Marine Carbonates in the Mantle Source of Oceanic Basalts: Pb Isotopic Constraints.

For almost fifty years, geochemists have been interpreting the clues from Pb isotopic ratios concerning mantle composition and evolution separately. The Pb isotopes of ocean island basalts (OIB) indicate that their mantle source is heterogeneous, most likely due to the presence of end-components derived from recycled crust and sediment. Some OIB have unusually high 206Pb/204Pb coming from one of the end-components with a long time-integrated high 238U/204Pb or µ (HIMU). Most OIB and many mid-ocean ridge basalts (MORB) also have high 206Pb/204Pb, indicating a HIMU-like source. Moreover, measured 232Th/238U (κ) for most MORB are lower than those deduced from their 208Pb/204Pb and 206Pb/204Pb. Such high µ and low κ features of oceanic basalts are inconsistent with the known geochemical behavior of U, Pb and Th and temporal evolution of the mantle; these have been respectively termed the 1st and 2nd Pb paradox. Here we show that subducted marine carbonates can be a source for HIMU and a solution to the Pb paradoxes. The results are consistent with the predictions of the marine carbonate recycling hypothesis that posits the Pb isotopes of oceanic basalts indicate a common origin and/or magma generation process.

Excessive daytime somnolence is associated with hypoglycemia in adult Latinos with type 2 diabetes mellitus.

OBJECTIVE: This study aimed to determine the frequency of sleep disorders in hypoglycemic diabetic patients and possible relationships with scores of sleep disorders and restless legs syndrome in mestizo population in Guayaquil, Ecuador. METHODS: A multicenter, cross-sectional study conducted at an outpatient endocrinology clinic in urban and rural Ecuador regions, included 290 participants with type 2 diabetes mellitus with severe hypoglycemic episodes, completed, validated, and culturally adapted sleep questionnaires to assess daytime sleepiness, risk of sleep apnea and restless legs syndrome. Logistic regression analysis was conducted to identify factors associated with severe hypoglycemia. RESULTS: The prevalence of EDS was 56.8%, RLS prevalence of 46.2%, and 38.6% prevalence of high risk Berlin score. Multivariate logistic regression indicated hypoglycemic T2DM in the range of 56-75 years old were more likely to have high ESS (p 0.0001). CONCLUSION: A high prevalence of sleep disorders in diabetic Latinos living in Ecuador was evidenced. The presence of somnolence in patients older than 56 years and high HbA1c levels should alert the clinician for the occurrence of hypoglycemic episodes.

Adult outcomes of three newborns with a combined weight of 1100 grams.

OBJECTIVE: To present the short- and long-term (20 years) growth and developmental outcomes of four micropremies (birth weight of less than 500 grams). METHOD: Retrospective review of medical records and prospective assessment/interview with patients and their families. RESULTS: One infant was lost at long-term follow-up. The other three showed a quite satisfactory health status and life style in early adulthood. CONCLUSIONS: Despite extreme low birth weight (less than 500 grams) normal outcomes are possible. In the case of micropremies, gestational age appears to be of greater importance than birth weight as well as female gender in the decision-making process regarding initiation of resuscitation.

Pathophysiology of REM sleep behaviour disorder and relevance to neurodegenerative disease.

REM sleep behaviour disorder (RBD) is a parasomnia characterized by the loss of normal skeletal muscle atonia during REM sleep with prominent motor activity accompanying dreaming. The terminology relating to RBD, and mechanisms underlying REM sleep without atonia and RBD based on data in cat and rat are presented. Neuroimaging data from the few published human cases with RBD associated with structural lesions in the brainstem are presented, in which the dorsal midbrain and pons are implicated. Pharmacological manipulations which alter RBD frequency and severity are reviewed, and the data from human neuropathological studies are presented. An anatomic framework and new schema for the pathophysiology of RBD are proposed based on recent data in rat regarding the putative flip-flop switch for REM sleep control. The structure in man analogous to the subcoeruleus region in cat and sublaterodorsal nucleus in rat is proposed as the nucleus (and its associated efferent and afferent pathways) crucial to RBD pathophysiology. The association of RBD with neurological disease ('secondary RBD') is presented, with emphasis on RBD associated with neurodegenerative disease, particularly the synucleinopathies. The hypothesized pathophysiology of RBD is presented in relation to the Braak staging system for Parkinson's disease, in which the topography and temporal sequence of synuclein pathology in the brain could explain the evolution of parkinsonism and/or dementia well after the onset of RBD. These data suggest that many patients with 'idiopathic' RBD are actually exhibiting an early clinical manifestation of an evolving neurodegenerative disorder. Such patients may be appropriate for future drug therapies that affect synuclein pathophysiology, in which the development of parkinsonism and/or dementia could be delayed or prevented. We suggest that additional clinicopathological studies be performed in patients with dementia or parkinsonism, with and without RBD, as well as in patients with idiopathic RBD, to further elucidate the pathophysiology and also characterize the clinical and pathophysiological relevance of RBD in neurodegenerative disease. Furthermore, longitudinal studies in patients with idiopathic RBD are warranted to characterize the natural history of such patients and prepare for future therapeutic trials.

