A New Experiment for Investigating Evaporation and Condensation of Cryogenic Propellants.

Passive and active technologies have been used to control propellant boil-off, but the current state of understanding of cryogenic evaporation and condensation in microgravity is insufficient for designing large cryogenic depots critical to the long-term space exploration missions. One of the key factors limiting the ability to design such systems is the uncertainty in the accommodation coefficients (evaporation and condensation), which are inputs for kinetic modeling of phase change. A novel, combined experimental and computational approach is being used to determine the accommodation coefficients for liquid hydrogen and liquid methane. The experimental effort utilizes the Neutron Imaging Facility located at the National Institute of Standards and Technology (NIST) in Gaithersburg, Maryland to image evaporation and condensation of hydrogenated propellants inside of metallic containers. The computational effort includes numerical solution of a model for phase change in the contact line and thin film regions as well as an CFD effort for determining the appropriate thermal boundary conditions for the numerical solution of the evaporating and condensing liquid. Using all three methods, there is the possibility of extracting the accommodation coefficients from the experimental observations. The experiments are the first known observation of a liquid hydrogen menisci condensing and evaporating inside aluminum and stainless steel cylinders. The experimental technique, complimentary computational thermal model and meniscus shape determination are reported. The computational thermal model has been shown to accurately track the transient thermal response of the test cells. The meniscus shape determination suggests the presence of a finite contact angle, albeit very small, between liquid hydrogen and aluminum oxide.

Bilateral cortical border-zone infarction. A pseudobrainstem stroke.

Acute bilateral weakness of the extremities with weakness of the tongue classically signals a medullary lesion. A patient had these signs, but at autopsy, bilateral cortical border-zone infarcts and an entirely normal brainstem were found. This case points out the importance of considering bilateral cortical border-zone infarction in the presence of bilateral motor or sensory signs, especially when there is sparing of facial motor function.

Hereditary paroxysmal ataxia: response to acetazolamide.

From early childhood, eight patients in a kindred had paroxysmal bouts of ataxia, dysarthria, and nystagmus. The disorder was inherited as an autosomal dominant. Attacks occurred weekly and lasted 1 to 6 hours; there were slight cerebellar signs between attacks. Although the etiology was not determined, a serendipitous trial of acetazolamide completely abolished attacks, and all patients have remained free of attacks for as long as 5 years.

Successful treatment of familial idiopathic lipid storage myopathy with L-carnitine and modified lipid diet.

We describe the clinical presentation, course, pathologic findings, and biochemical abnormalities found in three adult siblings with an idiopathic lipid storage myopathy. The major presenting symptoms were weakness and cramping, which were profound in one patient, moderate in the second patient, and mild in the third. All three individuals exhibited true myotonic discharges on EMG, normal or mildly depressed muscle free carnitine levels, and borderline delayed ketosis (40 hours) with fasting. Muscle biopsies from all three showed neutral lipid storage. Polymorphonuclear leukocytes and macrophages were vacuolated. No systemic abnormalities of glucose or fat metabolism were identified at rest, with fasting, or with exercise. The two more severely affected patients have responded to medium-chain triglyceride diet and oral carnitine with increased strength and muscle bulk and decreased histochemically observed neutral lipid stores in muscle. One patient has had a resolution of the electrical myotonia. Prednisone therapy in one patient resulted in a loss of cramping sensations but not improvement in strength. We suggest that some cases of idiopathic lipid storage myopathy may be safely and effectively treated with carnitine and medium-chain triglyceride diet.

Neuropathologic evaluation of 40 confirmed cases of Legionella pneumonia.

Autopsy examination of the brain was performed in 40 cases of Legionella pneumonia. Thirty-nine of 40 patients had underlying chronic or acute medical problems. Sixteen patients (40%) had neurologic signs or symptoms that were not explained by preexisting disease. CSF was normal in six of seven patients examined; CSF protein content was 66 mg/100 ml in one patient. Neuropathologic examination in all 40 patients demonstrated no lesions attributable to disseminated Legionella pneumophila. Mechanisms other than direct cerebral invasion by the causative organism must be sought to explain the neurologic manifestations of Legionella pneumonia.

Cerebral vasculitis associated with cocaine abuse.

A variety of central nervous system pathology has been associated with cocaine abuse, including cerebral vasculitis. We report a case of a 25-year-old woman who died of hypoxic encephalopathy following cardiac arrest due to cocaine abuse. Autopsy revealed a distinctive cerebral vasculitis with features characteristic of hypersensitivity drug included vasculitis. The significance of cerebral vasculitis associated with cocaine is reviewed.

Pain and suffering ... and unconsciousness.

Medical examiners and coroners, in their compassion for survivors, often certify the interval between injury and death as "instantaneous" only to be confronted in legal proceedings, especially civil proceedings, with the need to detail the actual events and time required to die or to lose consciousness. A review of "pain and suffering" and consciousness is undertaken here and an estimate of actual time to unconsciousness is presented. This clinical pathologic correlation may assist in the scientific determination of the duration of pain and suffering.

Trauma, sport, and malignant cerebral edema.

Sudden cerebral swelling and death secondary to craniocerebral trauma has been noted in children and young adults. This is due to an increase in intracerebral blood, either secondary to an increase in cerebral blood volume or a redistribution of intracranial blood from the pial to the intraparenchymal vessels. Sequential craniocerebral trauma has been associated with the syndrome of "malignant cerebral edema"; the possibility of a "compliance compromised brain" has been suggested as the cause. The additional possibility of asymptomatic encephalitis leading to a compliance compromised brain and malignant cerebral edema is discussed.