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Substantial progress has been made in the standardization of nomenclature for paediatric and congenital cardiac care. In 1936, Maude Abbott published her Atlas of Congenital Cardiac Disease, which was the first formal attempt to classify congenital heart disease. The International Paediatric and Congenital Cardiac Code (IPCCC) is now utilized worldwide and has most recently become the paediatric and congenital cardiac component of the Eleventh Revision of the International Classification of Diseases (ICD-11). The most recent publication of the IPCCC was in 2017. This manuscript provides an updated 2021 version of the IPCCC.
The International Society for Nomenclature of Paediatric and Congenital Heart Disease (ISNPCHD), in collaboration with the World Health Organization (WHO), developed the paediatric and congenital cardiac nomenclature that is now within the eleventh version of the International Classification of Diseases (ICD-11). This unification of IPCCC and ICD-11 is the IPCCC ICD-11 Nomenclature and is the first time that the clinical nomenclature for paediatric and congenital cardiac care and the administrative nomenclature for paediatric and congenital cardiac care are harmonized. The resultant congenital cardiac component of ICD-11 was increased from 29 congenital cardiac codes in ICD-9 and 73 congenital cardiac codes in ICD-10 to 318 codes submitted by ISNPCHD through 2018 for incorporation into ICD-11. After these 318 terms were incorporated into ICD-11 in 2018, the WHO ICD-11 team added an additional 49 terms, some of which are acceptable legacy terms from ICD-10, while others provide greater granularity than the ISNPCHD thought was originally acceptable. Thus, the total number of paediatric and congenital cardiac terms in ICD-11 is 367. In this manuscript, we describe and review the terminology, hierarchy, and definitions of the IPCCC ICD-11 Nomenclature. This article, therefore, presents a global system of nomenclature for paediatric and congenital cardiac care that unifies clinical and administrative nomenclature.
The members of ISNPCHD realize that the nomenclature published in this manuscript will continue to evolve. The version of the IPCCC that was published in 2017 has evolved and changed, and it is now replaced by this 2021 version. In the future, ISNPCHD will again publish updated versions of IPCCC, as IPCCC continues to evolve.
Quantitative plant biology is an interdisciplinary field that builds on a long history of biomathematics and biophysics. Today, thanks to high spatiotemporal resolution tools and computational modelling, it sets a new standard in plant science. Acquired data, whether molecular, geometric or mechanical, are quantified, statistically assessed and integrated at multiple scales and across fields. They feed testable predictions that, in turn, guide further experimental tests. Quantitative features such as variability, noise, robustness, delays or feedback loops are included to account for the inner dynamics of plants and their interactions with the environment. Here, we present the main features of this ongoing revolution, through new questions around signalling networks, tissue topology, shape plasticity, biomechanics, bioenergetics, ecology and engineering. In the end, quantitative plant biology allows us to question and better understand our interactions with plants. In turn, this field opens the door to transdisciplinary projects with the society, notably through citizen science.
To estimate the impact of California’s antimicrobial stewardship program (ASP) mandate on methicillin-resistant Staphylococcus aureus (MRSA) and Clostridioides difficile infection (CDI) rates in acute-care hospitals.
Centers for Medicare and Medicaid Services (CMS)–certified acute-care hospitals in the United States.
2013–2017 data from the CMS Hospital Compare, Provider of Service File and Medicare Cost Reports.
Difference-in-difference model with hospital fixed effects to compare California with all other states before and after the ASP mandate. We considered were standardized infection ratios (SIRs) for MRSA and CDI as the outcomes. We analyzed the following time-variant covariates: medical school affiliation, bed count, quality accreditation, number of changes in ownership, compliance with CMS requirements, % intensive care unit beds, average length of stay, patient safety index, and 30-day readmission rate.
In 2013, California hospitals had an average MRSA SIR of 0.79 versus 0.94 in other states, and an average CDI SIR of 1.01 versus 0.77 in other states. California hospitals had increases (P < .05) of 23%, 30%, and 20% in their MRSA SIRs in 2015, 2016, and 2017, respectively. California hospitals were associated with a 20% (P < .001) decrease in the CDI SIR only in 2017.
The mandate was associated with a decrease in CDI SIR and an increase in MRSA SIR.
This paper reviews current knowledge of the structure, genesis, cytochemistry and putative functions of the haplosporosomes of haplosporidians (Urosporidium, Haplosporidium, Bonamia, Minchinia) and paramyxids (Paramyxa, Paramyxoides, Marteilia, Marteilioides, Paramarteilia), and the sporoplasmosomes of myxozoans (Myxozoa – Malacosporea, Myxosporea). In all 3 groups, these bodies occur in plasmodial trophic stages, disappear at the onset of sporogony, and reappear in the spore. Some haplosporidian haplosporosomes lack the internal membrane regarded as characteristic of these bodies and that phylum. Haplosporidian haplosporogenesis is through the Golgi (spherulosome in the spore), either to form haplosporosomes at the trans-Golgi network, or for the Golgi to produce formative bodies from which membranous vesicles bud, thus acquiring the external membrane. The former method also forms sporoplasmosomes in malacosporeans, while the latter is the common method of haplosporogenesis in paramyxids. Sporoplasmogenesis in myxosporeans is largely unknown. The haplosporosomes of Haplosporidium nelsoni and sporoplasmosomes of malacosporeans are similar in arraying themselves beneath the plasmodial plasma membrane with their internal membranes pointing to the exterior, possibly to secrete their contents to lyse host cells or repel haemocytes. It is concluded that these bodies are probably multifunctional within and between groups, their internal membranes separating different functional compartments, and their origin may be from common ancestors in the Neoproterozoic.
