The 1933 Long Beach Earthquake (California, USA): Ground Motions and Rupture Scenario.

We present a synoptic analysis of the ground motions from the 11 March 1933 Mw 6.4 Long Beach, California, earthquake, the largest known earthquake within the central Los Angeles Basin region. Our inferred shaking intensity pattern supports the association of the earthquake with the Newport-Inglewood fault; it further illuminates the concentration of severe damage in the town of Compton, where accounts suggest vertical ground motions exceeding 1 g. We use a broadband simulation approach to develop a rupture scenario for this earthquake, informed by the damage distribution. The predicted shaking for a 25-km-long fault matches the intensity distribution, with an indication that non-linear site response on soft sediments in some near-field regions was stronger than predicted using a simple model to account for non-linearity. Our results suggest that the concentration of damage near Compton can be explained by a combination of local site amplification, source-controlled directivity, and three-dimensional basin effects whereby energy was channeled towards the deepest part of the Los Angeles Basin.

Effect of statins on bone mineral density and bone histomorphometry in rodents.

Statins have been postulated to affect bone metabolism. We investigated the effects of different doses of simvastatin (1, 5, 10, and 20 mg. kg(-1). d(-1)), atorvastatin (2.5 mg. kg(-1). d(-1)), and pravastatin (10 mg. kg(-1). d(-1)) administered orally for 12 weeks to intact female Sprague-Dawley rats and the effect of 20 mg. kg(-1). d(-1) simvastatin in sham-operated and ovariectomized rats on femoral bone mineral density (BMD) and quantitative bone histomorphometry (QBH) and compared them with controls. BMD was decreased by 1 mg. kg(-1). d(-1) simvastatin (P=0.042), atorvastatin (P=0.0002), and pravastatin (P=0.002). The effect on QBH parameters differed with different doses of simvastatin (ANOVA, P=0.00012). QBH parameters of both bone formation and resorption were equivalently and markedly increased by 20 mg. kg(-1). d(-1) simvastatin in 2 separate groups of intact rats and were reflected by a relatively unchanged BMD. At lower doses, 1 mg. kg(-1). d(-1) simvastatin decreased bone formation while increasing bone resorption, as reflected by a marked decrease in BMD. Ovariectomized animals receiving 20 mg. kg(-1). d(-1) simvastatin showed no change in BMD relative to the untreated, ovariectomized controls; their increase in bone formation was smaller than in sham-operated rats receiving simvastatin, and there was no change in bone resorption. Dose-response curves of simvastatin for bone formation and resorption differed. These studies indicate that (1) statins decrease BMD in rodents, (2) high-dose simvastatin increases bone formation and resorption, (3) low-dose simvastatin decreases bone formation and increases bone resorption, (4) the effects of simvastatin on QBH differ at different dosages, (5) the effects of simvastatin seen in intact rats are not observed in ovariectomized rats, and (6) simvastatin is unable to prevent bone loss caused by ovariectomy.

Recognition of fibronectin by the platelet integrin alpha IIb beta 3 involves an extended interface with multiple electrostatic interactions.

