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Ventral hernias are a common abdominal wall defect vulnerable to the gravid abdomen’s physiological changes. This case report describes a 38-year-old gravida 3 para 2002 female with a complex abdominal surgical history and a chronic infection of the abdominal wall at the site of prior hernia repair with mesh. She was managed conservatively with antibiotics until delivery. Abdominal wall debridement and repair was coordinated with her 39-week cesarean, which allowed for a successful delivery of her infant paralleled with surgical management of the infected mesh.

In January 2020, a novel betacoronavirus (family Coronaviridae ), named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was identified as the etiological agent of a cluster of pneumonia cases occurring in Wuhan City, Hubei Province, China 1 , 2 . The disease arising from SARS-CoV-2 infection, coronavirus disease 2019 (COVID-19), subsequently spread rapidly causing a worldwide pandemic. Here we examine the added value of near real-time genome sequencing of SARS-CoV-2 in a subpopulation of infected patients during the first 10 weeks of COVID-19 containment in Australia and compare findings from genomic surveillance with predictions of a computational agent-based model (ABM). Using the Australian census data, the ABM generates over 24 million software agents representing the population of Australia, each with demographic attributes of an anonymous individual. It then simulates transmission of the disease over time, spreading from specific infection sources, using contact rates of individuals within different social contexts. We report that the prospective sequencing of SARS-CoV-2 clarified the probable source of infection in cases where epidemiological links could not be determined, significantly decreased the proportion of COVID-19 cases with contentious links, documented genomically similar cases associated with concurrent transmission in several institutions and identified previously unsuspected links. Only a quarter of sequenced cases appeared to be locally acquired and were concordant with predictions from the ABM. These high-resolution genomic data are crucial to track cases with locally acquired COVID-19 and for timely recognition of independent importations once border restrictions are lifted and trade and travel resume. The combination of nearly real-time genome sequencing of SARS-CoV-2 in infected patients during the first 10 weeks of COVID-19 containment in Australia and epidemiological modeling is helping in understanding the dynamics of the COVID-19 pandemic and potentially guiding public health decisions.

In response to shortcomings in epidemic preparedness and response that were revealed by the COVID-19 pandemic, there have been numerous proposals for ways to improve preparedness and response financing. Included among these is the World Bank’s Pandemic Fund, formerly known as the Financial Intermediary Fund for Pandemic Prevention, Preparedness, and Response, which was launched in September 2022. This analysis piece examines the Pandemic Fund, where it fits into ongoing discussions surrounding financing for preparedness and response efforts and discusses emerging apprehensions about the new financing mechanism. Briefly, the Pandemic Fund is not the first time that the World Bank has hosted a financing mechanism to provide support for pandemic response. Notably the Pandemic Emergency Financing Facility (PEF)—which was launched in 2017 and closed in 2021—was criticised for generally failing to realise its potential. However, the Pandemic Fund seems to be addressing several of these critiques by placing a greater emphasis on prevention and preparedness financing, as opposed to response financing. Still, there is an important need for response funding mechanisms, and concerningly, the Pandemic Fund seems to support response efforts in name only. While it is clearly desirable to prepare for and prevent outbreaks for a multitude of reasons, it is also naive to assume that strengthening preparedness capacities will eliminate outbreaks and the need for response financing altogether. Accordingly, there is a need to complement this new financing mechanism with dedicated funding for responding to infectious disease outbreaks and to closely link this response financing with health security frameworks and instruments.

H9N2 avian influenza A viruses are endemic in poultry of many Eurasian countries and have caused repeated human infections in Asia since 1998. To evaluate the potential threat of H9N2 viruses to humans, we investigated the replication and transmission efficiency of H9N2 viruses in the ferret model. Five wild-type (WT) H9N2 viruses, isolated from different avian species from 1988 through 2003, were tested in vivo and found to replicate in ferrets. However these viruses achieved mild peak viral titers in nasal washes when compared to those observed with a human H3N2 virus. Two of these H9N2 viruses transmitted to direct contact ferrets, however no aerosol transmission was detected in the virus displaying the most efficient direct contact transmission. A leucine (Leu) residue at amino acid position 226 in the hemagglutinin (HA) receptor-binding site (RBS), responsible for human virus-like receptor specificity, was found to be important for the transmission of the H9N2 viruses in ferrets. In addition, an H9N2 avian-human reassortant virus, which contains the surface glycoprotein genes from an H9N2 virus and the six internal genes of a human H3N2 virus, showed enhanced replication and efficient transmission to direct contacts. Although no aerosol transmission was observed, the virus replicated in multiple respiratory tissues and induced clinical signs similar to those observed with the parental human H3N2 virus. Our results suggest that the establishment and prevalence of H9N2 viruses in poultry pose a significant threat for humans.

