MyHealthAvatar (MHA) is built on the latest information and communications technology with the aim of collecting lifestyle and health data to promote citizen's wellbeing. According to the collected data, MHA offers visual analytics of lifestyle data, contributes to individualised disease prediction and prevention, and supports healthy lifestyles and independent living. The iManageCancer project aims to empower patients and strengthen self-management in cancer diseases. Therefore, MHA has contributed to the iManageCancer scenario and provides functionality to the iManageCancer platform in terms of its support of lifestyle management of cancer patients by providing them with services to help their cancer management. This paper presents two different MHA-based Android applications for breast and prostate cancer patients. The components in these apps facilitate health and lifestyle data presentation and analysis, including weight control, activity, mood and sleep data collection, promotion of physical exercise after surgery, questionnaires and helpful information. These components can be used cooperatively to achieve flexible visual analysis of spatiotemporal lifestyle and health data and can also help patients discover information about their disease and its management.
BACKGROUND Computerized clinical decision support system is a solution to promote ATLS protocol for traumatic injuries. To study its design based on user requirements and usability, a Kano questionnaire research to survey perspectives of physicians was undergone. OBJECTIVE This study aims to elicit user requirements for a CDSS treating traumatic patients in a hospital setting and it’s usability by evaluating the features of TFA. METHODS We applied Kano mode research studying user requirements to further provide theoretical support for the development of the system. A 5-level questionnaire was designed based on the perspectives of Kano. The features of TFA were evaluated by pairs of questions: first a functional question and subsequently a dysfunctional question. The questionnaire along with system introduction and instructions were sent to the physicians in ED from five different hospitals that work as regional trauma centers and have ability to treat severe trauma patients. RESULTS A total of 63 physicians in ED responded the questionnaire completely and were concluded into the study including 16 physicians qualified with ATLS certificate and 47 having not passed the ATLS training. A total of 16 features were rated and classified using the Kano evaluation table. Five features are classified as indifferent (5/16, 31.3%), with five being one-dimensional (5/16, 31.3%), four being attractive (4/16, 25%) and two being must-be (2/16,12.5%). Both physicians with and without ATLS experience were indifferent to most of the evaluated features (11/16, 68.8%). A difference in user requirements between physicians with ATLS qualification and those without the qualification regarding 3,4,8,13,14 features. CONCLUSIONS The study provides recommendations to developers on the user requirements that need to be addressed when developing a CDSS for advanced trauma life support care in-hospital. Two features of must-be attributes must be incorporated in the TFA. In addition, four features (attractive attributes) would result in higher user satisfaction. Among those five one-dimensional features, ISS and knowledge database display high score in both positive and negative values that indicates developers to especially prioritize the features to be implemented when developing the CDSS.
Article Figures and data Abstract Editor's evaluation eLife digest Introduction Results Discussion Materials and methods Data availability References Decision letter Author response Article and author information Metrics Abstract Malaria parasites avoid immune clearance through their ability to systematically alter antigens exposed on the surface of infected red blood cells. This is accomplished by tightly regulated transcriptional control of individual members of a large, multicopy gene family called var and is the key to both the virulence and chronic nature of malaria infections. Expression of var genes is mutually exclusive and controlled epigenetically, however how large populations of parasites coordinate var gene switching to avoid premature exposure of the antigenic repertoire is unknown. Here, we provide evidence for a transcriptional network anchored by a universally conserved gene called var2csa that coordinates the switching process. We describe a structured switching bias that shifts overtime and could shape the pattern of var expression over the course of a lengthy infection. Our results provide an explanation for a previously mysterious aspect of malaria infections and shed light on how parasites possessing a relatively small repertoire of variant antigen-encoding genes can coordinate switching events to limit antigen exposure, thereby maintaining chronic infections. Editor's evaluation This is an important study addressing the mechanisms of variant gene expression and switching in the malaria parasite Plasmodium falciparum. The work provides solid evidence supporting the existence of a non-random, highly structured switch pathway for var genes and identifies one var gene, called var2csa, as a sink node in this network. The findings consolidate previous observations and further the understanding of the enigmatic mechanism that underlies the regulation of the var gene family and antigenic variation in P. falciparum, which is paramount for immune evasion and acquired immunity and further influences malaria pathology. https://doi.org/10.7554/eLife.83840.sa0 