Age structure and multi-model growth estimation of longnose stingray Hypanus guttatus (Dasyatidae: Myliobatoidei) from north-east Brazil

We collected 729 Hypanus guttatus from the northern coast of the state of Rio Grande do Norte (RN), of which 196 were used to estimate age and growth. Ninety-five were male (12.7 to 57.0 cm disc width; W_D) and 101 were female (13.0 to 88.5 cm W_D); females were significantly larger than males. Cross sections of vertebrae showed band-pairs ranging from 0 to > 14 in females and from 0 to 9 in males. New-borns presented an opaque edge at birth in vertebrae without a birthmark. The average percentage of error (APE; %E) for the entire sample provided evidence that ages were repeatable. The mean monthly marginal increment (I_M) indicates annual band-pair formation from August to November. The annual cycle model for one band-pair deposition provided the best fit to data based on the AIC, with peaks between August and October, similar to that found in the I_M analysis, suggesting an annual formation pattern. A multi-model approach that included four models based on the observed mean W_D at age indicated a modified von Bertalanffy growth model as the best for describing the species growth: W₀ (W_D at birth) = 14.6 cm for both sexes; females W_∞ = 98.61 cm (95% CI = 87.34–114.61 cm); k = 0.112 year⁻¹ (CI = 0.086–0.148 year⁻¹); males W_∞ = 60.22 cm (CI = 55.66–65.35 cm); k = 0.219 year⁻¹ (CI = 0.185–0.276 year⁻¹). The age-at-maturity in males and females is 5 years and 7 years, respectively. The age composition shows that most (84%) specimens were aged 0 to 2 years. The information provided here is essential for analytical assessments of H. guttatus, which is subject to significant fishing pressure mainly on new-borns and juveniles.     

Defining dysbiosis and its influence on host immunity and disease

Mammalian immune system development depends on instruction from resident commensal microorganisms. Diseases associated with abnormal immune responses towards environmental and self antigens have been rapidly increasing over the last 50 years. These diseases include inflammatory bowel disease (IBD), multiple sclerosis (MS), type I diabetes (T1D), allergies and asthma. The observation that people with immune mediated diseases house a different microbial community when compared to healthy individuals suggests that pathogenesis arises from improper training of the immune system by the microbiota. However, with hundreds of different microorganisms on our bodies it is hard to know which of these contribute to health and more importantly how? Microbiologists studying pathogenic organisms have long adhered to Koch's postulates to directly relate a certain disease to a specific microbe, raising the question of whether this might be true of commensal–host relationships as well. Emerging evidence supports that rather than one or two dominant organisms inducing host health, the composition of the entire community of microbial residents influences a balanced immune response. Thus, perturbations to the structure of complex commensal communities (referred to as dysbiosis) can lead to deficient education of the host immune system and subsequent development of immune mediated diseases. Here we will overview the literature that describes the causes of dysbiosis and the mechanisms evolved by the host to prevent these changes to community structure. Building off these studies, we will categorize the different types of dysbiosis and define how collections of microorganisms can influence the host response. This research has broad implications for future therapies that go beyond the introduction of a single organism to induce health. We propose that identifying mechanisms to re‐establish a healthy complex microbiota after dysbiosis has occurred, a process we will refer to as rebiosis, will be fundamental to treating complex immune diseases.     

Regulation of nuclear DNA damage response by mitochondrial morphofunctional pathway

Cells are constantly challenged by genotoxic stresses that can lead to genome instability. The integrity of the nuclear genome is preserved by the DNA damage response (DDR) and repair. Additionally, these stresses can induce mitochondria to transiently hyperfuse; however, it remains unclear whether canonical DDR is linked to these mitochondrial morphological changes. Here, we report that the abolition of mitochondrial fusion causes a substantial defect in the ATM-mediated DDR signaling. This deficiency is overcome by the restoration of mitochondria fusion. In cells with fragmented mitochondria, genotoxic stress-induced activation of JNK and its translocation to DNA lesion are lost. Importantly, the mitochondrial fusion machinery of MFN1/MFN2 associates with Sab (SH3BP5) and JNK, and these interactions are indispensable for the Sab-mediated activation of JNK and the ATM-mediated DDR signaling. Accordingly, the formation of BRCA1 and 53BP1 foci, as well as homology and end-joining repair are impaired in cells with fragmented mitochondria. Together, these data show that mitochondrial fusion-dependent JNK signaling is essential for the DDR, providing vital insight into the integration of nuclear and cytoplasmic stress signals.     

