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PURPOSE: A controlled study evaluated the effect of condensed tannins (CT) from Gymnopodium floribundum leaf meal (GF), infection with Haemonchus contortus (I) and their interaction, on feed intake, diet digestibility and retention of N (NR) and energy (ER) in hair sheep lambs. METHODS: Thirty-six, worm-free hair sheep lambs (14.9 ± 1.56 kg body weight) were housed in metabolic cages. Eighteen animals were infected with 6000 H. contortus L3, while other 18 lambs were kept non-infected. On day 28th post-infection (PI), infected lambs were assigned to three diet groups: a diet without GF (I-NONGF), a diet with GF (I + GF) and a diet with GF + polyethylene glycol (PEG) (I + GF + PEG). Non-infected (NI) lambs were assigned to similar diet groups: NI-NONGF, NI + GF and NI + GF + PEG. The packed cell volume (% PCV), ante-mortem faecal egg counts and post-mortem worm burdens were also evaluated. RESULTS: Infection did not affect digestibility, NR and ER. Meanwhile, CT intake from the GF diet reduced the digestibility of dry matter, organic matter and crude protein, as well as NR, compared to lambs consuming the NONGF and GF + PEG diets (P < 0.05). Although, the digestible energy was similar between lambs consuming NONGF and GF + PEG diets, the ER was higher for lambs consuming the control NONGF diet. Diets did not affect the PCV, or the ante-mortem and post-mortem parasitological variables. CONCLUSION: The costs on N and energy metabolism were mainly associated with the CT content of the GF diet, but other features of the diet such as the high lignin content, seemed to affect animals consuming GF meal. Meanwhile, the H. contortus infection had a non-significant impact.

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The objective of this study was to evaluate the reduction in nematode faecal egg count (FEC) in Pelibuey lambs segregated as resistant (RES), susceptible (SUS) and intermediate (INT) to gastrointestinal nematodes. Twenty-nine weaned Pelibuey lambs, aged five months old, free of nematode infection, were used. Nine lambs were RES, six were SUS and 14 were INT lambs. The study consisted of two phases: in Phase 1 the lambs were infected experimentally with Haemonchus contortus. In Phase 2, the lambs were naturally infected by grazing. Faecal and blood samples were taken every week. The packed cell volume and total protein were quantified. The FEC value (FECmax) per lamb was recorded together with a natural reduction in FEC in the two phases. The data were analysed with a model of measures repeated over time. During Phase 1, the RES lambs showed the lowest FEC (1061 ± 1053) compared to the other groups (INT: 2385 ± 1794 eggs per gram of faeces (EPG); and SUS: 3958 ± 3037 EPG). However, in Phase 2 no significant differences (p > 0.05) were observed between the groups of lambs (RES: 275 ± 498 EPG; SUS: 504 ± 1036 EPG; and INT: 603 ± 1061 EPG). At the end of Phase 1, the FEC of RES lambs was naturally reduced by 75.5% in respect to FECmax (p < 0.05), and at the end of Phase 2 the reduction in FEC was 90% in respect to FECmax (p > 0.05); the same behaviour was observed in RES and SUS lambs. It is concluded that the artificial infection in the lambs induced a more rapid immune response in RES than SUS lambs, and all lambs developed high acquired resistance by continuous infection.

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The sterilization processes of nanoparticles (NP) by autoclaving and filtration are two of the most utilized methods in the pharmaceutical industry but are not always a viable option. For this reason, the search for alternative options such as UV and gamma radiation is of interest. In this work, we evaluated both types of sterilization on two types of NP in solid state widely employed in the literature for biomedical applications, poly-(ε-caprolactone) and poly(D, L-lactide-co-glycolide) acid NP stabilized with polyvinyl alcohol. Physicochemical properties and cell viability were studied pre- and post-sterilization. The efficiency of irradiation sterilization was performed by a test of sterility using 1 × 108 CFU/mL of Escherichia coli, Staphylococcus aureus, and Candida albicans. Microbiological monitoring revealed that both methods were sufficient for sterilization. After the UV irradiation sterilization (100 µJ/cm2), no substantial changes were observed in the physicochemical properties of the NP or in the interaction or morphology of human glial cells, though 5 and 10 kGy of gamma irradiation showed slight changes of NP size as well as a decrease in cell viability (from 100 µg/mL of NP). At 5 kGy of radiation doses, the presence of trehalose as cryoprotectant reduces the cell damage with high concentrations of NP, but this did not occur at 10 kGy. Therefore, these methods could be highly effective and low-processing-time options for sterilizing NP for medical purposes. However, we suggest validating each NP system because these generally are of different polymer-composition systems.

