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Biomedical subjects

G Bryan

Publications and source records attributed to G Bryan.

17 recordsLinked to original sources
PubMed1998

IFNgamma inhibition of cell growth in glioblastomas correlates with increased levels of the cyclin dependent kinase inhibitor p21WAF1/CIP1.

Glioblastoma is a highly aggressive form of brain cancer characterized by uncontrolled cell growth resulting from a loss of cell cycle regulation. In this study we determined the antiproliferative effects of interferon gamma (IFNgamma) on the glioblastoma cell lines T98G, SNB-19 and U-373, focusing on the ability of IFNgamma to increase levels of p21WAF1/CIP1, an important negative regulator of cell cycle events. IFNgamma was found to inhibit the growth of all cell lines, with inhibition ranging from 82.2% to 45.4%. Flow cytometry analysis showed that IFNgamma treatment caused a cell cycle delay in the G1 or S phases. The strength of this delay varied, correlating with the degree by which IFNgamma inhibited proliferation of each cell line. IFNgamma treatment increased the production of the cyclin dependent kinase inhibitor (CKI) p21WAF1/ CIP1 in all cell lines, the level and kinetics of production of which correlated with the degree and stage of inhibition of cellular proliferation. Further, immunoprecipitation of p21WAF1/CIP1 in complexes of p21WAF1/CIP1/cyclin-dependent kinase 2 (cdk2)/cyclin showed that the amount of p21WAF1/CIP1 in the complexes and the inhibition of cdk2-cyclin kinase activity correlated with the level of p21WAF1/CIP1 produced in the cells by IFNgamma. These results show that IFNgamma has significant antiproliferative effects on the glioblastoma cell lines and suggest that p21WAF1/CIP1 plays a role in mediating these effects.

CDC2-CDC28 Kinases↗
PubMed1997

Immunization services for adolescents within comprehensive school health programs.

Every school day, more than 95% of the nation's five- to 17-year-olds attend one of almost 110,000 elementary and secondary schools where they receive instruction in how to avoid major health-threatening behaviors. School is also the place where children and adolescents can be given preventive health care services, including administration of vaccines and monitoring of immunization levels. This article addresses how expanding school health services could improve immunization levels of school-aged youth.

Adolescent↗
PubMed1997

Adolescent immunization: focus on implementation.

On March 11-12, 1996, a workshop on how to implement new adolescent immunization (AI) recommendations was held in Atlanta, Ga. Sponsored by the Centers for Disease Control and Prevention, it was a collaborative effort of the National Immunization Program, the Division of Adolescent and School Health/National Center for Chronic Disease Prevention and Health Promotion, and the Hepatitis Branch/National Center for Infectious Diseases. The workshop brought together organizations and individuals interested in adolescent health and immunizations so they could address how new AI recommendations can be implemented most effectively. This article offers an overview of their discussions and suggestions, including issues of cooperation, education, legislation, and AI program development among health provider organizations, health department, schools, community groups and various other agencies relating to adolescent health services.

Adolescent↗
PubMed1996

Acute effects of the human amylin analog AC137 on basal and insulin-stimulated euglycemic and hypoglycemic fuel metabolism in patients with insulin-dependent diabetes mellitus.

Amylin has been reported to decrease glycogen storage in rodent skeletal muscles and produce insulin resistance in intact rats. To test the acute effect of a human amylin analog (AC137) on glucose metabolism in man, seven IDDM patients were infused in a randomized, double blind, cross-over study with AC137 (100 micrograms/h, n = 1; 50 micrograms/h, n = 6) or placebo for 330 min during a two-step euglycemic clamp (insulin infusion rates, 0.2 and 0.6 mU/kg.min; basal and hyperinsulinemic period, respectively) followed by a hyperinsulinemic hypoglycemic clamp (insulin infusion rate, 1.5 mU/kg.min; hypoglycemic period). During euglycemia, no differences were found in glucose disposal (step 1, 2.43 +/- 0.20 vs. 2.03 +/- 0.26; step 2, 4.28 +/- 0.54 vs. 4.11 +/- 0.45 mg/kg.min; AC137 vs. placebo, mean +/- SEM), arteriovenous substrate balances across the forearm, or hepatic glucose production. During hypoglycemia, glucose fluxes were also similar. However, lactate release from the forearm was more pronounced (P < 0.05) with the analog than with placebo (area under the curve, -11.2 +/- 4.6 vs. -1.4 +/- 2.2 mmol/min.L). Despite similar plasma glucose nadirs (2.7 +/- 0.0 vs. 2.6 +/- 0.1 mmol/L; AC137 vs. placebo), circulating cortisol and GH rose to significantly higher levels during hypoglycemia with the amylin analog (P < 0.05). In conclusion, acute administration of the amylin analog AC137 did not influence insulin-stimulated glucose metabolism during euglycemic conditions. During imposed hypoglycemia, lactate release from skeletal muscle was, however, enhanced, and the rise in cortisol and GH was augmented.

Adult↗
PubMed1992

Athletic heart syndrome.

