Ultrastructural changes in the spiral organ of cochlea at various intervals after exposure to impulse noise were investigated. Guinea pigs were exposed to 10 impulses noise of 166 dB SPL peak level which had duration of 0.1 ms. Thirteen of the exposed animals were used to systematically measure threshold shift at regular intervals from 30 min to 30d post-exposure. The other fourteen animals who had been exposed to the same impulse noise were killed for transmission electron microscopy (TEM) examination at the same intervals, respectively. The recovery pattern of threshold shift showed a nonmonotonic type. There was a progressive deterioration of changes in the hair cells between 30 min and 8h after exposure. Intracellular degeneration reached a peak at 8h and marked edema and swelling leading to deformation of the outer hair cells (OHCs), fused stereocilia, large vesicles in cytoplasm and swollen submembraneous cisterns were found. After that time the extent of degeneration in the hair cells reduced. The time sequence of changes in the spiral organ of cochlea in the present study was associated with the recovery pattern of threshold shift.

Guinea pigs were exposed to either 110dB SPL white noise for 30min (ITS group )or 120 dB SPL for 150 nun (PTS group). At varying postexposure intervals, threshold shifts were assessed using auditory cortex evoked response to tone bursts and intracellular ultrastructural changes in the spiral organ of cochleae were exmained with a transmission electron microscope.. The threshold shifts induced by 110dB noise were reversible while those induced by 120dB noise were generally irreversible. In the TTS cochleae, damage was confined to the third row of OHCs where depolymerization of actin filaments within the stereocilia, slight celluar swelling and small vacuolization were found. The subnuclear area and nerve-endings were not involved. In the PTS cochleae, the inner hair cells (IHCs) and the first row of OHCs were affected. The abnormilities consisted of ruptures and holes in the cuticular plates, fusion of stereocilia, marked edema, tranclucence of subcuticular region, swelling of submembraneous cisterns and large vesiculation in the efferent nerve-endings blow OHCs. Based on the ultrastructural observations, structural bases in cochleae for TTS and PTS, sequence of pathological changes in hair cells as well as reversibility of specific pathologies were suggested.

Portal vein thrombosis (PVT) is commonly seen in patients with liver cirrhosis. Patients with varices complicated by portal vein thrombosis are more likely to experience bleeding, with higher failure rate of hemostasis and rebleeding rate, and the patients receiving liver transplantation may have a poorer prognosis. There are various risk factors for portal vein thrombosis, such as severity of liver dysfunction, use of non-selective beta blockers, and portal vein blood flow velocity. This article reviews the risk factors for portal vein thrombosis in patients with liver cirrhosis, in order to further understand the mechanism and risk level of portal vein thrombosis.