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The article discusses the selection of members for a medical mission with consideration of their unique qualities to ensure the team's wide cultural range and competence. Topics covered include the Synergy Model that pairs a nurse and patient based on common qualities, the required criteria for medical mission trip candidates, the scoring of candidates, and the team's composition. Also noted is a culturally competent team's ability to meet the needs of specific healthcare populations.

Within the uncertainties of involved astronomical and biological parameters, the Drake Equation typically predicts that there should be many exoplanets in our galaxy hosting active, communicative civilizations (ACCs). These optimistic calculations are however not supported by evidence, which is often referred to as the Fermi Paradox. Here, we elaborate on this long-standing enigma by showing the importance of planetary tectonic style for biological evolution. We summarize growing evidence that a prolonged transition from Mesoproterozoic active single lid tectonics (1.6 to 1.0 Ga) to modern plate tectonics occurred in the Neoproterozoic Era (1.0 to 0.541 Ga), which dramatically accelerated emergence and evolution of complex species. We further suggest that both continents and oceans are required for ACCs because early evolution of simple life must happen in water but late evolution of advanced life capable of creating technology must happen on land. We resolve the Fermi Paradox (1) by adding two additional terms to the Drake Equation: foc (the fraction of habitable exoplanets with significant continents and oceans) and fpt (the fraction of habitable exoplanets with significant continents and oceans that have had plate tectonics operating for at least 0.5 Ga); and (2) by demonstrating that the product of foc and fpt is very small (< 0.00003–0.002). We propose that the lack of evidence for ACCs reflects the scarcity of long-lived plate tectonics and/or continents and oceans on exoplanets with primitive life. [ABSTRACT FROM AUTHOR]

The Cadomian orogeny reflects S -directed subduction on the northern margin of Greater Gondwana in Ediacaran – Cambrian time (∼600-500 Ma). It is well known from the eastern seaboard of North America, western and southern Europe, Turkey and Iran but is rarely identified in what was its backarc in N. Africa and Arabia. Here I summarize evidence for the Cadomian across ∼6500 km of Arabia and N. Africa from Oman to Morocco. The beginning of the Cadomian in Afro-Arabia cuts across and overlaps in time with earlier Neoproterozoic orogenies leading to the formation of Greater Gondwana, so emphasis is on rocks <570 Ma. Three Cadomian backarc crustal tracts or segments are identified. The eastern segment (Oman, Persian Gulf, eastern Saudi Arabia) mostly consists of buried transtensional basins with little igneous activity. The central segment was characterized by lower crust magma underplating and strong uplift along a N –S axis (Jordan) accompanied by rifting leading to deposition of thick sediments reminiscent of a passive continental margin, and strong evidence for regional metasomatism (Israel). The Zenifim passive margin is 580–610 Ma, older than our arbitrary 570 Ma limit for identifying the Cadomian but clearly post-dates terminal continental collision to form the East African Orogen and so must be related to Cadomian back-arc rifting. Along with related NE-SW trending dike swarms in NE Egypt and Jordan, the orientation of the Zenifim rifted margin, orthogonal to the Cadomian convergent margin, is another indication of strong Cadomian transtension. In contrast, the western segment (Libya, Algeria, Morocco) experienced abundant igneous activity, with evidence for this found especially far south in Libya. Recognition of the Cadomian orogeny in northern Africa provides a useful first step in breaking out distinct tectonic episodes in the ∼300 m.y. long Pan-African orogeny, at least in the north. Finally, the orthogonal relationship between older N –S orogens in the interior of Greater Gondwana and the E -W Cadomian orogen illustrates how the Neoproterozoic plate mosaic grew by subduction initiation exploiting lithospheric weaknesses along its continental margin. Ten recommendations for future research are also suggested. • The ∼550 Ma Cadomian orogeny in N. Africa and Arabia is reviewed for the first time. • N. Africa-Arabia Cadomian crosscuts older Neoproterozoic structures. • N. Afro-Arabia Cadomian is mostly transtensional basins in E, magmatic rocks in W. • Rifted continental margin offshore Israel suggests Cadomian basins lie further W. • 10 suggestions for research are provided. [ABSTRACT FROM AUTHOR]

