Search

Patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) often receive antibacterial prophylaxis. Antibacterial agents can cause elevations in the prothrombin time and international normalized ratio (INR). The impact of prophylactic antibacterials on the coagulation profiles and bleeding risk in patients with AML/MDS is unknown. We evaluated patients with AML or MDS who were being admitted to the hospital. The cohort was divided into two groups of patients: (1) those receiving and (2) those not receiving prophylactic antibacterials, at the time of admission. We conducted a retrospective cohort study of adult patients with AML/MDS admitted to Yale-New Haven Hospital between 2015–2019. The study was approved by the Yale Institutional Review Board. Inclusion criteria included patients >18 years old with a diagnosis of AML or MDS admitted to the hospital. We identified 150 individual patient encounters with active AML/MDS admitted to Yale-New Haven of which 32 occurred while on and 118 while off antibacterial prophylaxis. Median duration of pre-admission antibacterial exposure was 2 (range: 0.07–24) months. Patients on antibacterial prophylaxis had higher INR (median 1.14 vs. 1.03, p = 0.0002), and higher partial thromboplastin time prolongation (median 26.5 vs. 24.3, p < 0.0014), than patients without antibacterial prophylaxis. Patients without antibacterial prophylaxis had higher rates of bleeding using the ISTH-defined criteria (24.6% vs. 6.3%, p = 0.043), including higher rates of ISTH major (2 vs. 0) and clinically relevant bleeding (9 vs. 0). Patients with AML/MDS on antibacterial prophylaxis were more likely to have an abnormal coagulation profile when compared with their counterparts not on prophylaxis. Conversely, rates of bleeding were higher in patients not on prophylaxis. These data suggest that prophylactic antibacterials do not increase bleeding risk in patients with AML/MDS.

Coarctation of aorta is a common condition usually diagnosed during childhood. During adulthood they are usually diagnosed during evaluation of secondary hypertension or resistant hypertension. We report a case of young female who was asymptomatic and found to have high blood pressure during routine clinical evaluation. During physical examination she had absent femoral pulses which lead to suspicion of presence of coarctation. She underwent surgical procedure with interposition graft. After follow up of one year she is doing well and her blood pressure under control with a single medication.

Radiocontrast material is among the common drugs causing allergic reaction. Mostly it is well tolerated. The symptoms range from mild with urticaria to fatal anaphylaxis, developing rapidly. Anaphylaxis is the most severe form of radiocontrast media (RCM) induced hypersensitivity reaction. With more use of diagnostic and therapeutic procedure, the use of the radiocontrast media is increasing. We report here two cases of severe anaphylactic reaction that occurred during the coronary intervention for myocardial infarction.

This paper proposes an enhanced time delay based current component identification method for single-phase systems to overcome the absence of filtering and poor grid frequency response of conventional method. The proposed technique integrates a delayed signal cancellation (DSC) with a time delay unit, to incorporate a dc offset rejection feature, while maintaining speedy and precise extraction of orthogonal current components. The frequency adaption is also developed through the incorporation of linear interpolation. The dynamic and steady-state performance of the proposed method is analysed and compared with two advanced second-order generalised integrator (SOGI) based methods, namely, modified SOGI and cascaded SOGI under different operating scenarios. The simulation and experimental results substantiate the advantage of zero steady-state error and lower settling time of the proposed solution while exhibiting comparable overshoot with advanced SOGI based methods.

Phase-locked loops (PLL) are widely used in the synchronization of grid interfaced power converters. One solution is based on orthogonal signal generation (OSG), which requires the grid frequency information for their appropriate operation. This article developed a new solution to achieve the PLL function for single-phase grid interconnection but eradicate additional frequency feedback loops in the traditional architecture of all-pass filter PLL (APF-PLL). Four new topologies are developed along with their small-signal modeling and dynamic analysis. A thorough comparison among them on their dynamic response, steady-state accuracy, implementation, and disturbance rejection capability is carried out. Finally, the best approach of frequency-fixed (FF) APF-PLL is experimentally evaluated with frequency adaptive APF-PLL and FF PLLs belonging to time delay (TD) and second-order generalized integrator (SOGI) families.