Decision letter eLife's review process eLife digest Malaria causes severe illness and deaths in hundreds of thousands of people each year. Most of them are young children in Sub-Saharan Africa. The disease is transmitted when a mosquito carrying single-celled Plasmodium parasites bites a human, introducing the parasites into the bloodstream, where they enter red blood cells. When a red blood cell becomes infected, the parasite presents a protein on the cell's surface that the immune system can recognize to start fighting the infection. Immune cells then produce antibodies that flag infected cells for destruction, relieving the symptoms of the disease. To avoid being destroyed in this manner, the parasites repeatedly 'change' the protein that ends up on the surface of the red blood cells. With each change, the number of parasites rebounds, symptoms return, and the immune system must produce new antibodies. As the parasites and immune system battle it out, patients may experience repeated flare-ups of symptoms for well over a year. To change the protein that is presented on the surface of red blood cells, Plasmodium parasites switch the genes in the var gene family on and off one at a time. Each of these genes encodes a different surface protein, and the parasites may cycle through the entire var gene family during an infection. However, it remains a mystery how the millions of infecting parasites coordinate to produce the same surface protein each time. Zhang et al. show that a gene from Plasmodium parasites called var2csa is responsible for coordinating protein switching through a set pattern that allows the parasites to synchronize which protein they switch to next. Deleting the var2csa gene in malaria parasites blocks protein switching and disables this coordinated immune evasion tactic. Zhang et al.'s experiments provide new insights about protein switching in malaria parasites. Further research may help scientists characterize each step in the process and identify which steps can be targeted to treat malaria. While not a cure, treatments that disable protein switching could reduce the number of times patients relapse and relieve symptoms. More generally, the results of Zhang et al. describe a mechanism for coordinated gene expression that may be used in organisms other than Plasmodium, including humans. Introduction Malaria is a disease of enormous historical significance that continues to exert a heavy burden on health and economic development in many regions of the world (World Health Organization, 2021). The most virulent of the human malaria parasites is Plasmodium falciparum, a mosquito-borne pathogen that infects the circulating red blood cells (RBCs) of its hosts. While resident within the RBC, the parasites modify the host cell cytoskeleton through the insertion into the RBC membrane of an adhesive protein called Plasmodium falciparum erythrocyte member protein 1 (PfEMP1) (Baruch et al., 1995; Smith et al., 1995; Su et al., 1995). This enables adhesion to the vascular endothelium (Gardner et al., 1996), thereby avoiding filtration and destruction in the spleen (David et al., 1983; Barnwell et al., 1983), however this also exposes PfEMP1 as a target for adaptive immunity (Bull et al., 1998; Giha et al., 2000). To escape clearance by antibodies that recognize PfEMP1, parasites systematically change the form of PfEMP1 they express, thus continuously altering their antigenic signature and promoting a chronic infection that can extend over a year (reviewed in Deitsch and Dzikowski, 2017). Different forms of PfEMP1 are encoded by individual members of the var gene family, a collection of highly variable, paralogous genes numbering between 45 and 90 and distributed throughout the parasite's genome, primarily within subtelomeric regions or as tandemly arranged clusters within the interior of the chromosomes (Otto et al., 2018). Epigenetic mechanisms ensure that only a single gene is actively transcribed at a time (Scherf et al., 1998; Deitsch et al., 1999), a process with parallels to allelic exclusion of immunoglobulin genes (Corcoran, 2005) or mutually exclusive expression within the olfactory receptor gene family in mammals (Rodriguez, 2013). However, unlike these systems in which selection of the active gene is part of the differentiation process and thus permanent, var gene activation and silencing are reversible, thereby enabling parasites to switch which var gene is expressed, thus changing the form of PfEMP1 on the infected cell surface. Many attributes of the epigenetic processes that control var gene expression, including the histone modifications that mark a gene for activation or silencing, are shared with model eukaryotes (Chookajorn et al., 2007; Lopez-Rubio et al., 2009; Flueck et al., 2009). However, the added complexity of switching which gene is active while maintaining mutually exclusive expression is largely without precedent outside of pathogenic organisms. Moreover, given that the number of var genes within the parasite's genome is relatively limited, switching events must be coordinated to avoid rapid exhaustion of the parasite's variant capacity. Specifically, uncoordinated, random var gene switching by individual parasites within a circulating population that can number in the billions would result in rapid exposure of the entire var repertoire. In contrast, P. falciparum infections are characterized by rising and falling waves of parasitemia, with each wave representing a population of parasites expressing a single or small number of var genes (Bachmann et al., 2011; Bachmann et al., 2019; Kaestli et al., 2004). Modeling studies have suggested that in semi-immune