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Marine mammals can play important ecological roles in aquatic ecosystems, and their presence can be key to community structure and function. Consequently, marine mammals are often considered indicators of ecosystem health and flagship species. Yet, historical population declines caused by exploitation, and additional current threats, such as climate change, fisheries bycatch, pollution and maritime development, continue to impact many marine mammal species, and at least 25% are classified as threatened (Critically Endangered, Endangered or Vulnerable) on the IUCN Red List. Conversely, some species have experienced population increases/recoveries in recent decades, reflecting management interventions, and are heralded as conservation successes. To continue these successes and reverse the downward trajectories of at-risk species, it is necessary to evaluate the threats faced by marine mammals and the conservation mechanisms available to address them. Additionally, there is a need to identify evidence-based priorities of both research and conservation needs across a range of settings and taxa. To that effect we: (1) outline the key threats to marine mammals and their impacts, identify the associated knowledge gaps and recommend actions needed; (2) discuss the merits and downfalls of established and emerging conservation mechanisms; (3) outline the application of research and monitoring techniques; and (4) highlight particular taxa/populations that are in urgent need of focus.

The conservation status of small cetaceans has significantly worsened since the 1980s, when the baiji was the only species of small cetacean listed as Endangered by IUCN. Now the baiji is almost certainly extinct and 13 other species, subspecies, or populations (hereafter units-to-conserve or units) of small cetaceans are listed as Critically Endangered (CR) on the IUCN Red List. Bycatch is the main threat to 11 of the CR units. Entanglement in gillnets contributed to the extinction of the baiji and is responsible for the imminent extinction of the vaquita. Unfortunately, there is no simple technical solution to the problem of bycatch of small cetaceans. If the 8 CR units with 100 or fewer remaining individuals are to be saved, conservation zones must be established where gillnets are eliminated and bans on their use are strictly enforced. Recent experience with the vaquita in Mexico demonstrates that enforcement of such conservation zones can be very difficult. Ineffective enforcement is also a problem for at least 4 of the other CR units. Time is very short and, unless major efforts are made now to address the bycatch problem, the prospects for CR small cetaceans and other at-risk aquatic megafauna are grim. The ultimate long-term solution to the bycatch problem is the development of efficient, inexpensive, alternative fishing gear that can replace gillnets without jeopardizing the livelihoods of fishermen. Good fishery governance and the direct involvement of fishing communities are also essential to the successful conservation of most threatened populations of small cetaceans.

Abstract Wildlife disease surveillance programs and research studies track infection and identify risk factors for wild populations, humans and agriculture. Often, several types of samples are collected from individuals to provide more complete information about an animal's infection history. Methods that jointly analyse multiple data streams to study disease emergence and drivers of infection via epidemiological process models remain underdeveloped. Joint‐analysis methods can more thoroughly analyse all available data, more precisely quantifying epidemic processes, outbreak status, and risks. We contribute a paired data modelling approach that analyses multiple samples from individuals. We use ‘characterization maps’ to link paired data to epidemiological processes through a hierarchical statistical observation model. Our approach can provide both Bayesian and frequentist estimates of epidemiological parameters and state. Our approach can also incorporate test sensitivity and specificity, and we propose model fit diagnostics. We motivate our approach through the need to use paired pathogen and antibody detection tests to estimate parameters and infection trajectories for the widely applicable susceptible, infectious, recovered (SIR) model. We contribute general formulas to link characterization maps to arbitrary process models and datasets and an extended SIR model that better accommodates paired data. We find via simulation that paired data can more efficiently estimate SIR parameters than unpaired data, requiring samples from 5 to 10 times fewer individuals. We use our method to study SARS‐CoV‐2 in wild white‐tailed deer (Odocoileus virginianus) from three counties in the United States. Estimates for average infectious times corroborate captive animal studies. The estimated average cumulative proportion of infected deer across the three counties is 73%, and the basic reproductive number (R0) is 1.88. Wildlife disease surveillance programs and research studies can use our methods to jointly analyse paired data to estimate epidemiological process parameters and track outbreaks. Paired data analyses can improve precision and accuracy when sampling is limited. Our methods use general statistical theory to let applications extend beyond the SIR model we consider and to more complicated examples of paired data. The methods can also be embedded in larger hierarchical models to provide landscape‐scale risk assessment and identify drivers of infection.

