Correspondence among informants on parenting: preschool children, mothers, and observers.

The authors examined the correspondence among preschool children's, mothers', and observers' descriptions of parenting in the mother-child relationship along 3 dimensions (structure, warmth-responsiveness, and hostility). Ninety-four children (mean age = 5 years, 3 months) and their mothers, who represent diverse ethnic and socioeconomic groups, participated in the project. Preschool children were interviewed about their mothers' parenting by means of a developmentally sensitive, age-appropriate research tool for assessing the subjective experience of preschool children. Mothers responded to a self-report measure on their own parenting, and observers rated mothers' parenting behavior during a series of interaction tasks designed to elicit the relevant dimensions of parenting. Results indicated significantly greater correspondence between observer and child report of parenting than that between mother and child and mother and observer reports. Explanations for the inconsistencies among informants and implications of this finding are discussed.

Adolescent development.

This chapter identifies the most robust conclusions and ideas about adolescent development and psychological functioning that have emerged since Petersen's 1988 review. We begin with a discussion of topics that have dominated recent research, including adolescent problem behavior, parent-adolescent relations, puberty, the development of the self, and peer relations. We then identify and examine what seem to us to be the most important new directions that have come to the fore in the last decade, including research on diverse populations, contextual influences on development, behavioral genetics, and siblings. We conclude with a series of recommendations for future research on adolescence.

Hydration of amino acid side chains: dependence on secondary structure.

Energy calculations have been used to study the hydration sites around the polar groups of serine, threonine and tyrosine side chains. These hydration sites depend not only on the hybridization of the polar group but also on the local secondary structure, the chi 1 side chain torsion angle and the position of the hydroxyl hydrogen atom. For tyrosine side chains, two solvent sites are found approximately in the plane of the ring. Even for serine and threonine side chains only two minimum energy sites are found in general of which one is in an expected position within hydrogen bonding of the hydroxyl hydrogen atom (unless this is blocked from interaction with solvent molecules by, for example, Oi-4 or Oi-3. The position of the second of these sites depends not only on the position of the hydroxyl oxygen but also on neighbouring main chain atoms to which it can also hydrogen bond. There is good agreement with the solvent distributions obtained from crystallographic data.

Mitral valve repair for bacterial endocarditis.

Twenty-two patients with mitral insufficiency resulting from native valve endocarditis underwent mitral valve repair. Six patients had acute endocarditis with positive blood cultures and active valve infection. Sixteen patients were cured of active infection, but mitral insufficiency developed as a result of prior infection. Mean age was 48.5 +/- 21.7 years; 13 (59%) were male. Mean New York Heart Association functional class was 2.6 +/- 1.2. Multiple valve lesions were present in 11 (50%) patients. Valve abnormalities included leaflet perforation in 13 patients, chordal rupture or elongation in 14, vegetations in 5; and annular abscess in 1. In patients with acute endocarditis all macroscopically infected tissue was excised. Multiple techniques were required to achieve valve competence. Suture or patch closure of perforation was done in 14 patients, chordal shortening or transfer in 9, leaflet resection and closure in 4, leaflet resection with pericardial patching in 5, and annuloplasty in 15. Mitral valvuloplasty was combined with other procedures in 11 (50%) patients. There were two (9%) hospital deaths, both occurring in patients with healed endocarditis. There was one (9%) death in a patient undergoing an isolated procedure and one (9%) in a patient undergoing a combined procedure. Mean follow-up was 24 +/- 16.8 months and was complete. Seventeen (85%) were in New York Heart Association functional class I, and three (15%) were in class II. There were no late deaths, reoperations, recurrent endocarditis, thromboembolic events, or other valve-related morbidity. We conclude that mitral valve repair for insufficiency resulting from bacterial endocarditis (1) is possible in acute and healed disease, (2) has a low operative mortality, and (3) has resulted in patients free of recurrent infection and valve-related morbidity and mortality. Mitral valve repair is an attractive alternate to valve replacement in bacterial endocarditis.

Glucose uptake and flux through phosphofructokinase in wounded rat skeletal muscle.

Skeletal muscle injured with lambda-carrageenan has increased aerobic glycolysis. To assess the regulation of this process, the tissue concentrations of glycolytic intermediates, the flux through phosphofructokinase (PFK), and the intracellular concentrations of PFK effectors were examined in wounded rat skeletal muscle and in macrophages, the predominant inflammatory cell in the early stages of this wound model. Autoradiography demonstrated increased 2-deoxy-D-glucose uptake in wounded tissue compared with nonwounded muscle. 2-Deoxy-D-glucose was localized to the cellular infiltrate. The glycolytic intermediate concentrations demonstrated a facilitation of PFK in macrophages and wounded tissue as compared with nonwounded muscle. Wounded tissue had twice the flux through PFK compared with nonwounded muscle (10.0 +/- 0.6 wounded vs. 4.9 +/- 0.4 mumol.h-1.g-1 nonwounded). Macrophages had the highest flux through PFK (63.7 +/- 5.7 mumol.h-1.g-1) and when coincubated with muscle, the combined flux through PFK was equal to that of wounded muscle. The increase in glycolysis associated with wounded tissue may be explained by increased glucose uptake and increased flux through PFK by the inflammatory cells present in wounded tissue.