Postprandial glycaemia and insulinaemia are important risk factors for type 2 diabetes. The prevalence of insulin resistance in adolescents is increasing, but it is unknown how adolescent participant characteristics such as BMI, waist circumference, fitness and maturity offset may explain responses to a standard meal. The aim of the present study was to examine how such participant characteristics affect the postprandial glycaemic and insulinaemic responses to an ecologically valid mixed meal. Data from the control trials of three separate randomised, crossover experiments were pooled, resulting in a total of 108 participants (fifty-two boys, fifty-six girls; aged 12·5 (SD 0·6) years; BMI 19·05 (SD 2·66) kg/m2). A fasting blood sample was taken for the calculation of fasting insulin resistance, using the homoeostatic model assessment of insulin resistance (HOMA-IR). Further capillary blood samples were taken before and 30, 60 and 120 min after a standardised lunch, providing 1·5 g/kg body mass of carbohydrate, for the quantification of blood glucose and plasma insulin total AUC (tAUC). Hierarchical multiple linear regression demonstrated significant predictors for plasma insulin tAUC were waist circumference, physical fitness and HOMA-IR (F(3,98) = 36·78, P < 0·001, adjusted R2 = 0·515). The variance in blood glucose tAUC was not significantly explained by the predictors used (F(7,94) = 1·44, P = 0·198). Significant predictors for HOMA-IR were BMI and maturity offset (F(2,102) = 14·06, P < 0·001, adjusted R2 = 0·021). In summary, the key findings of the study are that waist circumference, followed by physical fitness, best explained the insulinaemic response to an ecologically valid standardised meal in adolescents. This has important behavioural consequences because these variables can be modified.
The career of Ernst Fraenkel in Nazi Germany poses a dilemma. How did he accomplish as much as he did – as a covert pamphleteer, an overt political lawyer, and a scholar – and still avoid arrest? The resolution of this dilemma poses another question. What might Fraenkel’s accomplishments under the Nazi regime show about the possibilities of liberal lawyering in a dictatorship?
Fraenkel’s book The Dual State has stood out for the first and third of its three parts. The first part set forth a provocative analysis of the Nazi legal system, dividing it into the prerogative and normative states. The third part argued that Nazism served the needs of late monopoly capitalism, drawing the sting of later critics. But the middle part on Nazism’s legal doctrine, tucked between the earlier part with pioneering analysis and the later one with a dated interpretation, has, at least until recently, suffered neglect.
Fraenkel took two main approaches to resisting Nazi rule: opposition lawyering and underground writing. From the very beginning, in 1933, he assisted clients by providing defense in criminal prosecutions, representation in labor cases, and general legal advice, as well as by engaging in legal consultations with colleagues. He also never stopped analyzing political developments.
On September 11, 1933, in Samaden, Switzerland, outside St. Moritz, a German Jewish lawyer from Berlin shot himself to death. On January 30, Hitler had become Germany’s Chancellor; on February 27, a blazing fire gutted the main chamber of Germany’s Reichstag, its parliament building; and in late March the lawyer’s non-Jewish partner had told him that he intended to dissolve their practice together. The partner denied being an anti-Semite, of course, but times had changed and he needed to worry about his own family and his own responsibilities. Around the same time, a former client, now a member of the SA, the organization of Nazi paramilitary street fighters, warned the lawyer that he was no longer safe in Berlin and must leave.
hen the seventeenth-century English poet John Donne famously wrote in a Meditation that “no man is an island,” he was not contemplating the plight of opponents to a regime like Nazi Germany’s. But, in one sense, his vivid metaphor applies to them, too. Acting in a shrinking world, losing friends and opportunities, and knowing that their foes might lie in wait around any corner, Nazism’s opponents still rarely acted alone. They worked with others. Fraenkel often did. But if he was, in Donne’s words, still “a piece of the continent, a part of the main,” Fraenkel stood out. Among other things, he was unusual in relating his own direct experience resisting Nazi oppression to an attempt to set forth a logically developed theory justifying resistance.
On January 19, 1934, Fraenkel wrote to a certain Wally Höppner and Gertrud Neumann about what had happened to her husband. Having inquired at police headquarters, Fraenkel had learned of a warrant for her husband’s arrest for high treason for having conspired to maintain outlawed Social Democratic Party organizations. Fraenkel wrote that he expected that authorities would soon move the nearly fifty men already arrested in the affair to protective custody at Berlin’s central jail at Moabit.