Repetitive head impacts (RHIs) from football are associated with the neurodegenerative tauopathy chronic traumatic encephalopathy (CTE). It is unclear whether a history of traumatic brain injury (TBI) is sufficient to precipitate CTE neuropathology. We examined the association between TBI and CTE neuropathology in 580 deceased individuals exposed to RHIs from football. TBI history was assessed using a modified version of the Ohio State University TBI Identification Method Short Form administered to informants. There were 22 donors who had no TBI, 213 who had at least one TBI without loss of consciousness (LOC), 345 who had TBI with LOC, and, of those with a history of TBI with LOC, 36 who had at least one moderate-to-severe TBI (msTBI, LOC >30 min). CTE neuropathology was diagnosed in 405. There was no association between CTE neuropathology status or severity and TBI with LOC (odds ratio [OR] = 0.95, 95% confidence interval [CI] = 0.64–1.41; OR = 1.22, 95% CI = 0.71–2.09) or msTBI (OR = 0.70, 95% CI = 0.33–1.50; OR = 1.01, 95% CI = 0.30–3.41). There were no associations with other neurodegenerative or cerebrovascular pathologies examined. TBI with LOC and msTBI were not associated with CTE neuropathology in this sample of brain donors exposed to RHIs from American football. [ABSTRACT FROM AUTHOR]

The continental crust of Iran is dominated by abundant calc-alkaline and alkaline plutonic and volcanic rocks and by rifted basins filled with mostly terrigenous sedimentary rocks that formed at a Late Ediacaran to Cambrian extensional convergent plate margin along the northern margin of Gondwana. Here we present new zircon U–Pb age, geochemical, and isotopic data from plutonic (granite-granodiorite) and metamorphic (gneiss) rocks in the Kariznou region of NE Iran to provide insights into the nature of the Cadomian convergent margin of Iran. Geochemical data indicate calc-alkaline signatures, characterized by strong depletions in Nb, Ta, P, and Ti and arc-like trace element patterns. New zircon U–Pb ages show that calc-alkaline granitoids and granitic gneiss formed at ~564 to 537 Ma and 538 Ma, respectively. Bulk rock Sr-Nd isotopic data of calc-alkaline rocks have εNd(t) = –5.42 to −5.53 and −6.93 to −7.43 for granite and gneiss, respectively. The gneisses show stronger interaction with and/or re-melting of older continental crust than do granitic rocks. We interpret Kariznou magmatic rocks as forming in association with strong extension accompanied by crustal assimilation. Extension initiated ~570 Ma with the deposition of Late Ediacaran sediments, and magmatism began at 545–535 Ma, generating calc-alkaline magmas. The tectonomagmatic evolution of the Kariznou region encapsulates the prolonged transition of Cadomian Iran from a strongly extensional convergent margin, possibly as a result of oblique oceanic subduction and slab roll-back of the subducting Proto-Tethys oceanic lithosphere, culminating in the formation of an Early Palaeozoic passive margin on the northern side of Gondwana. [ABSTRACT FROM AUTHOR]