The relationship of purine metabolism to the macrophage-mediated increase of high energy phosphates in skeletal muscle.

Previous investigations have demonstrated that the high energy phosphate and adenine nucleotide content of wounded tissue are decreased. Purine metabolism was investigated in incubated lambda-carrageenan wounded skeletal muscle and in muscle exposed to peritoneal macrophages or macrophage-conditioned media. Wounded muscle released predominately uric acid into the incubation medium; whereas, nonwounded muscle released inosine, hypoxanthine, and xanthine as well as uric acid. Macrophages incubated with nonwounded muscle changed the purine release pattern toward one of wounded muscle. The conversion of inosine to allantoin and uric acid by macrophages increased linearly with the addition of up to 1 X 10(7) macrophages per incubation. Muscles incubated in macrophage-conditioned media had a decreased release of inosine and hypoxanthine and higher tissue levels of creatine phosphate, ATP, ADP, AMP, and adenosine compared to muscles incubated in standard media. These data suggest that the macrophage determines the pattern of purine release from wounded skeletal muscle in the incubated system and that in conditioned media a high energy phosphate promoting factor may exert its effect by mechanisms that augment the adenine purine pool.

A macrophage-mediated factor that increases the high energy phosphate content of skeletal muscle.

A marked cellular infiltrate accompanies wounding. The phagocytic and bacteriocidal activities of this infiltrate require increased substrate and O2 consumption. This rapid utilization of available oxygen and substrates could jeopardize an already compromised resident cellular component of a wound. Recent studies have demonstrated macrophage-mediated cell stimulatory agents which induce proliferation of nonlymphoid mesenchymal cells. This study was designed to examine macrophage-resident tissue interactions and their possible significance in wounded tissue. A reconstituted wound system was designed which combines the major components of a lambda-carrageenan skeletal muscle wound (muscle + macrophages). The extensor digitorum longi (EDL) of male Fisher rats were incubated in a standardized fashion. The groups of EDL were muscle incubated alone, muscle with the addition to the incubate of activated peritoneal macrophages or muscle with the addition of a conditioned supernatant from the incubation of activated or nonactivated peritoneal macrophages. Muscle ATP and CP content were noted to be increased 46 and 22%, respectively, when macrophages and skeletal muscle were coincubated. Macrophage-conditioned media from activated or nonactivated macrophages increased the ATP and CP muscle content 44 and 37%, respectively. Preliminary characterization of this high energy phosphate (HEP) promoting factor demonstrates it to be heat and cold stable and less than 10,000 Da. Therefore, a macrophage-mediated transferable factor is capable of increasing the HEP content of skeletal muscle in an in vitro system. This may have important consequences in maintaining host cell integrity following injury.

Abnormal insulin response in patients with small-vessel disease.

The insulin response to a glucose load has been investigated in twenty-five patients with small-vessel disease (ischaemic lesions of toes or feet in the presence of foot pulses). The clinical presentation was similar to that of juvenile diabetic microangiopathy, but in small-vessel disease there was no glucose intolerance. Unexpectedly in the patients with small-vessel disease there was no striking insulin secretion response to the stimulus of a glucose load. Controls increased their circulating insulin levels on average sixfold over fasting levels after 50 g. oral glucose: all the small-vessel-disease patients had increases of less than three times their fasting levels, and nine of them had completely flat curves throughout the test. Tolbutamide also did not stimulate insulin secretion. The refractory state of these patients' responses to the normal stimulus of insulin output has similarities to the picture in juvenile diabetes mellitus and may be important in the aetiology of the small-vessel lesions.

Insulin response to glucose in patients with peripheral vascular disease, arteritis, and Raynaud's phenomenon.

Twenty-three patients with peripheral vascular disease due to atheromatous blocks in large vessels, four patients with arteritis, and twenty patients with Raynaud's phenomenon were tested for insulin response to glucose. (In an earlier investigation patients with small-vessel peripheral vascular disease did not secrete insulin in response to a glucose load--a previously unreported finding.) Insulin output after glucose in patients with atheromatous blocks in large peripheral arteries fell into three categories: (1) normal glucose tolerance and insulin output, the insulin rise (peak/basal ratio) comparing well with the rise in controls; (2) carbohydrate intolerance with a prediabetic pattern of glucose-tolerance test, and raised circulating insulin levels both fasting insulin and after glucose, so that the insulin rise was lower than normal; or (3) the flat insulin responses after glucose that had been noted in small-vessel disease with normal glucose tolerance. Thus in these twenty-three patients with large-vessel blocks presenting with peripheral vascular disease the high and late insulin secretion after glucose reported by other workers for patients with atheroma could not be confirmed. High but not delayed insulin peaks were seen after a glucose stimulus in some patients with arteritis and with Raynaud's phenomenon.