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Background: An obesity epidemic has been documented among adult Latinos/as in Latin America and the United States (US); however, little is known about obesity among Latinos/as with HIV (PWH). Moreover, Latinos/as PWH in the US may have different weight trajectories than those in Latin America due to the cultural and environmental contexts. We assessed weight and body mass index (BMI) trajectories among PWH initiating antiretroviral therapy (ART) across 5 countries in Latin America and the Caribbean and the US. Methods: ART-naÿve PWH ≥18 years old, enrolled in Brazil, Honduras, Mexico, Peru, and Haiti (sites within CCA-SAnet) and the US (NA-ACCORD) starting ART between 2000 and 2017, with at least one weight measured after ART initiation were included. Participants were classified according to site/ethnicity as: Latinos/as in US, non-Latinos/as in US, Haitians, and Latinos/as in Latin America. Generalized least squares models were used to assess trends in weight and BMI. Models estimating probabilities of becoming overweight/obese (BMI ≥25 kg/m2) and of becoming obese (BMI ≥30 kg/m2) post ART initiation for males and females were fit using generalized estimating equations with a logit link and an independence working correlation structure. Findings: Among 59,207 PWH, 9% were Latinos/as from Latin America, 9% Latinos/as from the US, 68% non-Latinos/as from the US and 14% were Haitian. At ART initiation, 29% were overweight and 14% were obese. Post-ART weight and BMI increases were steeper for Latinos/as in Latin America compared with other sites/ethnicities; however, BMI at 3-years post ART remained lower compared to Latinos/as and non-Latinos/as in the US. Among females, at 3-years post ART initiation the greatest adjusted probability of obesity was found among non-Latinas in the US (15·2%) and lowest among Latinas in Latin America (8.6%). Among males, while starting with a lower BMI, Latinos in Latin America had the greatest adjusted probability of becoming overweight or obese 3-years post-ART initiation. Interpretation: In the Americas, PWH gain substantial weight after ART initiation. Despite environmental and cultural differences, PWH in Latin America, Haiti and Latinos and non-Latinos in the US share similar BMI trajectories on ART and high probabilities of becoming overweight and obese over time. Multicohort studies are needed to better understand the burden of other metabolic syndrome components in PWH across different countries.

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Epidemiological studies on schizophrenia have showed different age at onset between gender, in which male schizophrenics present symptoms earlier than females. However this gender effect is not observed within familial schizophrenia. The present study investigates the age at onset in 31 RDC-schizophrenics from 13 Brazilian families. No differences in age at onset were found between gender, confirming previous studies in other populations. This result may indicate genetic influences on age at onset in a subgroup of patients affected by schizophrenia and can be explored by molecular genetic studies.

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In order to compare imipenem-sensitive and -resistant Acinetobacter baumannii strains isolated from three patients, ribotyping, plasmid, beta-lactamase detection and outer-membrane analysis were performed. Ribotyping and the use of a beta-lactam during the period when the strains were isolated suggested that they had a common origin and that resistance occurred in vivo. Outer membrane analysis showed no difference between susceptible and resistant strains with the exception of an A2 imipenem-resistant strain that lost a protein band of 31-36 kDa. Beta-lactamases were detected using isoelectric focusing in all strains (pI of 7.4). In addition, two beta-lactamases (pI of 5.9 and 6.7) were found in imipenem-resistant isolates. The double-disc technique demonstrated the presence of a beta-lactamase capable of imipenem inactivation in resistant strains. Plasmid analysis showed that all susceptible strains had the same pattern, one resistant strain did not have any plasmid, one had the same plasmid pattern of its susceptible pair and only one had a different pattern when compared with its susceptible pair.

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OBJECTIVE: The relationship between GH, body composition and leptin in children remains ill-defined. We have therefore examined the impact of severe GH deficiency (GHD) due to a mutation in the GHRH receptor on serum leptin concentrations and body composition in childhood. PATIENTS: 12 affected children and young people (GHD) (4 M:8F, age 5.4-20.1 years, 8 Tanner stage (TS) 1-2, 4 TS 3-5) and 40 healthy controls (C) from the same region (13 M:27F, age 5.3-18.4 years, 20 TS 1-2, 20 TS 3-5). METHODS: Percent body fat was determined by infra-red interactance, from which the amounts of fat mass (FM, kg) and fat free mass (FFM, kg) were derived. Serum leptin concentrations were measured in a single fasted, morning serum sample and results expressed as a concentration and as leptin per unit fat mass (L/FM, ng/ml/kg). To control for differences in sex and pubertal maturation, leptin standard deviation scores (leptin SDS) were calculated using normative data from UK children. RESULTS: FFM was significantly lower in GHD children than in controls (TS 1-2 P < 0.05, TS 3-5 P < 0.001). FM did not differ significantly between the two groups. Serum leptin concentrations, leptin per unit fat mass and leptin SDS were significantly elevated in GHD children both peripubertal and pubertal compared with controls. Using all subjects, stepwise multiple linear regression with FM, FFM, age, puberty and sex as explanatory variables and leptin concentration as the dependent variable indicated that 59% of the variability in leptin could be accounted for by FM (+, 45%), FFM (-, 9%) and sex (+, 5%) (P < 0.001). However on inclusion of GH deficiency (coded GHD = 1, control = 2) as an explanatory variable 73% of the variability in leptin was explained by FM (+, 45%), GHD (-, 22%) and sex (+, 6%) (P < 0.001). CONCLUSIONS: These data indicate that severe GH deficiency in children is associated with elevated leptin concentrations, irrespective of sex or pubertal stage. This increase is not associated with differences in fat mass but is related to reduced fat free mass in GH deficiency. Furthermore in this population there may be an additional effect of GH deficiency on leptin, independent of the influences of sex and body composition.

