No abstract available.
Abetalipoproteinemia ; Humans ; Neuroacanthocytosis

No abstract available.
Abetalipoproteinemia ; Humans ; Neuroacanthocytosis

The short term beneficial effect of arthroscopic excision of synovial tissue in knees with rheumatoid arthritis have been well documented. The purpose of this study to report the results of synovectomy in patients with rheumatoid arthritis who have been observed at least 3 years. We analysed the clinical result with modified Laurin criteria, radiologic change and patients own satisfaction degree with survey. The results were as follows; 1. The preoperative symptoms were pain (100%), swelling (100%), decreased range of motion (83%) and joint tenderness (74%), and those were improved postoperatively to 43%, 60%, 11%, 43% each other. 2. Among the laboratory parameters, C-reactive protein (CRP) was improved most significantly (pvalue =0.026). 3. On simple supine A-P X-rays, the width of medial joint space and lateral joint space were compared to preoperatively and postoperatively. The width of medial joint space was 4.33mm preoperatively, and it was changed to 3.22mm at last follow up (p=0.032). Those of lateral joint space was changed from 4.24mm preoperatively to 3.27mm at last tollow up (p=0.106). 4. The grade of articular cartilage damage was related with severity of preoperative symptoms and the patients with low grade of articular cartilage damage showed more postoperative improvement. The result of operation was related to symptom duration, degree of X-ray change and degree of cartilage damage. 5. 58% ot patients were satisfied to results of synovectomy, 28% were answered neither satisfied nor ansatisfied and 14% were unsatisf'ied to operation. We concluded the arthroscopic synovectomy of the knee joints was effective procedure to improve the clinical symptoms, range of knee motion and to alleviate the inflammatory reaction at mid-term period al'ter the operation. So we consider this procedure is a palliative treatment that modified and alleviate the progression of rheumatoid arthritis of knee joints.
Arthritis, Rheumatoid* ; C-Reactive Protein ; Cartilage ; Cartilage, Articular ; Follow-Up Studies ; Humans ; Joints ; Knee Joint* ; Knee* ; Palliative Care ; Range of Motion, Articular

Bilateral calcifications of the basal ganglia, the thalami, the dentate nuclei of the cerebellum, and the white matter of the cerebral hemisphere characterize Fahr's disease. The common clinical manifestations of the disease are movement disorders accompanied by cognitive impairment and mood disorder. Herein we report a case of Fahr's disease with atypical clinical manifestations. The patient was a 48 year-old man who presented with behavioral changes. His neurological examination showed no focal neurological deficits except for frontal dysfunctions. Abnormal involuntary movement was absent. Neuroimaging work-ups were compatible with Fahr's disease.
Basal Ganglia ; Cerebellum ; Cerebrum ; Dyskinesias ; Frontal Lobe* ; Humans ; Middle Aged ; Mood Disorders ; Movement Disorders ; Neuroimaging ; Neurologic Examination

We report a case of calcific bursitis of the shoulder in four-year-old boy who had severe pain and limitation of motion of the left shoulder joint for three days. Radiographs revealed the oval radiopaque lesion in the subacormial space, and the MR signal intensity of the mass was moderate on T2WI. Histological examination of the mass showed acute necrotizing inflammation with calcification.
Bursitis ; Humans ; Inflammation ; Male ; Shoulder ; Shoulder Joint

PURPOSE: To present the first report describing lesions of osteoma cutis on the upper eyelid and medial canthus.CASE SUMMARY: A 4-year-old female complained of a right upper eyelid mass. The examination showed a well-delineated, mild bluish-colored, hard mass over the upper eyelid and the medial canthus measuring 10 × 10 mm and 2 × 2 mm. During the cutaneous examination, her forearm, left shin, right dorsum of the foot, neck, and abdominal wall also showed well-delineated, mild bluish-colored, immobile hard masses, similar to the upper eyelid mass. A right upper eyelid and medial canthus mass excision was performed and a biopsy specimen was collected. Hematoxyline and eosin staining showed a mature bone in the dermis with spicules of bone and osteoblasts. She was finally diagnosed with osteoma cutis on the upper eyelid and the medial canthus. CONCLUSIONS Osteoma cutis is a rare, benign skin disorder characterized by bone formation in the skin. Albright hereditary osteodystrophy, which causes a metabolic disorder, should also be considered to prevent complications.

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.