Purpose/ObjectivesZAP-X, a novel and dedicated radiosurgery (SRS) system, has recently emerged, while CyberKnife has solidified its position as a versatile solution for SRS and stereotactic body radiation therapy over the past two decades. This study aims to compare the dosimetric performance and delivery efficiency of ZAP-X and CyberKnife in treating brain metastases of varying target sizes, employing circular collimation.Methods and materialsTwenty-three patients, encompassing a total of 47 brain metastases, were included in the creation of comparative plans of ZAP-X and CyberKnife for analysis. The comparative plans were generated to achieve identical prescription doses for the targets, while adhering to the same dose constraints for organs at risk (OAR). The prescription isodose percentage was optimized within the range of 97–100% for each plan to ensure effective target-volume coverage. To assess plan quality, indices such as conformity, homogeneity, and gradient (CI, HI, and GI) were computed, along with the reporting of total brain volumes receiving 12Gy and 10Gy. Estimated treatment time and monitor units (MUs) were compared between the two modalities in evaluating delivery efficiency.ResultsOverall, CyberKnife achieved better CI and HI, while ZAP-X exhibited better GI and a smaller irradiated volume for the normal brain. The superiority of CyberKnife’s plan conformity was more pronounced for target size less than 1 cc and greater than 10 cc. Conversely, the advantage of ZAP-X’s plan dose gradient was more notable for target sizes under 10 cc. The homogeneity of ZAP-X plans, employing multiple isocenters, displayed a strong correlation with the target’s shape and the planner’s experience in placing isocenters. Generally, the estimated treatment time was similar between the two modalities, and the delivery efficiency was significantly impacted by the chosen collimation sizes for both modalities.ConclusionThis study demonstrates that, within the range of target sizes within the patient cohort, plans generated by ZAP-X and CyberKnife exhibit comparable plan quality and delivery efficiency. At present, with the current platform of the two modalities, CyberKnife outperforms ZAP-X in terms of conformity and homogeneity, while ZAP-X tends to produce plans with a more rapid dose falloff.

Abstract Fibrous dysplasia (FD) is a rare, disabling skeletal disease for which there are no established treatments. Growing evidence supports inhibiting the osteoclastogenic factor receptor activator of nuclear kappa-B ligand (RANKL) as a potential treatment strategy. In this study, we investigated the mechanisms underlying RANKL inhibition in FD tissue and its likely indirect effects on osteoprogenitors by evaluating human FD tissue pre- and post-treatment in a phase 2 clinical trial of denosumab (NCT03571191) and in murine in vivo and ex vivo preclinical models. Histological analysis of human and mouse tissue demonstrated increased osteogenic maturation, reduced cellularity, and reduced expression of the pathogenic Gαs variant in FD lesions after RANKL inhibition. RNA sequencing of human and mouse tissue supported these findings. The interaction between osteoclasts and mutant osteoprogenitors was further assessed in an ex vivo lesion model, which indicated that the proliferation of abnormal FD osteoprogenitors was dependent on osteoclasts. The results from this study demonstrated that, in addition to its expected antiosteoclastic effect, denosumab reduces FD lesion activity by decreasing FD cell proliferation and increasing osteogenic maturation, leading to increased bone formation within lesions. These findings highlight the unappreciated role of cellular crosstalk between osteoclasts and preosteoblasts/osteoblasts as a driver of FD pathology and demonstrate a novel mechanism of action of denosumab in the treatment of bone disease. TRIAL REGISTRATION: ClinicalTrials.gov NCT03571191

