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Biomedical subjects

C M Craven

Publications and source records attributed to C M Craven.

33 records · Page 2Linked to original sources
PubMed1990

Characterization of a transferrin-independent uptake system for iron in HeLa cells.

HeLa cells incubated in serum-free medium accumulated 59Fe ("non-transferrin iron") when incubated with either 59Fe-citrate, 59Fe-nitrilotriacetate, or 59Fe dissolved in Tricine ascorbate. Accumulation of iron was time-, concentration-, and Ca2+-dependent and was saturable. Uptake of non-transferrin (non-Tf) iron was transferrin-independent because of the fact that uptake occurred at pH 5.5, a pH at which transferrin binds iron poorly and at which transferrin is not internalized by cells. Uptake of non-Tf iron was less affected than uptake of transferrin iron by 1) exposure of cells to trypsin, a maneuver that cleaves Tf receptors, or 2) incubation of cells with phenylarsine oxide, an agent that inhibits both fluid- and receptor-mediated internalization. After exposure of cells to non-Tf iron at 37 degrees C, most of the cell-associated radioactivity was recovered in heme and ferritin, demonstrating that iron gained access to intracellular compartments and was not simply adsorbed to the cell surface. Uptake of non-Tf iron could be partially blocked by Cu2+ in a dose-dependent manner, while the accumulation of transferrin-bound iron was unaffected by Cu2+. Other transition metals, such as Zn2+, Cd2+, and Mn2+ were able to inhibit the uptake of non-Tf iron to different degrees. The accumulation of 109Cd was inhibited by incubation of cells with non-Tf iron, Cu2+, or Mn2+. The extent of inhibition was concentration- and metal-dependent. A number of cultured cell lines including HeLa, human skin fibroblasts, and Chinese hamster ovary cells demonstrated uptake of non-Tf iron and 109Cd. Additionally, an endosome acidification mutant of Chinese hamster ovary cells, which exhibited an increase in non-Tf iron uptake, also exhibited an increase in the uptake of Cd2+. These observations suggest that the characteristics of the non-Tf iron transport system in HeLa cells are similar if not identical to those reported for perfused rat liver (Wright, T. L., Brissot, P., Ma, W.-L., and Weisiger, P. A. (1986) J. Biol. Chem. 261, 10909-10914) and suggest the existence of a family of transition metal transport systems, each with a different metal specificity.

Arsenicals↗
PubMed1990

Malignant histiocytosis in a patient with acquired immunodeficiency syndrome-related complex.

A patient with acquired immunodeficiency syndrome-related complex was examined for fever and hepatosplenomegaly. During his hospitalization, liver failure developed in the patient, and he became infected with Pseudomonas and Staphylococcus. At autopsy, in addition to signs of bacterial infection, malignant histiocytic infiltrates were found that involved his liver, spleen, lymph nodes, and lungs. To our knowledge, malignant histiocytosis has not been reported in a patient with acquired immunodeficiency syndrome or acquired immunodeficiency syndrome-related complex.

AIDS-Related Complex↗
PubMed1990

Evaluation of a perinatal autopsy protocol: influence of the Prenatal Diagnosis Conference Team.

This study was designed to evaluate changes in the perinatal autopsy following the adoption of a new autopsy protocol. The University of Utah Medical Center has a Prenatal Diagnosis Conference Team composed of obstetricians, pediatricians, geneticists, and other health care professionals. These individuals are involved in the care of patients whose pregnancies are at risk for congenital malformations. An autopsy protocol was designed to increase the interaction of the pathologist with the Prenatal Diagnosis Conference Team in the evaluation of perinatal death. Two years, 1982 and 1987, before and after the protocol was implemented, were selected for retrospective review. The autopsies in 1987 made more specific diagnoses compared with those in 1982. Additional congenital anomalies were diagnosed, and increased numbers of patients were found to have well-described congenital disorders. The number of attempted postnatal autopsy chromosome studies increased and more chromosomal abnormalities were detected. The final autopsy diagnoses made in 1987 have provided more information to the physician for genetic or other patient counseling. After the protocol was adopted, increased numbers of cases were referred to the Medical Center for evaluation at autopsy. More of those who came to autopsy had been evaluated during life by members of the Prenatal Diagnosis Conference Team. Premortem sonograms had been done at an earlier gestational age and a greater number of anomalies were detected. Fewer of the fetuses had intrauterine death and more had pregnancy terminated by induction of labor. The gestational age at delivery declined.

Autopsy↗
PubMed1990

Three cases of fatal cardiac tamponade following ventricular endocardial biopsy.