hosts, an underlying structure or coordination to the switching process would be optimal for extending an infection (Recker et al., 2011; Noble and Recker, 2012; Noble et al., 2013) by limiting activation to a single or small number of genes at a time within the circulating parasite population. However, while communication between parasites has been suggested (Mantel et al., 2013; Regev-Rudzki et al., 2013), there is no evidence that this influences var gene expression patterns and there does not appear to be a strict switching order within the var gene family, therefore how this is accomplished remains entirely without explanation. In 2011, Recker et al. explored this phenomenon using mathematical modeling based on data from switching events observed in cultured parasites (Recker et al., 2011). They proposed that parasites do not switch directly from one gene to another, but rather that a population of parasites switches from a dominant var gene, through a switch-intermediate state in which many genes are transiently expressed, to either a new dominant transcript or back to the original. This model also predicted that specific genes could serve as either 'source' or 'sink' nodes and provide additional structure to the network. The model provided a compelling explanation for how a population of parasites that can reach up to 1010 individuals can display seemingly coordinated switching patterns without the need for communication between cells or a fixed order of gene activation. Further, it described both how parasites can extend a chronic infection as well as successfully reinfect individuals when partial immunity exists. However, to date no experimental data have provided a molecular basis for such a structured network, the hypothetical switch-intermediate state or the source/sink nodes predicted by this model. Here, we describe molecular genetic evidence that fulfils many of the predictions of the previously proposed mathematical model. We identified a universally conserved, unique var gene that displays characteristics of a sink node and plays a key role in coordinating transcriptional switching events. Deletion of this locus disrupts var gene switching, resulting in parasites that have a drastically reduced ability to change var gene expression, thus disabling the process of antigenic variation that is required to maintain a chronic infection. In addition, we describe an underlying pattern of biased var transcriptional activation which shifts overtime, providing the potential for a coordinated pattern of expression switching that could prevent premature exposure of the parasite's variant repertoire over the length of an infection. These data extend our understanding of antigenic variation beyond mathematical models and represent an important step forward in understanding the pathogenic nature of human malaria. Results Clonal parasite lines display either 'single' or 'many' var gene expression profiles and can transition between these two states The mathematical model derived by Recker et al. was based on observations of var expression patterns observed in recently isolated clonal parasite populations (Recker et al., 2011). The proposed transition from expression of a single var gene, through an intermediate state in which many genes are expressed, then back to a single gene that becomes dominant in the population is referred to as the 'single-many-single' model for var gene switching (Figure 1A). This is similar to the two-step model for olfactory receptor gene activation in vertebrates, which has recently been shown to involve an initial, transient state in which large numbers of genes are expressed at a low level, followed by selection of a single gene for stable expression (Tan et al., 2015). Given the observations from this model system and previous reports of var gene switching patterns, we attempted to experimentally validate the SMS model of structured switching and to determine the molecular requirements that underlie the hypothetical var gene network that forms the foundation for this pathway. Figure 1 with 2 supplements see all Download asset Open asset Detection of 'single' and 'many' var expression profiles in cultured parasite populations. (A) Schematic representation of the single-many-single (SMS) model for var gene transcriptional switching. Each circle represents expression of an individual var gene and arrows represent switches in expression. Switching events are hypothesized to transition from activation of a single gene (top) to a broad range of genes (middle) to a different single gene (bottom) or back to the original gene (reverse arrow). (B) var gene expression profiles for two clonal populations that display the single phenotype (clone 1, top) or the many phenotype (clone 2, bottom). var transcription levels were determined using a standardized quantitative real-time RT-PCR (qRT-PCR) protocol with the expression of each individual var gene displayed as relative copy number in the histogram. Error bars represent standard deviation of three biological replicates. (C) Total var expression for the two subclones shown in B, with transcripts from each individual var gene shown in a different color. For clone 1, transcripts from the dominant gene are marked, while both clones display similar levels of minor transcripts. (D) Clone tree of wildtype 3D7 parasites. Pie charts display the var expression profile for each subcloned population with each slice of the pie representing the expression level of a single var gene. Vertical and horizontal lines delineate sequential rounds of subcloning by limiting dilution. For parasite populations that display a dominantly expressed