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Biomedical subjects

M S Miller

Publications and source records attributed to M S Miller.

136 records · Page 8Linked to original sources
PubMedDate not supplied

Impact of HIV risk and infection on delivery of psychosocial treatment services in outpatient programs.

HIV risk and HIV infection have profoundly affected the delivery of psychosocial treatment services in outpatient drug treatment settings. First, HIV has changed the programmatic emphasis of outpatient treatment, from the intake process through the goals of care, and treatment program staff are being altered significantly. Second, HIV brings with it a pull to extend the reach of drug abuse treatment to the sexual partners and families of patients. Finally, for community and statewide planners, a debate is emerging between the idea that programs should provide high-quality services to a few targeted "high risk" or "vital category" patients versus providing minimal services to as many drug abusers as possible. There is a vital need for research studies that will add data to the decision-making process, at both the policy and programmatic levels.

Ambulatory Care↗
PubMedDate not supplied

Use of topical recombinant human platelet-derived growth factor-BB (becaplermin) in healing of chronic mixed arteriovenous lower extremity diabetic ulcers.

Lower extremity ulcers cause significant morbidity and mortality in patients with diabetes. The primary factors that contribute to the development of this type of ulcer are peripheral neuropathy and peripheral vascular disease, which are often accompanied by infection. Lower extremity diabetic ulcers are chronic and difficult to treat, in part due to underlying pathologic conditions in individuals with diabetes that can contribute to impaired wound healing. This article reports the author's experience with treatment of chronic lower extremity ulcers of mixed etiologies with recombinant human platelet-derived growth factor--BB [rhPDGF-BB, REGRANEX (becaplermin) Gel 0.01%] in a patient with multiple risk factors including long-standing insulin-dependent type 2 diabetes.

Administration, Topical↗
PubMedDate not supplied

Serum inorganic fluoride levels in obese patients during and after enflurane anesthesia.

Serum ionic fluoride levels in 24 markedly obese patients (127.6 +/- 6.0 kg) and seven nonobese control subjects (67.3 +/- 1.2 kg) were compared during and following enflurane anesthesia (less than 2.0 MAC hr). Peak serum fluoride levels were higher (28.0 +/- 1.9 vs 17.3 +/- 1.3 micrometers/L, p less than 0.01) and the rate at which fluoride levels increased was more rapid (slope 5.6 vs 2.5 micrometers/L/hr) in obese patients than in control patients. No clinical evidence of nephrotoxicity was found in either group. Vasopressin resistance tests were not performed, and thus it is inknown whether subclinical nephrotoxicity occurred in either study group. Possible reasons for increased enflurane metabolism in obesity are discussed. These possibilities include differences in fluoride ion kinetics, hepatic delivery and penetration of volatile anesthetics, and altered hepatic microsomal enzyme activity. Obesity rather than weight is an important determinant of anesthetic biotransformation.

Adult↗
PubMedDate not supplied

Molecular pathogenesis of transplacentally induced mouse lung tumors.

Previous studies from this and other laboratories have shown that treatment of pregnant mice with 3-methylcholanthrene (MC) caused lung tumors in the offspring, the incidence of which correlated with fetal inducibility of Cyp1a1. Analysis of paraffin-embedded lung tissue for Ki-ras-2 mutations indicated that 79% of the lesions examined contained point mutations in codons 12 and 13 of the Ki-ras-2 gene locus, the majority of which (84%) were G-->T transversions. The mutational spectrum was dependent on the tumor stage, as both the incidence of mutation and type of mutation produced correlated with malignant progression of the tumor. Mutations occurred in 60% of the hyperplasias, 80% of the adenomas, and 100% of the adenocarcinomas. In the tumors with mutations, GLY12-->CYS12 transversions occurred in 100% of the hyperplasias, 42% of the adenomas, and 14% of the adenocarcinomas. GLY12-->VAL12 transversions were not observed in hyperplasias and occurred in 42% of the adenomas and 57% of the adenocarcinomas. The remaining ASP12 and ARG13 mutations occurred only in adenomas (17%) and adenocarcinomas (29%). The tumors were also analyzed for alterations in the structure or function of the tumor suppressor genes Rb, p53, and Cdkn2a. No mutations were observed in exons 5-8 of the p53 gene. SSCP analysis demonstrated that 2 of 15 lung tumors contained shifted bands at the Cdkn2a gene locus. Sequence analysis had identified these as mutations in exon 2, with a CAC-->TAC transition at base 301 (HIS74-->TYR74) in tumor 23-1 and GGG-->GAG transition at base 350 (GLY90-->GLU90) in tumor 36-1. Northern blot analysis of the larger tumors revealed that 14 of 14 of these large lung tumors exhibited markedly decreased expression of Rb gene transcripts. These results were confirmed by immunohistochemistry. The larger tumors, which exhibited features of adenocarcinomas, showed a marked reduction or almost complete absence of nuclear pRb staining compared with smaller adenomas and normal lung tissue. The results suggest that Ki-ras-2 mutations are an early and frequent event in lung tumorigenesis, and that the type of mutation produced by environmental chemicals can influence the carcinogenic potential of the tumor. The results obtained with the Cdkn2a and Rb genes suggest that alterations in the Rb regulatory axis may play a key role in the pathogenesis of the pulmonary tumors and appear to occur later in the neoplastic process. It appears from these experiments that the combination of mutated Ki-ras-2 and alterations in the Rb regulatory gene locus, which are frequent alterations in human lung tumors, may be the preferred pathway for lung tumor pathogenesis in mice exposed transplacentally to environmental carcinogens.

Adenocarcinoma↗
PubMedDate not supplied

Effects of betamethasone on the in vitro and in vivo 2-hydroxylation of biphenyl in the rat.

The in vitro addition of betamethasone to rat liver microsomes caused a concentration-dependent stimulation of biphenyl 2-hydroxylation. At a 100 microM concentration of betamethasone, the formation of 2-hydroxybiphenyl was increased by approximately 4-fold in microsomes from 28-day-old rats and 10-fold in liver microsomes from 5-day-old rats. The steroid had little or no effect on the hydroxylation of biphenyl in the 3- or 4-position except at the highest concentration tested (1 mM), where a 20-30% inhibition was observed. The ip injection of 0.01 to 10 mumol of betamethasone to 5-day-old rats had little or no effect on the total body metabolism of 0.01 to 3.5 mumol of biphenyl-2-3H to 2-hydroxybiphenyl as measured by 3H2O formation. Although betamethasone had no effect on the 2-hydroxylation of biphenyl in the intact rat, this reaction was stimulated 4- to 9-fold by the addition of 100 microM betamethasone to hepatocyte monolayer cultures.

Aging↗