Three patients had perforation of the ventricular free wall and fatal cardiac tamponade following endocardial biopsy to evaluate congestive heart failure. The number of endocardial biopsies at this institution at the time of the third death was 2372, resulting in an overall mortality rate of 0.13%. Of the 2372 biopsies, 2136 (90%) were performed to evaluate cardiac graft rejection and 236 (10%) were performed for other reasons. All the patients who died belonged to the latter group. None of the cardiac transplant patients have had fatal ventricular perforation--a significant difference. At our institution, the frequency of mortality following endocardial biopsy in the noncardiac transplant patients is 1.3%. Patients who have ventricular endocardial biopsy of native hearts rather than transplanted hearts may be at increased risk for fatal perforation.

Adult↗
PubMed1989

Fatal Clostridium perfringens septicemia associated with gastrointestinal arteriovenous malformations (vascular ectasias).

Clostridial infections usually occur in association with trauma, malignancy, or intra-abdominal disease. A 72-year-old previously healthy man presented with abdominal distress and fever. He developed a hemolytic anemia, coagulopathy, and fulminant clostridial septicemia. The patient died less than 24 hours after presentation. At autopsy, no malignancy was detected. The patient had an acute clostridial hepatic abscess and multiple arteriovenous malformations (vascular ectasias) of the large and small bowel. The case suggests that these mucosal and submucosal vascular lesions, which usually cause hemorrhage, may also predispose to infection.

Aged↗
PubMed1989

A splicing defect in the mouse transferrin gene leads to congenital atransferrinemia.

We have analyzed the biochemical defect in a mutant line of mice that produces less than 1% of the normal level of serum transferrin. This mouse line (Hp) transcribes the transferrin gene in liver at the same rate observed in normal mice, but the steady state levels of transferrin mRNA sequences are less than 20% of normal. Further hybridization studies reveal that most of the transferrin mRNA sequences present in homozygous Hp mouse liver are in the form of a 5 kb nuclear precursor instead of the mature 2.5 kb transferrin mRNA seen in normal mice. Using several different exon and intron probes from the mouse transferrin gene, we have shown that the 5 kb RNA precursor retains the last two introns of the transferrin gene but that the 5' and middle introns have been removed by processing. The defect in transferrin mRNA processing also extends to nonhepatic tissues and we find the same lack of mature mRNA and increased precursor accumulation in brain RNA. Since Southern blot analysis does not reveal gross changes in the structure of the transferrin gene in Hp mice, we suggest that the Hp defect is due to a small deletion or point mutation that either disrupts splicing signals or uncovers cryptic splice signals that interfere with processing of the last two introns in the transferrin gene. This Hp mouse line provides an opportunity to study the effects of transferrin deficiency on development and iron homeostasis.

Anemia↗
PubMed1989

Severe myocarditis following high-dose interleukin-2 administration.

We observed a patient who developed unusually severe myocardial dysfunction during therapy for renal cell carcinoma with high-dose interleukin-2 (IL-2). Although cardiac isoenzymes became markedly elevated shortly after the completion of 14 doses of IL-2 (100,000 U/kg of IL-2 every eight hours), serial electrocardiograms revealed only nonspecific changes. Echocardiography documented diffuse myocardial dysfunction, with akinesis of the anteroseptal region, suggestive of myocardial infarction. This anteroseptal hypokinesis persisted over a five-day period. The patient died unexpectedly and postmortem evaluation of the heart revealed a severe, diffuse lymphocytic, and eosinophilic myocarditis with myocyte necrosis, especially prominent in the anteroseptal region. This is the first histologically confirmed case of myocarditis reported, to our knowledge, in association with IL-2 therapy for cancer.

Carcinoma, Renal Cell↗
PubMed1987

Tissue distribution and clearance kinetics of non-transferrin-bound iron in the hypotransferrinemic mouse: a rodent model for hemochromatosis.

