Slip deficit on the san andreas fault at parkfield, california, as revealed by inversion of geodetic data.

A network of geodetic lines spanning the San Andreas fault near the rupture zone of the 1966 Parkfield, California, earthquake (magnitude M = 6) has been repeatedly surveyed since 1959. In the study reported here the average rates of line-length change since 1966 were inverted to determine the distribution of interseismic slip rate on the fault. These results indicate that the Parkfield rupture surface has not slipped significantly since 1966. Comparison of the geodetically determined seismic moment of the 1966 earthquake with the interseismic slip-deficit rate suggests that the strain released by the latest shock will most likely be restored between 1984 and 1989, although this may not occur until 1995. These results lend independent support to the earlier forecast of an M = 6 earthquake near Parkfield within 5 years of 1988.

Surface displacements in the 1906 san francisco and 1989 loma prieta earthquakes.

The horizontal displacements accompanying the 1906 San Francisco earthquake and the 1989 Loma Prieta earthquake are computed from geodetic survey measurements. The 1906 earthquake displacement field is entirely consistent with right-lateral strike slip on the San Andreas fault. In contrast, the 1989 Loma Prieta earthquake exhibited subequal components of strike slip and reverse faulting. This result, together with other seismic and geologic data, may indicate that the two earthquakes occurred on two different fault planes.

Rapid intraplate strain accumulation in the new madrid seismic zone.

Remeasurement of a triangulation network in the southern part of the New Madrid seismic zone with the Global Positioning System has revealed rapid crustal strain accumulation since the 1950s. This area experienced three large (moment magnitudes >8) earthquakes in 1811 to 1812. The orientation and sense of shear is consistent with right-lateral strike slip motion along a northeast-trending fault zone (as indicated by current seismicity). Detection of crustal strain accumulation may be a useful discriminant for identifying areas where potentially damaging intraplate earthquakes may occur despite the absence of large earthquakes during historic time.

Rapid deformation of the South flank of kilauea volcano, hawaii.

The south flank of Kilauea volcano has experienced two large [magnitude (M) 7.2 and M 6.1] earthquakes in the past two decades. Global Positioning System measurements conducted between 1990 and 1993 reveal seaward displacements of Kilauea's central south flank at rates of up to about 10 centimeters per year. In contrast, the northern side of the volcano and the distal ends of the south flank did not displace significantly. The observations can be explained by slip on a low-angle fault beneath the south flank combined with dilation deep within Kilauea's rift system, both at rates of at least 15 centimeters per year.

Lifetime brain serotonin: regional effects of age and precursor availability.

In the rat, regional brain serotonin levels which do not change from 2-30 months of age are increased at 36 months. Corresponding catecholamine levels progressively decrease. Feeding a diet restricted in the amino acid tryptophan (the precursor of serotonin) from weaning to two years of age markedly reduces serotonin levels in all brain regions and lowers norepinephrine levels in the cerebral hemispheres. Regional activity of synthesizing (tyrosine and tryptophan hydroxylases) and catabolizing enzymes (MAO-A) does not change markedly with age or dietary manipulation except for sporadic increases in tryosine hydroxylase activity in pair-fed animals. Returning the tryptophan-deficient animals to a normal diet produces a certain degree of rehabilitation the effectiveness of which varies with the function considered: Impaired brain serotonin levels recover moderately but remain lower than controls as late as 36 months, growth is never completely compensated, and norepinephrine levels show a rebound increase.

Interrelations of dietary and hormonal effects in aging.

A model system is proposed which suggests that aging involves a genetically programmed process encoded within specific regions of the central nervous system and is characterized by a gradual ascendency of inhibitory over excitatory influences. The resulting neural suppression reduces tonic stimulation to the hypothalamus-pituitary-endocrine axis, the autonomic nervous system and the spinal cord, and promotes the secretion of inactive pituitary hormone, the involution of the somatic musculature (smooth, cardiac and striated) and the compromise of secretomotor function. Experimental observation from nutritional restriction studies which include the prolongation of the life-span and delays in reproductive and homeostatic aging, degenerative coat changes and the appearance of neoplasia, are considered from the perspective of this hypothesis.

Patho-physiologic findings after chronic tryptophan deficiency in rats: a model for delayed growth and aging.

Long-Evans female rats three weeks, three months and 13-14 months of age were placed on tryptophan-deficient diets for periods ranging from a few months to nearly two years. Growth was interupted during the period of tryptophan-deficiency, but when the animals were returned to a complete diet, they gained weight and grew to normal size. Ability to reproduce, as indicated by litter production, was present at 17-28 months of age in rats which had been deprived of tryptophan, whereas no controls over 17 months of age produced any offspring. Other signs of delayed aging in the experimental group included, at advanced ages, greater longevity, as well as later onset in the appearance of obvious tumors, and better coat condition and hair regrowth. Many of these effects were also seen in pair-fed controls (fed a diet equal in amount to that eaten by the tryptophan-deprived rats, but with 1-tryptophan added). It is hypothesized that tryptophan deficiency delays growth, development and maturation of the central nervous system (CNS), in particular, by decreasing the levels of the neurotransmitter serotonin, for which tryptophan is the necessary precursor. In a parallel experiment, chronic treatment with d, 1-parachlorophenylalanine, an inhibitor of brain serotonin synthesis, from weaning until adulthood, also inhibited growth (body weight) and delayed sexual maturation (age of vaginal opening). These observations suggest that diets deficient in tryptophan or restricted in calories can affect maturation and aging by interfering with CNS protein synthesis, or neurotransmitter metabolism, or both.

