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Biomedical subjects

G D Penick

Publications and source records attributed to G D Penick.

At least 19 recordsLinked to original sources
PubMed1993

Lethal bone dysplasia in a fetus with manifestations of atelosteogenesis I and Boomerang dysplasia.

Atelosteogenesis I (AT-I) and Boomerang dysplasia have been described as separate lethal bone dysplasias. The possibility of a common cause of both conditions was suggested by Hunter and Carpenter (Clin Genet 39(6): 471-480, 1991) in their report of a patient with apparent manifestations of both AT-I and Boomerang dysplasia. We report on a male fetus of 31 weeks gestation whose clinical, radiologic and histologic findings are compared to reported cases of AT-I, Boomerang dysplasia and the patient of Hunter and Carpenter (Clin Genet 39(6): 471-480, 1991). From the documentation of clinical and radiologic findings we demonstrate overlap of AT-I and Boomerang dysplasia in our patient, and, from histologic examination, suggest a defect of cartilage and bone formation as the basic abnormality in this lethal bone dysplasia.

Bone Diseases, Developmental↗
PubMed1993

Disseminated adenoviral infection presenting as acute pancreatitis.

Adenoviruses are gradually being recognized as a significant source of morbidity and mortality in the immunocompromised patient population. We report a bone marrow transplant patient who developed severe abdominal pain accompanied by marked elevations in serum pancreatic and hepatic enzyme levels. She died shortly thereafter. Autopsy revealed hemorrhagic pancreatitis and fulminant hepatic necrosis. Both the pancreas and liver contained intranuclear inclusions consistent with adenovirus; electron microscopy confirmed that there were, indeed, adenoviral particles. This report of adenoviral pancreatitis emphasizes the diversity of manifestations seen with adenoviral infection.

Acute Disease↗
PubMed1989

Prolonged elevation of alphafetoprotein and detectable acetylcholinesterase after death of an anomalous twin fetus.

Persistence of elevated alphafetoprotein (AFP) levels and the presence of an acetylcholinesterase (AChE) band in amniotic fluid have been reported to occur up to 11 weeks following intrauterine fetal demise (IUFD) of one twin (Bass et al., 1986). We now report a case where such prolongation of these findings was observed in a case of unrecognized monochorionic, monoamniotic twinning, in which case cord entanglement resulted in IUFD at an estimated 10-12 weeks and 25-26 weeks. The fetus suffering early demise (Fetus B) had multiple congenital anomalies, including a neural tube defect. The presence of this defect and/or fetal demise and bleeding into the amniotic sac is entertained as continuing sources of documented elevated AChE and AFP 9-11 weeks after the initial fetal death. We re-emphasize the possibility of unrecognized twinning as a cause of abnormal maternal serum and amniotic fluid study results in the face of one apparently normal fetus.

Acetylcholinesterase↗
PubMed1982

The association of hairy cell leukemia with unusual immunologic disorders.

Hairy cell leukemia is a rare disease, probably of B-lymphocyte origin, that has been reported to rarely occur with polyarteritis nodosa. The records of 31 patients with hairy cell leukemia were reviewed for an association with other disorders of the immune system; such an association was found more often than previously suspected. Four cases are discussed--one with hepatitis B surface antigen-positive polyarteritis nodosa and another with an IgA (kappa) monoclonal gammopathy and amyloidosis of the kidney, liver, and small bowel. The other two patients had cutaneous vasculitis, one of which was a rare form of leukocytoclastic angiitis--erythema elevatum diutinum. Because the number of patients in this study is small, it is impossible to say whether the association of hairy cell leukemia with any of these immunologic disorders adversely affects survival.

Adult↗
PubMed1979

Cutaneous and nasal allergic responses in ragweed hay fever: lack of clinical and histopathologic correlations with late phase reactions.

The present study was designed to test the hypotheses that late cutaneous and nasal responses to allergen in patients with ragweed hay fever were human correlates of cutaneous basophil hypersensitivity, and that late responses in the nose and skin reflect similar pathogenesis. Forty-seven patients with ragweed hay fever were studied during a ragweed season for peripheral basophilia and clinical patterns reflecting late responses. Provocative nasal challenge, skin testing, and biopsy were carried out subsequently in 21 of the same patients during the winter months. Conclusions were as follows: (1) no histologic features distinguish positive from negative late skin reactions at 24 hr in patients with immediate wheal-and-flare responses; (2) cutaneous basophil hypersensitivity, i.e., tissue basophilia, is not a distinguishing feature of late skin responses in ragweed pollenosis; (3) seasonal peripheral basophilia was not found; (4) late responses in the nose were difficult to document objectively and did not correlate with late skin reactions; and (5) lymphocyte responses to antigen failed to correlate with late responses in either the nose or the skin.

