Objective To investigate the etiology,clinical characteristics,diagnosis,and treatment strategies and efficacy of pulsatile tinnitus(PT)caused by vascular anatomy abnormality.Methods The clinical data of 45 patients w...Objective To investigate the etiology,clinical characteristics,diagnosis,and treatment strategies and efficacy of pulsatile tinnitus(PT)caused by vascular anatomy abnormality.Methods The clinical data of 45 patients with PT in our hospital from 2012 to 2019 were collected and retrospectively analyzed.Results All 45 patients had vascular anatomical abnormalities.The patients were divided into 10 categories according to the different locations of vascular abnormalities:sigmoid sinus diverticulum(SSD),sigmoid sinus wall dehiscence(SSWD),SSWD with high jugular bulb,pure dilated mastoid emissary vein,aberrant internal carotid artery(ICA)in the middle ear,transverse-sigmoid sinus(TSS)transition stenosis,TSS transition stenosis with SSD,persistent occipital sinus stenosis,petrous segment stenosis of ICA,and dural arteriovenous fistula.All patients complained of PT synchronous with heartbeat rhythm.Endovascular interventional therapy and extravascular open surgery were used according to the location of the vascular lesions.Tinnitus disappeared in 41 patients,was significantly relieved in 3 patients,and was unchanged in 1 patient postoperatively.Except for one patient with transient headache postoperatively,no obvious complications occurred.Conclusion PT caused by vascular anatomy abnormalities can be identified by detailed medical history and physical and imaging examination.PT can be relieved or even completely alleviated after appropriate surgical treatments.展开更多
Objective: To observe and compare the efficacy of intratympanic application of dexamethasone (DXM) for the treatment of refractory sudden sensorineural hearing loss (SSNHL), the DXM was given in three different ways: ...Objective: To observe and compare the efficacy of intratympanic application of dexamethasone (DXM) for the treatment of refractory sudden sensorineural hearing loss (SSNHL), the DXM was given in three different ways: by tympanic membrane injection, by drip through a ventilation tube, and by perfusion through a round window catheter. Methods: We conducted a nonrandomized retrospective clinical trial involving 55 patients with refractory SSNHL. For 21 patients (the perfusion group), DXM (2.5 mg/0.5 ml) was perfused transtympanically through a round window catheter using an infusion pump for 1 h twice a day for 7 d giving a total amount of 35.0 mg. For 23 patients (the injection group), DXM (2.5 mg/time) was injected by tympanic membrane puncture at intervals of 2 d on a total of four occasions giving a total amount of 10.0 mg. For 11 patients (the drip group), DXM (2.5 mg/0.5 ml) was dripped via a ventilation tube placed by myringotomy, once on the first day and twice a day for the remaining 6 d giving a total amount of 32.5 mg. Thirty-two patients with refractory SSNHL who refused to undertake further treatments were defined as the control group. Hearing recovery and complications were compared among the groups. Hearing results were evaluated based on a four-frequency (0.5, 1.0, 2.0, 4.0 kHz) pure tone average (PTA). Results: Post-treatment audiograms were obtained one month after treatments were completed. The improvements in average PTA for the perfusion, injection, and drip groups were 9.0, 8.6, and 1.7 dB, respectively. Hearing improvement was significantly greater in the perfusion and injection groups than in the control group (1.4 dB) (P<0.05). In the perfusion group, 8 out of 21 patients (38.1%) had a PTA improvement of 15?56 dB (mean 29.8 dB); in the injection group, 8 out of 23 patients (34.8%) had a PTA improvement of 16?54 dB (mean 24.9 dB); in the drip group, 1 of 11 patients (9.1%) had a PTA improvement of 26.0 dB; in the control group, 3 out of 32 patients (9.4%) had a PTA improvement of 15?36 dB (mean 14.9 dB). Conclusions: Topical intratympanic application of DXM is a safe and effective method for the treatment of SSNHL cases that are refractory to conventional therapies.展开更多