var gene, the annotation number is shown below the pie chart with the var type shown in parenthesis. The five subclones marked with an asterisk are further analysed in Figure 2. (E) Total var expression levels as determined by qRT-PCR for 74 subclones (see Figure 1—figure supplement 1). The median ± 95% confidence interval is shown, and an unpaired t-test indicates a ***p < 0.0001. The original proposal of the SMS model was based on analysis of var gene expression by Northern blotting and quantitative real-time RT-PCR (qRT-PCR) using the IT and 3D7 genetic backgrounds (Recker et al., 2011). Since this original description, the method for determining var expression patterns has become widely used for NF54 (Delemarre and van der Kaay, 1979) and 3D7 (Walliker et al., 1987) through the further refinement of a standardized qRT-PCR method developed specifically for this genetic background (Salanti et al., 2003). This standardized method enables rapid, quantitative assessment of the expression level of each var gene in the parasite's genome. We employed this method to examine var gene expression profiles obtained from recently cloned parasite lines derived from a single parent population of 3D7. Specifically, we determined the expression level of each var gene within each subcloned population approximately 5 weeks after cloning, the earliest time point from which we could obtain suitable parasite numbers. Interestingly, these subcloned populations displayed two fundamentally different expression patterns. Clones displayed either dominant, relatively high-level expression of a single var gene with low-level expression of other members of the family, as exemplified by clone 1 (Figure 1B, top panel), or alternatively they lacked expression of a dominant gene and instead only displayed heterogeneous, low-level expression of a large portion of the var gene family, as shown by clone 2 (Figure 1B, bottom panel). Measurement of the total level of var gene expression from all members of the family detected significantly fewer var transcripts in the expression profile of clone 2 (Figure 1C), consistent with the lack of a dominantly expressed gene and indicating that overall var expression is lower in this population in addition to being more heterogenous. Given that the number of generations after cloning was identical for both populations, these differences in var gene expression profiles presumably reflect differences in the initial var expression state or in switching frequency. Similar, rather dramatic differences in total var expression levels have been previously described for clonal lines derived from both the NF54 and IT parasite isolates (Merrick et al., 2015; Janes et al., 2011), suggesting this phenomenon is typical of cultured parasites of different genetic backgrounds. The two phenotypes, either high-level, stable expression of a dominant var gene or highly diverse, low-level expression of many genes, are consistent with the 'single' and 'many' expression states proposed in the SMS model (Recker et al., 2011). If parasites transition between the single and many states as part of var expression switching as proposed in the SMS model, and if this model applies to the two different var expression profiles we observed in our recently cloned lines, then the phenotypes should be reversible. Specifically, it should be possible to obtain 'single' parasites from a population of parasites that cumulatively expresses 'many' var genes, and vice versa. To test this hypothesis, we used serial subcloning by limiting dilution to isolate and examine a large number of additional subclones (Figure 1D). As predicted, we again obtained parasite populations that either displayed low-level expression of many var genes or high-level, stable expression of one or a small number of genes, regardless of which phenotype was displayed by the population from which the clone was derived (Figure 1D; additional clones are shown in Figure 2B). Thus, it appears that parasites can transition between these two states, leading to populations that display heterogenous expression of many var genes or relatively stable expression of a single, dominant var gene. We also anticipated that populations primarily consisting of parasites in the 'many' state would display lower total var expression levels than populations that express one or two dominant var transcripts. To test this prediction, a larger collection of 74 recently subcloned lines were examined and each subclone was determined to be primarily in either the 'single' or 'many' state (see Figure 1—figure supplement 1). Specifically, populations in which over 50% of the total var expression profile was derived from one or two genes were defined as 'singles' while populations with more diverse expression patterns were considered 'manys'. When total var transcript levels were determined by qRT-PCR, levels were significantly lower in the 'many' lines (Figure 1E), consistent with the initial observations shown in Figure 1B and the SMS model. To ensure that this phenomenon was not a property unique to parasites that had been in continuous culture for decades, we repeated the subcloning and var expression analysis with a line of NF54 (the original isolate from which 3D7 was derived) that had not been in culture for as many replicative cycles and that maintains many characteristics of parasites recently isolated from the field, for example gametocytogenesis and knob formation. These subcloned lines similarly displayed either the 'single' or 'many' phenotypes, with the 'singles' displaying higher levels of total var transcripts (Figure 1—figure supplement 2). Note that there is a very clear and