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Biomedical subjects

J Kirkpatrick

Publications and source records attributed to J Kirkpatrick.

At least 55 records · Page 3Linked to original sources
PubMed1982

The dilemma of defining diabetes mellitus in the aging population.

A total of 1,009 persons were given a 100-gram glucose solution orally after a three-day regimen of a diet preparation and an overnight fast. Fasting and two-hour plasma glucose levels were determined for each subject and the results tabulated. Most of the persons tested were in the sixth, seventh or eighth decade of life with 43 persons between 80 and 89 years of age. The frequency of fasting plasma glucose determinations above 140 mg per dl varied from 3 percent to 7 percent between the sixth and ninth decades. Those persons with two-hour plasma glucose values above 200 mg per dl represented 8 percent of the 50 to 59 year old group and the percentages rose respectively to 12 percent, 16 percent and 21 percent in the 60 to 69, 70 to 79 and 80 to 89 year old groups. Finally, those who had fasting plasma glucose levels below 140 mg per dl and two-hour glucose values between 140 and 200 mg per dl were tabulated according to decade of life. This group varied from 9 percent to 15 percent between ages 20 and 59 and represented 20 percent to 22 percent of those in the seventh, eighth and ninth decades. In light of the known deterioration of glucose tolerance with aging, some stratification of blood glucose concentrations should be applied with age, but to what degree and what diagnostic criteria should be applied are still unclear.

Adult↗
PubMed1981

Joseph disease and Huntington disease: protein patterns in fibroblasts and brain.

Proteins were separated on two-dimensional acrylamide gels obtained from brain samples of patients with Joseph disease, Huntington disease (HD) and multiple sclerosis. Similar protein separations were made from cultured skin fibroblasts of Joseph disease patients. Two major classes of proteins, one with a MW of 50,000 probably representing the glial filamentous acidic protein, or another class with a MW of 40,000 (proteins Jc, Jd, L1 and L2) were increased in the cerebellum of six Joseph disease patients. The same protein species were abnormally increased in HD brains, mainly in the basal ganglia and frontal cortex. These identical classes of protein changes were present in two nosologically separate autosomal dominant neurological disorders, Joseph disease (a spinocerebellar degeneration) and HD (a basal ganglia and cerebral cortical degeneration) and may reflect a biochemical correlation of gliosis and neuronal disease. However, these changes may be evidence that the two diseases are allelic mutations of the same gene. The dominantly inherited spinocerebellar degenerations may result from a primary deficit of glial-neuronal interaction, resulting in neuronal loss but with a compensatory increase in the number of glial cells attempting to provide additional trophic-metabolic support.

Adult↗
PubMed1979

Joseph disease: protein patterns in fibroblasts and brain.

The separation of brain and fibroblast proteins was analyzed on two-dimensional acrylamide gels. Proteins were examined from skin fibroblast cultures and brain homogenates from the frontal cerebral cortex, putamen, and cerebellum. Protein species from skin fibroblast cultures of controls and patients with Joseph disease or Huntington disease were not significantly different. The proteins from homogenates of the cerebral cortex, putamen, and cerebellum from controls differed from those of one Joseph disease patient. Two major classes of proteins were increased in the patient's putamen and cerebellum. Proteins of 40,000 and 50,000 daltons--including the glial filamentous acidic protein complex (molecular weight 50,000), and two proteins which migrated near actin--were increased in the cerebellum. The glial filamentous acidic protein complex increased 3.7-fold in the putamen of the patient. These protein changes probably represent gliosis, but may also be an expression of the primary genetic mutation.

Brain Diseases↗
PubMed1979

Dexamethasone and severe head injury. A prospective double-blind study.

A prospective double-blind study of the effects of dexamethasone administration on the outcome of patients with severe head injuries was performed. Patients were stratified for severity of neurological injury and were treated with placebo, low-dose dexamethasone (16 mg/day), or high-dose dexamethasone (96 mg/day) for a period of 6 days. Outcome was evaluated at 6 months following injury. Of the 76 patients available for analysis, a good outcome was achieved in 37% of placebo-treated patients, 44% of low-dose-treated patients, and 29% of high-dose-treated patients. These differences are not statistically significant. Similarly dexamethasone administration had no statistically significant effect on intracranial pressure patterns or serial neurological examinations during hospitalization. Gastrointestinal bleeding occurred in only one patient. Good outcome was associated with age under 10 years, lighter depth of coma on admission, and the preservation of brain-stem reflexes upon admission. A recalculation of data in previous clinical series purporting to show an improvement in outcome as a result of corticosteroid therapy shows no significant difference in outcome when steroid- and placebo-treated patients are compared. In our series, 90% of all deaths were caused by recurrent intracranial hematomas, medical complications, or diffuse brain injuries with parenchymal hemorrhage and tissue disruption -- causes of death which cannot be affected by corticosteroid therapy. The study suggests that dexamethasone in either high or low dosages has no significant effect on morbidity and mortality following severe head injury.

