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All patients with precranioplasty epileptogenic paroxysms showed better EEG tracings after the procedure. CONCLUSIONS In routine clinical practice, altered amplitudes were observed in the region of bone defects. Although cranioplasty reduced pathologic EEG status (epileptogenic paroxysms), it was not able to produce new EEG tracings that could predict changes in seizure discharge or reduce ES. BACKGROUND The MYH11 gene codes for smooth muscle myosin heavy chain, which has a critical function in maintaining vascular wall stability. Patients with this mutation most commonly have aortic and cardiac defects. Documented involvement of intracranial vessels is exceptional. CASE DESCRIPTION A 29-year-old woman with a history of patent ductus arteriosus and aortic dissection was found to have incidental bilateral stenosis of the terminal internal carotid arteries as well as the proximal anterior cerebral arteries, middle cerebral arteries, and posterior cerebral arteries on magnetic resonance angiography that was obtained for unrelated symptoms. There was no evidence of basal collateral formation, and a generalized straightening of the vessels was observed. These angiographic findings have been typically observed in patients with ACTA2 mutations. Thus, genetic testing was pursued, which uncovered the presence of an MYH11 mutation. Follow-up imaging at 51 months demonstrated that the intracranial stenosis remained stable without evidence of basal collateral formation. She did not experience any neurologic events during the follow-up interval. CONCLUSIONS Intracranial vessel involvement in patients with MYH11 mutations is rare. Vigilant cerebrovascular monitoring should be practiced in this population to guide appropriate management. Reporting of similar cases is important to improve understanding of the development of idiopathic intracranial stenosis in young individuals. OBJECTIVE 1) To investigate the association between MCs and endplate sclerosis; 2) To investigate the effect of MCs and endplate sclerosis on cage subsidence in OLIF stand-alone. METHODS We included 78 inpatients who underwent OLIF stand-alone from August 2015 to August 2017. All patients underwent CT and MRI. The presence and the types of MCs were assessed. Endplate sclerosis was evaluated from sagittal reconstructed CT images. Cage subsidence was evaluated at the 1, 3, 6, and 12-month follow-up. RESULTS Of 78 patients, 92 discs underwent OLIF without posterior instrumentation, 32/92(34.8%) had MCs; Type I, II, and III MCs were seen in 10 (10.9%), 19 (20.7%), and 3 (3.2%) endplates, respectively. Among 32 endplates with MCs, 10 (31.3%) showed evidence of sclerosis on CT images including 2/10 endplates (20%) with Type I MCs, 5/19 (26.3%) with Type II, and 3/3 (100%) with Type III. Among 60 endplates without MCs, 5 (8.3%) showed evidence of sclerosis. Cage subsidence rate in no-MCs group was higher than the MCs group (P less then 0.01). We found only 1 case of cage subsidence in the MCs group (n=32), which was classified as MCs type I, while 6 cases of cage subsidence were observed in the no-MCs group (n=60). HU ratios for sclerotic and no-sclerotic endplates were 2.2±0.3 and 1.1±0.1, respectively. No subsidence of cage was found in sclerotic endplates group (n=15), while 7 cases of cage subsidence were found in no-sclerotic group (n=77). CONCLUSION MCs associated with endplate sclerosis can prevent cage subsidence in OLIF stand-alone. BACKGROUND Ileal Transposition (IT) was developed as a model to study body weight reduction without the restrictive or malabsorptive aspects of other bariatric surgeries, but the exact mechanisms of the alterations in body weight after IT are not completely understood. OBJECTIVE To provide a detailed description of the surgical procedure of IT, and describe its effect on energy balance parameters. METHODS Adult male Lewis rats underwent either IT (IT+) or sham (IT-) surgery. Following surgery body weight and energy intake were monitored. After attaining weight stability (> 30 days), energy expenditure and its components were assessed using indirect calorimetry at a day of fasting, limited intake, and ad libitum intake. At the end of the study body composition analysis was performed. RESULTS IT+ resulted in transiently reduced energy intake, increased ingestion-related energy expenditure (IEE) and decreased body and adipose tissue weight when compared to IT-. At weight stability, neither energy budget (i.e., energy intake - energy expenditure), nor energy efficiency was different in IT+ rats compared to IT-. CONCLUSION Our data show that the primary cause of weight reduction following IT+ is a transient reduction in energy intake. If the increased IEE is related to a higher level of satiety, compensatory feeding to bridge body weight difference between IT+ and IT- rats is less likely to occur. The drive to eat is a component of appetite control, independent of the omnivorous habit of humans, and separate from food choice, satiety and food reward. The drive forms part of the tonic component of appetite and arises from biological needs; it is distinct from episodic aspects of appetite which are heavily influenced by culture and the environment (and which reflect the omnivorous habit). It is proposed that the tonic drive to eat reflects a need state generated by metabolic energy expenditure (EE) required to maintain the functioning and integrity of vital organs. Specifically, the tonic drive is quantitatively associated with fat-free mass (FFM) and resting metabolic rate (RMR). A rational proposition is that high metabolic rate organs (such as heart, liver, kidneys, brain) together with skeletal muscle generate a metabolic need which drives energy intake (EI). The basic phenomenon of a relationship between FFM, RMR and EI, first published in 2011, has been substantially replicated and there are at least 14 concordant published studies carried out in 9 different countries (and 4 continents) with various ethnic groups of lean and obese humans. These studies demonstrate that FFM and RMR represent major determinants of the drive to eat, and this is rational from an evolutionary perspective. The EE of bodily movements through skeletal muscle activity (namely physical activity and exercise) represents another driver which is clearly but more weakly associated with an increase in EI. This account of appetite control, developed within an energy balance framework, is consistent with the apparent inexorable escalation of fatness in individual humans, and for the progressive increase in the prevalence of obesity which, among other factors, reflects the difficulty of managing the biological drive to eat. check details
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