No Abstract Available.
Anti-HIV Agents* ; Complement System Proteins* ; HIV-1*

Osteitis pubis is a noninfectious, painful, inflammmatory condition affecting the periosteum, cartilage, and ligaments of the symphysis pubis. It has been associated with urologic and gynecologic procedures, pregnancy and rheumatologic disorders. Despite seven decades of speculation, its pathogenesis, diagnostic criteria, natural history and optimal therapy for osteitis pubis remain controversial. We had experienced two cases of osteitis pubis after laparoscopic Burch colposuspension using prolene mesh and Tacker(R). All cases of osteitis pubis were treated with conservative managements.
Cartilage ; Ligaments ; Natural History ; Osteitis* ; Periosteum ; Polypropylenes ; Pregnancy

BACKGROUND AND OBJECTIVES: Tuberculous otitis media is not commonly found nowadays, and therefore, the index of suspicion is often low. However, once contracted, it can cause significant morbidities, such as profound hearing loss, labyrinthitis, facial nerve palsy and so on, if early diagnosis and treatment are not performed. MATERIALS AND METHODS: In the chronic otitis media patients who visited Masan Samsung Hospital from Jan. 1993 to Jan. 1996, 37 cases of pathologically proven tuberculous otitis media were retrospectively reviewed. And temporal bone computerized tomography (TBCT) of 14 cases of tuberculous otitis media were compared to those of chronic suppurative otitis media and choronic otitis media with cholesteatoma. RESULTS: 1) Classic clinical findings of the disease such as multiple perforation, painless otorrhea, young age are not consistent with the clinical findings reviewed here. 2) Unexpectedly severe hearing loss, facial paralysis, eroded malleus handle, polypoid granulation or necrotic debris in middle ear cavity were significant clinical features. 3) In TBCT findings, soft tissue density in the entire middle ear cavity, soft tissue density extension to superior external auditory canal, poor sclerotic change of mastoid air cell were more common than other types of chronic otitis media. 4) Most of cases were confirmed by operative specimen pathologically. 5) Delayed healing of postoperative wound and formation of granulation tissue suggested tuberculous otitis media. 6) Antituberculous chemotherapy provided effective means of treatment. CONCLUSION: Early diagnosis by pathologic examination of biopsied tissue obtained at OPD was mandatory to avoid complication and postoperative morbidity. Postoperative specimen obtained from middle ear surgery must be confirmed pathologically.
Cholesteatoma ; Cytochrome P-450 CYP1A1 ; Drug Therapy ; Ear Canal ; Ear, Inner ; Ear, Middle ; Early Diagnosis ; Facial Nerve ; Facial Paralysis ; Granulation Tissue ; Hearing Loss ; Humans ; Labyrinthitis ; Malleus ; Mastoid ; Otitis Media* ; Otitis Media, Suppurative ; Otitis* ; Paralysis ; Retrospective Studies ; Temporal Bone ; Wounds and Injuries

The primary cilium, a microtubule-based cellular organelle present in certain kidney cells, functions as a mechano-sensor to monitor fluid flow in addition to various other biological functions. In kidneys, the primary cilia protrude into the tubular lumen and are directly exposed to pro-urine flow and components. However, their effects on urine concentration remain to be defined. Here, we investigated the association between primary cilia and urine concentration. Methods: Mice either had free access to water (normal water intake, NWI) or were not allowed access to water (water deprivation, WD). Some mice received tubastatin, an inhibitor of histone deacetylase 6 (HDAC6), which regulates the acetylation of α-tubulin, a core protein of microtubules. Results: WD decreased urine output and increased urine osmolality, concomitant with apical plasma membrane localization of aquaporin 2 (AQP2) in the kidney. After WD, compared with after NWI, the lengths of primary cilia in renal tubular epithelial cells were shortened and HDAC6 activity increased. WD induced deacetylation of α-tubulin without altering α-tubulin levels in the kidney. Tubastatin prevented the shortening of cilia through increasing HDAC6 activity and consequently increasing acetylated α-tubulin expression. Furthermore, tubastatin prevented the WD-induced reduction of urine output, urine osmolality increase, and apical plasma membrane localization of AQP2. Conclusions: WD shortens primary cilia length through HDAC6 activation and α-tubulin deacetylation, while HDAC6 inhibition blocks the WD-induced changes in cilia length and urine output. This suggests that cilia length alterations are involved, at least in part, in the regulation of body water balance and urine concentration.

The primary cilium protrudes from the cell surface and functions as a mechanosensor. Recently, we found that water intake restriction shortens the primary cilia of renal tubular cells, and a blockage of the shortening disturbs the ability of the kidneys to concentrate urine. Here, we investigate whether high water intake (HWI) alters primary cilia length, and if so, what is its underlying mechanism and its role on kidney urine production. Methods: Experimental mice were given free access to normal water (normal water intake) or 3% sucrose-containing water for HWI for 2 days. Some mice were administered with U0126 (10 mg/kg body weight), an inhibitor of MEK kinase, from 2 days before HWI, daily. The primary cilium length and urine amount and osmolality were investigated. Results: HWI-induced diluted urine production and primary cilium elongation in renal tubular cells. HWI increased the expression of α-tubulin acetyltransferase 1 (αTAT1), leading to the acetylation of α-tubulins, a core protein of the primary cilia. HWI also increased phosphorylated ERK1/2 (p-ERK1/2) and exocyst complex component 5 (Exoc5) expression in the kidneys. U0126 blocked HWI-induced increases in αTAT1, p-ERK1/2, and Exoc5 expression. U0126 inhibited HWI-induced α-tubulin acetylation, primary cilium elongation, urine amount increase, and urine osmolality decrease. Conclusion: These results show that increased water intake elongates the primary cilia via ERK1/2 activation and that ERK inhibition prevents primary cilium elongation and diluted urine production. These data suggest that the elongation of primary cilium length is associated with the production of diluted urine.