Normal platelet function is dependent on the ability of integrin alpha IIb beta 3 (glycoprotein IIb/IIIa) to interact with components of the subendothelial matrix, such as fibronectin (Fn), exposed at sites of vascular injury. Studies using synthetic peptides derived from human Fn sequences Asp(1373)--Thr(1383) and Arg(1493)--Asp(1495) have suggested a role for both the 9th (3fn9) and 10th (3fn10) type III repeats of this ligand in binding to alpha IIb beta 3. In this study, we have taken a charge-to-alanine mutagenesis approach to evaluate the importance of these sites, and other charged residues, within the context of recombinant 3fn9--10 modules for binding to alpha IIb beta 3. To identify residues that are involved in Fn binding to alpha IIb beta 3, recombinantly expressed 3fn9--10 module pairs with alanine substitutions introduced into each of the 38 charged residues were individually assayed for the ability to inhibit Fn binding to purified alpha IIb beta 3. Substitutions at Fn residues Arg(1493) and Asp(1495) of the RGD sequence were found to have the greatest effect on alpha IIb beta 3 binding, as expected. However, Fn residues Arg(1369), Arg(1371), Arg(1379), Arg(1445), and Arg(1448) were needed for optimal interaction of the 3fn9--10 module pair with alpha IIb beta 3. All Fn residues found to affect binding of 3fn9--10 to alpha IIb beta 3 are located on the same face and extend from the surface of the molecule. Additionally, the epitopes for two anti-Fn monoclonal antibodies that inhibit binding of this ligand to alpha IIb beta 3 were found to overlap the sites identified. These results demonstrate that alpha IIb beta 3--Fn binding involves multiple electrostatic interactions.

Osteoporosis Clinical Guideline. South African Medical Association--Osteoporosis Working Group.

OBJECTIVE: This Guideline aims to improve the efficacy of both diagnostic and therapeutic interventions for osteoporosis. All health care workers are targeted in the Guideline. A rather detailed summary, which is cross-referenced to the full guideline, is provided to cater for the busy general practitioner. The motivation for the development of this Guideline is based on the facts that: Osteoporosis is a common, costly disease which carries a significant morbidity and mortality, yet is still too often regarded as an inescapable part of normal ageing. Early detection and intervention will be more cost-effective than the treatment of advanced disease. Much confusion exists regarding diagnostic criteria, the assessment of fracture risk, and therapeutic intervention thresholds. A rational approach to drug selection is seldom considered. No consensus guideline on the diagnosis and management of osteoporosis has been published in this country. OUTCOMES: Prevention of fracture and a reduction in morbidity and mortality were the major considerations in the development of this Guideline. Although no formal economic analysis was undertaken, the cost-effectiveness of diagnostic and therapeutic interventions was considered in all recommendations. EVIDENCE: A combination of descriptive, boundary (minimum standards) and algorithmic guidelines was employed. The highest level of evidence (meta-analyses, randomised and controlled studies) was used as far as possible and isolated descriptive studies and expert opinions were largely ignored. A draft guideline was developed, debated at a consensus meeting and finalised on the basis of written comments following the distribution of a second draft. METHODOLOGY: See Annexure B. RECOMMENDATIONS: In the absence of a sound health economic justification for a screening policy, it is recommended that the prevention and treatment of osteoporosis is best managed using a case-finding approach. It is recommended that clinical risk factors--related to bone mineral density (BMD), bone strength or falls--provide indications for further assessment, in particular bone mass measurement. Axial, dual energy X-ray absorptiometry (DEXA) is the preferred technique to assess BMD, to diagnose osteoporosis and to assess rates of bone loss/gain. While the four diagnostic categories proposed by the World Health Organisation (WHO, 1994) provide a practical basis to identify those at risk of fracture, cognisance should be taken of its limitations. We recommend that the BMD of both spine and hip should be measured, that the NHANES III reference data for Caucasians be used for subjects of all races (until local reference ranges for different ethnic groups are established), and that the same absolute thresholds be employed to diagnose osteoporosis in men and women. Recommendations are also made regarding indications for bone mass measurement and selected routine laboratory tests. The differences between diagnostic criteria and intervention thresholds are emphasised. The need to treat should not depend on a BMD value alone, but should also be determined by the patient's age, general health and willingness to consider treatment; the presence of clinical risk factors; prevalent vertebral fractures; and the rate of bone loss/turnover; as well as the cost-effectiveness and side-effects of available treatment. Non-pharmacological measures to improve bone strength include a balanced diet, physical exercise, limiting alcohol consumption, the avoidance of smoking and bone toxic drugs and the prevention of falls. No ideal drug can be recommended for the prevention and treatment of osteoporosis in all patients. The choice of drug is largely determined by the nature of the disease (e.g. antiresorptive agents like calcium (+/- vitamin D) for mild osteopenia, hormone replacement therapy (HRT) or bisphosphonates for moderate bone loss and the addition of a bone formation-stimulating agent in patients with more severe osteoporosis) and the pati

Cellular disposition of sulphamethoxazole and its metabolites: implications for hypersensitivity.