The SARS-CoV-2 epidemic has rapidly spread outside China with major outbreaks occurring in Italy, South Korea, and Iran. Phylogenetic analyses of whole-genome sequencing data identified a distinct SARS-CoV-2 clade linked to travellers returning from Iran to Australia and New Zealand. This study highlights potential viral diversity driving the epidemic in Iran, and underscores the power of rapid genome sequencing and public data sharing to improve the detection and management of emerging infectious diseases.

A novel, swine-origin influenza H1N1 virus (H1N1pdm) caused the first pandemic of the 21st century. This pandemic, although efficient in transmission, is mild in virulence. This atypical mild pandemic season has raised concerns regarding the potential of this virus to acquire additional virulence markers either through further adaptation or possibly by immune pressure in the human host. Using the mouse model we generated, within a single round of infection with A/California/04/09/H1N1 (Ca/04), a virus lethal in mice--herein referred to as mouse-adapted Ca/04 (ma-Ca/04). Five amino acid substitutions were found in the genome of ma-Ca/04: 3 in HA (D131E, S186P and A198E), 1 in PA (E298K) and 1 in NP (D101G). Reverse genetics analyses of these mutations indicate that all five mutations from ma-Ca/04 contributed to the lethal phenotype; however, the D131E and S186P mutations--which are also found in the 1918 and seasonal H1N1 viruses-in HA alone were sufficient to confer virulence of Ca/04 in mice. HI assays against H1N1pdm demonstrate that the D131E and S186P mutations caused minor antigenic changes and, likely, affected receptor binding. The rapid selection of ma-Ca/04 in mice suggests that a virus containing this constellation of amino acids might have already been present in Ca/04, likely as minor quasispecies.

The emergence of distinct populations of Cryptococcus gattii in the temperate North American Pacific Northwest (PNW) was surprising, as this species was previously thought to be confined to tropical and semitropical regions. Beyond a new habitat niche, the dominant emergent population displayed increased virulence and caused primary pulmonary disease, as opposed to the predominantly neurologic disease seen previously elsewhere. Whole-genome sequencing was performed on 118 C. gattii isolates, including the PNW subtypes and the global diversity of molecular type VGII, to better ascertain the natural source and genomic adaptations leading to the emergence of infection in the PNW. Overall, the VGII population was highly diverse, demonstrating large numbers of mutational and recombinational events; however, the three dominant subtypes from the PNW were of low diversity and were completely clonal. Although strains of VGII were found on at least five continents, all genetic subpopulations were represented or were most closely related to strains from South America. The phylogenetic data are consistent with multiple dispersal events from South America to North America and elsewhere. Numerous gene content differences were identified between the emergent clones and other VGII lineages, including genes potentially related to habitat adaptation, virulence, and pathology. Evidence was also found for possible gene introgression from Cryptococcus neoformans var. grubii that is rarely seen in global C. gattii but that was present in all PNW populations. These findings provide greater understanding of C. gattii evolution in North America and support extensive evolution in, and dispersal from, South America. IMPORTANCE Cryptococcus gattii emerged in the temperate North American Pacific Northwest (PNW) in the late 1990s. Beyond a new environmental niche, these emergent populations displayed increased virulence and resulted in a different pattern of clinical disease. In particular, severe pulmonary infections predominated in contrast to presentation with neurologic disease as seen previously elsewhere. We employed population-level whole-genome sequencing and analysis to explore the genetic relationships and gene content of the PNW C. gattii populations. We provide evidence that the PNW strains originated from South America and identified numerous genes potentially related to habitat adaptation, virulence expression, and clinical presentation. Characterization of these genetic features may lead to improved diagnostics and therapies for such fungal infections. The data indicate that there were multiple recent introductions of C. gattii into the PNW. Public health vigilance is warranted for emergence in regions where C. gattii is not thought to be endemic. Cryptococcus gattii emerged in the temperate North American Pacific Northwest (PNW) in the late 1990s. Beyond a new environmental niche, these emergent populations displayed increased virulence and resulted in a different pattern of clinical disease. In particular, severe pulmonary infections predominated in contrast to presentation with neurologic disease as seen previously elsewhere. We employed population-level whole-genome sequencing and analysis to explore the genetic relationships and gene content of the PNW C. gattii populations. We provide evidence that the PNW strains originated from South America and identified numerous genes potentially related to habitat adaptation, virulence expression, and clinical presentation. Characterization of these genetic features may lead to improved diagnostics and therapies for such fungal infections. The data indicate that there were multiple recent introductions of C. gattii into the PNW. Public health vigilance is warranted for emergence in regions where C. gattii is not thought to be endemic.