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INTRODUCTION: Epidemiological studies have described a high comorbidity of substance use disorders with another psychiatric disorder, which has been called dual pathology. However, the aetiological mechanisms underlying this association are still not fully understood. AIM: To carry out a preliminary study of the effect of polymorphism rs1051730 of the gene group CHRNA5-CHRNA3-CHRNB4 through a case-control study. SUBJECTS AND METHODS: A total of 225 subjects were selected and divided into three groups: those diagnosed with bipolar disorder, those with nicotine dependence, and subjects without nicotine dependence or any other psychiatric disorder. Genotyping was performed by real-time polymerase chain reaction. Genetic association analysis was performed using chi-square tests and multivariate logistic regressions. RESULTS: On comparing allelic frequencies with the control group, we found that polymorphism rs1051730 was associated with nicotine dependence (p = 0.03), but not with bipolar disorder (p = 0.94). CONCLUSION: Variant rs1051730 was associated with nicotine dependence in the Mexican population and showed the same effect in dual pathology. However, further studies are recommended to obtain conclusive results.

TITLE: Analisis del polimorfismo rs1051730 de CHRNA3 en pacientes con patologia dual en poblacion mexicana.Introduccion. Estudios epidemiologicos han descrito una alta comorbilidad de los trastornos de uso de sustancias con otro trastorno psiquiatrico, al cual se le ha llamado patologia dual. Sin embargo, los mecanismos etiologicos de esta asociacion continuan siendo dificiles de entender. Objetivo. Realizar un estudio preliminar del efecto del polimorfismo rs1051730 del grupo de genes CHRNA5-CHRNA3-CHRNB4 a traves de un estudio de casos y controles. Sujetos y metodos. Se selecciono a un total de 225 sujetos, divididos en tres grupos: con diagnostico de trastorno bipolar, con dependencia a la nicotina y sujetos sin dependencia a la nicotina o cualquier otro trastorno psiquiatrico. La genotipificacion se realizo mediante reaccion en cadena de la polimerasa en tiempo real. El analisis de asociacion genetica se realizo mediante pruebas de chi cuadrado y regresiones logisticas multivariables. Resultados. Al comparar las frecuencias alelicas con el grupo control, encontramos que el polimorfismo rs1051730 se asocio con el grupo de dependencia a la nicotina (p = 0,03), pero no con el de trastorno bipolar (p = 0,94). Conclusion. La variante rs1051730 se asocio con dependencia a la nicotina en la poblacion mexicana y mostro el mismo efecto en la patologia dual. Sin embargo, se recomiendan estudios adicionales para tener resultados concluyentes.

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Myotonic dystrophy type 1 is caused by expansion of a CTG trinucleotide repeat situated in the DMPK gene. Worldwide genetic studies suggest a single or limited number of mutational events cause the disease. However, distribution of CTG alleles and disease incidence varies among ethnicities. Due to the great ethnic diversity of the Mexican population, the present study was aimed at analyzing the impact of different lineages in shaping the CTG-repeat allelic distribution in the contemporary Mexican-Mestizo population as well as to shed light on the DM1 ancestral origin. Distribution of CTG-repeat alleles was similar among Mestizo and Amerindian subpopulations with (CTG)11-13 being the most frequent alleles in both groups, which implies that Mexican-Mestizo allelic distribution has been modeled by Amerindian ancestry. We diagnosed a relatively high number of cases, consistent with the high frequency of large-normal alleles found in Mexican subpopulations. Haplotype analysis using various polymorphic-markers in proximity to DMPK gene indicates that a single founder mutation originates myotonic dystrophy type 1 in Mexico; however, Y-STR haplogroups data and the presence of pre-mutated and large normal alleles in Amerindians support the hypothesis that both European and Amerindian ancestral chromosomes might have introduced the disease to the Mexican population, which was further disseminated through mestizaje.

