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Biomedical subjects

M L Freedman

Publications and source records attributed to M L Freedman.

At least 55 records · Page 3Linked to original sources
PubMed1983

Organic brain syndromes in the elderly. When are they reversible?

Dementia, delirium, and depression are not part of normal aging but are organic brain syndromes that often are reversible. Thus, it is imperative that primary care physicians carefully look for a reversible cause in a patient with one of these disorders. Even an irreversible condition, such as Alzheimer's disease, can be effectively treated with drugs that are carefully chosen to minimize serious side effects. Patients with cognitive impairment deserve to be treated with dignity, and every effort should be made to maintain the highest level of function possible.

Aged↗
PubMed1983

Pneumococcal bacteremia in adults: age-dependent differences in presentation and in outcome.

In order to evaluate the effect of age on the presentation of and response to acute bacterial infection, the hospital charts of 187 adult patients with community-acquired pneumococcal bacteremia admitted to Bellevue Hospital over a nine-and-a-half year period were reviewed. Compared with younger patients, older patients (aged 65 or older) more frequently had (1) a lower fever in response to the infection, (2) an unclear history of illness, (3) a delay in diagnosis and/or therapy, and (4) a higher risk of dying. On admission, their leukocyte counts and heart rates were similar to those in a group of younger patients, which was composed largely of alcoholic patients and those addicted to intravenous drugs. Response to therapy was also similar in surviving older patients. Lower temperature and an unclear history were features most commonly associated with both delayed diagnosis and higher mortality. When patients with a history of alcohol abuse and those dying shortly after admission (i.e., presenting in a moribund state) were eliminated from the analysis, many of these age-related differences in presentation and outcome became even more evident.

Adult↗
PubMed1983

Dextran-induced aggregation in a mutant of Streptococcus sobrinus 6715-13.

A mutant of wild-type Streptococcus sobrinus 6715-13 has been isolated which resists aggregation by exogenous dextran. This variant is able to form adherent plaque deposits in vitro when cultured in the presence of sucrose and has dextranase activity. In these respects it is the complement of previously described isolates which are plaque formation defective but aggregation normal. Measurements of the incorporation of glucose from glucosyl-labeled sucrose into glucan by cell-associated glucosyltransferase enzyme activity and the thermal labilities of catalytic and receptor functions, as well as the binding of labeled dextrans to the cells, provide evidence that neither dextranase nor glucosyltransferase is the receptor involved in dextran-induced aggregation. Blockage of such bacterial aggregation by anti-glucosyltransferase or anti-dextranase sera suggests cross-reactivity between the antigenic determinants of proteins which recognize alpha(1-6) glucan linkages. A model is proposed, consistent with these and previous findings, in which enzymatic function precedes dextran receptor activity in emergence from the cell. It is also proposed that dextran receptor components of the multireactive glucosyltransferase enzyme(s) and dextranase(s) are spatially separate from, although functionally and antigenically related to, the receptors on the bacterial surface involved in dextran-induced aggregation.

Agglutination↗
PubMed1982

Age-related decline in the biosynthesis of mitochondrial inner membrane proteins.

Isolated mitochondria from rat livers of various ages show a gradual decline in the rate of inner membrane-matrix protein synthesis with advancing age of the animal. Rats at 112-120 weeks synthesize these proteins at only 40% of the rate of 2-8-week-old animals. The initial rates of incorporation of label were 145 cpm/mg/minute for the "old" animals, and 320 cpm/mg/minute for the "young" animal. No difference in either amino acid pool size or leakage of label through the mitochondrial membrane was detected in the two age groups. Treatment of the mitochondria with ferrous ammonium sulphate produced a 1.62 fold increase in mitochondrial protein synthesis in the young animal but not in the old. Hemin treatment produced a similar effect. These results suggest that the decrease in delta-aminolevulinic acid synthase activity seen with age (Paterniti et al., 1978) may be due to a decrease in the synthesis of mitochondrial inner membrane proteins.

5-Aminolevulinate Synthetase↗
PubMed1982

Effect of inhibitors and stimulators on isolated liver cell mitochondrial protein synthesis from young and old rats.

