Surface visco-elastic moduli of a Langmuir film of a polystyrene-polydimethyl siloxane block copolymer at the air-ethyl benzoate interface.

Surface quasi-elastic light scattering has been applied to a spread film of a block copolymer of polystyrene and polydimethyl siloxane. The influence of surface concentration (surface pressure) at a fixed surface wave number has been explored. The capillary wave frequency and damping showed a similar dependence on the surface concentration as values obtained earlier, but due to a more appropriate analysis of the correlation functions, surface visco-elastic moduli obtained were distinctly different. By correlating the values obtained with the variations in solvated polystyrene layer thickness from neutron reflectometry, the maximum in dilational modulus was shown to occur at the same nominal surface concentration where the layer begins to stretch and take on brush-like behaviour. This same surface concentration is where the relaxation time of the spread film also has a maximum value, the relaxation time being calculated using the standard linear model of visco-elasticity, which was found to fit the frequency dependence of the surface tension and dilational moduli at the resonant nominal surface concentration of 3.1 mg m(-2).

Baby-friendly hospital initiative improves breastfeeding initiation rates in a US hospital setting.

OBJECTIVE: Breastfeeding initiation rates were compared at Boston Medical Center before (1995), during (1998), and after (1999) Baby-Friendly policies were in place. Boston Medical Center, an inner-city teaching hospital that provides care primarily to poor, minority, and immigrant families, achieved Baby-Friendly status in 1999. METHODS: Two hundred complete medical records, randomly selected by a computer, were reviewed from each of 3 years: 1995, 1998, and 1999. Infants were excluded for medical records missing feeding data, human immunodeficiency virus-positive parent, neonatal intensive care unit admission, maternal substance abuse, adoption, incarceration, or hepatitis C-positive mother. All infant feedings during the hospital postpartum stay were tallied, and each infant was categorized into 1 of 4 groups: exclusive breast milk, mostly breast milk, mostly formula, and exclusive formula. RESULTS: Maternal and infant demographics for all 3 years were comparable. The breastfeeding initiation rate increased from 58% (1995) to 77.5% (1998) to 86.5% (1999). Infants exclusively breastfed increased from 5.5% (1995) to 28.5% (1998) to 33.5% (1999). Initiation rates increased among US-born black mothers in this population from 34% (1995) to 64% (1998) to 74% (1999). CONCLUSIONS: Full implementation of the Ten Steps to Successful Breastfeeding leading to Baby-Friendly designation is an effective strategy to increase breastfeeding initiation rates in the US hospital setting.

Identification of a new HLA-B*39 allele: HLA-B*3924.

We have identified a new HLA-B*39 allele through polymerase chain reaction (PCR) using sequence-specific primers (SSP) and sequence-based typing of exons 2 and 3. This novel allele was identified in three HLA-identical siblings of Turkish origin. This allele only differs from HLA-B*3903 at a unique single nucleotide substitution (T for C) at position 365 in exon 3 which results in an amino acid change in codon 98 of methionine (ATG) to threonine (ACG). The sequencing enabled the development of a monospecific PCR-SSP reaction which can be used to discriminate between HLA-B*3924 and other B*39 alleles.

Hunger in legal immigrants in California, Texas, and Illinois.

OBJECTIVES: This study determined the prevalence of food insecurity and hunger in low-income legal immigrants. METHODS: We conducted a cross-sectional survey of Latino and Asian legal immigrants attending urban clinics and community centers in California, Texas, and Illinois with a food security questionnaire. RESULTS: Among 630 respondents, 40% of the households were food insecure without hunger and 41% were food insecure with hunger. Independent predictors of hunger were income below federal poverty level (odds ratio [OR] = 2.72, 95% confidence interval [CI] = 1.72, 4.30), receipt of food stamps (OR = 2.53, 95% CI = 1.57, 4.09), Latino ethnicity (OR = 2.39, 95% CI = 1.49, 3.82), and poor English (OR = 1.76, 95% CI = 1.10, 2.82). CONCLUSIONS: The prevalence of hunger among low-income legal immigrants is unacceptably high. Access to food assistance programs is important for the health and well-being of this population.