150 years ago, Stanley Jevons introduced the concept of energy rebound: that anticipated energy efficiency savings may be “taken back” by behavioural responses. This is an important issue today because, if energy rebound is significant, this would hamper the effectiveness of energy efficiency policies aimed at reducing energy use and associated carbon emissions. However, empirical studies which estimate national energy rebound are rare and, perhaps as a result, rebound is largely ignored in energy-economy models and associated policy. A significant difficulty lies in the components of energy rebound assessed in empirical studies: most examine direct and indirect rebound in the static economy, excluding potentially significant rebound of the longer term structural response of the national economy. In response, we develop a novel exergy-based approach to estimate national energy rebound for the UK and US (1980–2010) and China (1981–2010). Exergy—as “available energy”—allows a consistent, thermodynamic-based metric for national-level energy efficiency. We find large energy rebound in China, suggesting that improvements in China’s energy efficiency may be associated with increased energy consumption (“backfire”). Conversely, we find much lower (partial) energy rebound for the case of the UK and US. These findings support the hypothesis that producer-sided economies (such as China) may exhibit large energy rebound, reducing the effectiveness of energy efficiency, unless other policy measures (e.g., carbon taxes) are implemented. It also raises the prospect we need to deploy renewable energy sources faster than currently planned, if (due to rebound) energy efficiency policies cannot deliver the scale of energy reduction envisaged to meet climate targets.

Background Hepatic steatosis (HS) increases morbidity and mortality associated with liver surgery (LS). Furthermore, patients with HS are more likely to require a blood transfusion, which is associated with worse short and long-term outcomes. Patients with HS requiring LS receive no specific dietary treatment or advice. A very low-calorie diet (VLCD) is commonly used before gallbladder and bariatric surgery to reduce liver volumes and associated intraoperative morbidity. These diets typically provide 800–1200 kcal/day over a 2–4-week period. Limited evidence suggests that a VLCD in patients with LS may result in better outcomes. Methods This study aims to test the feasibility of delivering a multi-centre randomised clinical trial to compare a dietary intervention (VLCD plus motivational instructions) versus treatment as usual (TAU) in people with HS having LS. This study will provide high-quality data to estimate screening rates, recruitment, randomisation, retention, and intervention adherence. The study will also determine the definitive trial’s most clinically relevant primary outcome. The study will also estimate resource use and costs associated with the delivery of the intervention. Seventy-two adults ≥ 18 who are scheduled to undergo elective LS and have a magnetic resonance imaging (MRI) identified HS will be recruited. Acceptability to the dietary intervention will be evaluated with food diaries and focus groups. Clinical and patient-reported outcomes will be collected at baseline, pre- and post-surgery, day of discharge, plus 30- and 90-day follow-up. Discussion This feasibility study will provide data on the acceptability and feasibility of a dietary intervention for patients with HS having LS. The intervention has been developed based on scientific evidence from other clinical areas and patient experience; therefore, it is safe for this patient group. Patients with experience of LS and VLCDs have advised throughout the development of the study protocol. The findings will inform the design of a future definitive study. Trial registration ISRCTN Number 19701345. Date registered: 20/03/2023. URL: https://www.isrctn.com/ISRCTN19701345 .

Little is known about the effects of blast exposure on the human brain in the absence of head impact. Clinical reports, experimental animal studies, and computational modeling of blast exposure have suggested effects on the cerebellum and brainstem. In US military personnel with isolated, primary blast-related 'mild' traumatic brain injury and no other known insult, we found diffusion tensor MRI abnormalities consistent with cerebellar white matter injury in 3 of 4 subjects. No abnormalities in other brain regions were detected. These findings add to the evidence supporting the hypothesis that primary blast exposure contributes to brain injury in the absence of head impact and that the cerebellum may be particularly vulnerable. However, the clinical effects of these abnormalities cannot be determined with certainty; none of the subjects had ataxia or other detected evidence of cerebellar dysfunction. The details of the blast events themselves cannot be disclosed at this time, thus additional animal and computational modeling will be required to dissect the mechanisms underlying primary blast-related traumatic brain injury. Furthermore, the effects of possible subconcussive impacts and other military-related exposures cannot be determined from the data presented. Thus many aspects of topic will require further investigation.