Complex coefficient filters (CCFs) are widely used for phase-locked loop (PLL) in three-phase power systems, while its usage is largely sparse in the single-phase domain. Single-phase CCF-PLLs so far reported in the literature do not yield satisfactory performances at off-nominal frequency conditions, which is a crucial PLL attribute. Whether they are a suitable filtering technique of choice for single-phase PLL is yet to be formally documented in a methodological way. In this regard, this article derives an enhanced version of the single-phase CCF-PLL (ECCF-PLL), which is able to provide accurate estimation of grid parameters in dynamically changing grid frequency environment. The proposed ECCF-PLL is then numerically and experimentally compared with few other single-phase PLLs to gauge its efficacy and suitability. The test shows the advantage of harmonic robustness from ECCF-PLL, which is specifically useful in a weak grid.

Episodes of Acute exacerbation (AE) of Idiopathic Pulmonary fibrosis (IPF) are important events in the disease trajectory of IPF, associated with punctuated decline in lung function with significant mortality and morbidity associated with it. These episodes are idiosyncratic, and often unpredictable and may have triggers. Our diagnostic criteria for these events, etiology, pathogenesis, risk factors and management continue to evolve over the years, with limited availability of qualitative research data to help guide management. Outcome in general is poor with no well-defined therapy but prevention may be possible with use of Nintedanib. Our chapter aims to explore the contemporary knowledge of the key aspects of this disease entity.

The mechanisms by which excessive systemic activation of adaptive T lymphocytes, as in cytokine release syndrome (CRS), leads to innate immune cell-mediated acute lung injury (ALI) or acute respiratory distress syndrome, often in the absence of any infection, remains unknown. Here, we investigated the roles of IFN-γ and IL-17A, key T-cell cytokines significantly elevated in patients with CRS, in the immunopathogenesis of CRS-induced extrapulmonary ALI. CRS was induced in wild-type (WT), IL-17A- and IFN-γ knockout (KO) human leukocyte antigen-DR3 transgenic mice with 10 μg of the superantigen, staphylococcal enterotoxin B, given intraperitoneally. Several ALI parameters, including gene expression profiling in the lungs, were studied 4, 24, or 48 hours later. Systemic T-cell activation with staphylococcal enterotoxin B resulted in robust upregulation of several chemokines, S100A8/A9, matrix metalloproteases, and other molecules implicated in tissue damage, granulocyte as well as agranulocyte adhesion, and diapedesis in the lungs as early as 4 hours, which was accompanied by subsequent neutrophil/eosinophil lung infiltration and severe ALI in IFN-γ KO mice. These pathways were significantly underexpressed in IL-17A KO mice, which manifested mildest ALI and intermediate in WT mice. Neutralization of IFN-γ worsened ALI in WT and IL-17A KO mice, whereas neutralizing IL-17A did not mitigate lung injury in IFN-γ KO mice, suggesting a dominant protective role for IFN-γ in ALI and that IL-17A is dispensable. Ruxolitinib, a Janus kinase inhibitor, increased ALI severity in WT mice. Thus, our study identified novel mechanisms of ALI in CRS and its differential modulation by IFN-γ and IL-17A.

The mechanisms by which excessive systemic activation of adaptive T lymphocytes, as in cytokine release syndrome (CRS), leads to innate immune cell-mediated acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), often in the absence of any infection, remains unknown. Here, we investigated the roles of interferon (IFN)- and IL-17A, key T cell cytokines that are significantly elevated in CRS patients, in the immunopathogenesis CRS-induced extrapulmonary ALI (eALI). CRS was induced in wild-type (WT), IL-17A- and IFN--knockout (KO) human leukocyte antigen (HLA)-DR3 transgenic mice with 10 g of the superantigen, staphylococcal enterotoxin B (SEB), given intraperitoneally. Several ALI parameters including gene expression profiling in the lungs were studied 4, 24 or 48 hours later. Systemic T cell activation with SEB resulted in robust upregulation of several chemokines, S100A8/A9, matrix metalloproteases and other molecules implicated in tissue damage, granulocyte as well as agranulocyte adhesion and diapedesis in the lungs as early as 4 hours, which was accompanied by subsequent neutrophil/eosinophil lung infiltration and severe ALI in IFN-KO mice. These pathways were significantly under-expressed in IL-17AKO mice which manifested mildest ALI and intermediate in WT mice. Neutralization of IFN- worsened ALI in WT and IL-17AKO mice, whereas neutralizing IL-17A did not mitigate lung injury in IFN-KO mice, suggesting a dominant protective role for IFN- in ALI and that IL-17A is dispensable. Ruxolitinib, a Janus kinase inhibitor, increased ALI severity in WT mice. Thus, our study identified novel mechanisms of ALI in CRS and its differential modulation by IFN- and IL-17A.