Basophils↗
PubMed1979

Immunoglobulin E, mast cells, and eosinophils in the skin of rhesus monkeys immunized with x-irradiated cercariae of Schistosoma japonicum.

Immunoglobulin E (IgE), mast cells, and eosinophils in the skin of rhesus monkeys immunized with highly X-irradiated cercariae of Schistosoma japonicum were studied. IgE was stained by the unlabeled antibody enzyme method and was found on mast cells. Before challenge, mast cells were found only in the dermis. Immediately after the challenge, mast cells were found in both the dermis and epidermis and many of them were degranulated. Soon after, margination and emigration of granulocytes, predominantly eosinophils, occurred along the blood capillaries in the dermis. Gradulally, preivascular infiltration of eosinophils was seen in the dermis and migration of eosinophils from the dermis into the epidermis appeared, resulting in the formation of minute eosinophilic abscesses in the epidermis. In addition, the IgE was found as a thin coat on the integument of the schistosomula. Deteriorated schistosomula were seen amid the eosinophilic abscesses in the epidermis and in eosinophilic infiltrations in the dermis. The present findings suggest the possibility that the reaction of IgE, mast cells, and eosinophils were integrated into one immunological effect, namely the schistosomulicidal action.

Animals↗
PubMed1978

Urinary cytology and bladder biopsy in patients with bladder cancer.

Two hundred fifty patients with bladder tumor were evaluated over a three-year period. Cystoscopy, cytology, and random bladder and tumor biopsy were part of the workup. The follow-up of these patients resulted in a total of 509 cystoscopies, 772 specimens of bladder washings and urinary cytologies, and 503 tumor or selected mucosal biopsies. The value of cytologic study of bladder washings and cystoscopic urine samples as well as the importance of selected site mucosal biopsies in detecting "field changes" in the bladder epithelium associated with bladder tumors are discussed.

Biopsy↗
PubMed1976

Evidence for an ester bond between thrombin and heparin cofactor.

Heparin cofactor, a thrombin inhibitor, is purified from human plasma by affinity chromatography on heparin-agarose. The nature of the binding between thrombin and the inhibitor is studied by treatment of the complex with 6 M guanidinium chloride, hydroxylamine, and dilute alkali. The complex is not dissociated during gel chromatography in 6 M guanidinium chloride. This result supports an earlier proposal that formation of the complex includes the formation of a covalent bond. Treatment of dodecyl sulfate-denatured complex with hydroxylamine results in dissociation of the complex to yield free thrombin and heparin cofactor. Hydroxylamine does not dissociate the complex unless it is denatured. The complex is also dissociated in dilute sodium hydroxide (pH 12) solutions. These results indicate that the covalent bond between thrombin and the inhibitor is a carboxylic ester.

Alkalies↗
PubMed1976

Factor VIII synthesis: hepatic and renal allografts in swine with von Willebrand's disease.

Transplantation experiments were utilized to study the possible sites of synthesis of von Willebrand factor (vWF) and factor VIII (F VIII) activities. Three normal kidney and two normal liver allografts were implanted into five swine with von Willebrand's disease (vWD) that survived for 1,6, and 7, and 4 and 9 days, respectively. The correction of the multiple hemostatic defects of vWD by organ transplantation was evaluated using the F VIII procoagulant activity, bleeding time, and platelet aggregating factor (PAF) levels; i.e., vWF levels. Normal kidney allografts produced no changes in the bleeding times or increases in F VIII or PAF. Transfusions for surgical hemostasis produced transient increases in F VIII and PAF. In animals receiving normal liver allografts, the levels of F VIII exceeded 100%, PAF was increased, and sustained correction of the bleeding time and maintenance of hemostasis was observed. These data suggest that the kidney is incapable of synthesizing either the vWF or the F VIII and that cells contained in the liver, possibly the endothelial cells, are one of the sites of synthesis of these factors.

Animals↗
PubMed1968

Genetic variants of hemophilia B: detection by means of a specific PTC inhibitor.

Hemophilia B can be divided into at least two mutant forms different from the mild, moderate, and severe categories previously described. In about 90% of hemophilia B patients, PTC-inhibitor-neutralizing activity is reduced in proportion to PTC clotting activity. In about 10% of the patients, PTC-inhibitor-neutralizing activity is fully effective, whereas PTC clotting activity is reduced. Extensive pedigree studies indicate that the presence or absence of inhibitor-neutralizing activity is genetically determined. It is suggested that those hemophilia B mutants with decreased inhibitor-neutralizing material produce decreased amounts of PTC-protein. It is further suggested that those with normal levels of inhibitor-neutralizing material produce normal amounts of PTC-protein, which is structurally altered so as to lose procoagulant activity but which retains inhibitor-neutralizing activity. The latter group may be analogous to CRM(+) mutants described in bacteria and Neurospora.

Factor IX↗