Amygdaloid-lesion hyperphagia: impaired response to caloric challenges and altered macronutrient selection.

Lesions of the most posterodorsal aspects of the amygdala in female rats result in hyperphagia and moderate obesity. In the present study, rats with amygdaloid lesions did not increase their daily food intake when their powdered diet was diluted with 25 or 50% nonnutritive bulk. Control animals adjusted their food intake appropriately. In a second study, rats with lesions ate less food (lab chow pellets) than controls when allowed to eat for only 1 h/day for 10 days. In experiment 3, rats were offered a three-choice macronutrient diet. Whereas four of six control animals preferred the high-fat diet, all eight of the rats with amygdaloid lesions displayed a distinct preference for the high-carbohydrate diet, including those that had preferred the high-fat diet before surgery. These results, along with the previous finding that identical lesions result in hyperinsulinemia, indicate that the amygdala is involved in both the homeostatic regulation of food (caloric) intake and the selection of macronutrients.

Amygdaloid lesion-induced obesity in rats in absence of finickiness.

Female rats with lesions of the most posterodorsal aspects of the amygdala were tested for their reaction to a variety of manipulations of their food and water supply. Compared to control animals, the rats with lesions were hyperphagic and displayed excess weight gain. However, they did not consume more of a high-fat diet or of a sucrose solution than did controls, nor did they consume less than controls when their food or water supply was adulterated with quinine or when switched from pellets to ground chow. On a fine-powder diet, control animals lost weight whereas rats with lesions gained weight. Rats with lesions consumed more saline than controls in a two-bottle preference test. These results are consistent with those of earlier studies of other species with amygdaloid damage. It is concluded that rats with lesions of the posterodorsal amygdala are hyperphagic in absence of the marked finickiness that characterizes some other brain lesion-induced obesity syndromes.

Posterodorsal amygdaloid lesions in rats: long-term effects on body weight.

Bilateral lesions in the most posterodorsal aspects of the amygdala in female rats resulted in immediate and dramatic weight gains on a standard lab chow diet. The rate of weight gain returned to normal by Day 20, but the difference in body weight between animals with amygdaloid lesions and those with sham lesions was maintained for the duration of the study (60 days). Because rats with posterodorsal amygdaloid lesions have also been found to be hyperinsulinemic, it is hypothesized that the lesions result in a similar, though smaller, version of the syndrome that follows lesions of the ventromedial hypothalamus.

Hyperinsulinemia in rats with obesity-inducing amygdaloid lesions.

Electrolytic lesions of the posterodorsal aspects of the medial division of the extended amygdala in female rats result in hyperphagia and excessive weight gain. In the present study, the effects of such lesions on plasma insulin, glucose, corticosterone, and adrenocorticotropic hormone were assessed during a period of food restriction and again after a 15-day period of food ad libitum. Compared with control animals, the rats with amygdaloid lesions were hyperinsulinemic under both conditions and gained substantially more weight when fed ad libitum. No difference between groups was observed for the other hormones. It is concluded that damage to the posterodorsal aspects of the medial amygdala results in a primary metabolic dysfunction that accounts, at least in part, for the overeating and excessive weight gain.

Temporal lobe lesion-induced obesity in rats: an anatomical investigation of the posterior amygdala and hippocampal formation.

Bilateral lesions centered in the posterodorsal amygdala of female rats resulted in hyperphagia and excessive weight gain (mean = 65.3 g in 20 days compared to 6.8 g for control animals). The brain damage always extended posteriorly into the ventral hippocampal formation. However, lesions that were confined to the ventral hippocampus or amygdalohippocampal area had no effect on daily food intake or body weight, nor did lesions at any other hippocampal site. In a previous study, lesions of the basolateral, corticomedial, and anterior groups of amygdaloid nuclei failed to affect food intake or body weight. It is concluded that the posterodorsal aspect of the amygdala is the critical site for this experimentally induced obesity syndrome. New coordinates for the effective site are presented.

Segregation analysis of NIDDM in Caucasian families.

