Tracking the Cracking: A Holistic Analysis of Rapid Ice Shelf Fracture Using Seismology, Geodesy, and Satellite Imagery on the Pine Island Glacier Ice Shelf, West Antarctica.

Ice shelves regulate the stability of marine ice sheets. We track fractures on Pine Island Glacier, a quickly accelerating glacier in West Antarctica that contributes more to sea level rise than any other glacier. Using an on-ice seismic network deployed from 2012 to 2014, we catalog icequakes that dominantly consist of flexural gravity waves. Icequakes occur near the rift tip and in two distinct areas of the shear margin, and TerraSAR-X imagery shows significant fracture in each source region. Rift-tip icequakes increase with ice speed, linking rift fracture to glaciological stresses and/or localized thinning. Using a simple flexural gravity wave model, we deconvolve wave propagation effects to estimate icequake source durations of 19.5-50.0 s and transient loads of 3.8-14.0 kPa corresponding to 4.3-15.9 m of crevasse growth per icequake. These long-source durations suggest that water flow may limit the rate of crevasse opening.

Alcohol abuse and dependence in the rural South.

We studied rural-urban differences in the prevalence of Diagnostic Interview Schedule (DIS)-DSM-III alcohol abuse or dependence from a community survey (part of the Epidemiologic Catchment Area program) of 3921 adults living in the Piedmont of North Carolina. Bivariate analyses disclosed that current alcohol-related problems, as identified by the DIS, were more common in the rural area (4.2% vs 2.6%). In a logistic regression analysis that controlled for potential confounders, including age, sex, race, socioeconomic status, and the DIS-DSM-III diagnoses of major depression and antisocial personality disorder, the elevated odds of alcohol abuse or dependence in the rural area remained significant for the interactive variable "rural blacks" (relative risk, 2.88). Factors leading to urban-rural differences in psychiatric disorders, such as current alcohol abuse or dependence, are therefore more complex than can be explained by geographic boundaries alone.

Aortic aneurysm with retroperitoneal fibrosis and ureteral obstruction.

Arteriosclerotic aneurysms of the abdominal aorta constitute a common clinical entity. Rarely are they associated with retroperitoneal fibrosis and ureteral obstruction requiring ureterolysis. Fifteen such cases have been reported, with resection successful in 5 of 7. A sixteenth case is presented complicated by the presence of a persistent left cardinal vein. It is the third aneurysm resected with such an anomaly, and to our knowledge the first to be associated with retroperitoneal fibrosis and ureteral obstruction. Ureterolysis with resection of the aneurysm was performed. The difficulties presented by these pathologic entities, as well as the anomalous venous pattern, are reviewed. Complete preoperative evaluation, including intravenous pyelogram, retrograde pyelography, aortography, and venacavography, for the definition of anatomic relationships and planning of the surgical approach is stressed.

Effects of dopamine metabolites on locomotor activities and on the binding of dopamine: relevance to the side effects of L-dopa.

L-dopa is the major treatment for Parkinson's disease (PD), but its efficacy is limited by the presence of dyskinesia. The dyskinesia develops over a period of exposure to L-dopa and is related to the dosage, therefore, the cause may involve inductive changes that produce toxic levels of metabolites, interfering with dopamine (DA) neurotransmission. Chronic L-dopa induces catechol-O-methyltransferase (COMT) and methionine adenosyl transferase (MAT), enzymes involved in the methylation of catecholamines (CA). In addition, high levels of 3-O-methyl-dopa have been reported in the plasma of dyskinetic PD patients, treated with L-dopa, as compared to non-dyskinetic patients, therefore, the methyl metabolites of CA may be increased during L-dopa therapy and may be involved in the dyskinesia. Since large amounts of DA are produced from L-dopa, and DA is extensively methylated, the methyl metabolites of DA, 3-methoxytyramine (3-MT) and 3,4-dimethoxyphenylethylamine (DIMPEA), may be also involved. The first step in knowing this, is to assess the behavioral and DA-receptor activities of 3-MT and DIMPEA. In the rat, the intraventricular injection of 0.5 micromol of DIMPEA increased the total distance traveled (TD) by over 100%, the number of movement (NM) made by 40% and the time spent moving (MT) by about 36%. Identical doses of 3-MT decreased the TD by 42%, NM by 22% and MT by 39%. DIMPEA (1 mM) increased the binding of DA with brain membranes by 44.7%, whereas 3-MT decreased it by 15.8%. The results show that 3-MT and DIMPEA are behaviorally active, and in parallel, they interact with the binding sites for DA, consequently, they may contribute to the side effects of L-dopa. L-dopa produces high levels of DA and induces MAT and COMT. It is proposed, therefore, that DA will be methylated to 3-MT and 3-MT to DIMPEA. At threshold level each product will inhibit, allosterically, its enzyme of methylation, causing sequential and rhythmic up and down regulation of its concentration. At peak levels these hydrophobic metabolites will modulate the actions of DA on synaptic membranes, causing abnormal movements, at times, resembling the "on-off effects".