Objective:To evaluate the effects of mitomycin on the growth of human dermal fibroblast and immortalized human keratinocyte line (HaCat cell),particularly the effect of mitomycin on intracellular messenger RNA (mRNA) ...Objective:To evaluate the effects of mitomycin on the growth of human dermal fibroblast and immortalized human keratinocyte line (HaCat cell),particularly the effect of mitomycin on intracellular messenger RNA (mRNA) synthesis of collagen and growth factors of fibroblast.Methods:The normal dermal fibroblast and HaCat cell were cultured in vitro.Cell cultures were exposed to 0.4 and 0.04 mg/ml of mitomycin solution,and serum-free culture medium was used as control.The cellular morphology change,growth characteristics,cell proliferation,and apoptosis were observed at different intervals.For the fibroblasts,the mRNA expression changes of transforming growth factor (TGF)-β1,basic fibroblast growth factor (bFGF),procollagen Ⅰ,and Ⅲ were detected by reverse transcription polymerase chain reaction (RT-PCR).Results:The cultured normal human skin fibroblast and HaCat cell grew exponentially.A 5-min exposure to mitomycin at either 0.4 or 0.04 mg/ml caused marked dose-dependent cell proliferation inhibition on both fibroblasts and HaCat cells.Cell morphology changed,cell density decreased,and the growth curves were without an exponential phase.The fibroblast proliferated on the 5th day after the 5-min exposure of mitomycin at 0.04 mg/ml.Meanwhile,5-min application of mitomycin at either 0.04 or 0.4 mg/ml induced fibroblast apoptosis but not necrosis.The apoptosis rate of the fibroblast increased with a higher concentration of mytomycin (p<0.05).A 5-min exposure to mitomycin at 0.4 mg/ml resulted in a marked decrease in the mRNA production of TGF-β1,procollagen Ⅰ and Ⅲ,and a marked increase in the mRNA production of bFGF.Conclusions:Mitomycin can inhibit fibroblast proliferation,induce fibroblast apoptosis,and regulate intracellular protein expression on mRNA levels.In additon,mitomycin can inhibit HaCat cell proliferation,so epithelial cell needs more protecting to avoid mitomycin's side effect when it is applied clinically.展开更多
基金supported by the Medical Science and Technology Project of Zhejiang Province(No.2019KY584)Traditional Chinese Medicine Science and Technology Project of Zhejiang Province(No.2023ZL648).
文摘Objective To investigate the etiology,clinical characteristics,diagnosis,and treatment strategies and efficacy of pulsatile tinnitus(PT)caused by vascular anatomy abnormality.Methods The clinical data of 45 patients with PT in our hospital from 2012 to 2019 were collected and retrospectively analyzed.Results All 45 patients had vascular anatomical abnormalities.The patients were divided into 10 categories according to the different locations of vascular abnormalities:sigmoid sinus diverticulum(SSD),sigmoid sinus wall dehiscence(SSWD),SSWD with high jugular bulb,pure dilated mastoid emissary vein,aberrant internal carotid artery(ICA)in the middle ear,transverse-sigmoid sinus(TSS)transition stenosis,TSS transition stenosis with SSD,persistent occipital sinus stenosis,petrous segment stenosis of ICA,and dural arteriovenous fistula.All patients complained of PT synchronous with heartbeat rhythm.Endovascular interventional therapy and extravascular open surgery were used according to the location of the vascular lesions.Tinnitus disappeared in 41 patients,was significantly relieved in 3 patients,and was unchanged in 1 patient postoperatively.Except for one patient with transient headache postoperatively,no obvious complications occurred.Conclusion PT caused by vascular anatomy abnormalities can be identified by detailed medical history and physical and imaging examination.PT can be relieved or even completely alleviated after appropriate surgical treatments.