Pneumonia causes a significant burden of disease worldwide. Although all populations are at risk of pneumonia, those at extremes of age and those with immunosuppressive disorders, underlying respiratory disease, and critical illness are particularly vulnerable. Although clinical practice guidelines addressing the management and treatment of pneumonia exist, few of the supporting studies focus on the crucial contributions of the host in pneumonia pathogenesis and recovery. Such essential considerations include the host risk factors that lead to susceptibility to lung infections; biomarkers reflecting the host response and the means to pursue host-directed pneumonia therapy; systemic effects of pneumonia on the host; and long-term health outcomes after pneumonia. To address these gaps, the Pneumonia Working Group of the Assembly on Pulmonary Infection and Tuberculosis led a workshop held at the American Thoracic Society meeting in May 2018 with overarching objectives to foster attention, stimulate research, and promote funding for short-term and long-term investigations into the host contributions to pneumonia. The workshop involved participants from various disciplines with expertise in lung infection, pneumonia, sepsis, immunocompromised patients, translational biology, data science, genomics, systems biology, and clinical trials. This workshop report summarizes the presentations and discussions and important recommendations for future clinical pneumonia studies. These recommendations include establishing consensus disease and outcome definitions, improved phenotyping, development of clinical study networks, standardized data and biospecimen collection and protocols, and development of innovative trial designs.

Acute respiratory distress syndrome (ARDS) is a life-threatening clinical condition defined by rapid onset respiratory failure following acute lung injury (ALI). Its increased incidence due to COVID-19 and high mortality rate (∼40%) make the study of ARDS pathogenesis a crucial research priority. CRTH2 is a G protein-coupled receptor with established roles in type 2 immunity and well-characterized inhibitors. Prior studies have shown it also promotes neutrophilic inflammation, indicating that CRTH2 inhibition may be a potential therapeutic strategy for ARDS. To test this hypothesis, we first examined the expression pattern of CRTH2 on murine neutrophils. We found it is expressed on neutrophils, but only after extravasation into the lung. Next, we showed that extravasated lung neutrophils generate inflammatory responses upon stimulation with the CRTH2-specific agonist DK-PGD2, as demonstrated by reactive oxygen species (ROS) production. This response was abrogated in CRTH2 KO neutrophils. Inhibition of CRTH2 with fevipiprant suppressed baseline ROS production, indicating an autocrine PGD2-CRTH2 signaling loop. We then evaluated the role of CRTH2 in vivo using a murine model of LPS-induced ALI. Despite the pro-inflammatory effects of CRTH2 on neutrophils in vitro, we observed worsening of lung injury in CRTH2-deficient mice in terms of neutrophilic inflammation, vascular leak, and survival. Bulk RNAseq of lung tissue indicated an impairment in type 2 immune signaling; qPCR and ELISA confirmed downregulation of the key type 2 effector cytokine, IL-4. Thus, CRTH2 appears to play a dual role in ALI, directly promoting neutrophil effector responses, but indirectly suppressing lung injury and neutrophilic inflammation through type 2 immunity. These findings reveal a novel protective function for CRTH2 during lung injury and argue against the use of CRTH2 inhibitors in ARDS.

