No abstract available.
Chondromatosis, Synovial* ; Knee Joint* ; Knee* ; Osteoarthritis*

Inflammatory bowel disease (IBD) is a chronic condition characterized by continuous inflam-mation of the gastrointestinal tract that varies in intensity over time. IBD is caused by several factors including aberrant gut flora, immunological dysregulation, altered environmental con-ditions, and genetic variations. However, the pathogenesis of IBD remains unclear. Studies have indicated that an imbalance between T helper 17 (Th17) and regulatory T (Treg) cells contributes significantly to the development of IBD. Intestinal Tregs suppress inflammation and are critical for maintaining tissue homeostasis. Th17 cells are known to play an import-ant role in the development and pathogenesis of IBD and provide non-inflammatory support for the integrity of the intestinal barrier against bacterial and fungal infections. Therefore, the Th17/Treg cell balance is crucial in the pathogenesis of IBD and gut integrity. The micro-environment of the intestinal mucosal immunity is regulated by the secretion of cytokines associated with Th17 cells and Tregs. Several studies have indicated that the gut bacteria contribute to the control of the immune milieu and play a key role in the regulation of Th17 cell development. Intestinal bacteria and cytokines control Th17 cell development. Th17 cells secrete cytokines that regulate the immune microenvironment in the gut mucosa. This review provides an overview of Th17 cells and examines the strategies for treating patients with IBD using Th17 cell-targeted drugs.

Inflammatory bowel disease (IBD) is a chronic condition characterized by continuous inflam-mation of the gastrointestinal tract that varies in intensity over time. IBD is caused by several factors including aberrant gut flora, immunological dysregulation, altered environmental con-ditions, and genetic variations. However, the pathogenesis of IBD remains unclear. Studies have indicated that an imbalance between T helper 17 (Th17) and regulatory T (Treg) cells contributes significantly to the development of IBD. Intestinal Tregs suppress inflammation and are critical for maintaining tissue homeostasis. Th17 cells are known to play an import-ant role in the development and pathogenesis of IBD and provide non-inflammatory support for the integrity of the intestinal barrier against bacterial and fungal infections. Therefore, the Th17/Treg cell balance is crucial in the pathogenesis of IBD and gut integrity. The micro-environment of the intestinal mucosal immunity is regulated by the secretion of cytokines associated with Th17 cells and Tregs. Several studies have indicated that the gut bacteria contribute to the control of the immune milieu and play a key role in the regulation of Th17 cell development. Intestinal bacteria and cytokines control Th17 cell development. Th17 cells secrete cytokines that regulate the immune microenvironment in the gut mucosa. This review provides an overview of Th17 cells and examines the strategies for treating patients with IBD using Th17 cell-targeted drugs.

Inflammatory bowel disease (IBD) is a chronic condition characterized by continuous inflam-mation of the gastrointestinal tract that varies in intensity over time. IBD is caused by several factors including aberrant gut flora, immunological dysregulation, altered environmental con-ditions, and genetic variations. However, the pathogenesis of IBD remains unclear. Studies have indicated that an imbalance between T helper 17 (Th17) and regulatory T (Treg) cells contributes significantly to the development of IBD. Intestinal Tregs suppress inflammation and are critical for maintaining tissue homeostasis. Th17 cells are known to play an import-ant role in the development and pathogenesis of IBD and provide non-inflammatory support for the integrity of the intestinal barrier against bacterial and fungal infections. Therefore, the Th17/Treg cell balance is crucial in the pathogenesis of IBD and gut integrity. The micro-environment of the intestinal mucosal immunity is regulated by the secretion of cytokines associated with Th17 cells and Tregs. Several studies have indicated that the gut bacteria contribute to the control of the immune milieu and play a key role in the regulation of Th17 cell development. Intestinal bacteria and cytokines control Th17 cell development. Th17 cells secrete cytokines that regulate the immune microenvironment in the gut mucosa. This review provides an overview of Th17 cells and examines the strategies for treating patients with IBD using Th17 cell-targeted drugs.

Inflammatory bowel disease (IBD) is a chronic condition characterized by continuous inflam-mation of the gastrointestinal tract that varies in intensity over time. IBD is caused by several factors including aberrant gut flora, immunological dysregulation, altered environmental con-ditions, and genetic variations. However, the pathogenesis of IBD remains unclear. Studies have indicated that an imbalance between T helper 17 (Th17) and regulatory T (Treg) cells contributes significantly to the development of IBD. Intestinal Tregs suppress inflammation and are critical for maintaining tissue homeostasis. Th17 cells are known to play an import-ant role in the development and pathogenesis of IBD and provide non-inflammatory support for the integrity of the intestinal barrier against bacterial and fungal infections. Therefore, the Th17/Treg cell balance is crucial in the pathogenesis of IBD and gut integrity. The micro-environment of the intestinal mucosal immunity is regulated by the secretion of cytokines associated with Th17 cells and Tregs. Several studies have indicated that the gut bacteria contribute to the control of the immune milieu and play a key role in the regulation of Th17 cell development. Intestinal bacteria and cytokines control Th17 cell development. Th17 cells secrete cytokines that regulate the immune microenvironment in the gut mucosa. This review provides an overview of Th17 cells and examines the strategies for treating patients with IBD using Th17 cell-targeted drugs.