Neural and endocrine development after chronic tryptophan deficiency in rats: II. Pituitary-thyroid axis.

Long-Evans female rats, 21 days of age, were weaned and placed on a control (Purina Rat Chow) diet, on a tryptophan deficient diet (T-) and on a diet complete in quality (Purina Rat Chow) but restricted to the daily amount consumed by the rats on the T- diet (pair-feeding). All animals were maintained on these diets for 1 and 2 months and then one group of T- rats was returned to the complete (Purina) diet and kept on this diet for several periods of time (up to 2 months). Growth was interrupted during the period of tryptophan deficiency and pair-feeding, but was restored to normal when the animals were returned to the Purina diet. In control rats, blood levels of TSH, T4 and T3 as determined by radio-immunoassay showed characteristic development patterns. In T- rats, hormonal developmental patterns were similar to those of controls after 1 month on the T- diet but levels fell significantly below control values after 2 months. On the other hand, hormonal levels of pair-fed rats were already significantly low 1 month after treatment and continued to remain low after 2 months. The decrease in thyroid function reported in these experiments as a result of severe dietary restrictions not only may explain the retardation of growth and development characteristic of nutritionally deficient animals, but also suggest some long-term interaction of nutrition and thyroid function on the aging process.

Histology and survival in age-delayed low-tryptophan-fed rats.

Diets containing tryptophan in concentrations 30 and 40 percent of those fed to controls from weaning to 24-30 months or more, can delay aging in Long-Evans female rats. Mortality among low-tryptophan-fed rats was greater in the juvenile period, but substantially less than controls at late ages. Histological biomarkers of aging were also delayed after tryptophan restriction in some organs (liver, heart, uterus, ovary, adrenal and spleen) but not in others (kidney, lung, aorta). Brain serotonin levels were low in tryptophan-deficient rats but showed remarkable capacity for rehabilitation. Effects on early and late mortality and brain levels of serotonin were proportional to the severity of the restriction.

Low tryptophan diets delay reproductive aging.

Newly weaned female rats fed diets severely deficient in the essential amino acid tryptophan show marked delays in reproductive aging, with conception and delivery occurring as late as 36 months. The rate of aging in these rats seems inversely related to both their early growth rates and the accessibility of brain tryptophan. The subsequent age retardation may depend on a reduction in both early cell loss and rate of brain maturation.

Neural and endocrine development after chronic tryptophan deficiency in rats: I. Brain monoamine and pituitary responses.

Caloric restriction and tryptophan deficient diets have been shown to delay aging in the immature laboratory rat. Studies of monoamine levels in the brain of developing female rats fed on these diets show changes in serotonin but not norepinephrine or dopamine levels: in tryptophan-restricted rats serotonin levels were reduced in all brain areas studied, whereas in caloric-restricted animals serotonin levels were increased in the cerebral hemispheres only. Another group of animals, in which growth and maturation was delayed by feeding d,1-parachlorophenylalanine (PCPA) showed decreases in serotonin, norepinephrine and dopamine concentrations in all brain regions investigated. All treatments employed to arrest growth and maturation resulted in pituitary alterations manifested by gross, histological and ultrastructural changes. It is postulated that there maturation- and age-retarding treatments delay the development of the central nervous system resulting in postponed maturation of the neuroendocrine axis, with consequent hypoactivity of certain pituitary functions and a resultant delay in the onset of maturation and senescence.

Incidence of new pulmonary perfusion defects after routine cardiac catheterization.

The incidence of pulmonary perfusion defects after routine cardiac catheterization was assessed in 57 patients by comparing ventilation-perfusion lung scans obtained before and 1 day after catheterization. Patients were prospectively randomized to two groups, one in which right heart catheterization was performed using an antecubital venous cutdown procedure and one in which the percutaneous femoral vein approach was used. Seven patients (12 percent) had new postcatheterization perfusion defects consistent with pulmonary emboli. These patients did not differ significantly from patients without new defects in clinical characteristics, duration of catheterization, hemodynamic variables or route of right heart catheterization. The data suggest that pulmonary embolism may be a more common complication of routine cardiac catheterization than previously appreciated.

Deep venous thrombosis of the upper extremity associated with use of the Swan-Ganz catheter.

