To investigate the difference of dry ear wax and wet ear wax, the lipid composition of wet ear wax was analyzed and compared with that of dry ear wax. In dry ear wax, squalene, steryl esters, wax esters, triglycerides free fatty acids and cholesterol were found. Squalene, triglycerides, free fatty acids and cholesterol formed the main demonstrable fractions in wet ear wax. In addition, three unidentified spots were always present in wet ear wax. Our results indicate that wet ear wax is due to the difference of quantity and composition of ear wax lipids.
Cerumen/metabolism* ; Ear Canal/metabolism ; Ear Diseases/metabolism* ; Human ; Lipids/metabolism*

OBJECTIVE: To detect the expression and localization of macrophages and BMP2 (bone morphogenetic protein 2) in the middle ear mucosa of TS, to explore its role in the pathogenesis of TS. METHOD: Seventeen patients with TS were studied and 17 matching cases with simple chronic suppurative otitis media (COM) were enrolled as control. Immunohistochemistry was performed to detect the expression and localization of CD68 (the symbol of macrophage) and BMP2 in the middle ear mucosa. And the expression difference in the TS and COM were analyzed. RESULT: Positive cells of CD68 was mainly localized in the submucosa layer. Each group had 12 cases with positive expression of CD68 (70.59%) and had no difference in the number of positive cells (TS: 6.94 +/- 6.08; COM: 7.59 +/- 7.84; P=0.79). All the specimens had positive expression of BMP2 and BMP2 protein was expressed in the mucosa layer and submucosa layer. There was statistical difference in the number of BMP2 expression between TS and COM group. In TS group, all the sclerotic plaques were surrounded with macrophages and BMP2 positive cells. The cells surrounding sclerotic plaques were synchronously expressing CD68 positive and BMP2 positive. CONCLUSION Macrophages should take part in the pathogenesis of TS. BMP2 secreted by macrophage was important in formation of TS.
Adolescent ; Adult ; Bone Morphogenetic Protein 2 ; metabolism ; Ear Diseases ; metabolism ; pathology ; Ear, Middle ; metabolism ; pathology ; Female ; Humans ; Macrophages ; metabolism ; Male ; Middle Aged ; Sclerosis ; metabolism ; pathology ; Young Adult

Mitochondria contain the respiratory chain enzyme complexes that carry out oxidative phosphorylation and produce the majority of cellular energy in the form of ATP. Mitochondrial disorders are either due to sporadic or inherited mutations of genes located in nuclear or mitochondrial DNA or due to other exogenous factors. Although several proteins related with signalling, assembling, transporting, and enzymatic function can be impaired in mitochondrial disorders, most frequently however, the activity of the respiratory chain protein complexes is primarily or secondarily affected, leading to impaired oxygen utilization and reduced energy production. Mitochondrial disorders usually show a chronic slowly progressive course and present with multiorgan involvement with varying onset between birth and late adulthood. They represent a diagnostic challenge because of their wide variation in presentation and course. Systems frequently affected in mitochondrial disorders are peripheral nervous system, brain, endocrine system, heart, eyes, ears, guts, kidney and bone marrow. Although there is no specific therapy and cure for mitochondrial disorders, the rapidly increasing understanding of the pathophysiological background of the disorders may further facilitate the diagnostic approach and open perspectives to, possibly causative therapies in future.
Adenosine Triphosphate ; Bone Marrow ; Brain ; DNA, Mitochondrial ; Ear ; Electron Transport ; Endocrine System ; Energy Metabolism ; Heart ; Kidney ; Mitochondria ; Mitochondrial Diseases* ; Oxidative Phosphorylation ; Oxygen ; Parturition ; Peripheral Nervous System

Mitochondria contain respiratory chain enzyme complexes that carry out oxidative phosphorylation and produce a main part of cellular energy in the form of ATP. Mitochondrial disorders occur either due to sporadic or inherited mutations of the genes located in the nuclear or mitochondrial DNA or due to other exogenous factors. Although several proteins related with signalling, assembling, transporting, and enzymatic functions can be impaired in mitochondrial disorders, most frequently the activity of the respiratory chain protein complexes is primarily or secondarily affected, leading to impaired oxygen utilization and reduced energy production. Mitochondrial disorders usually show a chronic and slowly progressive course and present with multiorgan involvement with varying onsets between birth and late adulthood. They represent a diagnostic challenge because of their wide variations in the presentation and the course. The systems frequently affected in mitochondrial disorders are the peripheral nervous system, brain, endocrine system, heart, eyes, ears, guts, kidneys and bone marrow. Although there is actually no specific therapy and cure for mitochondrial disorders, the rapidly increasing understanding of the pathophysiological background of mitochondrial disorders may further facilitate the diagnostic approach and open perspectives to the future and possibly causative therapies.
Adenosine Triphosphate ; Bone Marrow ; Brain ; DNA, Mitochondrial ; Ear ; Electron Transport ; Endocrine System ; Energy Metabolism ; Heart ; Kidney ; Mitochondria ; Mitochondrial Diseases* ; Oxidative Phosphorylation ; Oxygen ; Parturition ; Peripheral Nervous System

OBJECTIVETo observe the effect of different concentration of Tamoxifen ointment on the fibroblasts and transforming growth factor (TGF-beta2) of hypertrophic scar at rabbit ears, so as to explore the possibility of treatment of hypertrophic scar with Tamoxifen.

