Glioma, the most common primary intracranial tumor, has high morbidity and mortality. The detection of circulating tumor cells (CTCs) is an important part of the liquid biopsy of gliomas. CTCs, carrying the genetic and biological information of tumor tissue, provide a new perspective and dimension for the study of tumor metastasis, progression, chemotherapy sensitivity and drug resistance. Cerebrospinal fluid (CSF) circulates through the ventricle and spinal cord cistern, which can better maintain the original information of tumor cells compared with the complicated environments of tissues and plasma. Study on the dynamic changes of CTCs in the CSF of the central nervous system (CNS) is relatively rare. However, the analysis of CTCs in CSF can be used to guide the treatment of gliomas and reveal the pathophysiological and genetic mechanisms of tumor cell metastasis to the CSF. This paper reviews the progress in the research on CTC detection in gliomas.

Objective: bipolar cells (BCs) communicate with amacrine and ganglion cells of the retina via both transient and sustained neurotransmitter release in ribbon synapses. Reconstructing the published quantitative release data from electrical soma stimulation (voltage clamp experiments) of rat rod BCs were used to develop two simple models to predict the number of released vesicles as time series. In the experiment, the currents coming to the AII amacrine cell originating from releasing vesicles from the rod BC were recorded using paired-recordings in whole-cell voltage-clamp method. Method: one of the models is based directly on terminal transmembrane voltage, so-called ‘modelV’, whereas the temporally exacter modelCa includes changes of intracellular calcium concentrations at terminals. Result: the intracellular calcium concentration method replicates a 0.43 ms signal delay for the transient release to pulsatile stimulation as a consequence of calcium channel dynamics in the presynaptic membrane, while the modelV has no signal delay. Both models produce the quite similar results in low stimuli amplitudes. However, for large stimulation intensities that may be done during extracellular stimulations in retinal implants, the modelCa predicts that the reversal potential of calcium limits the number of transiently released vesicles. Adding sodium and potassium ion channels to the axon of the cell enable to study the impact of spikes on the transient release in BC ribbons. Conclusion: a spike elicited by somatic stimulation causes the rapid release of all vesicles that are available for transient release, while a non-spiking BC with a similar morphometry needs stronger stimuli for any transient vesicle release. During extracellular stimulation, there was almost no difference in transient release between the active and passive cells because in both cases the terminal membrane of the cell senses the same potentials originating from the microelectrode. An exception was found for long pulses when the spike has the possibility to generate a higher terminal voltage than the passive cell. Simulated periodic 5 Hz stimulation showed a reduced transient release of 3 vesicles per stimulus, which is a recovery effect.

Objective: to investigate the expression of yeast silencing information regulator 2 (Sirt2) in the secondary injury of intracerebral hemorrhage (ICH). Methods: twelve Sprague Dawley (SD) rats were randomly divided into a sham group and an ICH group, with six rats in each group. A rat model of ICH was established by injecting collagenase type IV into the right striatum of the rats. The expression of Sirt2 was measured by Western blot and immunohistochemistry after ICH. Result: the behavioral score of the ICH rats was the lowest at 48 h after the operation; therefore the rats at 48 h after surgery were selected as the model rats. The expression of Sirt2 was significantly higher in the striatal tissue of the ICH rats compared with the sham group (P＜0.05). Conclusion: the expression of Sirt2 around hematoma in ICH rats decreases, and Sirt2 is expected to become a new target for ICH treatment.

Subdural hematoma is often secondary to brain trauma and other diseases. The onset is hidden and the condition is critical. Timely detection and early treatment are particularly important. The patient denied a history of trauma, but had a history of consciousness loss after charcoal burning. The clinical symptoms were progressive cognitive impairment. The initial diagnosis was delayed encephalopathy caused by carbon monoxide poisoning. However, computed tomography (CT) scan of the brain showed a large area of subdural hematoma on the left side and the formation of a cerebral hernia, which was life-threatening. The patient’s symptoms gradually improved after an emergency operation.