Challenges in the profitability of small-scale broiler farming by avoiding injudicious use of drugs and additives.

The aim of the current study was to determine the present scenario of injudicious use of drugs and additives in small-scale broiler operations and whether broilers can be produced successfully and profitably without the injudicious use of drugs and additives. First, a survey was undertaken in relation to farmers' basic information and general management methods in commercial broilers, with special attention given to the usage of medications and additives in drinking water. Second, based on the survey data, an experimental trial was carried out to compare the growth performance and economic profitability of rearing broilers with and without the use of said drugs and additives. A total of 540 broiler DOCs were allotted into three treatments: T1 = self-formulated feed (SFF) with judicious use of drugs and additives; T2 = commercial feed with judicious use of drugs and additives (JUDA) and T3 = commercial feed with injudicious use of drugs and additives (InJUDA), with six replications (30 birds/replication) in each. The results showed that the farmers used a variety of drugs and additives in 35 days of broiler rearing; however, the farmers usually did not consult with veterinary practitioners, instead relying on and being instructed by local dealers and medicine company representatives. Although the medications and additives account for almost 6-8% of total production costs, the experimental trial clearly demonstrated that the broilers kept with either JUDA or InJUDA showed statistically (p < 0.05) similar BW (2181.93 g & 2222.53 g/bird), BWG (2110.0 g & 2129.91 g/bird), and FCR (1.62 & 1.57, respectively), whereas broilers in the SFF group showed significantly lower growth performances (BW = 1799.31 g/bird, BWG = 1746.19 g/bird, and FCR = 1.93, respectively). The net profit per kg bird in the JUDA group was substantially (p < 0.05) greater (BDT- 27.34/-), followed by the SFF group (BDT- 25.56/) and the InJUDA group (BDT- 24.49/-). Taken together, these findings suggest that profitable broiler farming is possible without the injudicious use of drugs and additives.

Suppression of FOXO1 attenuates inflamm-aging and improves liver function during aging.

The liver is a key metabolic organ that maintains whole-body nutrient homeostasis. Aging-induced liver function alterations contribute to systemic susceptibility to aging-related diseases. However, the molecular mechanisms of liver aging remain insufficiently understood. In this study, we performed bulk RNA-Seq and single-cell RNA-Seq analyses to investigate the underlying mechanisms of the aging-induced liver function changes. We found that liver inflammation, glucose intolerance, and liver fat deposition were aggravated in old mice. Aging significantly increased pro-inflammation in hepatic macrophages. Furthermore, we found that Kupffer cells (KCs) were the major driver to induce pro-inflammation in hepatic macrophages during aging. In KCs, aging significantly increased pro-inflammatory levels; in monocyte-derived macrophages (MDMs), aging had a limited effect on pro-inflammation but led to a functional quiescence in antigen presentation and phagosome process. In addition, we identified an aging-responsive KC-specific (ARKC) gene set that potentially mediates aging-induced pro-inflammation in KCs. Interestingly, FOXO1 activity was significantly increased in the liver of old mice. FOXO1 inhibition by AS1842856 significantly alleviated glucose intolerance, hepatic steatosis, and systemic inflammation in old mice. FOXO1 inhibition significantly attenuated aging-induced pro-inflammation in KCs partially through downregulation of ARKC genes. However, FOXO1 inhibition had a limited effect on aging-induced functional quiescence in MDMs. These results indicate that aging induces pro-inflammation in liver mainly through targeting KCs and FOXO1 is a key player in aging-induced pro-inflammation in KCs. Thus, FOXO1 could be a potential therapeutic target for the treatment of age-associated chronic diseases.

A Hyperparameter-Free, Fast and Efficient Framework to Detect Clusters From Limited Samples Based on Ultra High-Dimensional Features.

Clustering is a challenging problem in machine learning in which one attempts to group N objects into K0 groups based on P features measured on each object. In this article, we examine the case where N ≪ P and K0 is not known. Clustering in such high dimensional, small sample size settings has numerous applications in biology, medicine, the social sciences, clinical trials, and other scientific and experimental fields. Whereas most existing clustering algorithms either require the number of clusters to be known a priori or are sensitive to the choice of tuning parameters, our method does not require the prior specification of K0 or any tuning parameters. This represents an important advantage for our method because training data are not available in the applications we consider (i.e., in unsupervised learning problems). Without training data, estimating K0 and other hyperparameters-and thus applying alternative clustering algorithms-can be difficult and lead to inaccurate results. Our method is based on a simple transformation of the Gram matrix and application of the strong law of large numbers to the transformed matrix. If the correlation between features decays as the number of features grows, we show that the transformed feature vectors concentrate tightly around their respective cluster expectations in a low-dimensional space. This result simplifies the detection and visualization of the unknown cluster configuration. We illustrate the algorithm by applying it to 32 benchmarked microarray datasets, each containing thousands of genomic features measured on a relatively small number of tissue samples. Compared to 21 other commonly used clustering methods, we find that the proposed algorithm is faster and twice as accurate in determining the "best" cluster configuration.