Introduction/backgroundPhosphatase and tensin homolog (PTEN) genomic deletions and transmembrane protease, serine 2/v-ets avian erthyroblastosis virus E26 oncogene homolog (ERG) rearrangements are two of the most common genetic abnormalities associated with prostate cancer. Prior studies have demonstrated these alterations portend worse clinical outcomes. Our objective is to evaluate the impact of biopsy-determined PTEN losses and TMPRSS2-ERG fusion on biochemical progression-free survival (bPFS) and overall survival (OS) in patients who receive SBRT for localized prostate cancer.Methods/materialsPatients received SBRT for localized prostate cancer on a prospective quality-of-life (QoL) and cancer outcomes study. For each patient, the single biopsy core with the highest grade/volume of cancer was evaluated for PTEN and ERG abnormalities. Differences in baseline patient and disease characteristics between groups were analyzed using ANOVA for age and χ2 for categorical groupings. bPFS and OS were calculated using the Kaplan Meier (KM) method with Log-Rank test comparison between groups. Predictors of bPFS and OS were identified using the Cox proportional hazards method. For all analyses, p

Fibrous dysplasia (FD) is a mosaic skeletal disorder involving the development of benign, expansile fibro-osseous lesions during childhood that cause deformity, fractures, pain, and disability. There are no well-established treatments for FD. Fibroblast activation protein (FAPα) is a serine protease expressed in pathological fibrotic tissues that has promising clinical applications as a biomarker and local pro-drug activator in several pathological conditions. In this study, we explored the expression of FAP in FD tissue and cells through published genetic expression datasets and measured circulating FAPα in plasma samples from patients with FD and healthy donors. We found that FAP genetic expression was increased in FD tissue and cells, and present at higher concentrations in plasma from patients with FD compared to healthy donors. Moreover, FAPα levels were correlated with skeletal disease burden in patients with FD. These findings support further investigation of FAPα as a potential imaging and/or biomarker of FD, as well as a pro-drug activator specific to FD tissue.

Fibrous dysplasia (FD) is a mosaic skeletal disorder caused by somatic activating variants of GNAS encoding for Gαs and leading to excessive cyclic adenosine monophosphate signaling in bone-marrow stromal cells (BMSCs). The effect of Gαs activation in the BMSC transcriptome and how it influences FD lesion microenvironment are unclear. We analyzed changes induced by Gαs activation in the BMSC transcriptome and secretome. RNAseq analysis of differential gene expression of cultured BMSCs from patients with FD and healthy volunteers, and from an inducible mouse model of FD, was performed, and the transcriptomic profiles of both models were combined to build a robust FD BMSC genetic signature. Pathways related to Gαs activation, cytokine signaling, and extracellular matrix deposition were identified. To assess the modulation of several key secreted factors in FD pathogenesis, cytokines and other factors were measured in culture media. Cytokines were also screened in a collection of plasma samples from patients with FD, and positive correlations of several cytokines to their disease burden score, as well as to one another and bone turnover markers, were found. These data support the pro-inflammatory, pro-osteoclastic behavior of FD BMSCs and point to several cytokines and other secreted factors as possible therapeutic targets and/or circulating biomarkers for FD.

Recent data suggest that 3,4-methylenedioxypyrovalerone (MDPV) has neurotoxic effects; however, the cognitive and neurochemical consequences of MDPV self-administration remain largely unexplored. Furthermore, despite the fact that drug preparations that contain MDPV often also contain caffeine, little is known regarding the toxic effects produced by the co-use of these two stimulants. The current study investigated the degree to which self-administered MDPV or a mixture of MDPV+caffeine can produce deficits in recognition memory and alter neurochemistry relative to prototypical stimulants. Male Sprague Dawley rats were provided 90 min or 12 h access to MDPV, MDPV+caffeine, methamphetamine, cocaine, or saline for 6 weeks. Novel object recognition (NOR) memory was evaluated prior to any drug self-administration history and 3 weeks after the final self-administration session. Rats that had 12 h access to methamphetamine and those that had 90 min or 12 h access to MDPV+caffeine exhibited significant deficits in NOR, whereas no significant deficits were observed in rats that self-administered cocaine or MDPV. Striatal monoamine levels were not systematically affected. These data demonstrate synergism between MDPV and caffeine with regard to producing recognition memory deficits, highlighting the importance of recapitulating the manner in which drugs are used (e.g., in mixtures containing multiple stimulants, binge-like patterns of intake).

