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An unprecedented increase in earthquakes in the U.S. mid-continent began in 2009. Many of these earthquakes have been documented as induced by wastewater injection. We examine the relationship between wastewater injection and U.S. mid-continent seismicity using a newly assembled injection well database for the central and eastern United States. We find that the entire increase in earthquake rate is associated with fluid injection wells. High-rate injection wells (>300,000 barrels per month) are much more likely to be associated with earthquakes than lower-rate wells. At the scale of our study, a well's cumulative injected volume, monthly wellhead pressure, depth, and proximity to crystalline basement do not strongly correlate with earthquake association. Managing injection rates may be a useful tool to minimize the likelihood of induced earthquakes.

We have determined the structure of intact ATP synthase from bovine heart mitochondria by electron cryomicroscopy of single particles. Docking of an atomic model of the F 1 ‐c 10 subcomplex into a major segment of the map has allowed the 32 Å resolution density to be interpreted as the F 1 ‐ATPase, a central and a peripheral stalk and an F O membrane region that is composed of two domains. One domain of F O corresponds to the ring of c‐subunits, and the other probably contains the a‐subunit, the transmembrane portion of the b‐subunit and the remaining integral membrane proteins of F O . The peripheral stalk wraps around the molecule and connects the apex of F 1 to the second domain of F O . The interaction of the peripheral stalk with F 1 ‐c 10 implies that it binds to a non‐catalytic α–β interface in F 1 and its inclination where it is not attached to F 1 suggests that it has a flexible region that can serve as a stator during both ATP synthesis and ATP hydrolysis.

Seven cases of clinically symptomatic benign glial cyst of the pineal gland are reported. The cysts' size ranged from 1.0-4.5 cm in diameter. They were characterised by a golden or, less frequently, brown-reddish proteinaceous or haemorrhagic fluid content. The cyst wall, up to 2 mm thick, consisted of clusters of normal pineal parenchymal cells, often compressed and distorted, surrounded by reactive gliotic tissue which sometimes contained Rosenthal fibres. The presenting clinical features included headache (6/7), signs of raised intracranial pressure, partial or complete Parinaud's syndrome (5/7), cerebellar deficits (2/7), corticospinal and corticopontine fibre (2/7) or sensory (1/7) deficits, and emotional disturbances (2/7). CT and MRI (in 2/7 cases) scans showed a hypodense or nonhomogeneous lesion in the region of the pineal gland, with or without contrast enhancement. Surgical excision resulted in complete clearance of the symptoms in 5/7 patients. The previous literature is reviewed and the clinicopathological correlations and the possible pathogenetic mechanisms are discussed. The need to distinguish this benign lesion from other mass lesions of the pineal region, in particular from pinealocytoma, is stressed.

Cerebrovascular amyloid is the main constituent of the perivascular and neuritic plaques typical of Alzheimer disease, whereas neurofilaments and microtubule-associated tau protein have been considered primary contributors to the formation of the characteristic Alzheimer tangles. Plaques and tangles and their constituents have at times been ascribed a role in pathogenesis of the disease. Normally, neurofilaments become phosphorylated only upon axonal entry. In many neurologic disorders, neurofilament phosphorylation, as detected by any of the available monoclonal antibodies (mAbs) to neurofilament phosphorylated epitopes is shifted from an axonal to a cell-body location. An exception is provided by Alzheimer disease, where tangles (which are neuronal cell-body-derived structures) exhibit only one phosphorylated epitope. However, the very presence of neurofilaments in tangles and plaques has been questioned because of a reported cross-reaction of mAbs to phosphorylated neurofilaments with tau protein. On reinvestigating this cross-reactivity we found that four of five mAbs to phosphorylated neurofilaments and four of five mAbs to nonphosphorylated neurofilaments failed to react with tau protein. A fifth mAb (07-5) to phosphorylated neurofilament cross-reacted with partially denatured tau protein at an affinity 1/1700th of that for denatured neurofilaments; nondenatured tau protein in tissue sections did not cross-react. A fifth mAb (02-40) to nonphosphorylated neurofilament also cross-reacted weakly. In Alzheimer disease normal-appearing axons were revealed with all the mAbs to phosphorylated neurofilaments, but tangles were revealed with only one of them (mAb 07-5). mAb to tau protein did not stain or did so indistinctly. Four of five mAbs to nonphosphorylated neurofilaments failed to reveal axons. Upon dephosphorylation of tissue, staining by mAbs to phosphorylated neurofilaments disappeared, and axons were revealed with the mAb to tau protein and all mAbs to the nonphosphorylated neurofilaments. Tangles became stained with tau mAb and one mAb to the nonphosphorylated neurofilaments (mAb 10-1). Quantitative evaluation of immunocytochemical staining intensities and immunoblot cross-reactivity showed that neurofilaments are, indeed, constituents of tangles--apparently exceeding the concentration of tau protein 17-fold. Contribution of both conformation and primary structure to IgG specificity may explain the lack of any cross-reaction of mAbs to neurofilaments with tau protein in intact tissue and the appearance of cross-reaction in immunoblots where conformation specificity may be largely lost. The present data extend earlier findings of abnormal processing of neurofilaments and tau protein in Alzheimer disease and, together with reported abnormal processing of cerebrovascular amyloid β -protein, suggest that inhibition of the processing of multiple proteins is basic to the pathogenesis of Alzheimer disease, whereas formation of plaques and tangles could be merely the most striking histologic result.

Despite being located 21 kilometers from the epicenter of the 1994 Northridge earthquake (magnitude 6.7), the city of Santa Monica experienced anomalously concentrated damage with Mercalli intensity IX, an intensity as large as that experienced in the vicinity of the epicenter. Seismic records from aftershocks suggest that the damage resulted from the focusing of seismic waves by several underground acoustic lenses at depths of about 3 kilometers, formed by the faults that bound the northwestern edge of the Los Angeles basin. The amplification was greatest for high-frequency waves and was less powerful at lower frequencies, which is consistent with focusing theory and finite-difference simulations.

Three cases are reported of primary bronchial carcinoma with metastatic deposits in an intracranial glioma (two cerebral astrocytomas and one fourth ventricle ependymoma). The rarity of this phenomenon is emphasised and the literature critically reviewed.

An unprecedented increase in earthquakes in the U.S. mid-continent began in 2009. Many of these earthquakes have been documented as induced by wastewater injection. We examine the relationship between wastewater injection and U.S. mid-continent seismicity using a newly assembled injection well database for the central and eastern United States. We find that the entire increase in earthquake rate is associated with fluid injection wells. High-rate injection wells (>300,000 barrels per month) are much more likely to be associated with earthquakes than lower-rate wells. At the scale of our study, a well's cumulative injected volume, monthly wellhead pressure, depth, and proximity to crystalline basement do not strongly correlate with earthquake association. Managing injection rates may be a useful tool to minimize the likelihood of induced earthquakes.

A case of ependymoma of the cauda equina, presumably originating from the filum terminale in a girl aged 17 at the onset of illness, eventually developed remote metastases in the lungs, pleura, and one para-aortic lymph node. This case is compared with three other previously reported examples. The unusual features in the present instance were (1) the total length of the clinical history, amounting to 29 years; (2) the development, six years after the removal of the original spinal tumour, of another ependymomatous mass in the fourth ventricle, interpreted as a rostral metastasis that seeded via the cerebrospinal fluid; and (3) the demonstration of anaplastic cytological changes at the primary site, interpreted as the result of irradiation. The salient aspects of this and the three other reported cases are briefly reviewed, and the pathway of distant dissemination, resulting from venous permeation at the primary site, is emphasized.