severe trauma, or obstetric complications. However, a gynecological etiology, such as hysterectomy, in a patient with adenomyosis has rarely been reported. We describe a case of a 42-year-old women who presented with DIC and acute kidney injury after a total hysterectomy. We thought that the cause for the acute kidney injury might be small vascular thrombosis and acute tubulointerstital nephritis due to probable catastrophic antiphospholipid syndrome with DIC. The patient was successfully treated with steroid therapy.
Acute Kidney Injury ; Adenomyosis ; Adult ; Antiphospholipid Syndrome ; Blood Coagulation Factors ; Dacarbazine ; Disseminated Intravascular Coagulation ; Female ; Humans ; Hysterectomy ; Nephritis ; Thrombosis

Mutations in the transmembrane inner ear (Tmie) gene, which encodes the Tmie protein, have been attributed to deafness autosomal recessive 6 (DFNB6), an autosomal nonsyndromic recessive hearing loss disorder. Although the Tmie gene was identified a few years ago, little is known about subcellular localization of the Tmie protein. In order to address this, we developed a stable cell line expressing Tmie protein. The expression of Myc-tagged Tmie protein was confirmed by Western blot analysis using an anti-Myc antibody and localization of the Tmie protein was confirmed by immunostaining, using the anti-Myc antibody as well as the anti-tmie antibody. Our study demonstrates that the Tmie protein is localized mostly in the cellular membrane and to a lesser extent in cytoplasm. These results suggest that our Tmie expressing stable cell line provides a suitable in vitro model to explore Tmie synthesis and functions.
Blotting, Western ; Cell Line ; Cytoplasm ; Deafness ; Ear, Inner ; Hearing Loss ; Membranes

Hemorrhagic cystitis is a common complication in hematopoietic stem cell transplant recipients. We report a case of hemorrhagic cystitis after unrelated cord blood transplantation associated with adenovirus infection. Despite hydration, hematuria and large clots persisted. We instilled cidofovir into the bladder, which resulted in clearance of the adenovirus and significant clinical improvement. Our case emphasizes the effectiveness of intravesical cidofovir treatment for viral hemorrhagic cystitis.
Adenoviridae ; Adenoviridae Infections ; Cord Blood Stem Cell Transplantation ; Cystitis ; Cytosine ; Fetal Blood ; Hematopoietic Stem Cells ; Hematuria ; Organophosphonates ; Transplants ; Urinary Bladder

Renal artery pseudoaneurysm is an uncommon disease. A 47-year-old man complained of recently developed gross hematuria and left flank pain. The initial laboratory study and radiographic evaluation revealed acute pyelonephritis. After the treatment with antibiotics, gross hematuria was resolved and the patient was discharged. However, he revisited with repeated gross hematuria and throbbing left flank pain. The renal angiography revealed left intra-renal arterial pseudoaneurysm. Angiographic embolization by glue injection was successfully performed. Thereafter, gross hematuria and flank pain were disappeared. We report a successful glue embolization of intra-renal artery pseudoaneurym associated with acute pyelonephritis.
Adhesives ; Aneurysm, False ; Angiography ; Anti-Bacterial Agents ; Arteries ; Flank Pain ; Hematuria ; Humans ; Middle Aged ; Pyelonephritis ; Renal Artery