Objective: To examine the effects of a 6-month weight loss intervention on physical function, inflammatory biomarkers, and metabolic biomarkers in both those with and without osteoarthritis (OA). Design: 59 individuals ≥60 years old with obesity and a functional impairment were enrolled into this IRB approved clinical trial and randomized into one of two 6-month weight loss arms: a higher protein hypocaloric diet or a standard protein hypocaloric diet. All participants were prescribed individualized 500-kcal daily-deficit diets, with a goal of 10% weight loss. Additionally, participants participated in three, low-intensity, exercise sessions per week. Physical function, serum biomarkers and body composition data were assessed at the baseline and 6-month timepoints. Statistical analyses assessed the relationships between biomarkers, physical function, body composition, and OA status as a result of the intervention. Results: No group effects of dietary intervention were detected on any outcome measures (multiple p ​> ​0.05). During the 6-month trial, participants lost 6.2 ​± ​4.0% of their bodyweight (p ​

Bone maintenance in health and disease depends on bone-resorbing osteoclasts. Whitlock et al. demonstrate that an RNA chaperon -La protein- lives a second life as a key regulator of osteoclast size and function, suggesting a new therapeutic target.

Quantitative evaluation of human stability using foot pressure/force measurement hardware and motion capture (mocap) technology is expensive, time consuming, and restricted to the laboratory. We propose a novel image-based method to estimate three key components for stability computation: Center of Mass (CoM), Base of Support (BoS), and Center of Pressure (CoP). Furthermore, we quantitatively validate our image-based methods for computing two classic stability measures, CoMtoCoP and CoMtoBoS distances, against values generated directly from laboratory-based sensor output (ground truth) using a publicly available, multi-modality (mocap, foot pressure, two-view videos), ten-subject human motion dataset. Using Leave One Subject Out (LOSO) cross-validation, experimental results show: 1) our image-based CoM estimation method (CoMNet) consistently outperforms state-of-the-art inertial sensor-based CoM estimation techniques; 2) stability computed by our image-based method combined with insole foot pressure sensor data produces consistent, strong, and statistically significant correlation with ground truth stability measures (CoMtoCoP r = 0.79 p < 0.001, CoMtoBoS r = 0.75 p < 0.001); 3) our fully image-based estimation of stability produces consistent, positive, and statistically significant correlation on the two stability metrics (CoMtoCoP r = 0.31 p < 0.001, CoMtoBoS r = 0.22 p < 0.043). Our study provides promising quantitative evidence for the feasibility of image-based stability evaluation in natural environments.

Introduction Many extremely preterm newborns develop anaemia requiring a transfusion, with most receiving three to five transfusions during their admission. While transfusions save lives, the potential for transfusion-related adverse outcomes is an area of growing concern. Transfusion is an independent predictor of death and is associated with increased morbidity, length of hospital stay, risk of infection and immune modulation. The underlying mechanisms include adverse pro-inflammatory and immunosuppressive responses. Evidence supports an association between transfusion of washed red cells and fewer post-transfusion complications potentially through removal of chemokines, lipids, microaggregates and other biological response modifiers. However, the clinical and cost-effectiveness of washed cells have not been determined.Methods and analysis This is a multicentre, randomised, double-blinded trial of washed versus unwashed red cells. Infants 2, and; necrotising enterocolitis stage ≥2. To detect a 10% absolute reduction in the composite outcome from 69% with unwashed red blood cell (RBCs) to 59% with washed RBCs with 90% power, requires a sample size of 1124 infants (562 per group). Analyses will be performed on an intention-to-treat basis with a prespecified statistical analysis plan. A cost-effectiveness analysis will also be undertaken.Ethics and dissemination Ethics approval has been obtained from the Women’s and Children’s Health Network Human Research Ethics Committee (HREC/12/WCHN/55). The study findings will be disseminated through peer-reviewed articles and conferences.Trial registration number ACTRN12613000237785 Australian New Zealand Clinical Trials Registry.

