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Blunt vertebral artery injury occurs frequently in forensic practice. However, injuries of the vertebral artery are easily ignored or overlooked because of its relatively deep location. Through literatures review, this paper finds that the manners of blunt vertebral artery injury are varied and one or more injury mechanisms may be involved simultaneously. Patients often undergo immediate or delayed cerebral apoplexy as well as compression and injury of surrounding structures, due to direct injury or secondary aneurysm or dissection, resulting in disability or death. Diseases such as, vertebral atherosclerosis and dysplasia can increase the disability and death risk and the difficulty of forensic identification. In forensic identification, the details of the case should be considered. For cases of suspected vertebral artery injury, in addition to routine examination of intracranial segment, attention should be paid to the examination of extracranial segment. If conditions permit, angiography can be used prior to or during the autopsy to improve the identification efficiency and accuracy of opinions.

The ultrafine-palygorskite/copper composites(ultrafine-P/Cu) were prepared by mechanical ball milling. The extreme pressure properties and the effect of load and speed on tribological properties of ultrafine-P/Cu powders, as 150N base oil additive, were evaluated on a four ball friction wear tester. The morphologies, element distributions and micromechanical properties of the worn surface were investigated by means of scanning electron microscopy, energy dispersive spectrometry and X-ray photoelectron spectroscopy. The results indicate that ultrafine-P/Cu used as a lubricant additive can effectively improve the tribological properties of base oil. The non-seizure value PB of ultrafine-P/Cu lubricant is increased by 31.6% than the base oil and by 9.1% than the single particles. Load and speed can affect the tribological properties of ultrafine-P/Cu. Ultrafine-P/Cu exhibits the optimum friction-reducing property and anti-wear property at the load of 245N and speed of 1200r/min, respectively. The excellent tribological properties of ultrafine-P/Cu can be attributed to the porous auto-restoration film of palygorskite and extended film of Cu formed on the worn surface to compensate wear and repair friction.

Internal carotid arterial system is the main source of blood supply in brain. In forensic identification practice, blunt injures of internal carotid arterial system usually cause complications such as thrombus, aneurysm and arteriovenous fistula, etc. The deaths following delayed cerebral infarction or intracranial haemorrhage are not rare. At present, literature of deaths caused by blunt injuries of internal carotid arterial system mainly consist of case reports in China. This paper reviews related literature and case reports at home and abroad, and summarizes forensic medical features and identification method of the deaths caused by such injuries. The results show that blunt injures of internal carotid arterial system are related to the direct or indirect force on head and neck, which can result in exceed physiological range traction of head and neck, incision following basicranial fracture, etc. Such injuries are common in the cases as mechanical asphyxia, cervical manipulation, traffic accident and fall, etc. The artery should be examined carefully, and the relationship among injury, disease and death should be analysed correctly when no cause of infarction and hemorrhage was found in routine examination of such cases in forensic pratice. Because of the difficulty for exposing the artery completely in autopsy, angiography can be used to infer the location when necessary for improving the scientificity and reliability of the appraisal conclusion.

Connexin (Cx) 36 is known to be a component of gap junctions, and has been suggested to play an important role in epilepsy. In order to determine dynamic changes of Cx36 protein expression in epilepsy and investigate the role of Cx36 in electroencephalographic activity and pathogenesis, we utilized kainic acid (KA) to induce epileptogenesis. We found that epileptic discharges began 71.8 ± 23.7 s after KA administration. Spike frequency and amplitude of epileptiform activity reached maximal levels at 30 ± 5.2 min. The maximum level of spike frequency and amplitude of epileptiform activity was 13.9 ± 0.3 Hz and 198 ± 14.3mV respectively. Employing Western blotting and immunohistochemistry, we demonstrated that hippocampal Cx36 protein expression was significantly increased 6 h after KA kindling compared to control or sham groups, but decreased in 3 d and 7d groups. Our results suggested that the dynamic change of Cx36 expression may play an important role inepilepsy, and the specific manipulation of Cx36 expression may be a potential target for the treatment of epilepsy.

In this study we investigated the potential anti-epileptogenic effect of neuronal connexin Cx36 gap junction blockage via inhibition of microtubule-associated protein 2 (MAP-2) and synaptophysin (SYP) overexpression. Thirty adult male Wistar rats were divided into five groups (six animals per group): control, sham, carbenoxolone (CBX), quinine (QN), and quinidine (QND). An epilepsy model was produced by injecting kainic acid (KA) into the rat amygdala. Broad-spectrum and selective blockers of the Cx36 channel (CBX, QN, and QND) were administered via intraperitoneal injection. Expression of MAP-2 and SYP was assessed by immunofluorescent and immunohistochemical examination. Expression of MAP-2 and SYP was significantly increased after KA administration in the sham group compared with the control group. Expression of MAP-2 and SYP was significantly decreased in the CBX, QN, and QND groups compared with the sham group. The results provide new evidence regarding the key role of MAP-2 and SYP overexpression in three important mechanisms: the modulation of neuronal plasticity, hyperexcitability of the hippocampal neuronal network, and persistent seizure discharge. Furthermore, the reversal of MAP-2 and SYP overexpression following administration of Cx36 channel blockers indicates a potential role for Cx36 channel blockers in anti-epileptogenic treatment and in doing so, highlights a critical need for further investigation of these compounds.