ABSTRACT
BACKGROUND: A skull defect is inevitable after decompression treatment for traumatic brain injury. Titanium mesh as the most recognized skull repair material has good biocompatibility and has been widely used in clinical practice. However, the timing for skull repair after brain injury is still in dispute.OBJECTIVE: To compare the changes of brain perfusion and the recovery of neurological function in patients with skull defects before and after early and late-stage titanium mesh repair based on CT perfusion technique.METHODS: This was a single-center, prospective, observational clinical trial that was completed at the Taihe Hospital,Hubei University of Medicine in Hubei Province, China. Eighty-six patients with craniocerebral injury who had undergone decompression with removal of bone flap from January 2013 to January 2016 were recruited and subjected to skull repair using titanium mesh. All the patients were randomized into two groups: test group (n=40) with early skull repair within 1-3 months after decompression and control group (n=46) with late-stage skull repair within 6-12 months after decompression. CT perfusion technology was used to observe changes of brain perfusion at 3 days operatively and at 10 days postoperatively. The Barthel index was evaluated at 30 days postoperatively. The trial was registered with ClinicalTrial.gov (identifier: NCT03222297) on July 12th, 2017. The study protocol was approved by the Ethics Committee of Taihe Hospital with the approval No. 2012 (08), and performed in accordance with the Declaration of Helsinki,formulated by the World Health Organization and the hospital's ethical requirements for human research. All the patients and their families were voluntary to participate in the trial, were fully informed of the trial process, and then signed the informed consent prior to the initialization of the trial.RESULTS AND CONCLUSION: The postoperative cerebral blood volume and cerebral blood flow at the parietal cortex on the side of skull defect and at the cortex in the defect region were significantly higher in the two group than the baseline (P < 0.05), while the time to peak was lower than the baseline (P < 0.05). Compared with the control group,significantly higher cerebral blood volume and cerebral blood flow as well as shorter time to peak were observed in the test group (P < 0.05). The Barthel index of the test group was also significantly higher than that of the control group at 30 days postoepratively (P < 0.05). Overall, early skull repair with titanium mesh is helpful to improve the cerebral blood perfusion at the affected side and the recovery of neurological function. In addition, CT perfusion technology is a safe and effective method to monitor hemodynamic changes in the brain.
ABSTRACT
Aim To study the characteristics of KCNQ2/3 potassium channel expressed in CHO cells and its modulation by M_1 receptor.Methods KCNQ2 and KCNQ3 potassium channels and M_1 receptor were co-expressed in CHO cells.Whole cell patch-clamp techniques was used to observe the characteristics of KCNQ2/3 current,its modulation by the M_1 receptor,and the effects of the common potassium channel blockers.Results KCNQ2/3 current recorded in CHO cells was a slow-activation low-threshold non-inactivating,voltage-dependent outward potassium current.KCNQ2/3 current was elicited at about-60 mV,V_(1/2)(-26.8?1.2) mV and the deactivation current fitted two exponential function,with ?_(fast) of 101ms and ?_(slow) of 309 ms.The channel was not sensitive to common pharmacological blockers such as 4-AP,Ba~(2+) and TEA,but was inhibited significantly by linopirdine,with a IC_(50) of(6.5?0.83) ?mol?L~(-1).Acetylcholine suppressed the KCNQ2/3 current reversibly via M_1 receptor,with a IC_(50) of(0.7?0.05) ?mol?L~(-1).Conclusion KCNQ2 and KCNQ3 channels are the molecular basis of M-current observed in neuronal cells.KCNQ2/Q3 current expressed in CHO cells has similar characteristics as that seen in neuronal M-current.Linopirdine is a powerful blocker of KCNQ2/3 channel and acetylcholine inhibits the current by muscarinic M_1 receptor.This experiment has laid a solid basis for further study of M-current and KCNQ2/3 current,and is important for the study of neurological diseases relating to alteration of M-current,such as convulsion,epilepsy and Alzheimers disease.
ABSTRACT
As an outward,voltage-dependent potassium channel,M type channel is crucial in the regulation of neuronal excitability;it is modulated by a variety of factors in vivo and its dysfunction often results in neuronal system diseases.Great efforts have been made to elucidate the mechanism underlying M channel modulation since its discovery decades ago.It is generally accepted that the Phospholipase C(PLC) signaling pathway plays a significant role in the M channel modulation.This review highlights the relationship between PLC signaling pathway and M channel modulation,as well as some recent progresses in the research of this field.
ABSTRACT
Receptor tyrosine kinase(RTK),a membrane receptor superfamily with intrinsic protein tyrosine kinase activity,has many members and complicated signal transduction pathways.Activation of RTKs can trigger a series of signal transduction pathways and play essential roles in modulating cell growth,proliferation,differentiation and metabolism through influencing gene transcription and expression.Activation of RTK can also rapidly modulate some cellular functions including the modulation of ion channels.Potassium channels play a critical role in stabilization of membrane potential and regulation of cellular excitability.This review highlights the rapid modulation of potassium channels by RTKs and reviews the recent progress in related research.