Mitochondria isolated from the livers of old rats (26-30 months) were found to incorporate 41% less leucine into mitochondrial proteins as compared to those from young rats (2-3 months). The initial rates of incorporation of label were 145 cpm/mg/min for the "old" animals, and 320 cpm/mg/min for the young animal. No difference in either amino acid pool size or leakage of label through the mitochondrial membrane was detected in the two age groups. Young rats were treated in vivo with cycloheximide (10 mg/kg) followed by isolation and incubation of their mitochondria in vitro two hours later. There was a two-fold increase in incorporation of leucine into mitochondrial proteins. In contrast, mitochondria isolated from old rats showed a markedly blunted response to cycloheximide pre-treatment. When mitochondria isolated from young and old rats were exposed to inhibitors of mitochondrial protein synthesis, alpha-alpha-dipyridyl (2 x 10(-4)M) and ethanol (0.15M), the old mitochondria showed greater susceptibility to inhibition. These results suggest that the control of the biosynthesis of mitochondrial proteins is altered in the old animals.

2,2'-Dipyridyl↗
PubMed1982

Preemption of Streptococcus mutans 10449S colonization by its mutant 805.

Oral infection of rats with Streptococcus mutans mutant 805 was used to prevent the establishment of its highly virulent wild-type progenitor NCTC 10449S. The dose of wild-type cells required to colonize 100% of the specific pathogen-free Osborne-Mendel rats (21 to 43 days old) consuming caries test diet 2000 was greater than 4 x 10(5) but less than 4 x 10(6) cells. Therefore, the latter dose was used to challenge rats which had already been colonized by an oral dose of about 6 x 10(8) cells of mutant 805. This prior infection by 805 either completely protected rats from subsequent colonization by wild-type cells or greatly delayed and diminished their emergence. Rats in which wild-type cells became established showed much lower percentages of wild-type cells in their total recoverable floras than did rats that were not first infected by the mutant. Large doses of mutant 805, however, did not displace wild-type cells from rats once it became established. There was no evidence of reversion of the mutant, which is defective in intracellular polysaccharide synthesis and hence is less virulent than wild-type cells. The data indicate that the S. mutans cell which first colonizes rats gains the strongest ecological position and is difficult to displace. Also, they suggest the possible prophylactic utility of infection by this mutant of S. mutans.

Animals↗
PubMed1982

Physiology of "mutans-like" Streptococcus ferus from wild rats.

Strains of Streptococcus ferus isolated from the oral cavities of wild rodents inhabiting sucrose-rich and sucrose-poor environments have many traits in common with the "mutans" streptococci. Thus, S. ferus HD3 and 8S1, like cariogenic S. sobrinus 6715-13, from adherent, alpha (1 leads to 3) glucopyranosyl-glucose linkage-rich, plaquelike deposits in vitro and in vivo through the action of constitutive glucosyltransferase(s) enzymes on sucrose, produce and degrade intracellular polysaccharide, produce short-chain fatty acids from the catabolism of mono- and disaccharides, carry the c antigen of S. mutans, and penetrate, persist, and proliferate in a sucrose-augmented fashion in the oral cavities of specific-pathogen-free rodent caries models. However, unlike infection with common S. mutans, infection with tested S. ferus strains does not cause caries. This avirulence appeared to result more from the reduced aciduricity of S. ferus than from differences in glucosyltransferase complements. Studies showed that despite generally similar growth rates and extracellular glucan syntheses, the acidogenic metabolism of S. ferus was more inhibited by declining environmental pH than was cariogenic S. sobrinus 6715-13 and that, in vitro, less hydroxyapatite was solubilized by S. ferus metabolic end products. The physiology of these S. ferus strains demonstrated that, in addition to plaque formation and acid production, acid tolerance was crucial to the carious process.

Agglutination↗
PubMed1981

Evidence of prior hepatitis B and hepatitis A virus infections in an ambulatory geriatric population.