No abstract available.
Leukemia, Myeloid, Acute*

Purpose: This study examines errors in death certificates (DCs) issued to cases of poisoning. Methods: DCs issued in poisoning cases were retrospectively reviewed. Errors in the DC were classified as major and minor errors, and were evaluated in accordance with their impact on the process of selecting the cause of death (COD). Results: A total of 79 DCs were evaluated; 43 (54.4%) DCs were issued in the emergency department (ED), and 36 (45.6%) DCs were issued outside the ED. The average major and minor errors per DC were determined to be 0.4 and 3.3, respectively. Moreover, an average of 3.0 errors were discovered in DCs issued at the ED, and 4.4 errors in DCs issued outside the ED. The most common major errors were incorrect manner of death (11.4%, 9/79), followed by unacceptable COD (7.6%, 6/79), and the mode of dying as an underlying COD (5.1%, 4/79). The common minor errors most frequently encountered were incorrect time interval (86.1%, 68/79), followed by incorrect other significant conditions (73.4%, 58/79), and no record for date of onset (62.0%, 49/79). Conclusion Our results indicate that the total numbers of major errors, minor errors and cases of misjudged cause of death were greater in DCs issued outside the ED than in DCs issued at the ED. The most frequently quoted major error of DCs related to poisoning was determined to be the incorrect manner of death.

PURPOSE: We compared adductor canal block (ACB) alone and a combination of ACB and sciatic nerve block (SNB) to control early postoperative pain after total knee arthroplasty. MATERIALS AND METHODS: One hundred patients received continuous ACB alone (group A), and another 100 patients received continuous ACB and single popliteal SNB (group B). Pain was evaluated at rest and 45° knee flexion using the numeric rating scale (NRS). The number of times the patient pressed the intravenous patient-controlled analgesia (PCA) button, total PCA volume infused, and the total dosage of additional analgesics were evaluated. We also investigated complications associated with each pain control technique. RESULTS: The NRS score on postoperative day 1 was significantly lower in group B than in group A. The number of times patients pressed the PCA button on postoperative day 1 and the total infused volume were significantly lower in group B than in group A. Thirty-five (35%) patients in group B developed foot drop immediately after surgery; but they all fully recovered on postoperative day 1. CONCLUSIONS: SNB can be effective for management of early postoperative pain that persists even after ACB. Further research is needed to determine the proper dosage and technique for reducing the incidence of foot drop.
Analgesia, Patient-Controlled ; Analgesics ; Arthroplasty ; Arthroplasty, Replacement, Knee ; Foot ; Humans ; Incidence ; Knee ; Nerve Block ; Pain, Postoperative ; Passive Cutaneous Anaphylaxis ; Sciatic Nerve

A case of vaginal and cervical adenocarcinoma, mostly of clear cell type, in young women have been associated with intrauterine exposure to diethystillbestrol(DES) or other nonsteroidal estrogenic substances and vaginal adenosis. We have encountered a case of clear-cell adenocarcinoma of the cervix uteri of 27years young house wife, in which there was a history of intrauterine exposure to DES. We presented a case with a brief review of related literature.
Adenocarcinoma ; Adenocarcinoma, Clear Cell* ; Cervix Uteri* ; Estrogens ; Female ; Humans ; Spouses

The author has examined the effect of cortical spreading depression(CSD) on the changes in extracellular concetration of aspartate and glutamate in the neocortex of anesthetized rats using microdialysis and high performance liquid chromatography(HPLC). The rats were prepared by halothane anesthesia and artificial ventilation. Rats were placed in a stereotaxic frame, and craniotomies were performed over the frontal and parietal cortexes on one side. The CSD was elicited by local application of KCI-soaked small pellets to the frontal cortex. The CSD was monitored by the changes of direct current(DC) potential in the parietal cortex. The microdialysis probe was implanted in the anterior part of the parietal cortex. Amino acids were analyzed by HPLC and fluorescence detection. Baseline concentration of the aspartate was 34.9+/-15.9nM and that of glutamate was 189.8+/-29.1nM(mean standard deviation). The perfusate for analysis was obtained 30 minutes after the beginning of the 300mM KCl induced CSD. Aspartate was found to increase to 146+/-55% baseline, glutamate up to 173+/-30% baseline(mean standard deviation). The increment of glutamate was statistically significant(p<0.05). Then 2M KCI-doaked pellets were applied for more frequent CSD amd the samples were collected. Aspartate increased up to 258+/-97% baseline, glutamate up to 174+/-57% baseline(mean standard deviation), The increment of glutamate and aspartate accompanying 2M KCI induced CSD were also statistically significant(p<0.05). These data suggest that the excitatory amino acids were released during the CSD and this may explain the various aspects of CSD that could contribute to the secondary neuronal damage in the compromised nerve cell.
Amino Acids ; Anesthesia ; Animals ; Aspartic Acid* ; Cerebral Cortex* ; Chromatography, High Pressure Liquid ; Cortical Spreading Depression* ; Craniotomy ; Excitatory Amino Acids ; Fluorescence ; Glutamic Acid* ; Halothane ; Microdialysis ; Neocortex ; Neurons ; Rabeprazole ; Rats* ; Ventilation