1. Bioactivation of sulphamethoxazole (SMX) to chemically-reactive metabolites and subsequent protein conjugation is thought to be involved in SMX hypersensitivity. We have therefore examined the cellular metabolism, disposition and conjugation of SMX and its metabolites in vitro. 2. Flow cytometry revealed binding of N-hydroxy (SMX-NHOH) and nitroso (SMX-NO) metabolites of SMX, but not of SMX itself, to the surface of viable white blood cells. Cellular haptenation by SMX-NO was reduced by exogenous glutathione (GSH). 3. SMX-NHOH and SMX-NO were rapidly reduced back to the parent compound by cysteine (CYS), GSH, human peripheral blood cells and plasma, suggesting that this is an important and ubiquitous bioinactivation mechanism. 4. Fluorescence HPLC showed that SMX-NHOH and SMX-NO depleted CYS and GSH in buffer, and to a lesser extent, in cells and plasma. 5. Neutrophil apoptosis and inhibition of neutrophil function were induced at lower concentrations of SMX-NHOH and SMX-NO than those inducing loss of membrane viability, with SMX having no effect. Lymphocytes were significantly (P<0.05) more sensitive to the direct cytotoxic effects of SMX-NO than neutrophils. 6. Partitioning of SMX-NHOH into red blood cells was significantly (P<0.05) lower than with the hydroxylamine of dapsone. 7. Our results suggest that the balance between oxidation of SMX to its toxic metabolites and their reduction is an important protective cellular mechanism. If an imbalance exists, haptenation of the toxic metabolites to bodily proteins including the surface of viable cells can occur, and may result in drug hypersensitivity.

Fast and slow bone losers. Relevance to the management of osteoporosis.

A low bone mineral density (BMD) is presently regarded as the most important risk factor for the development of osteoporosis. BMD is a function of peak bone mass attained during growth and subsequent age-related bone loss. BMD can be measured accurately and precisely, although the rate of bone loss is more difficult to assess. When axial BMD was measured, the rate of bone loss was shown to increase by 2- to 4-fold at the menopause. Although this rate varies markedly between individuals, it is symmetrically distributed, which argues against the existence of a subpopulation of fast bone losers. Levels of biochemical markers of bone turnover (e.g. osteocalcin, bone specific alkaline phosphatase, deoxypyridinoline) also increase markedly at the menopause, and individuals with a high turnover tend to lose bone more rapidly. Moreover, since increased bone resorption also results in qualitative changes regardless of BMD, a high bone turnover constitutes an independent risk factor. Currently, large intraindividual variations (10 to 40%) in levels of biochemical markers and assay errors still limit our ability to correctly classify individual patients as fast or slow bone losers. The routine use of these markers as a screening tool to predict the risk of osteoporosis in individuals is of limited value, although their selective use in therapeutic decision-making is more promising.

Bone mineral density in long-term survivors of childhood cancer.