Parkinson's disease-like effects of S-adenosyl-L-methionine: effects of L-dopa.

The major symptoms of Parkinson's disease (PD) are due to degeneration of the nigrostriatal pathway and depletion of dopamine (DA). Tyrosine hydroxylase (TH), norepinephrine (NE), serotonin (5-HT), and melanin pigments are also decreased and acetylcholinergic activity increased. Biochemically, increased methylation can cause the depletion of DA, NE, 5-HT, and melanin pigments and also an increase of acetylcholine; thus, increased methylation can present a biochemical picture that resembles the biochemical changes that occur in PD. During the therapy of PD with L-dopa, it is well known that L-dopa reacts avidly with S-adenosyl-L-methionine (SAM), the biologic methyl donor, to produce 3-O-methyl-dopa. Correspondingly, L-dopa has been shown to deplete the concentration of SAM, and SAM has been found to induce PD-like motor impairments in rodents; therefore, an excess of SAM-dependent methylation may be associated with Parkinsonism. To further study the effects of methylation, SAM was injected into the lateral ventricle of rats. SAM caused tremors, rigidity, abnormal posture, and dose-related hypokinesia. Doses of 9.38, 50, and 400 nM/rat caused 61.9, 73.4, and 94.8% reduction, respectively, of motor activity. A 200-mg/kg IP dose of L-dopa, given before 50 nM SAM, blocked the SAM-induced hypokinesia. SAM also caused a decrease in TH immunoreactivity, apparent degeneration of TH-containing fibers, loss of neurons, and the accumulation of phagocytic cells in the substantia nigra. These results showed that excess SAM in the brain, probably due to its ability to increase methylation, can induce symptoms that resemble some of the changes that occur in PD.

Striatal dopamine depletion, tremors, and hypokinesia following the intracranial injection of S-adenosylmethionine: a possible role of hypermethylation in parkinsonism.

The major symptoms of Parkinson disease (PD) are tremors, hypokinesia, rigidity, and abnormal posture, caused by the degeneration of dopamine (DA) neurons in the substantia nigra (SN) and deficiency of DA in the neostriatal DA terminals. Norepinephrine (NE) and serotonin (5-HT) levels in the neostriatum and tyrosine hydroxylase and melanin pigments in the substantia nigra are also decreased, and brain cholinergic activity is increased. The cause of PD is unknown, but PD is an age-related disorder, suggesting that changes that occur during the aging process may help to precipitate PD. Methylation increases in aging animals. Increased methylation can deplete DA, NE, and 5-HT; increase acetylcholine; and cause hypokinesia and tremors. These effects are similar to changes seen in PD, and interestingly also, they are similar to some of the changes that are associated with the aging process. It is suggested, therefore, that increased methylation may be an inducing factor in parkinsonism. Accordingly, the effects of an increase in methylation in the brain of rats were studied. S-adenosylmethionine (AdoMet), the limiting factor in the methylation process, was injected into the lateral ventricle of rats. Specific behavioral changes that resemble changes seen in PD were investigated. The results showed that AdoMet caused tremors, rigidity, hypokinesia, and depleted DA. The hypokinetic effects of a single dose of AdoMet lasted for about 90 min. AdoMet has a dose-dependent hypokinetic effect. A dose of 9.4 nmol reduced movement time (MT) by 68.9% and increased rest time (RT) by 20.7%, and a dose of 400 nmol reduced MT by 92.4% and increased RT by 27.6%. The normethyl analog of AdoMet, S-adenosylhomocysteine, did not cause hypokinesia or tremors, but it blocked the AdoMet-induced motor effects. L-dopa, the precursor of DA, also blocked the AdoMet-induced motor effects. These data suggest that the methyl group of AdoMet as well as DA depletion are involved in the AdoMet-induced motor effects. A dose of 0.65 mumol of AdoMet depleted DA in the ipsilateral caudate nucleus (CN) or neostriatum by 50.1%, and DA in the contralateral CN was reduced by 9.3%. Double the dose of AdoMet did not increase the depletion of DA on the ipsilateral CN, but DA in the contralateral CN was decreased by 26.3%. Taken together, the results suggest that increased methylation may contribute to the symptoms of PD.

Identification of motor neurons for accessory muscles of inspiration and expiration, pectoralis, trapezius and external oblique: comparison with non-respiratory skeletal muscle.