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We studied the interethnic variation of the MMP-9 microsatellite in the Mestizo and Amerindian populations using blood samples collected from 435 healthy unrelated individuals from the Central Valley of Mexico. DNA samples were genotyped using the -90 (CA)12-27 repeat near the MMP transcriptional start site using capillary electrophoresis. Our data were compared with those from African, Asian, and European populations (N = 729). Both Mestizo and Amerindian populations were in Hardy-Weinberg equilibrium (P ≥ 0.05). However, strong genetic heterogeneity was found within the Mestizo population (94%, P ≤ 0.0001), which exhibited the highest frequency of Amerindian, African, and European alleles. Likewise, Amerindians showed 6.7% variation among populations (P ≤ 0.0001), suggesting a genetic substructure potentially associated with linguistic affiliations. These findings were corroborated with principal component and population differentiation analyses, which showed relative proximity among the Mestizos and their historical parental populations: Asian (FST ≥ 0.05), European (FST ≥ 0.09), and African (FST ≥ 0.02). Nevertheless, important differences were found between Mestizo and Nahuas (P ≤ 0.0001), and between Mestizo and Me'Phaas (P ≤ 0.0001). These findings highlight the importance of determining local-specific patterns to establish the population variability of MMP-9 and other polymorphic markers. Validation of candidate markers is critical to identifying risk factors; however, this depends on knowledge of population genetic variation, which increases the possibility of finding true causative variants. We also show that dissimilar ethnic backgrounds might lead to spurious associations. Our study provides useful considerations for greater accuracy and robustness in future genetic association studies.

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Spinocerebellar ataxia type 7 (SCA7) is an inherited neurodegenerative disorder characterized by progressive cerebellar ataxia associated with macular degeneration. We recently described one of the largest series of patients with SCA7 that originated from a founder effect in a Mexican population, which allowed us to perform herein the first comprehensive clinical, neurophysiological, and genetic characterization of Mexican patients with SCA7. In this study, 50 patients, categorized into adult or early phenotype, were clinically assessed using standard neurological exams and genotyped using fluorescent PCR and capillary electrophoresis. Patients with SCA7 exhibited the classical phenotype of the disease characterized by cerebellar ataxia and visual loss; however, we reported, for the first time, frontal-executive disorders and altered sensory-motor peripheral neuropathy in these patients. Semiquantitative analysis of ataxia-associated symptoms was performed using Scale for the Assessment and Rating of Ataxia (SARA) and the Brief Ataxia Rating Scale (BARS) scores, while extracerebellar features were measured employing the Inventory of Non-ataxia Symptoms (INAS) scale. Ataxia rating scales confirmed the critical role size of cytosine-adenine-guanine (CAG) repeat size on age at onset and disease severity, while analysis of CAG repeat instability showed that paternal rather than maternal transmission led to greater instability.

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Myotonic dystrophy type 1 (DM1) is a multisystem genetic disorder caused by a triplet nucleotide repeat expansion in the 3' untranslated region of the Dystrophia Myotonica-Protein Kinase (DMPK) gene. DMPK gene transcripts containing CUG expanded repeats accumulate in nuclear foci and ultimately cause altered splicing/gene expression of numerous secondary genes. The study of primary cell cultures derived from patients with DM1 has allowed the identification and further characterization of molecular mechanisms underlying the pathology in the natural context of the disease. In this study we show for the first time impaired nuclear structure in fibroblasts of DM1 patients. DM1-derived fibroblasts exhibited altered localization of the nuclear envelope (NE) proteins emerin and lamins A/C and B1 with concomitant increased size and altered shape of nuclei. Abnormal NE organization is more common in DM1 fibroblasts containing abundant nuclear foci, implying expression of the expanded RNA as determinant of nuclear defects. That transient expression of the DMPK 3' UTR containing 960 CTG but not with the 3' UTR lacking CTG repeats is sufficient to generate NE disruption in normal fibroblasts confirms the direct impact of mutant RNA on NE architecture. We also evidence nucleoli distortion in DM1 fibroblasts by immunostaining of the nucleolar protein fibrillarin, implying a broader effect of the mutant RNA on nuclear structure. In summary, these findings reveal that NE disruption, a hallmark of laminopathy disorders, is a novel characteristic of DM1.