Background: Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease characterized by hyperphosphorylated tau (p-tau) accumulation. The clinical features associated with CTE pathology are unclear. In brain donors with autopsy-confirmed CTE, we investigated the association of CTE p-tau pathology density and location with cognitive, functional, and neuropsychiatric symptoms. Methods: In 364 brain donors with autopsy confirmed CTE, semi-quantitative p-tau severity (range: 0–3) was assessed in 10 cortical and subcortical regions. We summed ratings across regions to form a p-tau severity global composite (range: 0–30). Informants completed standardized scales of cognition (Cognitive Difficulties Scale, CDS; BRIEF-A Metacognition Index, MI), activities of daily living (Functional Activities Questionnaire), neurobehavioral dysregulation (BRIEF-A Behavioral Regulation Index, BRI; Barratt Impulsiveness Scale, BIS-11), aggression (Brown-Goodwin Aggression Scale), depression (Geriatric Depression Scale-15, GDS-15), and apathy (Apathy Evaluation Scale, AES). Ordinary least squares regression models examined associations between global and regional p-tau severity (separate models for each region) with each clinical scale, adjusting for age at death, racial identity, education level, and history of hypertension, obstructive sleep apnea, and substance use treatment. Ridge regression models that incorporated p-tau severity across all regions in the same model assessed which regions showed independent effects. Results: The sample was predominantly American football players (333; 91.2%); 140 (38.5%) had low CTE and 224 (61.5%) had high CTE. Global p-tau severity was associated with higher (i.e., worse) scores on the cognitive and functional scales: MI (β standardized = 0.02, 95%CI = 0.01–0.04), CDS (β standardized = 0.02, 95%CI = 0.01–0.04), and FAQ (β standardized = 0.03, 95%CI = 0.01–0.04). After false-discovery rate correction, p-tau severity in the frontal, inferior parietal, and superior temporal cortex, and the amygdala was associated with higher CDS (β sstandardized = 0.17–0.29, ps < 0.01) and FAQ (β sstandardized = 0.21–0.26, ps < 0.01); frontal and inferior parietal cortex was associated with higher MI (β sstandardized = 0.21–0.29, ps < 0.05); frontal cortex was associated with higher BRI (β standardized = 0.21, p < 0.01). Regions with effects independent of other regions included frontal cortex (CDS, MI, FAQ, BRI), inferior parietal cortex (CDS) and amygdala (FAQ). P-tau explained 13–49% of variance in cognitive and functional scales and 6–14% of variance in neuropsychiatric scales. Conclusion: Accumulation of p-tau aggregates, especially in the frontal cortex, are associated with cognitive, functional, and certain neurobehavioral symptoms in CTE. [ABSTRACT FROM AUTHOR]

Objective: Exposure to repetitive head impacts (RHI) is associated with later‐life cognitive symptoms and neuropathologies, including chronic traumatic encephalopathy (CTE). Cognitive decline in community cohorts is often due to multiple pathologies; however, the frequency and contributions of these pathologies to cognitive impairment in people exposed to RHI are unknown. Here, we examined the relative contributions of 13 neuropathologies to cognitive symptoms and dementia in RHI‐exposed brain donors. Methods: Neuropathologists examined brain tissue from 571 RHI‐exposed donors and assessed for the presence of 13 neuropathologies, including CTE, Alzheimer disease (AD), Lewy body disease (LBD), and transactive response DNA‐binding protein 43 (TDP‐43) inclusions. Cognitive status was assessed by presence of dementia, Functional Activities Questionnaire, and Cognitive Difficulties Scale. Spearman rho was calculated to assess intercorrelation of pathologies. Additionally, frequencies of pathological co‐occurrence were compared to a simulated distribution assuming no intercorrelation. Logistic and linear regressions tested associations between neuropathologies and dementia status and cognitive scale scores. Results: The sample age range was 18–97 years (median = 65.0, interquartile range = 46.0–76.0). Of the donors, 77.2% had at least one moderate–severe neurodegenerative or cerebrovascular pathology. Stage III–IV CTE was the most common neurodegenerative disease (43.1%), followed by TDP‐43 pathology, AD, and hippocampal sclerosis. Neuropathologies were intercorrelated, and there were fewer unique combinations than expected if pathologies were independent (p < 0.001). The greatest contributors to dementia were AD, neocortical LBD, hippocampal sclerosis, cerebral amyloid angiopathy, and CTE. Interpretation: In this sample of RHI‐exposed brain donors with wide‐ranging ages, multiple neuropathologies were common and correlated. Mixed neuropathologies, including CTE, underlie cognitive impairment in contact sport athletes. ANN NEUROL 2024;95:314–324 [ABSTRACT FROM AUTHOR]