METHODSThe hypertrophic scar model was established in 96 New Zealand rabbits' ears. The wounds were divided into four groups (A, B, C and D), with 144 wounds in each group. Different concentration of tamoxifen ointment (0.5%, 1%, 2%) was topically administered in groups A, B and C respectively, and blank ointment in group D. On postoperative day 30, 60 and 90, the scar samples were harvested. The scar thickness, scar histological change and the content of TGF-beta2 were detected.

RESULTS(1) On the 30th day after operation, the difference of scar tissue thickness among groups A, D and B, C reached statistical significance (group A, D < group B < group C). However, there was a contrary tendency in fibroblasts density and TGF-beta2 content of the scar tissue simultaneously. (2) On 60th, 90th day after injury, there was statistical difference in scar thickness, fibroblasts density and the content of TGF-beta2 in scar of four groups (P < 0.05). The content of TGF-beta2 in group A, B, C, D was (43.97 +/- 3.63) microg/L, (41.92 +/- 3.91) microg/L, (36.69 +/- 4.15) microg/L, (54.90 +/- 4.71) microg/L, respectively, on 60th day; and (45.69 +/- 2.63) microg/L, (40.43 +/- 3.87) microg/L, (38.76 +/- 3.24) microg/L, (52.59 +/- 4.92) microg/L, respectively, on 90th day. The fibroblasts density of scar in groups A, B, C, D was (4392.07 +/- 327.84) point/mm2, (4208.57 +/- 329.76) point/mm2 (4 033.44 +/- 427.91) point/mm2, (4863.03 +/- 387.98) point/mm2, respectively, on 60th day; and (4418.41 +/- 432.52) point/mm2, (4077.65 +/- 386.70) point/mm2, (3844.53 +/- 354.29) point/mm2, (4838.64 +/- 390.52) point/mm2, respectively, on 90th day. The content of TGF-beta2 and fibroblasts density of scar were lined up as group D > group A > group B > group C (P < 0.05).

CONCLUSIONSTopical Tamoxifen can reduce the content of TGF-beta2 and fibroblast, decrease fibroblasts density and the formation of hypertrophic scar at rabbit ears. It offers a new way for the treatment of the hypertrophic scar.

Animals ; Cicatrix, Hypertrophic ; drug therapy ; metabolism ; pathology ; Disease Models, Animal ; Ear Diseases ; drug therapy ; metabolism ; pathology ; Fibroblasts ; drug effects ; pathology ; Ointments ; Rabbits ; Tamoxifen ; pharmacology ; Transforming Growth Factor beta2 ; metabolism

AIMTo investigate the expression of matrix metalloproteinase-9 (MMP-9) in mouse ears induced with croton oil and the inhibitory effect of dexamethasone, indomethacin and resveratrol on MMP-9 expression, and further explore the relationship between anti-inflammation and MMP-9 inhibition of these three medicines.

METHODSImmuno-histochemistry was used to detect the expression of MMP-9 in mouse ears. Expression of MMP-9 in U937 cells was analyzed by gelatin zymography.

RESULTSMouse ear edema induced with croton oil was inhibited significantly by dexamethasone and indomethacin at the dose of 10 mg.kg-1 and resveratrol at 50 mg.kg-1 administered subcutaneously. The inhibitory rate was 76.2% (P < 0.001), 56.7% (P < 0.001) and 36.9% (P < 0.001) respectively. The MMP-9 expression increased in mouse ears induced with croton oil and inhibited by dexamethasone, indomethacin and resveratrol at above doses. Gelatin zymography results showed that MMP-9 expression in U937 cells increased significantly after exposed to PMA at 1 x 10(-8) mol.L-1 (P < 0.001); MMP-9 expression induced with phorbol myristate acetate(PMA) was inhibited by dexamethasone at 1 x 10(-9), 1 x 10(-7) and 1 x 10(-5) mol.L-1, indomethacin at 1 x 10(-6) and 1 x 10(-5) mol.L-1 and resveratrol at 1 x 10(-6) and 1 x 10(-5) mol.L-1.

CONCLUSIONThe inhibition of MMP-9 expression may be one of the anti-inflammatory mechanisms of dexamethasone, indomethacin and resveratrol.

Animals ; Anti-Inflammatory Agents ; pharmacology ; Anti-Inflammatory Agents, Non-Steroidal ; pharmacology ; Croton Oil ; Dexamethasone ; pharmacology ; Ear Diseases ; chemically induced ; metabolism ; Edema ; chemically induced ; metabolism ; Humans ; Indomethacin ; pharmacology ; Male ; Matrix Metalloproteinase 9 ; metabolism ; Matrix Metalloproteinase Inhibitors ; Mice ; Mice, Inbred ICR ; Random Allocation ; Stilbenes ; pharmacology ; U937 Cells ; metabolism