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Dive into the research topics where Samuel K. Morgan is active.

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Featured researches published by Samuel K. Morgan.


Clinical Toxicology | 1979

Folinic acid rescue for vincristine toxicity.

Owen C. Grush; Samuel K. Morgan

Inadvertent vincristine sulfate overdosage was treated with folinic acid. The sequence of development of the signs and symptoms associated with known vincristine toxicity was accentuated; however, the duration of these toxicities was markedly compressed in time when compared with previous reports. The known pharmacologic and biologic activities of vincristine sulfate and presumed mechanism of counteractivity of folinic acid is presented.


Acta Paediatrica | 1972

FANCONI'S ANEMIA IN A NEONATE

Juan J. Gershanik; Samuel K. Morgan; Richard Akers

In the 44 years since Fanconi’s original description (2) in three male siblings, of a lethal familial anemia associated with microcephaly, brown skin pigmentation, hypogonadism, exaggerated reflexes and strabismus, over 150 cases have been added to the world literature. A broad range of embryonic developmental defects have been described in Fanconi’s anemia (4). This is a report of a case which demonstrates a singular combination of congenital anomalies with the early onset of hematologic manifestations and raises certain questions regarding variants of Fanconi’s anemia.


Clinical Immunology and Immunopathology | 1980

Immunological studies in sickle cell disease: I. Analysis of circulating T-lymphocyte subpopulations☆

Edwin W. Ades; Ann Hinson; Samuel K. Morgan

Abstract Patients with sickle cell disease have an increased risk of development of overwhelming bacterial infection. Although several defects in immunological function have been described, analysis of suppressor T (T G ) cells has not been studied. Of the sickle cell patients assessed, all had at least 50% less T cells than the normal controls. In 70% of the cases, these patients had increased percentages of suppressor (T G ) cells. When helper cells (T M ) were tested, these numbers were similar to control values. These preliminary findings suggest an important mechanism to explain sickle cell disease infections in addition to previously defined immunological disorders and the asplenic state.


Clinical Pediatrics | 1970

Ewing's sarcoma in children. Lessons from four cases.

Samuel K. Morgan; William G. Thurman

Case 1. This eight and ot~e-half-year-old Caucasian girl had progressively severer pain over the medial aspect of the left leg for six weeks. Physical examination was essentially negative except that the medial aspect of the left upper tibia was tender to palpation. She was diagnosed as having Ewing’s sarcoma of the left tibia on December 22, 1964 after open surgical biopsy. X-ray changes consistent with Ewing’s sarcoma were described on January 22, 1965 (Fig. 1). Treatment was initiated with 30 mg. phenylalanine mustard (PAM),*** an analogue of nitrogen mustard (HNs), using the technic of isolationperfusion. There was no immediate or delayed toxicity. This was followed with radiation therapy, 5,000 r. tumor dose to the entire left tibia in 27


Clinical Pediatrics | 1972

Is the Bone Marrow Uniformly Reactive in Pediatric Hematologic Conditions?: A Study of 53 Simultaneous Dual Aspirations in Children

Samuel K. Morgan; Ann M. Grooms; C.B. Loadholt

was allowed to spread in the angle formed by two slides. The top slide was then moved over the horizontal slide effecting the spread of the marrow. The slides were dried. Wright’s stain was applied. 200 nucleated cells from each aspiration specimen were counted under oil immersion by the same technologist. An AO Microstar binocular Series 10 microscope was used. A chi-square test of independence of proportions of cell types from the two locations sampled was then calculated for each of the cases. The statistical analysis of these counts was carried out on an IBM 360 Model 40 Computer. A significant chisquare would indicate that the proportions of cell types differ between locations.


The Journal of Clinical Pharmacology | 1978

Toxicity Study of Cytosine Arabinoside and Methotrexate in the Maintenance Therapy of Childhood Leukemia. A Southwest Oncology Group Study

Ruprecht Nitschke; Diane M. Komp; Samuel K. Morgan; Kenneth A. Starling; Teresa J. Vietti

In a toxicity study to determine the feasibility of treating patients with acute lymphocytic leukemia (ALL) using an intravenous combination of cytosine arabinoside (Ara-C) and methotrexate (MTX), the drugs were given either simultaneously or sequentially every two weeks. Twenty-nine patients were studied, 17 treated simultaneously, 12 treated sequentially. The tolerated doses of Ara-C and MTX were 60 mg/m2 and 90 mg/m2, respectively, for the simultaneous treatment schedule and 90 mg/m2 and 150 mg/m2, respectively, for the sequential treatment schedule. The dose-limiting factor of the drug combination was gastrointestinal toxicity. The observed recurrent vomiting on both schedules rendered the treatment unsuitable for maintenance therapy.


The Journal of Clinical Pharmacology | 1979

Streptozotocin (NSC‐85998) in Children with Acute Lymphocytic Leukemia. A Southwest Oncology Group Study

Paul G. Dyment; Rathi V. Iyer; Samuel K. Morgan; Charles Sexauer

Streptozotocin (NSC-85998), a nitrosourea antibiotic, was given to 18 children with acute lymphocytic leukemia in relapse in a dose of 500 mg/m2/day intravenously every day for five days. There were no responses in 14 fully evaluable patients. The principal toxicity consisted of gastrointestinal disturbances. Based on our findings and those of others in adults, steptozotocin appears to play no role in the management of acute lymphocytic leukemia.


Clinical Pediatrics | 1976

Leukapheresis: A Technique for Granulocyte Transfusion

Edmund J. Doering; Samuel K. Morgan; Anthony M. Moser

This eight-year-old girl was diagnosed in April, 1972 as having acute lymphoblastic leukemia. She was treated sequentially with vincristine, prednisone, methotrexate, and 6-MP. Craniospinal radiacion therapy was given for prophylaxis of CNS leukemia. After relapse in December, 1973, reinduction with vincristine and prednisone was unsuccessful. She was then hospitalized for more intensive therapy. At the time of admission, she was essentially asymptomatic. On physical examination, she was afebrile and had hepatosplenomegaly, but there were no other significant findings. Her hemoglobin level was 9.4 gm/100 ml; her white count, 2,900 cells/mm~ with 92 per cent polys and 8 per cent lymphocytes; platelets, 22,000 celllmm~. Bone marrow examination revealed complete replace-


Medical and Pediatric Oncology | 1978

Combination chemotherapy with MOPP in children with recurrent brain tumors

Ayten Cangir; Jan van Eys; D. H. Berry; Eva V. Hvizdala; Samuel K. Morgan


American Journal of Medical Genetics | 1989

Etiologic heterogeneity in dyskeratosis congenita

G. Shashidhar Pai; Samuel K. Morgan; Carl Whetsell; John M. Opitz; James F. Reynolds

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Owen C. Grush

Medical University of South Carolina

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Vita J. Land

Washington University in St. Louis

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Ann M. Grooms

Medical University of South Carolina

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Ayten Cangir

University of Texas MD Anderson Cancer Center

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D. H. Berry

University of Arkansas at Little Rock

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Teresa J. Vietti

Washington University in St. Louis

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