Adolescent↗
PubMed1979

The sepsis-glucose intolerance riddle: a hormonal explanation.

Glucose intolerance has been commonly observed in sepsis and has been attributed to a multitude of endocrine and metabolic disorders. From 1977 to 1978, 19 patients were studied using intravenous glucose tolerance tests to evaluate this phenomenon; 15 patients presented with ongoing sepsis and four patients served as stress controls. Glucose intolerance was found to be a significant finding in less than 40% of the septic group. This state of intolerance was noted to be associated with a high mortality rate (60%), whereas glucose tolerance in sepsis was associated with a much improved mortality rate (10%). Hormone levels were correlated with glucose tolerance curves using the parameters of insulin, glucagon, growth hormone, cortisol, and epinephrine levels. Glucose intolerance and a high mortality rate were linked to sustained hyperglucagonemia, which was unresponsive to glucose challenge, and to marked suppression of growth hormone. This apparently represents a decompensated peripheral metabolic energy deficit, which results in the increased mortality rate.

Bacterial Infections↗
PubMed1978

Bronchial atresia: a recognizable entity in the pediatric age group.

Bronchial atresia, a congenital lesion that develops after the 16th wk of fetal life, may be more common than previously believed, and this probably explains some cases of so-called congenital lobar emphysema. It may produce symptoms of pulmonary infection, wheezing, and respiratory distress severe enough to justify elective resection of that part of the lung distal to the atresia. The roentgenographic features that make this a recognizable entity are the following: (1) There is localized hyperinflation of lung in a segmental or lobar distribution, with a circular or oval parahilar radiodensity. Bronchography will demonstrate that there is no filling of the bronchus supplying this part of the lung. (2) The occasional neonate with this condition may present with an intrathoracic mass suggesting retained fetal lung fluid in lobar distribution. Bronchography will demonstrate that there is no filling of the bronchus to that part of the lung. (3) A plug of desquamated tissue and mucus in the cyst-like bronchus just distal to the point of atresia appears to be an unvarying component of the syndrome. It most commonly presents as a round or oval density, but in some cases it may be shaped like a rod or tree and rarely contains an air-fluid level.

Adolescent↗
PubMed1977

Hypothermia and persisting capacity to develop fever. Occurrence in a patient with sarcoidosis of the central nervous system.

A patient with central nervous system and systemic sarcoidosis had profound hypothermia and dementia with associated lymphadenopathy and hypernatremia. His capacity to develop fever remained; despite the persistent marked hypothermia, sweating and shivering in response to peripheral heating and cooling were maintained. Postmortem neuropathologic studies indicated that the hypothalamic region, generally considered to contain the primary temperature control, had been severely damaged by granulomatous sarcoid disease. These results confirm and extend previous findings of temperature disturbance in hypothalamic sarcoidosis and suggest that the integrity of the primary control of body temperature is not essential to fever production and "broad-band" regulation against environmental temperature extremes.

Central Nervous System Diseases↗
PubMed1976

Periostitis and pseudoperiostitis.

Increased metabolic activity with the periosteum is demonstrated radiographically by the presence of a linear shadow of bone paralleling the cortex, most commonly reflecting increased osteoblastic activity and thus representing periosteal new bone. This is frequently seen in psoriatic arthritis and Reiter's syndrome. A similar picture occurs with increased osteoclastic activity and reflects rapid demineralization, simulating periostitis. This change must be recognized as a reflection of osteoporosis, lest the condition be misdiagnosed as inflammatory disease.

Arthritis↗
PubMed1976

alpha-L-iduronidase deficiency and possible Hurler-Scheie genetic compound. Clinical, pathologic, and biochemical findings.

The enzymatic delineation of the mucopolysaccharidoses has revealed that certain syndromes, although phenotypically distinct, share the same enzymatic defect. Patients with the classic Hurler and Scheie syndromes or other phenotypic variations of these two disorders have a deficiency of alpha-L-iduronidase. We are reporting a patient with alpha-L-iduronidase deficiency whose phenotypic abnormalities did not resemble either the Hurler or Scheie syndrome and who may have had either the Hurler-Scheie genetic compound described by McKusick or an allelic disorder. Our patient was a 25-year-old woman whose initial presentation was due to acute paranoia and who was subsequently found to have many morphologic, neurologic, radiographic, and neuropathologic findings consistent with a mucopolysaccharide disorder. To our knowledge, complete neuropathologic findings have not been previously described in this hybrid group of patients. A distinctive feature of this patient's illness is that the underlying disorder was not clinically apparent until adulthood, but presented with sever bony abnormalities of the skull and deposition of mucopolysaccharides in the meninges.

Adult↗