The late Middle Pleistocene, starting at around 300 ka, witnessed large-scale biological and cultural dynamics in hominin evolution across Africa including the onset of the Middle Stone Age that is closely associated with the evolution of our species-Homo sapiens. However, archaeological and geochronological data of its earliest appearance are scarce. Here we report on the late Middle Pleistocene sequence of Wadi Lazalim, in the Sahara of Southern Tunisia, which has yielded evidence for human occupations bracketed between ca. 300-130 ka. Wadi Lazalim contributes valuable information on the spread of early MSA technocomplexes across North Africa, that likely were an expression of large-scale diffusion processes.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8933421 | PMC |
| http://dx.doi.org/10.1038/s41598-022-07816-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Ritlecitinib, a JAK3 /TEC inhibitor, modulates the markers of celiac autoimmunity in alopecia areata and vitiligo patients.
Arch Dermatol Res
January 2025
Division of Gastroenterology and Hepatology, 200 1st Street SW, Rochester, MN, 55905, USA.
Background: Celiac disease (CeD) has shown an association with autoimmune disorders including vitiligo and alopecia areata (AA). Ritlecitinib, a JAK3 and TEC kinase family inhibitor, has been approved for treatment of patients with AA and is in late-stage development for vitiligo. Ritlecitinib inhibits cytotoxic T cells, NK cells, and B cells which play a role in the pathogenesis of CeD.
View Article and Find Full Text PDFComparison of the amyloid plaque proteome in Down syndrome, early-onset Alzheimer's disease, and late-onset Alzheimer's disease.
Acta Neuropathol
January 2025
Department of Neurology, NYU Grossman School of Medicine, New York, NY, USA.
Down syndrome (DS) is strongly associated with Alzheimer's disease (AD) due to APP overexpression, exhibiting Amyloid-β (Aβ) and Tau pathology similar to early-onset (EOAD) and late-onset AD (LOAD). We evaluated the Aβ plaque proteome of DS, EOAD, and LOAD using unbiased localized proteomics on post-mortem paraffin-embedded tissues from four cohorts (n = 20/group): DS (59.8 ± 4.
View Article and Find Full Text PDFOutcome prediction for late-onset sepsis after premature birth.
Pediatr Res
January 2025
Neonatal Intensive Care Unit, University Hospital of Modena, Via del Pozzo, 41124, Modena, Italy.
Background: Our aim was to develop a quantitative model for immediately estimating the risk of death and/or brain injury in late-onset sepsis (LOS) in preterm infants, based on objective and measurable data available at the time sepsis is first suspected (i.e., time of blood culture collection).
View Article and Find Full Text PDFProgression of Amyloid Accumulation in Late Adulthood Among People With Childhood-Onset Epilepsy.
Neurology
February 2025
Departments of Child Neurology and General Practice, University of Turku and Turku University Hospital, Finland.
Background And Objectives: Previous research has demonstrated increased brain amyloid plaque load in individuals with childhood-onset epilepsy in late middle age. However, the trajectory of this process is not yet known. The aim of this study was to determine whether individuals with a history of childhood-onset epilepsy show progressive brain aging in amyloid accumulation in late adulthood (Turku Adult Childhood-Onset Epilepsy study, TACOE).
View Article and Find Full Text PDFDelayed Progression of Ataxia with a Static Cerebellar Lesion- Consider SCA27B.
Cerebellum
January 2025
Department of Neurology, Donders Institute for Brain, Cognition & Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
Repeat expansions in the fibroblast growth factor 14 gene (FGF14), associated with spinocerebellar ataxia type 27B (SCA27B), have emerged as a prevalent cause of previously unexplained late-onset cerebellar ataxia. Here, we present a patient with residual symptom of gait ataxia after complicated meningioma surgery, who presented with progressive symptoms of oculomotor disturbances, speech difficulties, vertigo and worsening of gait imbalance, twelve years post-resection. Neuroimaging revealed a surgical resection cavity in the dorsolateral side of the left cerebellar hemisphere, accompanied by gliosis in left cerebellar hemisphere extending into the vermis, extensive non-specific supratentorial periventricular white matter abnormalities, and mild atrophy of the cerebellar vermis.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!