Accurate determination of hepatic fat content is essential for investigating the quantitative association between hepatic steatosis and multiple metabolic disorders,and is of great significance in determining the beginning and goal for clinical intervention.More attention has been focused on establishing a non-invasive,simple and accurate method for determining hepatic fat content.Recently,a computer-aided ultrasound quantitative method may provide a new way for single and accurate estimation of hepatic fat content.

An early diagnosis of nonalcoholic fatty liver disease ( NAFLD) is meaningful to the prevention and cure of diabetes and cardiovascular disease ( CVD). The sensitivity and specificity of qualitative methods vary greatly, and these methods do not quantify liver fat content. Pathological diagnosis is a quantitative method, but it is invasive and inappropriate for clinical application. The establishment of H Magnetic Resonance Spectrum (1H MRS) opened up a brand-new era for noninvasive liver fat quantification. This review systemically introduces the new progress in noninvasive diagnosis of NAFLD.

The purpose of the present work is to observe cGMP positive cells after cerebral ischemia-reperfusion in the gerbil hip-pocampus. Immunofluorescent methods were used in gerbil hippocampal tissue slices. The results showed that after cerebral is-chemia cGMP synthesis in the CAi-a subfields was increased, cGMP positive cells were distributed mainly in CA1 subfield. Mostof cGMP positive cells were astrocytes. The number of small round cGMP positive cells were increased after recirculation follow-ing ischemia in the dentate gyrus. These results indicate that after cerebral ischemia cGMP synthesis was increased in the CA1-asubfield, It is possible that astrocytes play an important role in the regulation of metabolism in the early stage after ischemia-reperfusion.

AIM: To investigate the effect of Ginkgo biloba extrac (GBE) on cerebral ischemia during early stage of subarachnoid hemorrhage (SAH). METHODS: Noncraniotomy models of SAH in Wistar rats were used and animals were divided into sham-operated group, SAH group and SAH+GBE group. Dynamic change of regional cerebral blood flow (rCBF) was detected. Brain endothelin-1(ET-1) and calcium contents were also determined at different time point during 24 hours after the operation. Pathological change of neurons of hippocampus CA1 region was observed. RESULTS: In SAH group, rCBF decreased immediately and persistently after induction of SAH. Values of brain ET-1 content and calcium content at 1 hour, 6 hours and 24 hours were significantly higher than those in sham-operated group. Neurons of hippocampus CA1 region were damaged severely 3 days after onset of SAH. Above abnormal changes in SAH+GBE group were much slighter than those in SAH group. CONCLUSION: GBE may relieve cerebral ischemic damage after SAH.

AIM: To investigate the changes of somatosensory evoked potential(SEP), nitric oxide (NO) levels both in serum and in brain tissue after subarachnoid hemorrhage(SAH) and the influence of Ginkgo biloba extract(GBE) on them. METHODS: Wistar rats were divided into sham-operated group, pure SAH group and GBE-treated group. Dynamic changes of regional cerebral blood flow( rCBF),SEP, and NO levels both in serum and in brain tissue were detected within 24 hours after operation. RESULTS: In pure SAH group, rCBF decreased immediately after operation, with no tendency to recover within 24 hours. Latency of SEP delayed progressively from 1 hour to 24 hours after SAH.NO levels in serum and in brain tissue decreased and increased respectively from 1 hour to 24 hours after SAH. GBE effectively antagonized the changes of above parameters. CONCLUSION: SEP is useful in the judgement of cerebral ischemic damage after SAH. Decrease of serum NO and increase of brain NO are important factors leading to cerebral vasospasm and neural damage respectively after SAH. GBE relieves cerebral ischemic damage by reversing the pathological alterations of NO.

AIM: To investigate the pathological feature of neuron in the process of lymphostatic cerebro dema.METHODS: The model of lyphostatic cerebro edema was established by occluding and removing both the shallow and deep cervical lymph nodes in rats. The tissues of their brains were studied at different times after the operation, under light-microscope (HE stain and TUNEL stain) and electron-microscope.RESULTS: Cerebroedema appeared 2 days after the blockage of cervical lymphatic. Apoptosis and necrosis of neuron were observed in cerebral cortical of parietal lobus and hippocampal CA1 sector mainly. The alterations above were most noticeable at fifths day after the blockage. CONCLUSION: The blockage of the drainage of the cerebral lymphatic can lead to lymphastatic cerebroedema. Neuronal apoptosis and necrosis was the main pathological feature in the brain.

AIM: To investigate the changes of somatosensory evoked potential(SEP), nitric oxide (NO) levels both in serum and in brain tissue after subarachnoid hemorrhage(SAH) and the influence of Ginkgo biloba extract(GBE) on them. METHODS: Wistar rats were divided into sham-operated group, pure SAH group and GBE-treated group. Dynamic changes of regional cerebral blood flow( rCBF),SEP, and NO levels both in serum and in brain tissue were detected within 24 hours after operation. RESULTS: In pure SAH group, rCBF decreased immediately after operation, with no tendency to recover within 24 hours. Latency of SEP delayed progressively from 1 hour to 24 hours after SAH.NO levels in serum and in brain tissue decreased and increased respectively from 1 hour to 24 hours after SAH. GBE effectively antagonized the changes of above parameters. CONCLUSION: SEP is useful in the judgement of cerebral ischemic damage after SAH. Decrease of serum NO and increase of brain NO are important factors leading to cerebral vasospasm and neural damage respectively after SAH. GBE relieves cerebral ischemic damage by reversing the pathological alterations of NO.

AIM: To investigate the changes of bcl-2, bax expression and neuron apoptosis of cerebral cortex in lymphostatic encephalopathy of rats. METHODS: The model of lymphostatic encephalopathy was established by occluding and removing both the shallow and deep cervical lymph nodes in rats. The animals were sacrificed at 1, 2, 3, 5, 7 and 14 days after operation. HE staining was used to observe the structure of brain tissues and TUNEL staining was used to detect in situ cell apoptosis. The expressions of bcl-2 and bax were examined by RT-PCR. RESULTS: Cerebroedema appeared at the second day and was the most serious at the 5th day after blockage of cervical lymphatics. The number of TUNEL positive cells and the expression of bax began to increase at the 2nd day, reached a peak at the 5th day and dropped to control level at the 14th day. The expression of bcl-2 began to increase at the 1st day, reached a peak at the 5th day and dropped to control level at the 7th day. The increasing extent of bax was higher than that of bcl-2. CONCLUSION: The blockage of cervical lymphatics can lead to lymp[JP2]hostatic encephalopathy. Apoptosis is the main form of neuron death in the cortex and has relation to the increasing expression of bcl-2 and bax. [JP]

AIM: To investigate the role of nitric oxide in the development of brain edema after subarachnoid hemorrhage(SAH), and the influence of L-arginine on them. METHODS: Noncraniotomy models of SAH in Wistar rats were used and animals were divided into sham-operated group, SAH group and SAH plus L-arginine group. Dynamic changes of regional cerebral blood flow within 24 hours were measured. Serum nitric oxide level, brain water and sodium content at different time points within 24 hours were also detected. RESULTS: Regional cerebral blood flow and serum nitric oxide level at every time point after operation in SAH group were lower than those in sham-operated group, while brain water content and sodium content in the former group were higher than those in the latter group. Above pathological alterations in SAH plus L-arginine group were not so obvious as in SAH group. CONCLUSION: Decrease in serum nitric oxide plays a role in the development of brain edema after SAH, which may be partly reversed by administration of L-arginine.