Non-insulin-dependent diabetes mellitus (NIDDM) has a substantial genetic component, but the mode of inheritance and the molecular basis are unknown. We have undertaken segregation analysis of NIDDM after studying 247 subjects in 59 Caucasian nuclear pedigrees ascertained without regard to family history of the disorder. The analyses were performed using POINTER and COMDS, which are computer programs which apply statistical models to the data. POINTER analysis was performed defining the phenotype as a presence or absence of hyperglycaemia. Among single locus hypothesis, the analyses rejected a recessive model and favoured a dominant model, but could not statistically show that this fitted better than a mixed model (a single locus against a polygenic background) or a polygenic model. COMDS analysis assumed a continuum of hyperglycaemia from normality to NIDDM, classified family members into a series of diathesis classes with increasing plasma glucose levels and compared the distribution with that found by screening the normal population. This analysis improved the likelihood of a dominant single locus model and suggested a gene frequency of 7.4%. It raised the possibility of a second locus, but cannot identify or exclude a polygenic model. In conclusion, two types of segregation analyses rejected a recessive model and favoured a dominant model of inheritance, although they could not statistically show that this fitted better than the polygenic model. The results raised the possibility of a common dominant gene with incomplete penetrance, but genetic analysis of NIDDM needs to take into account the likelihood of polygenic inheritance with genetic heterogeneity.

Non-linkage of the glucagon-like peptide 1 receptor gene with maturity onset diabetes of the young.

Glucagon-like peptide-1 (GLP-1) is a hormone derived from the preproglucagon molecule that is secreted by intestinal L cells and stimulates insulin secretion from beta cells. The GLP-1 receptor is a candidate gene for diabetes mellitus, as mutations may induce the impaired insulin response that is a characteristic feature of NIDDM. To study the relationship between the GLP-1 receptor gene and NIDDM, linkage of a microsatellite polymorphism flanking the GLP-1 receptor gene with diabetes was investigated in three Caucasian families with MODY and in the nuclear families of 12 NIDDM probands. A cumulative LOD score -8.50 excludes linkage in these MODY pedigrees. A LOD score of -1.24 in the NIDDM nuclear pedigrees makes linkage improbable. Mutations in or near the GLP-1 receptor gene are unlikely to be the major cause of the inherited predisposition to NIDDM in Caucasian pedigrees, but we cannot exclude a role for this locus in a polygenic model or a major role in some pedigrees.

Microsatellite polymorphisms at the glucokinase locus: a population association study in Caucasian type 2 diabetic subjects.

Glucokinase has a central role in glucose metabolism in pancreatic beta cells and hepatocytes and is an important candidate gene for Type 2 diabetes. Mutations of the glucokinase gene have been reported in Caucasian pedigrees with maturity-onset diabetes of the young and late-onset Type 2 diabetes. In population studies of American Blacks and Mauritian Creoles an association between alleles of a glucokinase polymorphism and Type 2 diabetes has been described. Two microsatellite polymorphisms (GCK 1 and GCK 2) flanking the glucokinase gene were investigated in Caucasian subjects. There was no significant linkage disequilibrium between the alleles of the two polymorphisms. The overall allelic frequencies for GCK 1 and the combined haplotyes did not significantly differ between 95 Type 2 diabetic and 76 normoglycaemic subjects. In an expanded cohort of 151 diabetic subjects the allelic frequencies at GCK 2 were also similar to controls. These results suggest that a single mutation of the glucokinase gene is not a common cause of Type 2 diabetes in English Caucasians.

Availability of type II diabetic families for detection of diabetes susceptibility genes.

Type II diabetes is a familial disorder, as evidenced by the increased prevalence in monozygotic cotwins and first-degree relatives of affected subjects; however, its genetic etiology is largely unknown. Well-characterized pedigrees are an essential resource for the study of susceptibility genes for type II diabetes. This study describes a 5-yr search for type II diabetic families in Oxfordshire, U.K. We interviewed 950 type II diabetic subjects concerning the availability of first-degree relatives; 127 Caucasian families ascertained through a proband with type II diabetes were studied, and 589 first-degree relatives were characterized. Three large pedigrees with maturity-onset diabetes of the young, and 8 multiplex multigenerational type II diabetic pedigrees were identified. We identified 12 sib-pairs in which both siblings had type II diabetes; however, only 7 sib-pairs had both parents alive, and 2 of these had both parents affected. If one also considers one sib having diabetes and one sib having glucose intolerance as being an affected sib-pair, we identified 30 sib-pairs of which 7 had both parents affected and probably had bilineal inheritance. We identified 76 complete nuclear families with both parents and offspring available for study, but only 6 were of optimal structure for linkage analysis. In conclusion, multiplex pedigrees and type II diabetic sib-pairs with living parents are uncommon, and their ascertainment requires a substantial investment of resources. Large-scale collaborative multicenter initiatives would be needed to collect a large resource of family material for the study of susceptibility genes for type II diabetes.

