Notes

Bilateral massive cellular cancer involving tendo Achilles: In a situation collection upon renovation by peroneus brevis : tibialis posterior plantar fascia.
es are of different value depending on the section type and are not directly comparable. Naïvely using the body text of articles along with abstract text degrades the overall quality of the search. The proposed log odds ratio scores normalize and combine the contributions of occurrences of query tokens in different sections. By including full text where available, we gain another 0.67%, or 7% relative improvement over abstract alone. We find an advantage in the more accurate estimate of the value of BM25 scores depending on the section from which they were produced. Taking the sum of top three section scores performs the best.
Brain functional network abnormalities are reported in posttraumatic stress disorder (PTSD). Most resting-state functional magnetic resonance imaging (rs-fMRI) studies have assumed that the functional networks remain static during the scan. How these might change dynamically in PTSD remains unclear.

Rs-fMRI data were collected from 71 noncomorbid treatment-naïve PTSD patients and 70 demographically-matched trauma-exposed non-PTSD (TENP) controls. Network switching rate was used to characterize dynamic changes of individual resting-state functional networks. Results were analyzed by comparing switching rates between PTSD and TENP, for diagnosis-by-sex interactions, and by correlation with individual PTSD symptom severity.

At the global level, PTSD showed significantly lower network switching rates than TENP. These were observed mainly in the fronto-parietal, default-mode, and limbic networks at the subnetwork level, and in the frontal and temporal regions at the nodal level. These network switching rate alterations were correlated with PTSD symptom severity. There were no significant effects of sex.

These disruptions of dynamic functional network stability, reflected by lower network switching rate in the resting state, are a feature of PTSD, and suggest that the fronto-parietal, default mode and limbic networks may play a critical role in the underlying neural mechanisms.
These disruptions of dynamic functional network stability, reflected by lower network switching rate in the resting state, are a feature of PTSD, and suggest that the fronto-parietal, default mode and limbic networks may play a critical role in the underlying neural mechanisms.
Adult patients with mild traumatic brain injury (mTBI) exhibit distinct phenotypes of emotional and cognitive functioning identified by latent profile analysis of clinical neuropsychological assessments. When discerned early after injury, these latent clinical profiles have been found to improve prediction of long-term outcomes from mTBI. The present study hypothesized that white matter (WM) microstructure is better preserved in an emotionally resilient (ER) mTBI phenotype compared with a neuropsychiatrically distressed (ND) mTBI phenotype.

The present study used diffusion MRI to investigate and compare WM microstructure in major association, projection, and commissural tracts between the two phenotypes and over time. Diffusion MR images from 172 mTBI patients were analyzed to compute individual diffusion tensor imaging (DTI) maps at 2 weeks and 6 months postinjury.

By comparing the DTI parameters between the two phenotypes at global, regional, and voxel levels, the present study showed that the ER patients have higher axial diffusivity (AD) compared to their ND counterparts early after mTBI. Longitudinal analysis revealed greater compromise of WM microstructure in ND patients, with greater decrease of global AD and more widespread decrease of regional AD during the first 6 months after injury compared to their ER counterparts.

These results provide neuroimaging evidence of WM microstructural differences underpinning mTBI phenotypes identified from neuropsychological assessments and show differing longitudinal trajectories of these biological effects. These findings suggest diffusion MRI can provide short- and long-term imaging biomarkers of resilience.
These results provide neuroimaging evidence of WM microstructural differences underpinning mTBI phenotypes identified from neuropsychological assessments and show differing longitudinal trajectories of these biological effects. These findings suggest diffusion MRI can provide short- and long-term imaging biomarkers of resilience.
Although corporal punishment is a common form of punishment with known negative impacts on health and behavior, how such punishment affects neurocognitive systems is relatively unknown.

To address this issue, we examined how corporal punishment affected neural measures of error and reward processing in 149 adolescent boys and girls of ages 11 to 14 years (mean age [SD]= 11.02 [1.16]). Corporal punishment experienced over the lifetime was assessed using the Stress and Adversity Inventory. In addition, participants completed a flankers task and a reward task to measure the error-related negativity and reward positivity, respectively, as well as measures of anxiety and depressive symptoms.

As hypothesized, participants who experienced lifetime corporal punishment reported more anxiety and depressive symptoms. Experiencing corporal punishment was also related to a larger error-related negativity and blunted reward positivity. Importantly, corporal punishment was independently related to a larger error-related negativity and a more blunted reward positivity beyond the impact of harsh parenting and lifetime stressors.