statistically significant difference in total var expression levels between populations categorized as 'single' or 'many', however there is some overlap. We hypothesize this is because no population is completely homogeneous and that parasites in the single state contribute disproportionately to the overall expression profile of a population due to their higher expression level. Thus, mixed populations will display intermediate expression levels. Nonetheless the trend is very clear and statistically significant. Figure 2 Download asset Open asset Detection of var gene minor transcript expression profiles in clonal populations overtime. (A) Heatmap of var minor transcripts for clones 2–6. The clones were all derived from the same parent population as shown in Figure 1D. Pie charts show the initial var gene expression profiles above the heatmap. The annotation numbers for each var gene are shown to the left of the heatmap and organized according to var type (left, var2csa is considered separately in Figure 3). Six time points are included for each clone. Two genetically identical parasite populations (clones 7 and 8) also originally derived from 3D7 but grown separately for several years are shown for comparison. For clones 5 and 6, the dominant transcript (PF3D7_1240600 and PF3D7_0421100, respectively, marked by black boxes in the heatmap) was removed from the analysis to enable visualization of the minor transcripts. (B) Clone tree of wildtype 3D7. The tree is organized into three 'subclone generations' derived from initial clone 4 (top row). Pie charts display the var expression profile for each subclone. (C) Heatmap of var minor transcripts for the individual clones from each generation shown in B with the pattern of the parent population (clone 4) shown at the left for comparison. The annotation numbers for each var gene are shown to the left of the heatmap, and the gene order was organized according to var type. The order from left to right of each column in the heatmap corresponds to the order from left to right of the pie charts for each subclone generation shown in B. For parasites expressing the 'single' phenotype, the dominant transcript (marked by black boxes in the heatmap) was removed to enable visualization of the minor transcripts. Distinct semi-conserved pattern of var gene transcription underlies the 'single' and 'many' states and shifts slowly over time In our var expression analysis of recently cloned parasites populations, we observed that populations in both the 'many' and 'single' states expressed a subset of the var gene family at a low level (Figure 1C). Importantly, the entire var gene family is not equally represented within the subset of minor transcripts, suggesting that this low-level var gene activation is consistently biased toward certain var genes. If such intrinsic switching biases shift over time, they could shape the trajectory of var gene expression over the course of an infection and provide a model for how large populations of parasites could systematically cycle through their complement of var genes. This would lead to semi-coordinated var gene switching, thereby avoiding antibody-mediated clearance while protecting the majority of the variant repertoire. If true, this hypothesis provides a key insight into how antigenic variation with a small repertoire of genes can maintain a chronic infection, however direct evidence for shifting switching biases within the context of the SMS model has been lacking. To specifically examine minor transcript expression, we compared the patterns of minor transcripts from five of the newly isolated clonal populations shown by asterisks in Figure 1D that displayed both the 'single' and 'many' expression profiles. RNA was obtained on days 0, 20, 45, 90, 116, and 147 after initiation of the experiment and the expression level of each var gene determined by qRT-PCR. The dominant var transcript was removed from the expression profile of 'single' populations and the expression levels of the remainder of the var gene family displayed in a heatmap, thus enabling easy visualization of the minor transcript expression pattern. var2csa is a unique var gene that often dominates cultured parasite populations and therefor was considered separately in Figure 3. We used this method to determine if a distinct pattern exists and if it shifts overtime (Figure 2A). The heatmap shows that there are subsets of var genes that are more highly represented within the profiles of minor transcripts, and this pattern is largely shared within this group of closely related subclones. However, the pattern is not fixed and displays variation between subclones and over time. Two additional parasite populations that are genetically identical but had been cultured separately for several years (clones 7 and 8) displayed entirely different patterns of minor transcripts, providing additional evidence that the pattern is not fixed (Figure 2A). The similarity of the patterns displayed by the five subclones examined here likely reflects that these populations originated from a common original clonal population. Figure 3 Download asset Open asset Convergence to var2csa expression in long-term cultures and targeted deletion of the var2csa locus. (A) Changes in var expression over time in five clonal parasite populations, three 'manys' (clones 2–4) and two 'singles' (clones 5 and 6), over several months of continuous culture. Expression of var2csa is shown in red. (B) Schematic diagram showing the truncation of the end of chromosome 12 by telomere healing. Telomere repeats are shown as slanted lines and the telomere-associated repeat elements (TAREs) are shown as