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The objective of this review is to highlight changes in body composition in rodent models as a result of healthy aging in order to enhance translational research. Aging is associated with alterations in body composition, particularly fat mass and fat-free mass, which may be accompanied by adverse health effects, especially nearing middle age to old age. In humans, it is generally understood that fat mass tends to increase while fat-free mass concurrently declines with aging. However, the effect of aging on body composition in rodent models is less well studied, and how these changes compare and contrast with observations in humans has not yet been fully elucidated. Though, it appears as though the constituent-level alterations occur in humans and rodents at different life phases thereby having a potential effect on the outcomes of basic biomedical research. Though highly strain-dependent, this review suggests that FM changes begin at a much earlier life phase in rodents than in humans. Conversely, FFM appears to increase throughout middle age and into old age in rodents, whereas middle age is associated with the initiation the subsequent decline of FFM in humans. Given the essentiality of rodent models in basic biomedical research, careful consideration of these differences in age-related BC findings is imperative when the research is aimed for human translation.

Aeroallergen sensitization and virus-induced wheezing are risk factors for asthma development during early childhood, but the temporal developmental sequence between them is incompletely understood. To define the developmental relationship between aeroallergen sensitization and virus-induced wheezing. A total of 285 children at high risk for allergic disease and asthma were followed prospectively from birth. The timing and etiology of viral respiratory wheezing illnesses were determined, and aeroallergen sensitization was assessed annually for the first 6 years of life. The relationships between these events were assessed using a longitudinal multistate Markov model. Children who were sensitized to aeroallergens had greater risk of developing viral wheeze than nonsensitized children (hazard ratio [HR], 1.9; 95% confidence interval [CI], 1.2-3.1). Allergic sensitization led to an increased risk of wheezing illnesses caused by human rhinovirus (HRV) but not respiratory syncytial virus. The absolute risk of sensitized children developing viral wheeze was greatest at 1 year of age; however, the relative risk was consistently increased at every age assessed. In contrast, viral wheeze did not lead to increased risk of subsequent allergic sensitization (HR, 0.76; 95% CI, 0.50-1.1). Prospective, repeated characterization of a birth cohort demonstrated that allergic sensitization precedes HRV wheezing and that the converse is not true. This sequential relationship and the plausible mechanisms by which allergic sensitization can lead to more severe HRV-induced lower respiratory illnesses support a causal role for allergic sensitization in this developmental pathway. Therefore, therapeutics aimed at preventing allergic sensitization may modify virus-induced wheezing and the development of asthma.

Virus-induced wheezing episodes in infancy often precede the development of asthma. Whether infections with specific viral pathogens confer differential future asthma risk is incompletely understood. To define the relationship between specific viral illnesses and early childhood asthma development. A total of 259 children were followed prospectively from birth to 6 years of age. The etiology and timing of specific viral wheezing respiratory illnesses during early childhood were assessed using nasal lavage, culture, and multiplex reverse transcriptase-polymerase chain reaction. The relationships of these virus-specific wheezing illnesses and other risk factors to the development of asthma were analyzed. Viral etiologies were identified in 90% of wheezing illnesses. From birth to age 3 years, wheezing with respiratory syncytial virus (RSV) (odds ratio [OR], 2.6), rhinovirus (RV) (OR, 9.8), or both RV and RSV (OR , 10) was associated with increased asthma risk at age 6 years. In Year 1, both RV wheezing (OR, 2.8) and aeroallergen sensitization (OR, 3.6) independently increased asthma risk at age 6 years. By age 3 years, wheezing with RV (OR, 25.6) was more strongly associated with asthma at age 6 years than aeroallergen sensitization (OR, 3.4). Nearly 90% (26 of 30) of children who wheezed with RV in Year 3 had asthma at 6 years of age. Among outpatient viral wheezing illnesses in infancy and early childhood, those caused by RV infections are the most significant predictors of the subsequent development of asthma at age 6 years in a high-risk birth cohort.

Introduction: Anterior cruciate ligament (ACL) injuries pose significant challenges to football (soccer) players resulting in prolonged absence from play and immediate and long-term disability. Due to the lack of consensus and conflicting findings in the current literature regarding the role of fatigue in ACL injuries, this study aimed to explore the relationship between player in-match exposure and ACL injury occurrence in professional female football matches Methods: This was a prospective cohort study involving professional female football players who suffered ACL injuries during official matches during the 2021–2024 seasons. A significant difference in the pre-and post-45 min (first and second half) of gameplay was noted (p=0.02) with survival analysis showing a declining risk of ACL injury as the game continued, resulting in a 25% likelihood of injury occurring after the 54th min of gameplay.

All costs were inflated to 2020 prices using the total health price index and converted to Australian dollars where necessary. Discussion: This is the first study to project the lifetime costs of ACL reconstructions of football players within Australia. Along with player adherence, the study model does not account for the number of the population that are aware of the program (injury prevention program’s reach), players and coaches using the program correctly (implementation) and stakeholders continuing to use the program long-term (maintenance).

Participants completed online questionnaires at baseline (anytime within first 6 months post-injury, asking about participant characteristics [age, sex, metropolitan or rural living area, private insurance coverage, pre-injury physical activity (PA) level based on Tegner activity scale (TAS), prior knee injury(ies) history] and injury characteristics [meniscus or other concomitant injuries]) and 6-month post-injury (asking if they had undergone ACLR). Additionally, the bias for surgery in this group may be driven by access and affordability of surgery given their private health insurance coverage. Impact/Application to the field: - In the Australian context, a younger age, higher PA level and private insurance coverage led to increased odds of undergoing early surgery post-ACL injury. - Since younger, more active, and privately insured patients are more likely to undergo early surgery, clinicians should ensure they are informed about the evidence showing comparable outcomes between early ACLR and rehabilitation alone (with the option of delayed surgery).

Respiratory viruses of human origin infect wild apes across Africa, sometimes lethally. Here we report simultaneous outbreaks of two distinct human respiratory viruses, human metapneumovirus (MPV; Pneumoviridae: Metapneumovirus) and human respirovirus 3 (HRV3; Paramyxoviridae; Respirovirus, formerly known as parainfluenza virus 3), in two chimpanzee (Pan troglodytes schweinfurthii) communities in the same forest in Uganda in December 2016 and January 2017. The viruses were absent before the outbreaks, but each was present in ill chimpanzees from one community during the outbreak period. Clinical signs and gross pathologic changes in affected chimpanzees closely mirrored symptoms and pathology commonly observed in humans for each virus. Epidemiologic modelling showed that MPV and HRV3 were similarly transmissible (R 0 of 1.27 and 1.48, respectively), but MPV caused 12.2% mortality mainly in infants and older chimpanzees, whereas HRV3 caused no direct mortality. These results are consistent with the higher virulence of MPV than HRV3 in humans, although both MPV and HRV3 cause a significant global disease burden. Both viruses clustered phylogenetically within groups of known human variants, with MPV closely related to a lethal 2009 variant from mountain gorillas (Gorilla beringei beringei), suggesting two independent and simultaneous reverse zoonotic origins, either directly from humans or via intermediary hosts. These findings expand our knowledge of human origin viruses threatening wild chimpanzees and suggest that such viruses might be differentiated by their comparative epidemiological dynamics and pathogenicity in wild apes. Our results also caution against assuming common causation in coincident outbreaks.