Ninety-five randomly selected patients attending an ambulatory geriatric medical clinic were tested for the presence in their sera of hepatitis B surface antigen and of antibody to hepatitis B and A viruses. Such evidence of past hepatitis infection was correlated with current liver function and history of having received blood transfusions. The results showed that 94% of patients had antibody to hepatitis A virus, and 32% had antibody to hepatitis B virus. Patients with abnormal liver function tests, or those with a history of blood transfusions were no more likely to have hepatitis B antibody than patients with normal liver function tests or those with no history of transfusion.

Aged↗
PubMed1981

Colonization and cariogenicity of Streptococcus ferus in rats.

Streptococcus ferus, which is indigenous to wild rats, is a member of the mutans group of streptococci. We tested its ability to colonize and to cause caries in laboratory rats by comparing two strains of S. ferus with the very cariogenic Streptococcus sobrinus strain 6715. Groups of rats were fed either finely ground mouse chow or a 56% sucrose diet, or they were switched from chow to the sucrose diet. All three strains colonized the mouths of rats regardless of diet. However, the infectants reached higher proportions of the total flora more quickly in the rats consuming sucrose. Similarly, the percentage of the oral flora represented by an infecting organism increased numerically when rats originally fed chow were switched to the sucrose diet. S. ferus formed plaques on the teeth of the rats, but these plaques did not proliferate over smooth tooth surfaces as extensively as did those of S. sobrinus. Although S. ferus colonized and accumulated, it was non-cariogenic in rats fed sucrose compared both with rats fed similarly but infected with S. sobrinus 6715 and with uninfected controls. In vitro measurements suggested the S. ferus produced acid less rapidly than S. sobrinus. Thus, the lack of cariogenicity in S. ferus may result from an inability to form copious plaques on smooth tooth surfaces and from low acid production and, therefore, may represent a natural absence of the pathogenic potential usually inherent in the mutans streptococci.

Animal Nutritional Physiological Phenomena↗
PubMed1980

Iron requirement for isolated rat liver mitochondrial protein synthesis.

Isolated rat liver mitochondrial protein synthesis was severly inhibited by alpha, alpha-dipyridyl (a ferrous iron-chelating agent), chloramphenicol and hemin (10(-7) M or greater). In contrast, gamma, gamma-dipyridyl (a non-iron-chelating analogue of alpha, alpha-dipyridyl), cycloheximide and lower concentrations of hemin were non-inhibitory. The inhibitory action of alpha, alpha-dipyridyl was reversed by addition of Fe(NH4)2(SO4)2 while ZnCl2, CuCl2 and CoCl2 were ineffective. Hemin, however, did not protect against the alpha, alpha-dipyridyl inhibition of mitochondrial protein synthesis. These results indicate that ferrous iron is required for mitochondrial protein synthesis and suggests that it is through a mechanism independent of hemin concentration.

2,2'-Dipyridyl↗
PubMed1979

Induction of liver cell haem oxygenase in iron-overloaded rats.

Rats were chronically iron-overloaded by intraperitonel injections of iron-dextran. Electron microscopy revealed that the excess iron was deposited in ferritin-like particles packed in lysosomes and scattered in hepatic cytoplasm. No mitochondrial iron deposition or damage was seen. Furthermore, mitochondrial preparations from chronically iron-overloaded animals were found to be contaminated with lysosomes, which could explain previously reported increases in mitochondrial iron by chemical analysis. Mitochondrial function, as measured by cytochromes a-a3, b and c concentrations as well as activity of the rate-limiting enzyme of haem synthesis, delta-aminolaevulinate synthetase, was not diminished by chronic iron-overloading. Microsomal haem was decreased by 30% at the time that haem oxygenase, the rate-limiting enzyme of haem degradation, was increased approx. 3-fold. Animals were given a single intraperitoneal injection of iron-dextran and the activities of delta-aminolaevulinate synthetase and haem oxygenase were measured over 24 h. delta-Aminolaevulinate synthetase activity increased approx. 2-fold in these acutely iron-overloaded rat livers, but at a time after the increase in haem oxygenase. These results suggest that an early consequence of excess iron in liver is acceleration of the rate of haem degradation, possible by haem oxygenase.

5-Aminolevulinate Synthetase↗