THE RED SEA — GULF OF ADEN: BIOSTRATIGRAPHY, LITHOSTRATIGRAPHY AND PALAEOENVIRONMENTS

Sediments of Palaeozoic, Mesozoic and early Palaeogene ages experienced a similar geological history in Ethiopia, Yemen and Somalia. During the late Eocene, however, uplift and differential erosion took place, prior to rift development in the middle Oligocene, when the proto-Gulf of Aden became established. To a certain extent, a similar sequence of events had also taken place in those regions of Egypt, Sudan, Ethiopia, Yemen and Saudi Arabia which border the Red Sea, but post-Eocene subsidence is now believed to have commenced during the late Oligocene in the southern Red Sea and progressed later, during the early Miocene, in the northern Red Sea and Gulf of Suez. Timing of this progressive development of the Gulf of Aden rift complex through the Red Sea and Gulf of Suez is well constrained by biostratigraphy, and provides a new approach to the understanding of lithological variations within the region.
These lithological variations have, until now, only been considered on a country-specific basis, thus hindering establishment of a regional history of sedimentation. The well-understood and well-documented lithostratigraphic nomenclature of the Miocene succession of the Gulf of Suez has been used as a reference, or type, with which the lateral facies variations within the Red Sea have been compared. By this method only has it been possible to produce palaeoenvironmental maps for the entire study region, and for each formation and member. Lateral equivalents of the Gulf of Suez Nukhul, Rudeis, Kareem, Belayim, South Gharib. Zeit, Wardan and Shagara Formations have been identified within the Red Sea syn-rift and post-rift episodes.     

A review of the pathophysiology of cervical spondylotic myelopathy with insights for potential novel mechanisms drawn from traumatic spinal cord injury

Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction. Despite advances in diagnosis and surgical treatment, many patients still have severe permanent neurologic deficits caused by this condition. An improved understanding of the pathophysiology of cervical spondylotic myelopathy, particularly at a cellular and molecular level, may allow improved treatments in the future. A detailed review of articles in the literature pertaining to cervical spondylotic myelopathy was supplemented by an analysis of relevant mechanisms of spinal cord injury. The pathologic course of cervical spondylotic myelopathy is characterized by early involvement of the corticospinal tracts and later destruction of anterior horn cells, demyelination of lateral and dorsolateral tracts, and relative preservation of anterior columns. Static and mechanical factors and ischemia are critical to the development of cervical spondylotic myelopathy. Free radical-and cation-mediated cell injury, glutamatergic toxicity, and apoptosis may be of relevance to the pathophysiology of cervical spondylotic myelopathy. To date, research in cervical spondylotic myelopathy has focused exclusively on the role of mechanical factors and ischemia. Fundamental research at a cellular and molecular level, particularly in the areas of glutamatergic toxicity and apoptosis may result in clinically relevant treatments for this condition.     

Use of tests for acidification of methyl-alpha-D-glucopyranoside and susceptibility to efrotomycin for differentiation of strains of Enterococcus and some related genera

A total of 107 Enterococcus strains, 10 Vagococcus fluvialis strains, and 8 Lactococcus garvieae strains were tested for acidification of methyl-alpha-D-glucopyranoside (MGP) and susceptibility to 100-microg efrotomycin (EFRO) disks. All 26 strains of Enterococcus casseliflavus, including 3 nonmotile and 2 nonpigmented strains, acidified MGP and were resistant to EFRO. All 22 strains of Enterococcus gallinarum, including 5 nonmotile strains, also acidified MGP and were resistant to EFRO. None of the 26 strains of Enterococcus faecium acidified MGP, and all were susceptible to EFRO. Although all 12 Enterococcus faecalis strains were also negative in the MGP test, they were resistant to EFRO. Other enterococcal strains gave variable results. All 10 strains of V. fluvialis and all 8 strains of L. garvieae gave positive and negative results, respectively, in the MGP test and were, respectively, resistant and susceptible to EFRO. These results indicate that tests of the production of acid from MGP and susceptibility to EFRO can be used as adjunct tests in the identification of typical and atypical strains of enterococci in the clinical microbiology laboratory.     