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Spinocerebellar ataxias (SCA) are a heterogeneous group of neurodegenerative disorders. CAG (cytosine-adenine-guanine) trinucleotide repeat expansions in the causative genes have been identified as the cause of different SCA. In this study, we simultaneously genotyped SCA1, SCA2, SCA3, SCA6, and SCA7 applying a fluorescent multiplex polymerase chain reaction assay. We analyzed 10 families with SCA (64 patients) from five different communities of Veracruz, a Mexican southeastern state, and identified 55 patients for SCA7 and 9 for SCA2, but none for SCA1, SCA3, or SCA6. To our knowledge, this sample represents one of the largest series of SCA7 cases reported worldwide. Genotyping of 300 healthy individuals from Mexican population and compiled data from different ethnicities showed discordant results concerning the hypothesis that SCA disease alleles arise by expansion of large normal alleles.

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BACKGROUND: The competence model states that what is most important is to have the elements to solve problems since abstract training does not provide enough tools to solve them. Therefore, it uses key and auxiliary competences that are linked to values such as attitudes. This study was performed to explore these competences. MATERIAL AND METHODS: This is a cross sectional, observational and descriptive trial. An anonymous survey with profile data of Orthopedics and Trauma residents was given, it contained 14 questions for residents of different academic levels. RESULTS: 24 residents participated out of the 35 registered in the course. 100% agreed to answer the survey, 54% was in the second year, 29% in the first year and 17% in the fourth year. 75% expressed auxiliary competences, 13% did not respond, 8% developed key competences and 4% don't know. CONCLUSIONS: Three main factors that are a negative influence to improve the knowledge of orthopedics were expressed. The most relevant is that residents describe a bad attitude from attending physicians, lack of willingness to teach and, poor interpersonal relationships. Awareness should be raised among orthopedics specialists so they understand that having the knowledge and skills is not enough to approach health issues in a comprehensive manner for each patient and the development of better competences should be fostered, especially key competences.

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We evaluated the effect of feeding dietary tannins from Lysiloma latisiliquum fresh forage on the saliva tannin-binding capacity of hair sheep lambs without previous exposure to tannin-rich (TR) fodder. Twenty-four hair sheep lambs (13.6±3.04 kg LW) were fed a tannin-free diet at the beginning of the experimental period (from day 10 to 13). On day 14, lambs were distributed into three groups (n=8): control group (CG), fed with the tannin-free diet (from D10 to D112); tannin short-term group (TST), fed the basal diet and 650 g of L. latisiliquum forage (from D14 to D55); tannin long-term group (TLT), fed the basal diet and 650 g of L. latisiliquum forage (from D14 to D112). Saliva samples were collected from the mouth of each lamb in the morning before feeding time on D10 and D14 (baseline period), on D49 and D56 (period 1) and on D97 and D112 (period 2). The tannin binding response of salivary protein (∆% turbidity) was determined with the haze development test (HDT) using either tannic acid or L. latisiliquum forage acetone extract. A turbidity protein index (TPI) was calculated as (∆% turbidity/[salivary protein (mg)]). Differences in HDT and TPI in the different groups were compared by repeated measures ANOVA using Proc Mixed. All groups had similar ∆% turbidity throughout the experiment (P>0.05). At baseline and period 1, the TPI of the different groups was similar (P>0.05). On period 2 the TLT group showed higher TPI compared with CG (P<0.05). Meanwhile, CG and TST showed similar salivary TPI. The saliva of hair sheep lambs consuming TR L. latisiliquum fresh fodder (TLT group) increased their TPI compared with control lambs not exposed to tannins.