Helicobacter pylori bab Paralog Distribution and Association with cagA,vacA, and homA/B Genotypes in American and South Korean Clinical Isolates

Helicobacter pylori genetic variation is a crucial component of colonization and persistence within the inhospitable niche of the gastric mucosa. As such, numerous H. pylori genes have been shown to vary in terms of presence and genomic location within this pathogen. Among the variable factors, the Bab family of outer membrane proteins (OMPs) has been shown to differ within subsets of strains. To better understand genetic variation among the bab genes and to determine whether this variation differed among isolates obtained from different geographic locations, we characterized the distribution of the Bab family members in 80 American H. pylori clinical isolates (AH) and 80 South Korean H. pylori clinical isolates (KH). Overall, we identified 23 different bab genotypes (19 in AH and 11 in KH), but only 5 occurred in greater than 5 isolates. Regardless of strain origin, a strain in which locus A and locus B were both occupied by a bab gene was the most common (85%); locus C was only occupied in those isolates that carried bab paralog at locus A and B. While the babA/babB/- genotype predominated in the KH (78.8%), no single genotype could account for greater than 40% in the AH collection. In addition to basic genotyping, we also identified associations between bab genotype and well known virulence factors cagA and vacA. Specifically, significant associations between babA at locus A and the cagA EPIYA-ABD motif (P<0.0001) and the vacA s1/i1/m1 allele (P<0.0001) were identified. Log-linear modeling further revealed a three-way association between bab carried at locus A, vacA, and number of OMPs from the HOM family (P<0.002). En masse this study provides a detailed characterization of the bab genotypes from two distinct populations. Our analysis suggests greater variability in the AH, perhaps due to adaptation to a more diverse host population. Furthermore, when considering the presence or absence of both the bab and homA/B paralogs at their given loci and the vacA genotype, an association was observed. Our results highlight the multifactorial nature of H. pylori mediated disease and the importance of considering how the specific combinations of H. pylori virulence genes and their multiple interactions with the host will collectively impact disease progression.     

Role of Weight History on Functional Limitations and Disability in Late Adulthood: The ARIC Study

Objective: To examine associations of weight history with functional limitations and disability in white and African‐American men and women. Research Methods and Procedures: Data were from the Atherosclerosis Risk in Communities study (n = 11, 177). Associations of recalled weight status at age 25 and weight change from age 25 to ages 45 to 64 with functional limitations, activities of daily living (ADLs), and instrumental activities of daily living (IADLs) at follow‐up (ages 52 to 75) were examined using logistic regression. Results: Obesity (BMI ≥ 30 kg/m²) at age 25 was associated with functional limitations and ADL and IADL impairment at follow‐up in white and African‐American men and women. For example, obese compared with normal weight (BMI, 18.5 to 24.9 kg/m²) white women had higher odds of mild [odds ratio (95% confidence interval), 1.97 (1.18 to 3.29)] and severe [9.81 (5.92 to 16.27)] functional limitations and ADL [3.48 (2.36 to 5.13)] and IADL [2.95 (2.00 to 4.33)] impairment. In African‐American women, obesity was associated with higher odds of mild [2.71 (1.14 to 6.41)] and severe [6.01 (2.53 to 14.26)] functional limitations and ADL [1.82 (1.10 to 3.00)] and IADL [2.39 (1.47 to 3.90)] impairment. Similar associations were found in men. Compared with weight maintenance (±10 lbs), large weight gain (>30 lbs) from age 25 to ages 45 to 64 was also associated with functional limitations and ADL and IADL impairment in white and African‐American men and women. Discussion: Maintenance of a healthy body weight throughout adulthood may play a role in preventing or delaying the onset of functional limitations and disability, resulting in increased quality of life and decreased health care costs.