文摘Objective: To observe and compare the efficacy of intratympanic application of dexamethasone (DXM) for the treatment of refractory sudden sensorineural hearing loss (SSNHL), the DXM was given in three different ways: by tympanic membrane injection, by drip through a ventilation tube, and by perfusion through a round window catheter. Methods: We conducted a nonrandomized retrospective clinical trial involving 55 patients with refractory SSNHL. For 21 patients (the perfusion group), DXM (2.5 mg/0.5 ml) was perfused transtympanically through a round window catheter using an infusion pump for 1 h twice a day for 7 d giving a total amount of 35.0 mg. For 23 patients (the injection group), DXM (2.5 mg/time) was injected by tympanic membrane puncture at intervals of 2 d on a total of four occasions giving a total amount of 10.0 mg. For 11 patients (the drip group), DXM (2.5 mg/0.5 ml) was dripped via a ventilation tube placed by myringotomy, once on the first day and twice a day for the remaining 6 d giving a total amount of 32.5 mg. Thirty-two patients with refractory SSNHL who refused to undertake further treatments were defined as the control group. Hearing recovery and complications were compared among the groups. Hearing results were evaluated based on a four-frequency (0.5, 1.0, 2.0, 4.0 kHz) pure tone average (PTA). Results: Post-treatment audiograms were obtained one month after treatments were completed. The improvements in average PTA for the perfusion, injection, and drip groups were 9.0, 8.6, and 1.7 dB, respectively. Hearing improvement was significantly greater in the perfusion and injection groups than in the control group (1.4 dB) (P<0.05). In the perfusion group, 8 out of 21 patients (38.1%) had a PTA improvement of 15?56 dB (mean 29.8 dB); in the injection group, 8 out of 23 patients (34.8%) had a PTA improvement of 16?54 dB (mean 24.9 dB); in the drip group, 1 of 11 patients (9.1%) had a PTA improvement of 26.0 dB; in the control group, 3 out of 32 patients (9.4%) had a PTA improvement of 15?36 dB (mean 14.9 dB). Conclusions: Topical intratympanic application of DXM is a safe and effective method for the treatment of SSNHL cases that are refractory to conventional therapies.
基金supported by the Social Development of Science and Technology Program of Ningbo City(No.2010C50031)the Ningbo Natural Science Foundation(No.2013A610261),China
文摘Objective:To evaluate the effects of mitomycin on the growth of human dermal fibroblast and immortalized human keratinocyte line (HaCat cell),particularly the effect of mitomycin on intracellular messenger RNA (mRNA) synthesis of collagen and growth factors of fibroblast.Methods:The normal dermal fibroblast and HaCat cell were cultured in vitro.Cell cultures were exposed to 0.4 and 0.04 mg/ml of mitomycin solution,and serum-free culture medium was used as control.The cellular morphology change,growth characteristics,cell proliferation,and apoptosis were observed at different intervals.For the fibroblasts,the mRNA expression changes of transforming growth factor (TGF)-β1,basic fibroblast growth factor (bFGF),procollagen Ⅰ,and Ⅲ were detected by reverse transcription polymerase chain reaction (RT-PCR).Results:The cultured normal human skin fibroblast and HaCat cell grew exponentially.A 5-min exposure to mitomycin at either 0.4 or 0.04 mg/ml caused marked dose-dependent cell proliferation inhibition on both fibroblasts and HaCat cells.Cell morphology changed,cell density decreased,and the growth curves were without an exponential phase.The fibroblast proliferated on the 5th day after the 5-min exposure of mitomycin at 0.04 mg/ml.Meanwhile,5-min application of mitomycin at either 0.04 or 0.4 mg/ml induced fibroblast apoptosis but not necrosis.The apoptosis rate of the fibroblast increased with a higher concentration of mytomycin (p<0.05).A 5-min exposure to mitomycin at 0.4 mg/ml resulted in a marked decrease in the mRNA production of TGF-β1,procollagen Ⅰ and Ⅲ,and a marked increase in the mRNA production of bFGF.Conclusions:Mitomycin can inhibit fibroblast proliferation,induce fibroblast apoptosis,and regulate intracellular protein expression on mRNA levels.In additon,mitomycin can inhibit HaCat cell proliferation,so epithelial cell needs more protecting to avoid mitomycin's side effect when it is applied clinically.