Genetically hypotransferrinemic mice accumulate iron in the liver and pancreas. A similar pattern of tissue iron accumulation occurs in humans with hereditary hemochromatosis. In both disorders, there is a decreased plasma concentration of apotransferrin. To test the hypothesis that nontransferrin-bound iron exists and is cleared by the parenchymal tissues, the tissue distribution of 59Fe was studied in animals lacking apotransferrin. Two groups of animals were used: normal rats and mice whose transferrin had been saturated by an intravenous injection of nonradiolabeled iron, and mice with congenital hypotransferrinemia. In control animals, injected 59Fe was found primarily in the bone marrow and spleen. In the transferrin iron-saturated animals, injected 59Fe accumulated in the liver and pancreas. Gastrointestinally absorbed iron in hypotransferrinemic or transferrin iron-saturated mice was deposited in the liver. This indicates that newly absorbed iron is released from mucosal cells not bound to transferrin. Clearance studies demonstrated that transferrin-bound 59Fe was removed from the circulation of rats with a half-time of 50 min. In transferrin iron-saturated animals, injected 59Fe was removed with a half-time of less than 30 s. Analysis of the distribution of 59Fe in serum samples by polyacrylamide gel electrophoresis demonstrated the presence of 59Fe not bound to transferrin. These results demonstrate the existence of and an uptake system for non-transferrin-bound iron. These observations support the hypothesis that parenchymal iron overload is a consequence of reduced concentrations of apotransferrin.

Animals↗
PubMed1986

Acid phosphatase positivity in childhood acute lymphocytic leukemia.

The Pediatric Oncology Group analyzed 103 cases of childhood acute lymphocytic leukemia (ALL) with an acid phosphatase stain and with a series of immunologic markers. As reported by others, the authors demonstrated a high correlation of acid phosphatase (AP) positivity and T-ALL. However, a subset of T-ALL was acid phosphatase negative, and some non-T, non-B, non-pre-B-ALL cases were AP positive. The predictive value of the AP test was, therefore, poor as a marker of T-ALL. AP-negative T-ALL cases appeared to be a distinctive subset of T-ALL, and AP negativity an intrinsic characteristic of this subset, rather than a failure of the test system. AP-positive n-ALL cases demonstrated no difference from AP-negative cases and, in particular, no evidence of early T-ALL differentiation.

Acid Phosphatase↗
PubMed1985

Institutional performance in application of the FAB classification of acute leukemia. The Southwest Oncology Group experience.

Institutional performance in application of the French-American-British (FAB) classification of acute leukemia in The Southwest Oncology Group is presented, demonstrating a disparity between institutional and expert performance. A significant improvement is shown with an educational effort coupled with experience in use of the classification, and the importance of cytochemistry in the use of the classification is illustrated. A simplification of the classification, merging M1, M2, and M4 as M7, is proposed. This simplification improves institutional performance in use of the classification, while preserving distinctions that appear clinically important.

Acute Disease↗
PubMed1985

Reproducibility of the French-American-British classification of acute leukemia: the Southwest Oncology Group Experience.

After initial French-American-British (FAB) diagnosis by a multiinstitutional Southwest Oncology Group panel, slides of acute leukemia cases were recirculated to panel members for second review. The reproducibility of the FAB classification is analyzed. The classification is reproducible in the 70% range in panel reviewer hands and allows remarkable reproducibility in the morphologic and cytochemical distinction of acute lymphoid leukemia (ALL) from acute myeloid leukemia (AML). The limitations of a morphologic and cytochemical classification of acute leukemia are discussed. A simplification of the FAB system, merging M1, M2, and M4 as M7, is proposed; this simplification improves the system's reproducibility.

Acute Disease↗
PubMedDate not supplied

Lateral placental growth occurs by trophoblast cell invasion of decidual veins.

During human pregnancy, growth of the placenta is proportionally greater than the growth of the decidual surface, suggesting that trophoblast cells invade the decidua at the placenta's margin. We hypothesized that a method of lateral placental growth was trophoblast cell invasion of decidual veins. This was investigated in two in situ pregnancies and in tissues from 100 women undergoing elective termination at 8-12 weeks of gestation. Decidua was compared to normal secretory endometrium. Histological sections were stained by immunohistochemistry to identify trophoblast cell and vascular antigens, as well as vascular cell adhesion molecule (VCAM), integrin subunits beta(1)and beta(4), and oncofetal fibronectin. Dilated veins were observed in all decidua but not in the secretory endometrium. Decidual and myometrial veins contained villi, trophoblast cell islands and syncytial elements. Decidual endothelial cells expressed vascular cell adhesion molecule (VCAM). Villous trophoblast cells were integrin subunits beta(4)positive and beta(1)negative. Trophoblast cell islands in the placenta and within decidual veins were integrin subunits beta(1)positive and beta(4)negative. Trophoblast cell islands and villi attached to veins, and mononuclear cells, invaded decidual stroma. Oncofetal fibronectin was present at sites of trophoblast invasion. These findings suggest that a method of lateral placental growth is trophoblast cell invasion of veins.

Cell Movement↗