Campaign '92: three more years!

Creative planning and well-executed graphics produced an upbeat approach to preparing staff for a JCAHO accreditation visit. Five humorous and highly visible strategies were used in a coordinated eight-week "campaign." Not only did the institution "pass the test" but there was a consensus among staff nurses that they had felt comfortable, confident and in control during interviews with the JCAHO surveyor.

Hyperglycaemic progression in subjects with impaired glucose tolerance: association with decline in beta cell function.

Impaired glucose tolerance is associated with an increased risk of Type 2 diabetes. This prospective cohort study has examined the variables associated with hyperglycaemic progression in order to elucidate the aetiology of this deterioration. The 5 mg glucose.kg ideal body weight.min-1 continuous infusion of glucose with model assessment (CIGMA) test was used to quantitate glucose tolerance, beta cell function, and insulin sensitivity. Twenty-two Caucasian subjects who had impaired glucose tolerance identified on two separate tests underwent repeat testing after a median period of 24 months. At follow-up, 2 of the 22 subjects (9%) had Type 2 diabetes, 18 (82%) had impaired glucose tolerance, and 2 (9%) were normoglycaemic. The fasting and achieved (60-min) glucose levels were significantly higher at follow-up (mean +/- SD) (5.7 +/- 0.8 vs 5.5 +/- 0.5 mmol l-1, p = 0.029 and 10.0 +/- 0.9 vs 9.6 +/- 0.6 mmol l-1, p = 0.021, respectively), and beta cell function was significantly lower (median and interquartile range): 75% (50-93%) vs 90% (70-135%), p = 0.009. The changes in fasting plasma glucose were found to correlate with change in body mass index (rs = 0.46, p = 0.03). We conclude that impaired glucose tolerance is associated with decline in beta cell function, and denotes substantial risk of hyperglycaemic progression. Randomized controlled trials are warranted to determine whether exercise programmes, dietary advice, and attentive follow-up and effective preventive strategies for subjects with impaired glucose tolerance.

Association of low birth weight with beta cell function in the adult first degree relatives of non-insulin dependent diabetic subjects.

OBJECTIVE: To examine the relation between birth weight and beta cell function in the first degree relatives of non-insulin dependent diabetic subjects. DESIGN: Cross sectional study of 101 adults of known birth weight from 47 families which had at least one member with non-insulin dependent diabetes. SUBJECTS: 101 white adults aged mean 43 (SD 7) years. SETTING: Oxfordshire, England. MAIN OUTCOME MEASURES: Glucose tolerance was measured by continuous infusion glucose tolerance test. beta cell function and insulin sensitivity were calculated from the fasting plasma glucose and insulin concentrations with homeostasis model assessment. beta cell function was standardised to allow for the confounding effects of age and obesity. RESULTS: Twenty seven subjects had non-insulin dependent diabetes, 32 had impaired glucose tolerance, and 42 were normoglycaemic. Birth weight correlated with the beta cell function of the complete cohort (rs = 0.29, p = 0.005), the non-insulin dependent diabetic subjects (rs = 0.50, p = 0.023), and the non-diabetic subjects (rs = 0.29, p = 0.013). The non-insulin dependent diabetic (n = 27) and the non-diabetic (n = 74) subjects had similar mean (inter-quartile range) centile birth weight 50% (19%-91%), and 53% (30%-75%) respectively. Non-insulin dependent diabetic subjects had significantly lower beta function than the non-diabetic subjects: 69% (48%-83%) v 97% (86%-120%), p < 0.001. CONCLUSIONS: The cause of the association between low birth weight and reduced beta cell function in adult life is uncertain. Impaired beta cell function in non-insulin dependent diabetic subjects was not accounted for by low birth weight, and genetic or environmental factors are likely to be necessary for development of diabetes.