RationaleAsthma is a chronic airway disease driven by multiple immunologic pathways that determine the clinical response to therapy. Current diagnostic methods are incapable of discriminating subtypes of asthma and guiding targeted treatment. We hypothesized that sputum cytokine profiles could help to identify immunologically-defined disease subtypes and individualize therapy in patients with severe asthma.ObjectivesDefine asthma subtypes associated with sputum alarmin and cytokine levels.MethodsCross-sectional analysis of clinical features and sputum from 200 asthmatic patients was performed. 10 cytokines belonging to alarmin, T2, and non-T2 pathways were measured. Pearson correlation was used to identify cytokine modules. Latent class analysis was used to cluster patients by cytokine expression.Measurements and Main ResultsThree modules of highly correlated cytokines were identified including a non-T2 module, the IL-1βmod (IL-1β, IL-6, GCSF), and two distinct T2 modules: TSLPmod (TSLP, IL-4, IL-5, IL-9) and IL-33mod (IL-33, IL-13, IL-21). The TSLPmod was associated with asthma severity, airway obstruction, eosinophilia, and elevated FeNO. Patient clustering revealed three subgroups; two different subgroups showed expression of T2 modules.ConclusionsAnalysis of sputum cytokines revealed three discrete signaling modules in patients with asthma. Unexpectedly, the inclusion of alarmins led to separation of canonical T2 cytokines into two unique modules; IL-5 grouped with TSLP, while IL-13 grouped with IL-33. In addition, patient clustering revealed two distinct endotypes associated with T2 immune signaling. These findings indicate a new layer of immunologic heterogeneity within the T2 paradigm, and suggest that sputum cytokine profiling may hold diagnostic utility for patients with asthma.

Patients hospitalized with COVID-19 are at significant risk for superimposed bacterial pneumonia. However, diagnosing superinfection is challenging due to its clinical resemblance to severe COVID-19. We therefore evaluated whether the immune biomarker, procalcitonin, could facilitate the diagnosis of bacterial superinfection. To do so, we identified 185 patients with severe COVID-19 who underwent lower respiratory culture; 85 had superinfection. Receiver operating characteristic curve analysis showed that procalcitonin at the time of culture was incapable of distinguishing patients with bacterial infection (AUC, 0.52). We conclude that static measurement of procalcitonin does not aid in the diagnosis of superinfection in severe COVID-19.

Case Presentation A 62-year-old nonsmoking woman with no medical history initially presented with a 3-month history of rash. A painful, erythematous exanthem had progressed from her forehead, cheeks, and upper chest to her eyes (heliotrope rash) and hands, primarily involving the extensor surface finger joints with prominent digital ulceration.

IntroductionProcalcitonin expression is thought to be stimulated by bacteria and suppressed by viruses via interferon signalling. Consequently, during respiratory viral illness, clinicians often interpret elevated procalcitonin as evidence of bacterial coinfection, prompting antibiotic administration. We sought to evaluate the validity of this practice and the underlying assumption that viral infection inhibits procalcitonin synthesis.MethodsWe conducted a retrospective cohort study of patients hospitalised with pure viral infection (n=2075) versus bacterial coinfection (n=179). The ability of procalcitonin to distinguish these groups was assessed. In addition, procalcitonin and interferon gene expression were evaluated in murine and cellular models of influenza infection.ResultsPatients with bacterial coinfection had higher procalcitonin than those with pure viral infection, but also more severe disease and higher mortality (pDiscussionThese studies reveal that procalcitonin rises during pure viral infection in proportion to disease severity and is not suppressed by interferon signalling, in contrast to prior models of procalcitonin regulation. Applied clinically, our data suggest that procalcitonin represents a better indicator of disease severity than bacterial coinfection during viral respiratory infection.

All-pass filter (APF) offers a simpler implementation for orthogonal signal generation (OSG) and has widely featured in single-phase phase locked loop (PLL) applications. However, they have two prominent issues, the absence of filtering capability and reliance on grid frequency information for yielding 90° phase shifted signal. This paper proposes an enhanced APF-PLL based on frequency fixed configuration for abnormal grid voltage scenarios addressing both the aforementioned concerns. The suggested structure utilizes a modified transformation for attaining frequency-independent APF-PLL, while a frequency-fixed bandpass filter (BPF) is appended as a prefilter to serve the filtering objective. Thus obtained PLL structure, is then evaluated against some recently proposed OSG-PLLs. The simulation and experimental results demonstrate improved performance (dynamic and steady-state) in different operating scenarios.