T lymphocyte responses to anti-neutrophil cytoplasmic autoantibody (ANCA) antigens are present in patients with ANCA-associated systemic vasculitis and persist during disease remission

The cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel has been identified in the cardiac muscle of a number of mammalian species, including humans. The goal of this study was to begin quantifying the structural requirements necessary for arylaminobenzoate block of the CFTR channel. The cardiac cAMP-dependent Cl- current (ICl) was measured using the whole-cell arrangement of the patch-clamp technique in guinea pig ventricular myocytes during stimulation of protein kinase A with forskolin. At drug concentrations below the IC50 value for channel block, reduction of ICl by the arylaminobenzoates occurred in a strongly voltage-dependent manner with preferential inhibition of the inward currents. At higher drug concentrations, block of both the inward and outward ICl was observed. Increasing the length of the carbon chain between the benzoate and phenyl rings of the arylaminobenzoates resulted in a marked increase in drug block of the channel, with IC50 values of 47, 17, and 4 microM for 2-benzylamino-5-nitro-benzoic acid, 5-nitro-2-(2-phenylethylamino)-benzoic acid, and 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), respectively. Increasing the carbon chain length further with the compound 5-nitro-2-(4-phenylbutylamino)-benzoic acid, caused no additional increase in the potency of drug block (IC50 = 4 microM). Inhibition of ICl by the arylaminobenzoates was modulated by the pH of the external solution; increasing the pH from 7.4 to 10.0 greatly weakened NPPB block, whereas decreasing the pH to 6.4 enhanced block. In addition, block of ICl was observed during intracellular dialysis of NPPB, and this action was not affected by raising the external pH.     

Finite element modeling of three-dimensional pulsatile flow in the abdominal aorta: relevance to atherosclerosis

The infrarenal abdominal aorta is particularly prone to atherosclerotic plaque formation while the thoracic aorta is relatively resistant. Localized differences in hemodynamic conditions, including differences in velocity profiles, wall shear stress, and recirculation zones have been implicated in the differential localization of disease in the infrarenal aorta. A comprehensive computational framework was developed, utilizing a stabilized, time accurate, finite element method, to solve the equations governing blood flow in a model of a normal human abdominal aorta under simulated rest, pulsatile, flow conditions. Flow patterns and wall shear stress were computed. A recirculation zone was observed to form along the posterior wall of the infrarenal aorta. Low time-averaged wall shear stress and high shear stress temporal oscillations, as measured by an oscillatory shear index, were present in this location, along the posterior wall opposite the superior mesenteric artery and along the anterior wall between the superior and inferior mesenteric arteries. These regions were noted to coincide with a high probability-of-occurrence of sudanophilic lesions as reported by Cornhill et al. (Monogr. Atheroscler. 15:13-19, 1990). This numerical investigation provides detailed quantitative data on hemodynamic conditions in the abdominal aorta heretofore lacking in the study of the localization of atherosclerotic disease.     

CCR5/delta(ccr5) heterozygosity: a selective pressure for the syncytium-inducing human immunodeficiency virus type 1 phenotype. NIAID AIDS Clinical Trials Group Protocol 241 Virology Team

Mechanisms underlying the delay in dominance of syncytium-inducing (SI) phenotype HIV-1 (human immunodeficiency virus type 1) in vivo are unknown. Both random mutational events and selective pressures operative only late in the disease process have been suggested to underlie the shift from CCR5 to alternative coreceptor usage. Among the moderately advanced patients who entered AIDS Clinical Trials Group protocol 241, SI viral phenotype was more common among CCRS/delta(ccr5) heterozygotes (7/7, 100%) than among CCR5/CCR5 homozygotes (29/88, 33%; P < .001, Fisher's exact test). Other characteristics did not differ at study entry by CCR5 genotype, including median CD4 cell counts, plasma RNA levels, and infectious HIV-1 titers in circulating cells. These data indicate that CCR5/delta(ccr5) heterozygosity, which decreases cell-surface levels of CCR5 available to serve as an HIV-1 entry coreceptor, is a selective pressure for evolution of T cell line-tropic viruses that use an alternative coreceptor.     

Head trauma: CT scan interpretation by radiology residents versus staff radiologists

The determination of diagnostic features in recorded heart sounds was investigated with Carpentier-Edwards (CE) bioprosthetic valves. Morphological features, extracted using the Choi-Williams distribution, achieved between 96 and 61% correct classification. The time-scale wavelet-transform feature set achieved 100% correct classification with native valve populations, and 87% with the CE replacements.