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Spinocerebellar ataxia type 7 (SCA7) is a neurodegenerative disorder characterized by progressive cerebellar ataxia associated with macular degeneration that leads, in the majority of patients, to loss of autonomy and blindness. The cause of the disease has been identified as (CAG) n repeat expansion in the coding sequence of the ATXN7 gene on chromosome 3p21.1. SCA7 is one of the least common genetically verified autosomal dominant cerebellar ataxias found worldwide; however, we previously identified the Mexican population showing high prevalence of SCA7, suggesting the occurrence of a common founder effect. In this study, haplotype analysis using four SCA7 gene-linked markers revealed that all 72 SCA7 carriers studied share a common haplotype, A-254-82-98, for the intragenic marker 3145G/A and centromeric markers D3S1287, D3S1228, and D3S3635, respectively. This multiloci combination is uncommon in healthy relatives and Mexican general population, suggesting that a single ancestral mutation is responsible for all SCA7 cases in this population. Furthermore, genotyping using 17 short tandem repeat markers from the non-recombining region of the Y chromosome and further phylogenetic relationship analysis revealed that Mexican patients possess the Western European ancestry, which might trace the SCA7 ancestral mutation to that world region.

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Primary osteoarthritis (OA) is a multifactorial disorder with several genetics factors involved. Calcitonin (CT) has been suggested to possess chondroprotective effects and could play an important role in the pathogenesis of OA. The aim of this study was to investigate whether genetic variations in or adjacent to the CT gene may be associated with primary OA of the knee in Mexican mestizo population. We conducted a case-control study to investigate the association between six single nucleotide polymorphisms at the CT locus and OA of the knee in 107 cases and 106 controls. Cases were patients >40 years of age, with a body mass index (BMI) ≤ 27 and a radiologic score for OA of the knee ≥ 2. Controls were subjects >40 years of age with a radiologic score <2. Non-conditional logistic regression was developed to evaluate risk magnitude. The G allele and GT genotype frequencies of the G-706T polymorphism and the C allele and CC genotype of the C-778T polymorphism were significantly higher in patients with OA than in control subjects. The GG genotype of the G-706T was associated with lower risk of the development of OA of the knee. According to the results, the G-706T and the C-778T polymorphisms were related to the Cdx1 and Mzf1 transcription factor binding sites, respectively. Therefore, these could be related to regulation sequences in the CT gene promoter. In conclusion, G-706T and C-778T polymorphisms in the CT gene are significantly associated with the development of primary OA of the knee.

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Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant genetic disease characterized by cerebellar dysfunction associated with slow saccades, early hyporeflexia, severe tremor of postural or action type, peripheral neuropathy, cognitive disorders, and other multisystemic features. SCA2, one of the most common ataxias worldwide, is caused by the expansion of a CAG triplet repeat located in the N-terminal coding region of the ATXN2 gene, which results in the incorporation of a segment of polyglutamines in the mutant protein, being longer expansions associated with earlier onset and more sever disease in subsequent generations. In this review, we offer a detailed description of the clinical manifestations of SCA2 and compile the experimental evidence showing the participation of ataxin-2 in crucial cellular processes, including messenger RNA maturation and translation, and endocytosis. In addition, we discuss in the light of present data the potential molecular mechanisms underlying SCA2 pathogenesis. The mutant protein exhibits a toxic gain of function that is mainly attributed to the generation of neuronal inclusions of phosphorylated and/or proteolytic cleaved mutant ataxin-2, which might alter normal ataxin-2 function, leading to cell dysfunction and death of target cells. In the final part of this review, we discuss the perspectives of development of therapeutic strategies for SCA2. Based on previous experience with other polyglutamine disorders and considering the molecular basis of SCA2 pathogenesis, a nuclei-acid-based strategy focused on the specific silencing of the dominant disease allele that preserves the expression of the wild-type allele is highly desirable and might prevent toxic neurodegenerative sequelae.