Neurocysticercosis and oncogenesis.

Recent studies suggest that neurocysticercosis may be a risk factor for human cancer. Pathogenetic mechanisms explaining possible oncogenic effects of cysticerci include the following: (a) parasite-induced modulation of the host immune response that may be associated with loss of regulatory mechanisms implicated in the immunological surveillance against cancer; (b) transfer of genetic material from the parasite to the host, causing DNA damage and malignant transformation of host cells, and (c) chronic inflammation with liberation of nitric oxide and inhibition of tumor suppressor genes. Further research is needed to confirm the potential role of cysticercosis in the development of cancer. These studies should determine the presence of cysticercotic factors responsible for the transfer of genetic material and potential mutations in the tumor suppressor genes in proliferating astrocytes surrounding cysticercotic lesions. Additionally, the complex interaction between the immune state of the host with variable cytokine release and the presence of inflammatory cells releasing nitric oxide that cause DNA damage and impair tumor suppressive mechanisms needs to be investigated.

Worst headache and subarachnoid hemorrhage: prospective, modern computed tomography and spinal fluid analysis.

STUDY OBJECTIVE: This study investigated the hypothesis that modern computed tomographic (CT) imaging is sufficient to exclude subarachnoid hemorrhage (SAH) in patients with severe headache. METHODS: All 38,730 adult patients who presented to Hermann Hospital in Houston, Texas, during a 16-month period were prospectively screened to detect those with "the worst headache of my life." Two neuroradiologists blinded to the study hypothesis interpreted the CT scans. Patients with negative scans underwent comprehensive cerebrospinal fluid (CSF) analysis including cell count in first and last tubes, visual and spectrophotometric detection of xanthochromia, and CSF D-dimer assay. RESULTS: A chief complaint of headache was elicited in 455 patients, and 107 of these had "worst headache" and were enrolled in the study. CT-confirmed SAH was found in 18 of the 107 (17%). Only 2 patients (2.5%, 95% confidence interval, .3% to 8.8%) had SAH detected by CSF analysis among those with negative CT imaging result. CSF spectrophotometric detection was the most sensitive test for blood. Three patients with less than 6 red blood cells in tube 1 had positive spectrophotometric results, but in all 3, tube 4 was negative on spectrophotometric analysis, suggesting a high false-positive rate. CONCLUSION: Modern CT imaging is sufficient to exclude 97.5% of SAH in patients presenting to the ED with "worst headache" symptoms.

Neurocysticercosis among patients with cerebral gliomas.

BACKGROUND: Parasites have been implicated in the pathogenesis of human cancer. Anecdotal reports have suggested an association between neurocysticercosis and brain tumors. OBJECTIVE: To determine whether neurocysticercosis is a risk factor for cerebral glioma. DESIGN: Case-control study. SETTING: A university general hospital and a cancer referral center. PATIENTS: Forty-three consecutive patients with a cerebral glioma and 172 controls matched for age, sex, and socioeconomic status. METHODS: We determined the ratio between the frequency of neurocysticercosis in patients with a cerebral glioma and in matched controls. We also evaluated differences in the characteristics of the patients and in the histological type of the neoplasm among case patients with and without neurocysticercosis. In addition, we noted relationships between the location of the cerebral glioma and that of parasitic lesions. RESULTS: Eight (16.8%) of 43 patients with a glioma and 5 (2.9%) of 172 controls had neurocysticercosis (P < .001). The odds ratio for this association was 7.63 (95% confidence interval, 2.03-31.09). Patients with glioma and neurocysticercosis were older than those without neurocysticercosis (mean [+/-SD] age, 62.75 +/- 18.34 years vs 44.69 +/- 14.04 years; P = .02). Glioblastoma multiforme was more frequent among case patients with neurocysticercosis than among those without neurocysticercosis (87.5% vs 48.6%); however, this difference was not statistically significant (P = .24). Six of the 8 patients with neurocysticercosis and a cerebral glioma had calcified parasitic lesions within and around the tumor. CONCLUSIONS: Results from this study suggest that neurocysticercosis is a risk factor for cerebral glioma. The intense astrocytic gliosis that surrounds calcified cysticerci, together with the suppression of the cellular immune response induced by cysticerci, may contribute to the development of malignant glial cells in patients with neurocysticercosis.