Mitochondrial ATPase 6,8 Associated with Brain Tumours in Patients Compared to Adjacent Normal Brain Cells

Abstract | Background: Brain cancer is considered one of the most prevalent types of cancer in the world. Primary brain tumours consist of two types. Studies provide some deficiencies in mitochondrial functions that could cause different genetic. Objective: This study aimed to determine the association of ATPase 6,8 alterations of brain tumour cells in comparison with the adjacent healthy tissue cells. Methods: A group of patients was examined, and their disease was identified during precise examinations. These persons were sampled for their affected brain tissues, and these were compared with their adjacent healthy cells. Besides, the populations of 300 healthy controls were selected as the control. The DNA of the brain tumour cells was extracted and analysed using sequencing methods. Result: After the sequence analysis, T8473C, G8584A, A8701G, A8730G and A8860G variants were found—all of them had been reported in other diseases. Also, they were observed in patients with brain tumours, as compared with the adjacent normal tissues. Discussion: The A8860G variant was one of the most prevalent polymorphisms between all these alterations in brain cancer. It seems that the ATPase 6 subunit is more prone to brain cancer. The analysis shows that amongst all the five variants determined in this research, the T8473C, G8584A and A8730G variants—with the p value<0.05—were considered to affect brain tumours

Outcome after Neuro-interventional Treatment of Intracranial Aneurysm (as a First Treatment Modality)

Endovascular treatment is widely applied as the first-line treatment for intracranial aneurysms and includes simple coiling (SC), stent-assisted coiling (SAC), flow diversion stent, and flow disruption stent. The present study is a retrospective cohort study performed in Imam Khomeini Hospital, Department of Neurovascular Intervention, between March 2016 and March 2021. A total number of 229 patients with intracranial aneurysms who underwent therapeutic intravascular interventions were enrolled, of which 89 were treated with SC, 111 with SAC, 25 with flow diversion stent, and 4 with flow disruption stent. The mean age of the subjects was 51.8±12.6 years, and 51.1% were male. Modified Raymond-Roy classification (MRRC) was used to define the occlusion outcome. The success rate, considered as Class I and Class II of MRRC at treatment time was 89% (94.4% in SC, and 84.7% in SAC), which was increased to 90.9% (94% in SC, 93% in SAC, 69.6% in flow diversion stenting, 100% in flow disruption) at 6-month follow-up, and 84.6% (80.8% in SC, 87.8% in SAC, 78.3% in flow diversion stenting, and 100% in flow disruption) at 12-month follow-up. The mean modified Rankin Scale (mRS) before the procedure was 0.05±0.26 which was increased to 0.22±0.76 after the procedure, 0.22±0.76 at 6 months, and 0.30±0.95 at 12 months (P<0.001). Similar to previous studies, the present study demonstrates that neurovascular intervention can treat ruptured aneurysms as the first therapeutic modality with favourable outcomes. A double-blind, randomized clinical trial is needed to eliminate the confounding factors and better demonstrate the outcome

Place fields of single spikes in hippocampus involve Kcnq3 channel-dependent entrainment of complex spike bursts

Hippocampal pyramidal cells encode an animal's location by single action potentials and complex spike bursts. The authors show that Kcnq3-containing M-channels synergistically with GABAergic inputs coordinate complex spike bursts during theta oscillations, which is a key mechanism for spatial coding by single spikes. Hippocampal pyramidal cells encode an animal's location by single action potentials and complex spike bursts. These elementary signals are believed to play distinct roles in memory consolidation. The timing of single spikes and bursts is determined by intrinsic excitability and theta oscillations (5-10 Hz). Yet contributions of these dynamics to place fields remain elusive due to the lack of methods for specific modification of burst discharge. In mice lacking Kcnq3-containing M-type K+ channels, we find that pyramidal cell bursts are less coordinated by the theta rhythm than in controls during spatial navigation, but not alert immobility. Less modulated bursts are followed by an intact post-burst pause of single spike firing, resulting in a temporal discoordination of network oscillatory and intrinsic excitability. Place fields of single spikes in one- and two-dimensional environments are smaller in the mutant. Optogenetic manipulations of upstream signals reveal that neither medial septal GABA-ergic nor cholinergic inputs alone, but rather their joint activity, is required for entrainment of bursts. Our results suggest that altered representations by bursts and single spikes may contribute to deficits underlying cognitive disabilities associated with KCNQ3-mutations in humans

Chen_et_al_SpikeTrains_BetaTimes.mat

Spike trains (samples at 20 KHz) of units recorded in the lateral hypothalamus (LH), the medial prefrontal cortex (mPFC) and ventral tegmental area (VTA, a subset of putative dopamine cells) in behaving mice concurrently with beta oscillations (15-30 Hz) in the lateral hypothalamus (for LH and mPFC units) or in the VTA (for VTA units). Times of beta oscillations (at 20 KHz) for each unit: first and third columns represent beginning and end of each beta epoch, respectively, the second column is the time of the beta peak of the maximal amplitude.</p