Phase-locked loop (PLL) is commonly utilised for AC power systems to detect phase and frequency. With the increasing use of small-scale distributed power generation, the technique becomes widely available for grid interconnection of renewable power source into single-phase AC distribution network. Through comprehensive analysis and design, this study proposed a new approach that includes dual independent control loops to enhance the transfer delay-based PLL capability in terms of speed and accuracy. The effectiveness and advantages of the proposed PLL structure are demonstrated by numerical simulation and verified by experimental test.

Variation in hospital mortality has been described for coronavirus disease 2019 (COVID-19), but the factors that explain these differences remain unclear.Our objective was to utilize a large, nationally representative dataset of critically ill adults with COVID-19 to determine which factors explain mortality variability.In this multicenter cohort study, we examined adults hospitalized in intensive care units with COVID-19 at 70 United States hospitals between March and June 2020. The primary outcome was 28-day mortality. We examined patient-level and hospital-level variables. Mixed-effects logistic regression was used to identify factors associated with interhospital variation. The median odds ratio (OR) was calculated to compare outcomes in higher- vs. lower-mortality hospitals. A gradient boosted machine algorithm was developed for individual-level mortality models.A total of 4,019 patients were included, 1537 (38%) of whom died by 28 days. Mortality varied considerably across hospitals (0-82%). After adjustment for patient- and hospital-level domains, interhospital variation was attenuated (OR decline from 2.06 [95% CI, 1.73-2.37] to 1.22 [95% CI, 1.00-1.38]), with the greatest changes occurring with adjustment for acute physiology, socioeconomic status, and strain. For individual patients, the relative contribution of each domain to mortality risk was: acute physiology (49%), demographics and comorbidities (20%), socioeconomic status (12%), strain (9%), hospital quality (8%), and treatments (3%).There is considerable interhospital variation in mortality for critically ill patients with COVID-19, which is mostly explained by hospital-level socioeconomic status, strain, and acute physiologic differences. Individual mortality is driven mostly by patient-level factors. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Summary: Many US states published crisis standards of care (CSC) guidelines for allocating scarce critical care resources during the COVID-19 pandemic. However, the performance of these guidelines in maximizing their population benefit has not been well tested. In 2,272 adults with COVID-19 requiring mechanical ventilation drawn from the Study of the Treatment and Outcomes in Critically Ill Patients with COVID-19 (STOP-COVID) multicenter cohort, we test the following three approaches to CSC algorithms: Sequential Organ Failure Assessment (SOFA) scores grouped into ranges, SOFA score ranges plus comorbidities, and a hypothetical approach using raw SOFA scores not grouped into ranges. We find that area under receiver operating characteristic (AUROC) curves for all three algorithms demonstrate only modest discrimination for 28-day mortality. Adding comorbidity scoring modestly improves algorithm performance over SOFA scores alone. The algorithm incorporating comorbidities has modestly worse predictive performance for Black compared to white patients. CSC algorithms should be empirically examined to refine approaches to the allocation of scarce resources during pandemics and to avoid potential exacerbation of racial inequities.

Single phase dq (park) transformation finds widespread application in grid interfaced converter current control, phase locked loop, reference current generation and active/reactive power calculation. The method requires additional signal to create orthogonal set and transform it to rotating frame. This is generally achieved using orthogonal signal generation(OSG) unit. As park transformation is instantaneous, associated dynamic and steady state performance depends on how fast and accurately OSG can generate orthogonal signal set while eliminating noises and disturbance signal. Moreover, power calculation in stationary frame also necessitates orthogonal sets of voltage and current signal. This paper presents a comprehensive comparative study of several OSG mechanisms reported in literature and applied to single phase systems. Various aspects of OSGs are assessed including dynamic response, accuracy, disturbance rejection feature, frequency adaptability and implementation. Moreover, issues in complex coefficient filter based OSG are identified and a generalized time delay transformation with reduced computation is also suggested. The discussions presented are substantiated via simulation results.