Corporal punishment appears to potentiate neural response to errors and decrease neural response to rewards, which could increase risk for anxiety and depressive symptoms.
Corporal punishment appears to potentiate neural response to errors and decrease neural response to rewards, which could increase risk for anxiety and depressive symptoms.Involuntary interruptions of upper limb movements, referred to as "upper limb freezing" (ULF) belong to the most disabling symptoms of Parkinson's disease (PD). Our study aimed to explore the cortical neuronal mechanisms underlying the reinstation of regular movement after a freezing episode and to control them by voluntary stops. We hypothesized that this movement recovery after a freeze would be accompanied by a decrease of beta power (13-30 Hz) over the primary sensorimotor cortex (electrode "C3"). We recorded a 62-channel surface EEG in 14 PD patients during a repetitive finger tapping task. After performing time-frequency analysis of the EEG data we segmented it to i) regular finger taps, ii) ULF episodes, and iii) voluntary movement stops (VS). We analysed cortical activity during each movement modality and later focused on the last 500 ms of ULF and VS and the first half of the following regular tap. At the beginning of regular finger taps we found decreased alpha power (6-12 Hz) over C3 (P = 0.01). During ULF, there was no significant activity modulation in the alpha and beta frequency bands, whereas beta power increased over C3 during VS (P = 0.0038). When tapping was reinstated after a freeze, we found that 100 ms before movement onset beta power decreased first present over C3, followed by fronto-central electrodes and then reaching the ipsilateral right fronto-temporal electrodes when reinstating regular tapping (P = 0.0256). Initiating movement after a VS showed a different pattern with a decrease of parieto-occipital beta activity 200 ms prior to the first tap (P = 0.044). Our findings suggest that PD freezers make use of different cortical pathways when re-initiating movement after ULF or VS. This includes either fronto-central or parieto-occipital pathways. These findings may help to customize novel neuromodulation strategies to counteract freezing behaviour.Early-life seizures (ELS) are associated with persistent cognitive deficits such as ADHD and memory impairment. These co-morbidities have a dramatic negative impact on the quality of life of patients. Therapies that improve cognitive outcomes have enormous potential to improve patients' quality of life. Our previous work in a rat flurothyl-induction model showed that administration of adrenocorticotropic hormone (ACTH) at time of seizure induction led to improved learning and memory in the animals despite no effect on seizure latency or duration. Administration of dexamethasone (Dex), a corticosteroid, did not have the same positive effect on learning and memory and has even been shown to exacerbate injury in a rat model of temporal lobe epilepsy. We hypothesized that ACTH exerted positive effects on cognitive outcomes through beneficial changes to gene expression and proposed that administration of ACTH at seizure induction would return gene-expression in the brain towards the normal pattern of expression in the Control animals whereas Dex would not. Twenty-six Sprague-Dawley rats were randomized into vehicle- Control, and ACTH-, Dex-, and vehicle- ELS. Rat pups were subjected to 60 flurothyl seizures from P5 to P14. After seizure induction, brains were removed and the hippocampus and PFC were dissected, RNA was extracted and sequenced, and differential expression analysis was performed using generalized estimating equations. Differential expression analysis showed that ACTH pushes gene expression in the brain back to a more normal state of expression through enrichment of pathways involved in supporting homeostatic balance and down-regulating pathways that might contribute to excitotoxic cell-damage post-ELS.Drug resistance is a major challenge in the treatment of epilepsy. CCT251545 Drug-resistant epilepsy (DRE) accounts for 30% of all cases of epilepsy and is a matter of great concern because of its uncontrollability and the high burden, mortality rate, and degree of damage. At present, considerable research has focused on the development of predictors to aid in the early identification of DRE in an effort to promote prompt initiation of individualized treatment. While multiple predictors and risk factors have been identified, there are currently no standard predictors that can be used to guide the clinical management of DRE. In this review, we discuss several potential predictors of DRE and related factors that may become predictors in the future and perform evidence rating analysis to identify reliable potential predictors.Endochondral bone formation from the growth plate plays a critical role in vertebrate limb development and skeletal homeostasis. Although miR-1 is mainly expressed in the hypertrophic region of the growth plate during this process, its role in the endochondral bone formation is unknown. To elucidate the role of miR-1 in cartilage development, chondrocyte-specific transgenic mice with high expression of miR-1 were generated (Col2a1-Cre-ERT2-GFPfl/fl-RFP-miR-1). Transgenic mice showed short limbs and delayed formation of secondary ossification centers. In the tibia growth plate of miR-1-overexpressing transgenic mice, the chondrocytes in the proliferative zone were disorganized and their proliferation decreased, and the ColX, MMP-13 and Indian Hedgehog (IHH) in chondrocytes showed a downward trend, resulting in decreased terminal differentiation in the hypertrophic zone. In addition, the apoptosis index caspase-3 also showed a downward trend in the tibia growth plate. It was concluded that miR-1 overexpression affects chondrocyte proliferation, hypertrophic differentiation, and apoptosis, thereby delaying the formation of secondary ossification centers and leading to short limbs.
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