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OBJECTIVES: To determine among adult patients with type-2 diabetes mellitus the proportion diagnosed with diabetic polyneuropathy (DPN) by clinical evaluation and by the Hoffmann reflex (H-reflex). In addition, the predictive value of the H-reflex in the diagnosis of DPN was evaluated. METHODS: Studies were carried out on 150 adult patients referred for neuropathy screening. Diagnostic criteria for DPN were at least two abnormalities in clinical neurophysiological examinations and electrophysiological testing (H-reflex and nerve conduction velocity). Logistic regression analysis was performed to identify unique contributions of study characteristics to positive versus negative outcomes. RESULTS: H-reflex was absent in 39.3% (59/150) and latency was prolonged in 43.3% (65/150) of patients. Ulnar nerve motor branch nerve conduction showed prolonged latency in 9.3% (14/150) of patients. Logistic regression analysis indicated that the H-reflex was significantly associated with positive outcomes. CONCLUSION: The H-reflex could have a predictive value in DPN, providing more quantitative information regarding diagnosis than conventional nerve conduction studies.

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Myotonic dystrophy type 1 (DM1), the most common form of adult muscular dystrophy, is caused by anormal expansion of CTG trinucleotide repeats located in the 3'-untranslated region of the DMPK gene. The clinical features of DM1 are multisystemic and highly variable, and the unstable nature of CTG expansion causes wide genotypic and phenotypic presentations. In this study, we described to our knowledge for the first time the molecular diagnosis of myotonic dystrophy type 1 patients in the Mexican population, applying a fluorescent PCR method in combination with capillary electrophoresis analysis of the amplified products. We identified expanded alleles in 45 out of 50 patients (90%) with clinical features of myotonic disease. Furthermore, genotyping of 400 healthy subjects revealed the presence of 25 different alleles, ranging in size from 5 to 34 repeats. The most frequent allele was 13 CTG repeats (38.87%) and the frequency for alleles over 18 CTG repeats was 6.7%. Molecular test is essential for DM1 diagnosis and distribution of the CTG repeat alleles present in the Mexican population are significantly different from those of other populations.

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Osteoarthritis (OA) is the most common form of destructive joint disease that is characterized by the degeneration of the articular cartilage, synovial membrane, joint capsule, and subchondral bone. The knee is a joint commonly affected for OA. Calcitonin (CT) has been suggested to have chondroprotective effects; therefore, could play a role in the pathogenesis of OA of the knee. Genetic variations in or adjacent to the CT gene may be associated with primary OA development. We conducted a case-control association study in which we examined the correlation between a dinucleotide (cytosine-adenine, CA) repeat polymorphism at the CT locus and OA of the knee in 88 patients with OA and in 111 control subjects from the Mexican mestizo population. Allele A and genotype AG frequencies were significantly higher in patients with OA than in control subjects (56.3 vs. 43.2%; p<0.001 and 40.9 vs. 26.1%; p=0.027, respectively), and were associated with the presence of OA of the knee (odds ratio [OR], 2.62; 95% confidence interval [95% CI], 1.30-5.27, and OR, 1.93; 95% CI, 1.04-3.58, respectively) using a logistic regression model adjusted for gender, age and Body mass index (BMI). The GG genotype was associated with a lower risk of OA development of the knee; thus, it may constitute a protective factor against this disease (OR, 0.40; 95% CI, 0.16-0.98). In summary, we conclude that the dinucleotide CA polymorphism in the CT gene may become a useful marker for genetic studies of OA of the knee in Mexican population.