Distribution of type II diabetes in nuclear families.

Type II diabetes has a substantial genetic component, but the mode of inheritance and the molecular basis of this inheritance are uncertain. This study documents the familial distribution of the disease in the parents and siblings of a consecutive series of type II diabetic subjects. We studied 66 first-degree relatives of 20 white subjects with type II diabetes and both parents alive. They were tested with a continuous infusion of glucose (5 mg.kg IBW-1.min-1) (n = 49) or FPG and hemoglobin A1c (n = 17). Seven probands had neither parent affected with diabetes or IGT, 10 had one parent affected (6 with diabetes and 4 with IGT), and 3 had both parents affected. The probands with affected and those with unaffected parents were phenotypically similar. These findings indicate that a sizable subgroup of type II diabetic subjects may have neither parent affected with a demonstrable abnormality of glucose tolerance. The assumption of autosomal dominance with complete penetrance is not supported, although it remains possible that a dominant gene of low penetrance may play a role in some pedigrees. Polygenic inheritance would appear likely, and genetic heterogeneity may occur. The inheritance of diabetic traits from phenotypically normal parents needs to be considered in the analysis of genetic linkage with type II diabetes.

Linkage analysis of glucokinase gene with NIDDM in Caucasian pedigrees.

NIDDM has a strong genetic component, as evidenced by the high level of concordance between identical twins. The nature of the genetic predisposition has remained largely unknown. Recently, the glucokinase gene locus on chromosome 7p has been shown to be linked to a subtype of NIDDM known as MODY in French and British pedigrees, and glucokinase mutations have been identified. To study the relationship between the glucokinase gene and NIDDM, we performed a linkage analysis in 12 Caucasian pedigrees ascertained through a proband with classical NIDDM. The LINKAGE program was used under four models, including autosomal dominant and recessive, with individuals with glucose intolerance counted as either affected or of unknown status. Linkage was significantly rejected with the dominant models (LOD scores -4.65, -4.25), and was unlikely with the recessive model when glucose intolerance was considered as affected (LOD score -1.38). These findings suggest that mutations in or near the glucokinase gene are unlikely to be the major cause of the inherited predisposition to NIDDM in Caucasian pedigrees, but do not exclude a role for this locus with a polygenic model, or a major role in some pedigrees.

Can life-styles of subjects with impaired glucose tolerance be changed? A feasibility study.

Thirty-one subjects with impaired glucose tolerance were randomly allocated to a group receiving advice to improve their diet and physical activity levels over 6 months (n = 23) or to a control group (n = 8). At 6 months, 18 of the 23 subjects receiving 'healthy living' advice were re-examined (five subjects had withdrawn). Fourteen of the 18 subjects showed an alteration in diet or an increase in exercise. The 18 subjects re-evaluated showed a reduction in systolic blood pressure (118 +/- 15 vs 124 +/- 15 mmHg, p less than 0.05) and decrease in total plasma cholesterol (4.5 +/- 1 vs 5.2 +/- 1 mmol l-1, p less than 0.01) and LDL-cholesterol levels (2.8 +/- 0.9 vs 3.2 +/- 0.9 mmol l-1, p less than 0.05). Plasma glucose levels were unchanged. One subject withdrew from the control group. At 6 months, the seven control subjects examined showed no significant change in metabolic parameters, with little measurable change in diet or exercise. At 2 years, 17 of the 23 'healthy living' subjects were reassessed. Nine of the subjects had continued to exercise or maintained a decreased weight compared to baseline. Fasting plasma glucose levels had increased (6.0 +/- 1.2 vs 5.5 +/- 0.6 mmol l-1, p less than 0.05), with the only continued improvement being a reduced LDL level (2.8 +/- 0.7 vs 3.1 +/- 0.9 mmol l-1, p less than 0.05). At 2 years, a similar proportion of the control group were taking regular exercise compared with the 'healthy living' group.(ABSTRACT TRUNCATED AT 250 WORDS)