Bias due to censoring of deaths when calculating extra length of stay for patients acquiring a hospital infection.

BACKGROUND: In many studies the information of patients who are dying in the hospital is censored when examining the change in length of hospital stay (cLOS) due to hospital-acquired infections (HIs). While appropriate estimators of cLOS are available in literature, the existence of the bias due to censoring of deaths was neither mentioned nor discussed by the according authors. METHODS: Using multi-state models, we systematically evaluate the bias when estimating cLOS in such a way. We first evaluate the bias in a mathematically closed form assuming a setting with constant hazards. To estimate the cLOS due to HIs non-parametrically, we relax the assumption of constant hazards and consider a time-inhomogeneous Markov model. RESULTS: In our analytical evaluation we are able to discuss challenging effects of the bias on cLOS. These are in regard to direct and indirect differential mortality. Moreover, we can make statements about the magnitude and direction of the bias. For real-world relevance, we illustrate the bias on a publicly available prospective cohort study on hospital-acquired pneumonia in intensive-care. CONCLUSION: Based on our findings, we can conclude that censoring the death cases in the hospital and considering only patients discharged alive should be avoided when estimating cLOS. Moreover, we found that the closed mathematical form can be used to describe the bias for settings with constant hazards.

Psychiatric case notes: symptoms of mental illness and their attribution at the Maudsley Hospital, 1924-35.

Case notes of patients treated at the Maudsley Hospital during the interwar period provided data about diagnosis, symptoms and beliefs about mental illness. In the absence of effective treatments, patients were investigated in detail in the hope that connections between disease processes might be revealed. We analysed a randomly-selected sample of 700 patients taken equally from 1924, 1928, 1931 and 1935. Eight groups (three representing psychosis and five indicating psychological disorders) were identified on the basis of symptom clusters. Formal diagnosis did not correlate with clusters. Although there was a measure of agreement between patients and doctors about the cause of mental illness, stigma may have inhibited discussion of some themes. Psychiatric diagnosis was informed by symptoms but not determined by them. In an era before classification systems were tested for reliability, diagnosis was fluid, reflecting changing hypotheses about causation, pathology and treatment. Attributions were associated with diagnosis rather than symptoms.

The Maudsley Hospital and the Rockefeller Foundation: the impact of philanthropy on research and training.

Opened in February 1923 to raise the status of academic psychiatry in the UK, the Maudsley Hospital struggled to secure grant income. Without a track record of published research and lacking internationally recognized clinicians, it failed to impress the British Medical Research Council. To challenge leading U.S. and German departments of neuropsychiatry, Edward Mapother, the medical superintendent, looked overseas for investment in an "institute of psychiatry." Intense lobbying and a modified strategy for research and training designed to meet the Rockefeller Foundation's prioritization of psychiatry and medical specialization ultimately led to a significant endowment. Alan Gregg and Daniel O'Brien at the Foundation played a pivotal role in re-defining the Maudsley's programs of research and teaching. Pressure on Mapother to attract funding was matched by that on administrators required to show that their philanthropy had yielded tangible gains in public health. While wealthy charities, like the Rockefeller, often had a vision of the direction that they wished to pull medical science, and they provided much needed income, the impact of their policy agenda was not without drawbacks. Institutions unwilling to embrace a charity's philosophy were unlikely to secure grants, while those that did might find themselves drawn into less optimal areas.

Managing the 'unmanageable': interwar child psychiatry at the Maudsley Hospital, London.

When opened as a post-graduate teaching and research hospital in 1923, the Maudsley made virtually no provision for the treatment of children. Yet its children's department saw sustained growth during the interwar period. This expansion is explored in relation to novel behaviourist hypotheses and the forging of formal links with local government and charitable bodies. The recruitment of psychologists, educators and specialist social workers fostered a multidisciplinary approach through case conferences. This development would structure the theoretical origins of child psychiatry, in particular influencing the role and interpretation of psychoanalytic theory within it. The theoretical orientation of child psychiatry and the practical treatment of children represented an area of dynamic change and innovation at a time when adult psychiatry struggled to discover effective treatments or achieve breakthroughs in causal understanding.