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The estrogen receptor gene (ER alpha) has been implicated in the development of osteoporosis. In this study, the association of two ER alpha gene polymorphic markers (a TA dinucleotide repeat and a single nucleotide polymorphism, G2014A) with osteoporosis was tested in 70 osteoporotic women, 70 non-osteoporotic women and 500 subjects from the Mexican population. According to the genetic analysis of the Mexican population using eight unlinked polymorphic markers, we found that our population is structured into three subpopulations; therefore, the allele-phenotype relationship was analyzed with a statistical method that considered population stratification. We found that the G2014A polymorphism is associated with the presence of osteoporosis while the TA dinucleotide repeat is not. The G allele and the GG genotype frequencies of the G2014A marker were significantly higher in osteoporotic than in non-osteoporotic women. Likewise, subjects bearing the G allele in heterozygous or homozygous displayed lower values for lumbar bone mineral density and T score than those who did not present any G allele. The effect of confounders for osteoporosis on the association of G allele-osteoporosis was ruled out. In summary, we conclude that the G2014 polymorphism may become a useful marker for genetic studies of osteoporosis in the Mexican population.

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Calcitonin (CT) plays a role in the pathogenesis of osteoporosis and genetic variations in or adjacent to the CT gene may be associated with loss of bone mineral density (BMD). The correlation between a dinucleotide (cytosine-adenine) repeat polymorphism at the CT locus and BMD was examined in 70 osteoporotic women, 70 non-osteoporotic women and 500 subjects from the Mexican population. The allele A and genotype AA frequencies were significantly higher in osteoporotic women than in non-osteoporotic women (60% vs 32%; p < 0.0001 and 41% vs 14%; p = 0.0007, respectively). Genotype AA was associated with the presence of osteoporosis [odds ratio 2.58; 95% confidence interval (CI); 1.62-4.12]. Likewise, the loss of lumbar BMD and T scores were related to the presence of allele A: subjects with a single A allele displayed lower values for lumbar BMD and T score (84.02% and -1.51, respectively) than those who do not present any A allele (89.61% and -0.88, respectively). Individuals with two alleles A showed the lowest lumbar BMD and T-score values (73.77% and -2.51, respectively). Analysis of potential confounder demonstrated that aging has a significant effect on osteoporosis development (odds ratio 1.1; 95% CI; 1.1052-1.152).

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The objective of this study was to evaluate the body weights up to 18 months of age of 12 breed groups of Zebu (Z), Brown Swiss (BS) and Charolais heifers (CH), and their crosses under tropical conditions. A total of 1434 data on weaning weights adjusted to 240 days (WW8), average daily gain to 240 days (ADG8) and 1025 body weights adjusted to 550 days (BW18) and average postweaning daily gain (ADG18) of heifers born from 1981 to 1995 were used. Cows and calves remained together from birth to weaning and grazed on Guinea grass (Panicum maximum). Years of birth were grouped in three periods, because of the small numbers of observations per year (1981-85, 1986-90 and 1991-95). Similarly, months of birth were grouped in three seasons: dry (February to May), rainy (June to September) and windy and rainy (October to January). Ages of dams were classified in six groups (or=8 years). Breed groups were animals with 12.5%, 25.0%, 50.0%, 62.5%, 75.0% and 100% BS genes and 25.0%, 50.0%, 75.0% and 100% CH genes and also Z and undefined crossbred animals. Data were analysed using a fixed model that included effects of period, and season of birth, age of dam and breed group of heifer. Analyses of variance showed significant (p < 0.05) effects of period, season and breed group for all traits. However, parity was significant (p < 0.05) only for WW8 and ADG8. Interactions among main factors were not significant (p > 0.05). Z heifers gained the least weight to weaning but were similar to BS at 18 months of age. CH were heavier at 18 months of age than BS heifers, but not at weaning. Body weights at 18 months of age of 1/8 and 1/4 BS crossbred heifers were similar (p > 0.05) and lower than F1 (BS x Z) (p < 0.05); however, the later and higher grades of BS had the highest body weights at 18 months of age and were similar to CH and 1/4 CH x 3/4 Z heifers. Undefined crossbred heifers had better performance than the Z breed group. Environmental factors were important sources of variation for pre- and postweaning traits. Under the conditions of this study, crossbred heifers generally performed better than Z heifers up to 18 months of age.

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