Introduction Severe bronchopulmonary dysplasia (BPD) is a well-known factor consistently associated with impaired cognitive outcomes. Regarding reported benefits on long-term neurodevelopmental outcomes, the potential adverse effects of high-dose docosahexaenoic acid (DHA) supplementation on this short-term neonatal morbidity need further investigations in infants born very preterm. This study will determine whether high-dose DHA enteral supplementation during the neonatal period is associated with the risk of severe BPD at 36 weeks’ postmenstrual age (PMA) compared with control, in contemporary cohorts of preterm infants born at less than 29 weeks of gestation.Methods and analysis As part of an Australian–Canadian collaboration, we will conduct an individual participant data (IPD) meta-analysis of randomised controlled trials targeting infants born at less than 29 weeks of gestation and evaluating the effect of high-dose DHA enteral supplementation in the neonatal period compared with a control. Primary outcome will be severe grades of BPD (yes/no) at 36 weeks’ PMA harmonised according to a recent definition that predicts early childhood morbidities. Other outcomes will be survival without severe BPD, death, BPD severity grades, serious brain injury, severe retinopathy of prematurity, patent ductus arteriosus and necrotising enterocolitis requiring surgery, sepsis, combined neonatal morbidities and growth. Severe BPD will be compared between groups using a multivariate generalised estimating equations log-binomial regression model. Subgroup analyses are planned for gestational age, sex, small-for-gestational age, presence of maternal chorioamnionitis and mode of delivery.Ethics and dissemination The conduct of each trial was approved by institutional research ethics boards and written informed consent was obtained from participating parents. A collaboration and data sharing agreement will be signed between participating authors and institutions. This IPD meta-analysis will document the role of DHA in nutritional management of BPD. Findings will be disseminated through conferences, media interviews and publications to peer-reviewed journals.PROSPERO registration number CRD42023431063.Trial registration number NCT05915806.

X-linked hypophosphatemia (XLH) is a rare, progressive, genetic disease with multisystem impact that typically begins to manifest in early childhood. Two treatment options exist: oral phosphate in combination with active vitamin D (“conventional therapy”) and a fully human monoclonal anti-FGF23 antibody, burosumab. The clinical benefit of conventional therapy in adults is limited, and poor tolerance and complications are common. Burosumab was first approved as a treatment for XLH in 2018 and its disease-modifying benefits in clinical trials in children suggest burosumab treatment could also alter the disease course in adults. Without long-term clinical data on multiple XLH-related sequelae available, the results of an elicitation exercise are reported, in which eight global experts in XLH posited how long-term treatment with burosumab is anticipated to impact the life course of clinical sequelae in adults with XLH. Based on their clinical experiences, the available evidence and their disease understanding, the experts agreed that some long-term benefits of using burosumab are likely in adults with XLH even if they have a misaligned skeleton from childhood. Burosumab treatment is anticipated to reduce the incidence of fractures and halt the progression of clinical sequelae associated with conventional therapy. While the trajectories for established dental abscesses are not expected to improve with burosumab treatment, dental abscess development may be prevented. Starting treatment with burosumab in childhood to increase the likelihood of an aligned skeleton and continuation into and throughout adulthood to maintain euphosphatemia may optimize patient outcomes, although future real-world investigation is required to support this hypothesis.