AHS is a benign condition consisting of physiologic adaptations to the increased cardiac work load of exercise. Its primary features are biventricular hypertrophy and bradycardia associated with normal systolic and diastolic function. In addition, the alterations in cardiac structure are related to the type of training with dynamic training causing proportionally greater dilation and static training primarily increased wall thickness. AHS is associated with abnormalities in ECG, radiograph, and echocardiographic findings. It is important to be aware of these changes so that they are not misinterpreted to represent pathologic states. In particular, the distinction between AHS and HCM can be difficult, although certain historic and echocardiographic features can help differentiate the two.

Animals↗
PubMed1990

Insertion and excision of the transposable element mariner in Drosophila.

The transposable element mariner is active in both germline and somatic cells of Drosophila mauritiana. Activity of the element is greatly enhanced in the presence of Mos1, a genetic factor identified as an autonomous copy of mariner. A strain of D. mauritiana containing Mos1 and other copies of mariner was used to initiate a screen for visible mutations. More than 20 mutations were obtained, including alleles of white, yellow and vermilion. Six alleles were characterized at the molecular level, and all were found to contain a mariner element inserted into the affected gene. Four insertions into the white locus were sequenced to determine the exact site of insertion of mariner. There appears to be little sequence specificity requirement for mariner insertion, other than an absolute requirement for the dinucleotide TA, which is duplicated upon insertion. Sequences of phenotypically wild-type germline and somatic revertants obtained from various white alleles, including the previously isolated wpch allele, were obtained using the polymerase chain reaction. Mariner excision is imprecise in both germline and soma, and the most frequent excision events are the same in the two tissues. Mutant derivatives of wpch were also studied, and were found to exhibit a wide range of molecular structures and phenotypes.

Alleles↗
PubMed1985

Hallucinogenic amphetamine selectively destroys brain serotonin nerve terminals.

(+/-)-3,4-Methylenedioxyamphetamine (MDA), an amphetamine analog with hallucinogenic activity, produced selective long-lasting reductions in the level of serotonin, the number of serotonin uptake sites, and the concentration of 5-hydroxyindoleacetic acid in rat brain. Morphological studies suggested that these neurochemical deficits were due to serotonin nerve terminal degeneration. These results show that MDA has toxic activity for serotonin neurons in rats and raise the question of whether exposure to MDA and related hallucinogenic amphetamines can produce serotonin neurotoxicity in the human brain.

3,4-Methylenedioxyamphetamine↗
PubMed1978

Dare we count the cost of cancer chemotherapy?

During 1972-1976, when the incidence of cancer rose only slightly in the United Kingdom and the number of cancer patients seen at a large metropolitan teaching hospital and oncological centre remained largely unchanged, the use of cytotoxic drugs rose from 5.1% to 14% of the hospital's total drug budget. Most of the rise in cost can be ascribed to the increased use and increased unit cost of four effective but expensive drugs. Although the cost of drugs is but a small proportion of the cost of care of the cancer patient, it is argued that cytotoxic chemotherapy cannot offer a "cheap alternative" to surgery and radiotherapy. In a health service with cash spending limits the use of the more expensive cytotoxic drugs should be limited to the treatment of patients in whom "cure" or long-term ablation of disease is being attempted or to protocol studies in which their effectiveness is compared with that of other, possibly less expensive, drugs. Further studies are required of the use of the less expensive cytotoxic drugs in order to maximise their usefulness in the palliative treatment of advanced disease.

Antineoplastic Agents↗
PubMed1975

Carcinogenicity of 5-nitrofurans and related compounds with amino-heterocyclic substituents.

Carcinogenicity of eight 5-nitrofurans with heterocyclic substituents at the 2-position of the furan ring was investigated by feeding the chemicals to Sprague-Dawley female rats. N-[5-(5-nitro-2-furyl)-1,3,4-thiadiazol-2-yl]acetamide induced in 30 rats the highest incidence of tumors with the greatest number of tissues involved: forestomach squamous cell tumors (22), kidney pelvis transitional cell carcinomas (15), pulmonary alveolar cell carcinomas (16), hemangioendothelialsarcomas (20) of the intestine, mesentery, liver, lung, and pancreas, and a few tumors of other tissues. 2-Amino-5-(5-nitro-2-furyl)-1,3,4-thiadiazole, 2-amino-5-(5-nitro-2furyl)-1,3,4-oxadiazole, and trans-2-[dimethylamino)methylimino]-5-[2-(5-nitro-2-furyl)vinyl]-1,3,4-oxadiazole produced high incidences of mammary tumors. The other four 5-nitrofurans tested: N-[4-(5-NITRO-2-FURYL)-2-THIAZOLYL]ACETAMIDE;2,3,4-TRIFLUORO-N-[4-(5-NITRO-2-furyl)-2-thiazoly]acetamide;5-(5-nitro-2-furyl)-1,3,4-oxadiazol-2-ol; and N-( [3-(5-nitro-2-furyl)-1,2,4-oxadiazol-5-yl]methyl)acetamide were associated with tumor incidences of 40-60%. Two other chemicals were also tested: 2-Amino-5-nitrothiazole caused a low incidence of breast and kidney pelvis tumors, and 2-amino-4-(p-nitrophenyl)thiazole induced a high incidence of breast and salivary gland adenocarcinomas and lymphomas.

Adenocarcinoma↗