Stilesberntsen0322
Moreover, CDX-LIPO promoted M1-macrophage polarization and facilitated mTOR-mediated reprogramming of glucose metabolism in glioma.
This study developed a potential combinatory therapeutic strategy by regulation of TIME and a 'three-birds-one-stone'-like glioma-targeting drug delivery system.
This study developed a potential combinatory therapeutic strategy by regulation of TIME and a 'three-birds-one-stone'-like glioma-targeting drug delivery system.
To test the hypothesis that absence seizures can evolve to generalized tonic-clonic seizures, we documented electroclinical features of this novel seizure type.
In 4 large video-EEG databases, we identified recordings of seizures starting with impaired awareness that, without returning to baseline interictal state, evolved to generalized tonic-clonic seizures. We extracted the detailed semiologic and electrographic characteristics of these seizures, and we documented the clinical background, diagnoses, and therapeutic responses in these patients.
We identified 12 seizures from 12 patients. All seizures started with a period of impaired awareness and bursts of generalized spike or polyspike and slow-wave discharges, the hallmark of absence seizures. https://www.selleckchem.com/products/cinchocaine.html Without returning to baseline, the nonmotor (absence) phase was followed by tonic-clonic convulsions. We called this novel generalized seizure type absence-to-bilateral-tonic-clonic seizure. Most patients had idiopathic generalized epilepsies, although with a high incidence of unusual features and poor therapeutic response.
Absence-to-bilateral-tonic-clonic seizures are a novel generalized seizure type. Clinicians should be aware of this seizure for correctly diagnosing patients. This novel seizure type may further elucidate generalized ictogenesis.
Absence-to-bilateral-tonic-clonic seizures are a novel generalized seizure type. Clinicians should be aware of this seizure for correctly diagnosing patients. This novel seizure type may further elucidate generalized ictogenesis.
To assess the relationship between diet pattern and prodromal Parkinson disease (PD) features.
These analyses include 47,679 participants from the Nurses' Health Study and the Health Professionals Follow-up Study. Since 1986, both cohorts have collected dietary information every 4 years and calculated scores for adherence to different diet patterns, including the alternate Mediterranean diet (aMED) and the Alternative Healthy Eating Index (AHEI). In 2012, participants responded to questions regarding constipation and probable REM sleep behavior disorder. For a subset of 17,400 respondents to the 2012 questionnaire, 5 additional prodromal features of PD were assessed in 2014 to 2015. We used multinomial logistic regression to estimate the association between baseline (1986) diet pattern score quintiles and number of prodromal features (0, 1, 2, or ≥3) in 2012 to 2015. Additional analyses investigated the association between long-term adherence to these dietary patterns over 20 years and prodromal features suggestive of PD.
In a comparison of extreme aMED diet quintiles, the odds ratio for ≥3 vs 0 features was 0.82 (95% confidence interval [CI] 0.68-1.00, false discovery rate [FDR]-adjusted
= 0.03) at baseline and 0.67 (95% CI 0.54-0.83, FDR-
< 0.001) for long-term diet; results were equally strong for the association with AHEI scores. Higher adherence to these diets was inversely associated with individual features, including constipation, excessive daytime sleepiness, and depression.
The inverse association between these diet patterns and prodromal PD features is consistent with previous findings and suggests that adherence to a healthy diet may reduce the occurrence of nonmotor symptoms that often precede PD diagnosis.
The inverse association between these diet patterns and prodromal PD features is consistent with previous findings and suggests that adherence to a healthy diet may reduce the occurrence of nonmotor symptoms that often precede PD diagnosis.
To explore the causal relationships between sleep, major depressive disorder (MDD), and Alzheimer disease (AD).
We conducted bidirectional 2-sample Mendelian randomization analyses. Genetic associations were obtained from the largest genome-wide association studies currently available in UK Biobank (n = 446,118), Psychiatric Genomics Consortium (n = 18,759), and International Genomics of Alzheimer's Project (n = 63,926). We used the inverse variance-weighted Mendelian randomization method to estimate causal effects and weighted median and Mendelian randomization-Egger for sensitivity analyses to test for pleiotropic effects.
We found that higher risk of AD was significantly associated with being a "morning person" (odds ratio [OR] 1.01,
= 0.001), shorter sleep duration (self-reported β = -0.006,
= 1.9 × 10
; accelerometer based β = -0.015,
= 6.9 × 10
), less likely to report long sleep (β = -0.003,
= 7.3 × 10
), earlier timing of the least active 5 hours (β = -0.024,
= 1.7 × 10
), and a smaller number of sleep episodes (β = -0.025,
= 5.7 × 10
) after adjustment for multiple comparisons. We also found that higher risk of AD was associated with lower risk of insomnia (OR 0.99,
= 7 × 10
). However, we did not find evidence that these abnormal sleep patterns were causally related to AD or for a significant causal relationship between MDD and risk of AD.
We found that AD may causally influence sleep patterns. However, we did not find evidence supporting a causal role of disturbed sleep patterns for AD or evidence for a causal relationship between MDD and AD.
We found that AD may causally influence sleep patterns. However, we did not find evidence supporting a causal role of disturbed sleep patterns for AD or evidence for a causal relationship between MDD and AD.For half a century now, the barrel cortex of common laboratory rodents has been an exceptionally useful model for studying the formation of topographically organized maps, neural patterning, and plasticity, both in development and in maturity. We present a historical perspective on how barrels were discovered, and how thereafter, they became a workhorse for developmental neuroscientists and for studies on brain plasticity and activity-dependent modeling of brain circuits. What is particularly remarkable about this sensory system is a cellular patterning that is induced by signals derived from the sensory receptors surrounding the snout whiskers and transmitted centrally to the brainstem (barrelettes), the thalamus (barreloids), and the neocortex (barrels). Injury to the sensory receptors shortly after birth leads to predictable pattern alterations at all levels of the system. Mouse genetics have increased our understanding of how barrels are constructed and revealed the interplay of the molecular programs that direct axon growth and cell specification, with activity-dependent mechanisms.