Cutaneous skeletal hypophosphatemia syndrome (CSHS) is a mosaic RASopathy characterized by the association of dysplastic skeletal lesions, congenital skin nevi of epidermal and/or melanocytic origin, and FGF23-mediated hypophosphatemia. The primary physiological source of circulating FGF23 is bone cells. However, several reports have suggested skin lesions as the source of excess FGF23 in CSHS. Consequently, without convincing evidence of efficacy, many patients with CSHS have undergone painful removal of cutaneous lesions in an effort to normalize blood phosphate levels. This study aims to elucidate whether the source of FGF23 excess in CSHS is RAS mutation–bearing bone or skin lesions. Toward this end, we analyzed the expression and activity of Fgf23 in two mouse models expressing similar HRAS/Hras activating mutations in a mosaic-like fashion in either bone or epidermal tissue. We found that HRAS hyperactivity in bone, not skin, caused excess of bioactive intact FGF23, hypophosphatemia, and osteomalacia. Our findings support RAS-mutated dysplastic bone as the primary source of physiologically active FGF23 excess in patients with CSHS. This evidence informs the care of patients with CSHS, arguing against the practice of nevi removal to decrease circulating, physiologically active FGF23.

ObjectivesWe aimed to compare the effects of nutrient-enriched formula with standard term formula on rate of body weight gain of late preterm infants appropriately grown for gestational age.Study designA multi-center, randomized, controlled trial. Late preterm infants (34–37 weeks' gestation), with weight appropriate for gestational age (AGA), were randomized to nutrient enriched formula (NEF) with increased calories (22 kcal/30 ml) from protein, added bovine milk fat globule membrane, vitamin D and butyrate or standard term formula 20 kcal/30 ml (STF). Breastfed term infants were enrolled as an observational reference group (BFR). Primary outcome was rate of body weight gain from enrollment to 120 days corrected age (d/CA). Planned sample size was 100 infants per group. Secondary outcomes included body composition, weight, head circumference and length gain, and medically confirmed adverse events to 365 d/CA.ResultsThe trial was terminated early due to recruitment challenges and sample size was substantially reduced. 40 infants were randomized to NEF (n = 22) and STF (n = 18). 39 infants were enrolled in the BFR group. At 120 d/CA there was no evidence of a difference in weight gain between randomized groups (mean difference 1.77 g/day, 95% CI, −1.63 to 5.18, P = 0.31). Secondary outcomes showed a significant reduction in risk of infectious illness in the NEF group at 120 d/CA [relative risk 0.37 (95% CI, 0.16–0.85), P = 0.02].ConclusionWe saw no difference in rate of body weight gain between AGA late preterm infants fed NEF compared to STF. Results should be interpreted with caution due to small sample size.Clinical Trial RegistrationThe Australia New Zealand Clinical Trials Registry (ACTRN 12618000092291). “mailto:maria.makrides@sahmri.com” maria.makrides@sahmri.com.

Summary: Elucidating a basic blueprint of osteoclast-osteoblast coordination in skeletal remodeling and understanding how this coordination breaks down with age and disease is essential for addressing the growing skeletal health problem in our aging population. The paucity of simple, activatable, biologically relevant models of osteoclast-osteoblast coordination has hindered our understanding of how skeletal remolding is regulated. Here, we describe an inducible ex vivo model of osteoclast-osteoblast progenitor coordination. Induction activates the release of osteoclastogenic factors from osteoprogenitors, which elicits the differentiation and fusion of neighboring preosteoclasts. In turn, multinucleated osteoclasts release soluble coupling factors, RANK+ extracellular vesicles and promote osteoprogenitor proliferation, recapitulating aspects of perturbed coordination in diseases underpinned by excessive osteoclast formation. We expect this model to expedite the investigation of cell-cell fusion, osteoclast-osteoblast progenitor coordination, and extracellular vesicle signaling during bone remodeling and offer a powerful tool for evaluating signaling cascades and novel therapeutic interventions in osteoclast-linked skeletal disease.

