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Biomedical subjects

R Griffin

Publications and source records attributed to R Griffin.

6 recordsLinked to original sources
PubMed1991

Structural studies of the mineral phase of calcifying cartilage.

The calcified cartilage of the epiphyseal growth plate of young calves has been studied by x-ray diffraction. Fourier transform infrared spectroscopy, magic angle 31P nuclear magnetic resonance spectroscopy, and chemical composition. The powdered tissue was separated by density centrifugation as a function of mineral content and thus qualitatively of the age of the calcium-phosphorus mineral phase. The individual density centrifugation fractions were examined separately. X-ray diffraction of the samples, especially of the lowest density fractions, revealed very poorly crystalline apatite. Fourier transform infrared spectroscopy and 31P nuclear magnetic resonance spectroscopy revealed the presence of significant amounts of nonapatitic phosphate ions. The concentration of such nonapatitic phosphates increases during the early stages of mineralization but then decreases as the mineral content steadily rises until full mineralization is achieved. The total concentration of carbonate ions was found to be much lower in calcified cartilage than in bone from the same organ (scapula). The carbonate ions are located in both A sites (OH-) and B sites (PO4(3-)), with a distribution similar to that found in bone mineral. However, discrepancies between infrared resolution factors of phosphate and carbonate bands are consistent with a heterogeneous distribution of carbonate ions in poorly organized domains of the solid phase of calcium phosphate. These initial studies permit one to characterize the calcium phosphate mineral phase as a very poorly crystalline, immature calcium phosphate apatite, rich in labile nonapatitic phosphate ions, with a low concentration of carbonate ions compared with bone mineral of the same animal, indeed from the bone of the same organ (scapula).

Animals↗
PubMed1991

Eosinophilic fasciitis is clinically distinguishable from the eosinophilia-myalgia syndrome and is not associated with L-tryptophan use.

Induration of the skin develops in a majority of patients with the eosinophilia-myalgia syndrome associated with L-tryptophan, and bears striking clinical and histopathological resemblance to eosinophilic fasciitis (EF). These similarities have led to the suggestion that eosinophilia-myalgia syndrome and EF are the same disease. To study the relationship of eosinophilia-myalgia syndrome and EF, we ascertained the prevalence of L-tryptophan use in a cohort of patients with EF, and compared their clinical and laboratory findings to those of patients with eosinophilia-myalgia syndrome associated cutaneous involvement. None of 11 patients who were diagnosed as having EF between 1970 and 1989 used L-tryptophan containing preparations prior to the onset of their illness. Marked clinical and laboratory test differences were observed between patients with EF and eosinophilia-myalgia syndrome. Patients with eosinophilia-myalgia syndrome had a more acute onset, more severe symptoms, higher frequency of rash and of pulmonary, cardiac, gastrointestinal, neurologic, myopathic and thyroid involvement compared to patients with EF. Corticosteroid therapy resulted in improvement of cutaneous involvement in 88% of patients with EF but it was only partially successful in patients with eosinophilia-myalgia syndrome. Hospitalization and fatalities occurred only among patients with eosinophilia-myalgia syndrome. These observations demonstrate that eosinophilia-myalgia syndrome is a more severe disease with multisystemic involvement that can be clinically distinguished from EF. In contrast to eosinophilia-myalgia syndrome, EF is not associated with L-tryptophan ingestion.

Adrenal Cortex Hormones↗
PubMed1978

Alcoholic liver disease presenting with marked elevation of serum alkaline phosphatase. A combined clinical and pathological study.

Twenty patients with longstanding alcoholism and biopsy-proven alcoholic liver disease presented with marked elevation of serum alkaline phosphatase (in excess of four times the upper limit of normal). None had a past or present history to suggest pancreatitis or biliary tract disease, nor had any of these patients recently taken medication which could be implicated in cholestatic jaundice. Thirteen (65%) of this group either had radiologic or post mortem confirmation of nonobstructed biliary systems. The histologic findings in this group of patients were compared with those of a group of patients with alcoholic liver disease and normal or only mild elevation of serum alkaline phosphatase. Significantly more hepatocellular necrosis (P less than 0.05), alcoholic hyaline (P less than 0.02), and cholestasis (P less than 0.002) were noted in the severely hyperphosphatasemic group. Minimal degrees of steatosis were found in both groups. These data indicate that intrahepatic cholestasis occurs in patients with alcoholic liver disease, and this may often be secondary to alcoholic hepatitis. Overemphasis has previously been given to alcoholic fatty liver as a cause of this syndrome.

Adult↗
PubMed1975

The influence of ascorbic acid on platelet structure and function.

To determine the effect on platelet behavior of transient exposure of platelets to ascorbic acid, studies of platelet function and ultrastructure were done before exposure to ascorbic acid at pH 6.5, during exposure to pH 6.5, and after restoration of pH to pre-acidification levels. The effect of ascorbic acid (A.A.) was compared to that of HCl and citric acid (C.A.). ADP- and collagen-induced aggregation of normal platelets were significantly impaired by both A.A. and C.A. but were less affected by HCl. The release of 14C-serotonin was significantly reduced by each agent. The ultrastructure of normal platelets brought to pH 6.5 by A.A. was normal. After neutralization, there was marked dilatation of the open channel system and loss of the disc shape. When platelets were brought to pH 6.5 by A.A., then neutralized, the aggregates which formed after stimulation by ADP or collagen were smaller than normal, the platelets were less closely approximated, and degranulation was less complete. The data show that exposure of platelets to ascorbic acid for short intervals impairs their function when measured after restoration of pH to levels compatible with maximal responses. Platelet survival studies using autologous platelets labelled with 51Cr in the presence or absence of ascorbic acid showed that the recovery of normal platelets was unaffected by ascorbic acid, whereas recovery of platelets from patients with idiopathic thrombocytopenic purpura, idiopathic thrombocythemia, and alcohol-related thrombocytopenia was markedly reduced. The injury resulting from the use of ascorbic acid in preparing platelets for studies of platelet survival in patients with disorders affecting platelets may impair the recovery of the cells, resulting in artifactual changes in the survival studies.

Adenosine Diphosphate↗