Bone mineral density (BMD) of the lumbar spine was measured in 97 long-term survivors of childhood cancer 5-23 years after diagnosis using dual-energy X-ray absorptiometry (DXA). They had been treated for acute leukemia (n = 22), brain tumors (n = 16), lymphomas (n = 16), Wilms' tumor (n = 10), neuroblastoma (n = 7) and other cancers (n = 26). The correlations between BMD and the Z-scores for weight for height, height for age and weight for age at diagnosis and follow-up were evaluated with stepwise multiple regression. Correlations with cumulative corticosteroid and radiation dose were examined with Spearman's correlation coefficient. The number of nature of fractures were noted. A BMD Z-score of below -2 was present in 13 and a BMD Z-score of -1 to -2 in 31 children. In total, a low BMD was observed in 45% of children. Height for age at follow-up correlated significantly with BMD Z-score. Increasing doses of cranial irradiation (18-54 Gy) were associated with lower BMD (p = 0.001, Spearman). This was true also for 22 children with acute lymphoblastic leukemia (ALL) who had received 18-24 Gy cranial irradiation (p = 0.04, Spearman). Fractures occurred in 14 children following trauma. The difference in BMD Z-scores of children with and without fractures did not achieve statistical significance although the majority of the children with fractures had low BMD Z-scores. The significant inverse correlation between height for age at follow-up and BMD must be interpreted with the realization that DXA is not a volumetric measurement of BMD and that short stature is associated with a smaller skeletal mass.

Partial purification and localization of platelet-activating factor acetylhydrolase from bovine seminal plasma.

Platelet-activating factor (PAF) is a potent lipid mediator that is inactivated by platelet-activating factor acetylhydrolase (PAF-AH). Platelet-activating factor bioactivity has been detected in bovine sperm phospholipids and PAF-AH activity is extraordinarily high in bovine seminal plasma. The purpose of this study was to purify and characterize partially the PAF-AH in bovine seminal plasma. Platelet-activating factor acetylhydrolase was partially purified from bovine seminal plasma using gelatin-agarose and ion-exchange chromatography and nondenaturing polyacrylamide gel electrophoresis (PAGE). Enzyme activity was increased 11-fold over seminal plasma with a yield of 11%. Platelet-activating factor acetylhydrolase activity was eluted from a single band with a R(f) of 0.258 from a nondenaturing preparative PAGE gel along with several other proteins of varying molecular weights. Following separation by sodium dodecyl sulfate (SDS)-PAGE under reducing conditions, PAF-AH was identified as a approximately 60-kD band by western blotting using antiserum directed against human blood PAF-AH. N-terminal sequencing of the approximately 60 kD band, followed by amino acid-sequence similarity searching, demonstrated a single-sequence match with PAF-AH from bovine blood. Based on western blotting, a approximately 60-kD band corresponding to PAF-AH was detected in seminal vesicle fluid but not in samples of washed, sonicated sperm or sperm plasma membranes where activity was low (<5% and <0.3%, respectively, of that in seminal plasma), suggesting that seminal plasma PAF-AH does not bind tightly to sperm. Specific PAF-AH activity measured in seminal vesicle fluid was in the lower range of that in seminal plasma. These results demonstrate that PAF-AH activity in bovine seminal plasma is due to PAF-AH secreted by the seminal vesicles with sequence homology to the enzyme in human blood.

The relationship between the disposition and immunogenicity of sulfamethoxazole in the rat.

Idiosyncratic toxicity associated with sulfamethoxazole (SMX) is thought to be a consequence of bioactivation to the hydroxylamine metabolite (SMX-NOH) and further oxidation to the ultimate reactive metabolite, nitroso-sulfamethoxazole (SMX-NO). To establish the link between the formation of the ultimate reactive metabolite and SMX hypersensitivity, we have undertaken metabolism and immunogenicity studies in the rat by use of SMX and its metabolites. SMX was excreted in urine as N4-acetyl SMX and SMX-NOH, with approximately 10% remaining unchanged as parent amine. After administration of SMX-NOH (54 mg x kg(-1)) and SMX-NO (10 mg x kg(-1)), 38.3% and 46.1% of the doses, respectively, were excreted in urine as SMX and N4-acetyl SMX, which indicated extensive reduction of these metabolites in vivo. The immunogenic potential of SMX and its metabolites, SMX-NOH and SMX-NO, were assessed in rats by analyzing serum samples for the presence of anti-SMX IgG antibodies during a 4-week dosing period. No antibodies to SMX were detected in either control or SMX-treated rats. In contrast, a high titer of SMX-specific IgG antibody was present in sera from all the rats administered SMX-NO, reaching a maximum 14 to 21 days after the initial dose. Rats administered SMX-NOH only produced a weak IgG response after 3 weeks of dosing. These findings indicate that SMX-NO is highly immunogenic and may be responsible for the hypersensitivity reactions associated with SMX. Both SMX-NOH and SMX-NO undergo extensive reduction in vivo which may afford protection against SMX toxicity.