an open box. The interior of the chromosome is displayed as a dashed line. A ~60 kb deletion, including three var genes (blue), three rif genes (green), and the acs7 gene is shown. (C) Schematic diagram showing the var2csa locus and the plasmid containing homology blocks for targeted integration (hb1 and hb2). The crossed lines linking the plasmid to the chromosome signify sites of double cross over recombination leading to deletion of approximately 2.5 kb upstream of the va2csa gene, including the promoter. To further investigate the shifting pattern of var minor transcript expression, we employed a parallel approach. We again performed serial subcloning starting from clone 4, thereby obtaining additional closely related populations. If the pattern of minor transcripts is semi-conserved and shifts slowly over time, it should be largely shared in all the subcloned populations, regardless of whether they display a 'single' or 'many' var expression profile, or if they express different dominant var genes. Rather than following individual populations overtime, we instead isolated three 'subclone generations' (Figure 2B) and determined both the dominant var transcript as well as the pattern of minor var transcripts for each subcloned population. Similar to our previous observations, the subcloned populations displayed both 'single' and 'many' expression patterns, and the dominant var gene varied among the 'single' subclones (Figure 2B). Comparison of the var minor transcripts once again detected the existence of a distinct expression pattern that was semi-conserved but not fixed within this group of closely related populations (Figure 2C). Switching events converge overtime to var2csa, a conserved var locus Previously, Mok et al. observed that after extended growth in culture, most parasite populations eventually converged to stable expression of a unique, highly conserved var gene called var2csa (UpsE), proposing that this gene could represent a default choice for var gene switching (Mok et al., 2008). We similarly previously observed convergence to var2csa expression when we artificially induced accelerated var gene switching by altering the activity of histone modifiers (Ukaegbu et al., 2014; Ukaegbu et al., 2015), further suggesting that the var2csa locus could occupy a unique position in the var switching hierarchy. To determine if var2csa likewise displayed preferential activation in our recently subcloned parasite populations, we more closely examined var transcript prevalence over time in the expression profiles for the five clonal lines shown in Figure 2A. Consistent with previous observations (Mok et al., 2008; Ukaegbu et al., 2015), all the clones, regardless of their initial switching frequency, eventually displayed significant expression levels of var2csa (Figure 3A). While how quickly each population converged to var2csa expression varied, in each instance, switching to var2csa was highly favored, suggesting that this var gene might occupy a unique position within the var gene switching hierarchy. The var2csa locus is required for efficient var gene switching With respect to the SMS model, var2csa displays the properties of a sink node, and is by far the most likely var gene to become highly activated in our cultures (Figure 3A). This gene also displays several other properties that make it an atypical member of the family, including universal conservation extending to related species that infect chimpanzees and gorillas (Zilversmit et al., 2013; Gross et al., 2021) and the presence of a unique upstream regulatory region that includes an upstream open reading frame (uORF) resulting in translational repression of the mRNA (Amulic et al., 2009; Bancells and Deitsch, 2013; Chan et al., 2017). The gene can therefore transcribe mRNA without producing PfEMP1 and thus could be transcriptionally activated repeatedly over the course of an infection without generating an antibody response by the host. Based on these unusual properties, we hypothesized that var2csa represents the dominant sink node at the center of the SMS network. If correct, we predicted that loss of var2csa would significantly alter how parasites undergo var gene switching. We recently isolated numerous independent clonal parasite lines in which the entire subtelomeric region surrounding var2csa was deleted from the parasite's genome and the chromosome end 'healed' through de novo telomere addition (Figure 3B; Zhang et al., 2019). To complement this set of deletions, we employed CRISPR/Cas9-mediated genome editing to replace the var2csa upstream region with a plasmid construct that included a drug selectable marker, thereby deleting the entire promoter region and rendering the gene non-functional (Figure 3C). Several independent clones were obtained from independent transfections of both 3D7 and NF54 that had this integration event and the structure of the resulting l
To investigate the effective method in treatment of pediatric chronic sinusitis.Two hundred and ten children were clinically diagnosed as chronic sinusitis and randomly divided into three groups as pulmicort, rhinocort and routine treatment group, respectively. All the patients in different group were systemic treated by corresponding method for two weeks.The effective rates were 84% for pulmicort treatment group, 61% for rhinocort treatment group and 48% for routine treatment group, so the effective rate for the patients treated with pulmicort were significantly higher than that with either rhinocort or routine treatment.Pulmicort can be used to treat pediatric chronic sinusitis with higher effective rate.
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