The motor neurons for the accessory muscles of respiration, pectoralis, trapezius, external oblique, and the rectus abdominis were studied in the spinal cord. The objective was to determine if the localization and morphology of the motor neurons for these muscles bear any distinct relationship to the specialized function of these muscles, serving both as supportive skeletal muscles and as accessory respiratory muscles. In addition, it was of interest to know if the inspiratory role of the pectoralis and trapezius muscles and the expiratory role of the external oblique and rectus abdominis are related to the spatial organization of the motor neurons; this knowledge may be important in the discrimination of influences from afferent connections. The motor neurons for these muscles were retrogradely labeled with true blue and were compared with the triceps motor neurons. All neurons occurred ipsilateral and most labeling occurred in C6-7. The motor neurons for the accessory muscles were mainly confined to the ventrolateral tip of the ventral gray matter. The triceps neurons were dorsolateral to the respiratory related neurons in C6-7. Within the confines of the ventrolateral area, the majority of neurons for the pectoralis were localized medial to ventromedial, those for the trapezius were ventrolateral, and those for the external oblique were in the extreme ventrolateral to ventral sections of C7. No neurons were observed in C2 to T2 for the rectus abdominis. A second neuronal column occurred medioventrally in the ventral gray of C4-6 for the trapezius, and is distinct and separated from the C6-7 cell column.(ABSTRACT TRUNCATED AT 250 WORDS)

Psychosocial risk factors and urban/rural differences in the prevalence of major depression.

The Piedmont Health Survey interviewed 3798 adult community residents in a region of North Carolina. Current major depression was nearly three times more common in the urban than in the rural counties; rural residence decreased the risk of major depression for some, but not all, demographic subgroups. The risk of major depression was decreased for young rural residents, compared with their urban age peers; rural residence was more protective for young women than for young men. Rural residence appears to be a buffer against major depression.

S-adenosyl-L-methionine decreases motor activity in the rat: similarity to Parkinson's disease-like symptoms.

S-Adenosyl-L-methionine has been shown to cause Parkinson's disease-like effects that include hypokinesia, tremor, rigidity, and abnormal posture. S-Adenosyl-L-methionine is the rate-limiting endogenous methyl donor. Its biochemical role, which includes the metabolism of dopamine and the synthesis of acetylcholine, also resembles the changes that occur in Parkinson's disease. Therefore, S-adenosyl-L-methionine may play a role in Parkinson's disease-like motor impairments. In this study we manipulated the levels of S-adenosyl-L-methionine in the brain of rats and quantified the changes in hypokinetic type motor activity that seems to occur also in Parkinsonism. Male Sprague-Dawley rats were anesthetized with chloral hydrate (400 mg/kg/rat), cannulated, injected into the lateral ventricle with S-adenosyl-L-methionine or saline, and their motor activity was measured in a Digiscan Animal Activity Monitor. Other behaviors were also observed. S-Adenosyl-L-methionine caused hypokinesia, tremor, rigidity, and abnormal posture in rats. Motor activity was significantly decreased within 2 min postinjection. The hypokinesia was maximal at 60 min, at which time a 65, 75, and 90% decrease for total distance, number of movements, and the ratio of total distance to the number of movements occurred, respectively. The hypokinetic effect of S-adenosyl-L-methionine was dose dependent. A 65.0 and 51.3% decrease in total distance and number of movements, respectively, were observed following 9.38 x 10(-9) mol. The 5.0 x 10(-8) mol caused a reduction of 73.42 and 57.66% and 4.0 x 10(-7) mol/rat caused a 94.9 and 78.43% decrease, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of L-dopa on the activity of methionine adenosyltransferase: relevance to L-dopa therapy and tolerance.

L-dopa, the major treatment for Parkinson's disease (PD), depletes S-adenosyl-L-methionine (SAM). Since SAM causes PD-like symptoms in rodents, the decreased efficacy of chronic L-dopa administered to PD patients may result from a rebound increase in SAM via methionine adenosyl transferase (MAT), which produces SAM from methionine and ATP. This was tested by administering intraperitoneally saline, or L-dopa to mice and assaying for brain MAT activity. As compared to controls, L-dopa (100 mg/kg) treatments of 1 and 2 times per day for 4 days did not significantly increase MAT activity. However, treatments of 3 times per day for 4 and 8 days did significantly increase the activity of MAT by 21.38% and 28.37%, respectively. These results show that short interval, chronic L-dopa treatments significantly increases MAT activity, which increases the production of SAM. SAM may physiologically antagonize the effects of L-dopa and biochemically decrease the concentrations of L-dopa and dopamine. Thus, an increase in MAT may be related to the decreased efficacy of chronic L-dopa therapy in PD.