One of the distinctive languages of Central Maluku, Naka’ela, was once spoken by a remnant language community on the north coast of Seram. Relying on data collected in Seram in 1978, Naka’ela has been among the Central Maluku languages included in studies of morphophonology (Collins 1983a, 1983b), areal phonology shift (1982, 2018a), and language classification (Collins 1983a). A fallacious, mechanistic classification of Naka’ela (Mahsun et al. 2008; Mukhamdanah 2015) was also published and has been recently disproven (Collins 2019a, 2019b). This essay will review some of the aspects of the Naka’ela language system by exploring what we can discern about verbal conjugation systems and genitive paradigms in this Central Maluku language. Based on contemporary reports from Seram (Sadrach Latue, p.c., 27-10-2018), the Naka’ela language, like so many others in Central Maluku, is no longer spoken; nor are there “rememberers” of this extinct language. In this setting of dead and forgotten languages, we recall the brutal genocides and culture murders in Australia (Daniel Nettle and Suzanne Romaine 2000). Recently, Dianne Biritjalawuy Gondarra, a Yolngu woman from northern Australia, explained that “culture is a shadow, it’s something that follows your everywhere, and part of culture is language, which connects me back to my land” (James Griffths 2020). This essay is intended to shed more light on Naka’ela and the complex setting of fading multilingualism in Central Maluku. The displaced, disregarded Naka’ela community survives in Seram, their land, but their language is only a shade, a ghostly memory.

In this review we outline the current evidence for the use of hydrogel rectal spacers in the treatment paradigm for prostate cancer with external beam radiation therapy. We review their development, summarize clinical evidence, risk of adverse events, best practices for placement, treatment planning considerations and finally we outline a framework and rationale for the utilization of rectal spacers when treating unfavorable risk prostate cancer with dose escalated Stereotactic Body Radiation Therapy (SBRT).

Abstract Background Preterm infants born 30 to 33 weeks’ gestation often require early support with intravenous fluids because of respiratory distress, hypoglycemia or feed intolerance. When full feeds are anticipated to be reached within the first week, risks associated with intravenous delivery mode and type must be carefully considered. Recommendations are for parenteral nutrition to be infused via central venous lines (because of the high osmolarity), however, given the risks associated with central lines, clinicians may opt for 10% glucose via peripheral venous catheter when the need is short-term. We therefore compare a low osmolarity peripheral intravenous parenteral nutrition (P-PN) solution with peripheral intravenous 10% glucose on growth rate in preterm infants born 30 to 33 weeks’ gestation. Methods In this parallel group, single centre, superiority, non-blinded, randomised controlled trial, 92 (P-PN 42, control 50) infants born 30+ 0 to 33+ 6 weeks’ gestation, were randomised within 24 h of age, to receive either P-PN (8% glucose, 30 g/L amino acids, 500 IU/L heparin and SMOFlipid®) or a control of peripheral intravenous 10% glucose. Both groups received enteral feeds according to hospital protocol. The primary outcome was rate of weight gain from birth to 21 days of age. Results The rate of weight gain was significantly increased in P-PN infants compared with control (P-PN, n = 42, 18.7, SD 6.6 g/d vs control, n = 50, 14.8, SD 6.0 g/d; adjusted mean difference 3.9 g/d, 95% CI 1.3 to 6.6; P = 0.004), with the effect maintained to discharge home. Days to regain birthweight were significantly reduced and length gain significantly increased in P-PN infants. One infant in the P-PN group had a stage 3 extravasation which rapidly resolved. Blood urea nitrogen and triglyceride levels were significantly higher in the P-PN group in the first week of life, but there were no instances of abnormally high levels. There were no significant differences in any other clinical or biochemical outcomes. Conclusion P-PN improves the rate of weight gain to discharge home in preterm infants born 30 to 33 weeks gestation compared with peripheral intravenous 10% glucose. Trial registration Australian New Zealand Clinical Trials Registry ACTRN12616000925448 . Registered 12 July 2016.