Relationship between androstenedione-induced myometrial contractions and platelet-activating factor acetylhydrolase in late gestation in pregnant rhesus monkeys.

An association between platelet-activating factor (PAF) and myometrial contractions has been established. Estrogens regulate PAF activity via reduction in the activity of plasma PAF acetylhydrolase (PAF-AH), the enzyme that catalyzes PAF inactivation. Administration of androstenedione to pregnant monkeys leads to sustained increases in maternal plasma estradiol (E2), with persistent nocturnal myometrial contractions. The present study tested the hypothesis that androstenedione-induced contractions are associated with a fall in maternal plasma PAF-AH activity in monkeys. Eight monkeys (132-136 days gestation, dGA) were instrumented under halothane anesthesia with maternal vascular catheters and uterine electromyogram electrodes. At 138-142 dGA, two baseline maternal arterial samples were taken for E2 and PAF-AH measurements. The following day a continuous i.v. androstenedione infusion was started in 4 monkeys while 4 control monkeys received i.v. infusions of vehicle alone. Arterial blood sampling was repeated 1 and 3 days after the start of either infusion. Despite an increase in maternal E2 to term levels and established myometrial contractions, no change in maternal plasma PAF-AH activity occurred after androstenedione treatment. Maternal plasma E2, PAF-AH activity, and contractions remained unchanged from baseline in control monkeys. In conclusion, androstenedione-induced increases in maternal plasma E2 and myometrial contractions are not associated with a fall in maternal plasma PAF-AH specific activity.

Body fat distribution as a risk factor for osteoporosis.

OBJECTIVE: The aim of this study was to compare the body fat distribution of patients with osteoporosis (OP) with that of an appropriately matched non-OP control group. DESIGN: Case control study. SETTING: Department of Endocrinology and Metabolism, Tygerberg Hospital. Participants. A total of 56 patients with histologically proven idiopathic OP, of whom 39 were women (mean age 61 +/- 11 years) and 17 men (49 +/- 15 years), were compared with 125 age- and sex-matched non-OP (confirmed by dual energy X-ray absorptiometry) subjects, 98 women (60 +/- 11 years) and 27 men (51 +/- 16 years). OUTCOME MEASURES: Anthropometric data, including weight, height, skinfold measurements, mid-upper arm, waist and hip circumferences, as well as elbow breadth. RESULTS: The men and women with OP were significantly shorter (P = 0.04 and P = 0.03 respectively) and of lower body mass (P = 0.04 and P = 0.02 respectively) than the control subjects, although their mean body mass indices were comparable. The OP population had significantly lower skinfold, elbow breadth and arm circumference values, although the majority of subjects in both groups fell within the 15-85th percentiles. Despite their lower body mass, both the OP women (P = 0.009) and men (P = 0.002) had significantly higher waist/hip ratios than corresponding controls. CONCLUSION: Whatever the underlying pathogenesis, this new finding suggests that, should these results be confirmed by larger studies, OP can be added to the list of diseases associated with a waist fat distribution.

Earthquakes in the los angeles metropolitan region: a possible fractal distribution of rupture size.