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease caused by repetitive head impacts (RHI) and pathologically defined as neuronal phosphorylated tau aggregates around small blood vessels and concentrated at sulcal depths. Cross-sectional studies suggest that tau inclusions follow a stereotyped pattern that begins in the neocortex in low stage disease, followed by involvement of the medial temporal lobe and subcortical regions with significant neocortical burden in high stage CTE. Here, we define a subset of brain donors with high stage CTE and with a low overall cortical burden of tau inclusions (mean semiquantitative value ≤1) and classify them as cortical-sparing CTE (CSCTE). Of 620 brain donors with pathologically diagnosed CTE, 66 (11%) met criteria for CSCTE. Compared to typical high stage CTE, those with CSCTE had a similar age at death and years of contact sports participation and were less likely to carry apolipoprotein ε4 (p < 0.05). CSCTE had less overall tau pathology severity, but a proportional increase of disease burden in medial temporal lobe and brainstem regions compared to the neocortex (p’s < 0.001). CSCTE also had lower prevalence of comorbid neurodegenerative disease. Clinically, CSCTE participants were less likely to have dementia (p = 0.023) and had less severe cognitive difficulties (as reported by informants using the Functional Activities Questionnaire (FAQ); p < 0.001, meta-cognitional index T score; p = 0.002 and Cognitive Difficulties Scale (CDS); p < 0.001,) but had an earlier onset age of behavioral (p = 0.006) and Parkinsonian motor (p = 0.013) symptoms when compared to typical high stage CTE. Other comorbid tauopathies likely contributed in part to these differences: when cases with concurrent Alzheimer dementia or frontal temporal lobar degeneration with tau pathology were excluded, differences were largely retained, but only remained significant for FAQ (p = 0.042), meta-cognition index T score (p = 0.014) and age of Parkinsonian motor symptom onset (p = 0.046). Overall, CSCTE appears to be a distinct subtype of high stage CTE with relatively greater involvement of subcortical and brainstem regions and less severe cognitive symptoms. [ABSTRACT FROM AUTHOR]

Former American football players are at risk for chronic traumatic encephalopathy (CTE) which may have parkinsonism as a clinical feature. Former football players were prospectively assessed for parkinsonism. 120 former professional football players, 58 former college football players, and 60 same-age asymptomatic men without repetitive head impacts, 45–74 years, were studied using the MDS-UPDRS to assess for parkinsonism, and the Timed Up and Go (TUG). Traumatic encephalopathy syndrome (TES), the clinical syndrome of CTE, was adjudicated and includes parkinsonism diagnosis. Fisher's Exact Test compared groups on parkinsonism due to small cell sizes; analysis of covariance or linear regressions controlling for age and body mass index were used otherwise. Twenty-two (12.4%) football players (13.3% professional, 10.3% college) met parkinsonism criteria compared with two (3.3%) in the unexposed group. Parkinsonism was higher in professional (p = 0.037) but not college players (p = 0.16). There were no differences on the MDS-UPDRS Part III total scores. Scores on the individual MDS-UPDRS items were low. TUG times were longer in former professional but not college players compared with unexposed men (13.09 versus 11.35 s, p < 0.01). There were no associations between years of football, age of first exposure, position or level of play on motor outcomes. TES status was not associated with motor outcomes. Parkinsonism rates in this sample of football players was low and highest in the professional football players. The association between football and parkinsonism is inconclusive and depends on factors related to sample selection, comparison groups, and exposure characteristics. • Parkinsonism/motor finding prevalence did not differ in former American football players compared to asymptomatic unexposed men. • Former players did have slowness on the Timed Up and Go (TUG) compared to the asymptomatic unexposed men. • TUG times were slower in former football players with TES-CTE probable compared to those with no TES and TES-CTE possible. [ABSTRACT FROM AUTHOR]