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Measurement of the insulin-like growth factors (IGFs) and their binding proteins has become commonplace in the indirect assessment of the integrity of the GH axis. However, the relative effect of GH deficiency (GHD) on each component of the IGF axis and the merit of any one parameter as a diagnostic test have not been defined in a homogeneous population across all ages. We therefore measured IGF-I, IGF-II, IGF-binding protein-1 (IGFBP-1), IGFBP-2, IGFBP-3, and acid labile subunit (ALS) in 27 GHD subjects (aged 5-82 yr) from an extended kindred in Northeast Brazil with an identical GHRH receptor mutation and in 55 indigenous controls (aged 5-80 yr). The effect of GHD on the theoretical distribution of IGFs between the IGFBPs and the ternary complex was also examined. All components of the IGF axis, measured and theoretical, showed complete separation between GHD and control subjects, except IGFBP-1 and IGFBP-2 concentrations, which did not differ. The most profound effects of GHD were on total IGF-I, IGF-I in the ternary complex, and ALS. The proportion of IGF-I associated with IGFBP-3 remained constant throughout life, but was significantly lower in GHD due to an increase in IGF-I/IGFBP-2 complexes. IGF-I in the ternary complex was determined principally by concentrations of ALS in GHD and IGFBP-3 in controls, implying that ALS has greater GH dependency. In the controls, IGF-II was associated primarily with IGFBP-3 and to a lesser extent with IGFBP-2, whereas in GHD the reverse was found. There was also a dramatic decline in the proportion of free ALS in GHD adults that was not evident in controls. As diagnostic tests, IGF-I in the ternary complex and total IGF-I provided the greatest separation between GHD and controls in childhood. Similarly, in older adults the best separation was achieved with IGF-I in the ternary complex, with free ALS being optimal in younger adults. Severe GHD not only reduces the amounts of IGFs, IGFBP-3, and ALS, but also modifies the distribution of the IGFs bound to each IGFBP. Diagnostic tests used in the investigation of GHD should be tailored to the age of the individual. In particular, measurement of IGF-I in the ternary complex may prove useful in the diagnosis of GHD in children and older adults, whereas free ALS may be more relevant to younger adults.

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Since 1969, several classical linkage studies suggested an X-chromosome locus for bipolar affective disorder. However, methods using highly polymorphic DNA markers have provided conflicting evidence for linkage, and an X-chromosomal locus for bipolar disorder remains controversial. More recently, Pekkarinen et al. (1995) found a maximum LOD score of 3.54 at the marker DXS994 in a large bipolar Finnish kindred. In the present study, we attempted to replicate this finding using 43 families multiply affected by bipolar affective disorder. These families were selected for the absence of male-to-male transmission of the disease, and were genotyped for two microsatellte markers, DXS1227 and DXS1062 (which is about 2 cM telomeric to DXS994). Linkage to this region was excluded either using a two-point lod score method with two plausible genetic models, or by a model-free lod score analysis which does not require specification of a particular mode of transmission. We conclude that there is no evidence of a common major gene for bipolar affective disorder at Xq25-q27 in our set of families.

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Straub et al. (1994: Nature Genet. 8. 291-296) have suggested that a susceptibility gene for bipolar affective disorder is located at chromosome 21q22.3, on the basis of linkage analysis in one large family. This result has been supported by Gurling et al. (1995: Nature Genet. 10, 8-9) who also found some evidence for linkage to this region under locus heterogeneity. In order to investigate the validity of these results and to estimate how broadly applicable they are, we performed a linkage study between bipolar affective disorder and two DNA markers (D21S171 and PFKL) from 21q22.3 using 60 bipolar pedigrees from three European centres and Brazil. The most positive result obtained was a maximised admixture lod score of 1.2 for the marker PFKI, under the assumption of locus heterogeneity, dominant transmission and a diagnostic classification which included recurrent unipolar depression. However, since lod scores obtained for both markers were substantially negative overall, we conclude that there is no common major gene for bipolar affective disorder at 21q22.3. It remains possible that a gene of major effect in this region operates in a minority of families.

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A family is reported in which four of five adult patients with Becker muscular dystrophy (BMD) also have schizophrenia or related spectrum disorders. Although the estimated lod scores are not sufficient to conclude the existence of linkage between BMD and schizophrenia, it is suggested that there may be an association between these two disorders. Two alternative hypotheses are proposed to explain such an association: (1) the existence of a susceptibility locus for schizophrenia and spectrum disorders on the short arm of the X chromosome at Xp21; (2) that these psychiatric disorders may result from an abnormality in the expression of the dystrophin gene in the brain.

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