Although there is debate on the maximum size of earthquake that is possible on any of several known fault systems in the greater Los Angeles metropolitan region, it is reasonable to assume that the distribution of earthquakes will follow a fractal distribution of rupture areas. For this assumption and an overall slip-rate for the region of approximately 1 centimeter per year, roughly one magnitude 7.4 to 7.5 event is expected to occur every 245 to 325 years. A model in which the earthquake distribution is fractal predicts that, additionally, there should be approximately six events in the range of magnitude 6.6 in this same span of time, a higher rate than has occurred in the historic record.

Platelet-activating factor acetylhydrolase activity in seminal plasma from the bull, stallion, rabbit, and rooster.

Platelet-activating factor (PAF) acetylhydrolase, which inactivates PAF, has been detected in human and bovine seminal plasma and may represent a mechanism for regulating sperm-derived PAF. This study was designed to characterize further PAF acetylhydrolase in seminal plasma from domestic animal species. Sperm-free seminal plasma from the bull, stallion, rabbit, and rooster was assayed for acetylhydrolase activity based on the release of [3H]acetate from PAF. As reported previously for bull seminal plasma, activity in stallion, rabbit, and rooster seminal plasma was linear with both time and protein concentration, with specific activities of 97.4, 1.2, and 0.33 nmol PAF hydrolyzed/mg protein/min, respectively. Activity in seminal plasma from the bull, rabbit, and rooster was calcium-independent whereas activity in stallion seminal plasma increased with added calcium (p < 0.01). Addition of EDTA partially inhibited acetylhydrolase activity in stallion seminal plasma but increased the specific activity in rabbit seminal plasma (p < 0.01). Enzyme activity in bull seminal plasma was nondialyzable (50,000 molecular weight cutoff), stable at pH 5.0, and heat-labile (> or = 60 degrees C). Very little activity was associated with bull seminal plasma lipoproteins isolated by KBr flotation or by precipitation with polyanions. These results demonstrate that PAF acetylhydrolase activity is present in seminal plasma from different species, with large differences in specific activity among species. These differences may be related to species differences in the physiological role of PAF and its regulation in sperm and male tract fluids.

Static bone histomorphometry in preterm and term babies.

The nature and pathophysiology of the bone loss which occurs in term and especially preterm neonates are poorly understood, and it is unclear whether this neonatal osteopenia results from impaired bone formation or increased bone resorption. This study compared the static bone histomorphometry of preterm and term babies, employing iliac crest bone biopsy specimens obtained postmortem. All the babies died within the first 6 days of life and none had any clinical, biochemical or radiologic evidence of metabolic bone disease. The trabecular bone volume, as well as static parameters of bone formation (OV/TV, OV/BV, OS/BS, OB.S/BS) did not differ significantly in preterm and term babies. Although time-spaced tetracycline labelling could not be employed in the present study, evidence of rickets was not apparent. Parameters of bone resorption in preterm babies were, however, significantly higher (p = 0.01) than those of term babies, suggesting that increased bone resorption and not impaired formation, underlies the development of osteopenia in the preterm neonate.

High turnover osteopenia in preterm babies.

Osteopenia is common in preterm babies, but its pathogenesis is uncertain. In this study bone density in babies was quantitated, postnatal bone mineralization compared to expected intrauterine bone mineralization and the pathogenesis of osteopenia investigated. Healthy babies (103 term, 76 preterm) were examined clinically, biochemically and radiologically the day after birth and at a time corresponding to expected full term gestation. Appendicular bone density was quantitated by magnification radiogrammetry, using the humeral cortical index (CI). The CI of preterm and term babies was similar the day after birth. In preterm babies elevated serum alkaline phosphatase and high urinary hydroxyproline indicated increased bone turnover. The CI of preterm babies at expected full term gestation was lower (p = 0.0001) than that of term babies at birth, implying that postnatal bone mineralization lagged behind expected intrauterine bone mineralization. Radiologic data suggested increased endosteal resorption rather than decreased bone formation. At expected full term gestation the preterm babies had higher serum alkaline phosphatase and urinary calcium, phosphate, c-AMP and hydroxyproline (p = 0.0001) than term babies at birth, and 15% had periosteal reactions. The biochemical as well as the radiologic data therefore indicated high turnover osteopenia in preterm babies. We conclude that postnatal bone mineralization in preterm babies lagged significantly behind expected intrauterine bone mineralization and that the osteopenia observed in preterm babies is caused by increased bone resorption and not by decreased bone formation. The cause(s) of this high turnover osteopenia, however, remains to be ascertained.