Two patients who developed unilateral neck vein distention following insertion of a Swan-Ganz catheter are described. One patient developed unilateral swelling of the arm used for catheter insertion. Following removal of the Swan-Ganz catheter in this patient, venograms of both upper extremities revealed internal jugular vein thrombosis and subclavian vein thrombosis of the involved extremity. The other patient had thrombosis of the internal jugular veins and subclavian veins bilaterally, as well as superior vena cava thrombosis.

Glutamic acid decarboxylase activity in discrete hypothalamic nuclei during the development of rats.

We have assessed the activity (nmol/mg protein/h) of glutamic acid decarboxylase (GAD) in discrete hypothalamic nuclei before and after sexual maturation in the developing female rat. Activity in other brain regions including the cortex, septum and caudate-putamen was also assessed. While there appears to be a general rise (approximately 30%), with age, in GAD activity, the rise is most marked, and highly significant (P less than 0.001), in the anterior portion of the hypothalamus (56%). In contrast, no significant increase of GAD activity was found in the medical basal hypothalamus.

Long-term tryptophan restriction and aging in the rat.

Growth-retarded rats fed a tryptophan deficient diet at 21 days for periods of 6-22 months were shown to reach normal body weight when subsequently fed Purina Rat Chow. They demonstrated an increased ability over similar aged controls to recover from hypothermia induced by 3-minute whole-body ice water immersion, were able to bear litters at 17--28 months of age, showed a delay in the age of onset of visible tumors, and indicated an increase in their average lifespan at late ages. Animals fed on this diet from 3 months of age revealed a similar ability to reproduce at advanced ages, but not as marked as those placed on the diet earlier. The average lifespan (in months +/- the standard error of the mean) of the rats recovering from the long-term tryptophan-deficient diets was 36.31 +/- 2.26 while the control rats survived an average of 30.5 +/- 1.90 months. The last of 8 rats surviving the period of tryptophan-deficiency died at 45.50 months (1387 days) while the last of 14 control rats died at 41.75 months (1266 days). It is hypothesized that some kind of subtle mechanism exerts its influence on the rats during the period of tryptophan deficiency which caused an accelerated morbidity and mortality as they approached senescence approximately 1 to 2 years after refeeding. This is parallel to the situation with immature animals subjected to long-term caloric restriction and then fed on normal diets.

Age-related changes in the thermoregulatory capacity of tryptophan-deficient rats.

From a larger study seeking to develop indexes of physiological aging, the present experiment was designed 1) to test thermoregulatory capacity in the aging and old rat subjected to 3 minutes of whole-body ice water immersion, and 2) using this index of physiological age, to determine whether tryptophan deficiency from time of weaning can retard the onset of senescence. Results indicate a progressive prolongation of temperature recovery time from young to middle age to old, and tryptophan-deficient animals restored to commercial diet at middle age show the thermoregulatory capacity of young adults. The implications of tryptophan deficiency with respect to brain development, serotonin metabolism, and temperature regulation are also discussed in terms of the possibility of intervening with the aging process.

Low temperature preservation and space medicine.

Cold maintenance may be an option for compromised space-borne astronauts. Contemporary aneurysm surgery can involve cooling below 20 degrees C for nearly one hour. Dogs and baboons have survived blood-substituted hypothermia for 1-3 hours. Hamsters have recovered from partial-freezing below -1 degree C, and supercooling at -5 degrees C. Laboratory frogs have survived partial-freezing from -9 degrees C, while in nature, frogs may overwinter in these states. While some invertebrates can tolerate freezing to cryogenic temperatures, no vertebrate has survived complete freezing. The following studies (hypothermia and sub-zero experiments) were conducted to explore low temperature preservation of rodents, dogs and baboons.

Cardiac-pulmonary edema and low pulmonary capillary wedge pressure.

We describe a patient who presented with acute massive pulmonary edema, clinically and on chest roentgenogram. Two hours later the patient became hypotensive and was found to have a low pulmonary capillary wedge pressure (PCWP). The blood pressure returned to normal after administration of fluids. Acute pulmonary edema develops if PCWP rises higher than 25 to 30 mm Hg. In our patient, the elevated PCWP fell to low normal within two hours, when chest roentgenogram and clinical examination still suggested severe pulmonary edema. A phase lag existed between lowering of the pulmonary capillary wedge pressure and clearing of fluid from the alveolar and interstitial spaces in the lungs. At least three different pathogenetic mechanisms in patients with coronary artery disease can produce this phase lag. Transient global ischemia of the left ventricle was thought to be the responsible mechanism in our patient.

Pulmonary edema with nifedipine in primary pulmonary hypertension.

Despite occasional case reports, vasodilator therapy of primary pulmonary hypertension remains unsatisfactory. Nifedipine, a calcium channel antagonist, has recently been recommended for the treatment of primary pulmonary hypertension. Transient mild side effects to this drug have been known. In this report we describe a case of primary pulmonary hypertension in whom oral nifedipine use was followed by fatal pulmonary edema. We suggest that nifedipine has the potential of causing life-threatening complications of pulmonary edema in patients with severe primary pulmonary hypertension, and in this condition it should be used cautiously.