Platelet-activating factor acetylhydrolase activity in bovine seminal plasma.

Platelet-activating factor (PAF) is a potent signaling molecule that has been detected in mammalian sperm from several species. The biological function of sperm-derived PAF and mechanisms controlling its production have not been clearly defined. In the remodeling pathway for PAF biosynthesis, PAF is produced by phospholipase A2 hydrolysis of 1-O-alkyl phospholipids followed by acetylation by PAF acetyltransferase. PAF is inactivated by PAF acetylhydrolase. PAF acetylhydrolase activity has been detected recently in human seminal plasma, where it may play a role in regulating PAF production or content by sperm. The purpose of this study was to measure and partially characterize PAF acetylhydrolase in bovine seminal plasma. Acetylhydrolase activity was detected in seminal plasma, was linear with time and protein concentration, and had a specific activity of 122 nmol/minute/mg protein. The enzyme was cation independent and was not inhibited by phosphatidylcholine but was inhibited by p-bromophenacylbromide and partially inhibited by phenylmethylsulfonylfluoride. Very little acetylhydrolase activity was detected in caudal epididymal fluid or caudal epididymal sperm. Enzyme activity associated with ejaculated sperm was largely removed by their centrifugation through Percoll and subsequent washing. These results demonstrate very high PAF acetylhydrolase activity in bovine seminal plasma. The enzyme appears to be of accessory gland origin and has properties similar to those of the enzyme from other sources.

Survival of bull spermatozoa seeded and frozen at different rates in egg yolk-tris and whole milk extenders.

Six factorially arranged experiments were designed to study effects of seeding, freezing, and thawing rates in whole milk and egg yolk-Tris extenders commonly used for commercial cryopreservation of bull sperm. In these extenders, semen normally is supercooled to -13 or -14 degrees C unless the sperm are seeded. When sperm were supercooled or seeded, either mechanically or with immobilized silver iodide, and frozen to -196 degrees C, the postthaw percentages of motile sperm were 59, 57, and 64%, respectively. Freezing rates of -15, -25, and -35 degrees C/min gave similar sperm survival rates and were superior to -5 degrees C/min. For milk, the critical freezing temperature extended to -75 degrees C before transfer to liquid nitrogen gave good results. For egg yolk-Tris extender, transfer to liquid nitrogen was less critical once -50 degrees C had been attained. Thawing of sperm in water baths at 25 and 45 degrees C gave similar results, and both temperatures were superior to 5 degrees C. The postthaw percentage of motile sperm in egg yolk-Tris was equal or superior to that of sperm frozen in milk. A freezing rate of -15 degrees C/min to -100 degrees C and thawing at 25 degrees C consistently gave good results.

Near-field investigations of the landers earthquake sequence, april to july 1992.

The Landers earthquake, which had a moment magnitude (M(w)) of 7.3, was the largest earthquake to strike the contiguous United States in 40 years. This earthquake resulted from the rupture of five major and many minor right-lateral faults near the southern end of the eastern California shear zone, just north of the San Andreas fault. Its M(w) 6.1 preshock and M(w) 6.2 aftershock had their own aftershocks and foreshocks. Surficial geological observations are consistent with local and far-field seismologic observations of the earthquake. Large surficial offsets (as great as 6 meters) and a relatively short rupture length (85 kilometers) are consistent with seismological calculations of a high stress drop (200 bars), which is in turn consistent with an apparently long recurrence interval for these faults.