This paper proposes a high-efficiency and high conversion gain dc-dc converter to integrate alternative energy sources into dc nanogrid. The proposed configuration takes advantage of the coupled inductor technique to attain high voltage gain and reduced switch voltage stress. The voltage stress on the switch is substantially minimized compared to the high output voltage. Therefore, a low voltage rating switch is employed to enhance conversion efficiency. Furthermore, the coupled inductor utilization eliminates the reverse recovery losses of diodes. The operation principle and steady-state analysis of the proposed converter are elaborated. A prototype is developed to substantiate the experimental performance of the proposed converter. The experimental results demonstrate coherence with the theoretical study and simulation results. The converter shows a 96.3% peak conversion efficiency.

BackgroundPatients with active acute myelogenous leukemia (AML) are at risk for leukemic infiltration (LI) into the lung and acute tumor lysis pneumopathy (ATLP) following chemotherapy. Fulminant presentations of these leukemic lung diseases are well-described, but indolent forms have not yet been studied. Therefore, we sought to elucidate the clinical features of mild-to-moderate LI and ATLP.MethodsA retrospective cohort analysis was performed on 51 hospitalized patients with AML, circulating blast count ≥3%, non-critical illness, and receipt of bronchoscopy between 2015-2019. Diagnoses of LI and ATLP were made via retrospective chart review by a multidisciplinary team of physicians.Results19 cases of leukemic lung disease were identified: 14 with LI and 5 with ATLP. The clinical presentations closely resembled pneumonia, with the majority demonstrating respiratory symptoms (63%), hypoxemia (63%), fever (84%), and pulmonary opacities (100%). All patients were presumptively diagnosed with infection, leading to an average of 18 days of broad-spectrum antibiotic therapy and multiple instances of delayed chemotherapy in treatment candidates. Although most patients were near the end-of-life (90% died within 1 year), transitions to comfort care were infrequent (25%) and hospitalizations were protracted (median 25 days).ConclusionsLI and ATLP are common yet under-recognized pulmonary complications in patients with active AML. When presenting indolently, these conditions are difficult to distinguish from lung infection, leading to missed diagnosis, inappropriate antibiosis, chemotherapy deferrals, and prolonged hospitalizations. Greater awareness and consensus definitions of LI and ATLP are therefore needed to improve care of this population.

The past two decades have witnessed a resurgence in neutrophil research, inspired in part by the discovery of neutrophil extracellular traps (NETs) and their myriad roles in health and disease. Within the lung, dysregulation of neutrophils and NETosis have been linked to an array of diseases including pneumonia, cystic fibrosis, acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), and severe asthma. However, our understanding of pathologic neutrophil responses in the lung remains incomplete. Two methodologic issues have contributed to this gap: first, an emphasis on studying neutrophils from blood rather than the lung and second, the technical difficulties of interrogating neutrophil responses in mice, which has largely restricted basic murine research to specialized laboratories. To address these limitations, we have developed a suite of techniques for studying neutrophil effector functions specifically in the mouse lung. These include ex vivo assays for phagocytosis and NETosis using bronchoalveolar neutrophils and in situ evaluation of NETosis in a murine model of pneumonia. Throughout, we have prioritized technical ease and robust, quantitative readouts. We hope these assays will help to standardize research on lung neutrophils and improve accessibility to this burgeoning field.

Understanding the mechanisms of bacterial cell wall synthesis is essential for microbiology and medicine alike. A key step in this process is peptidoglycan crosslinking, which confers mechanical strength to the cell wall and represents a target for numerous classes of antibiotics. However, the biology of crosslinking remains poorly understood due to a lack of tools for studying the reaction in vivo. Recently, we developed a class of synthetic probes called fluorescent stem peptide mimics (FSPMs) that meet this need, allowing quantification and localization of crosslinking activity in live bacteria. We have utilized FSPMs to describe novel aspects of peptidoglycan synthesis in the human pathogen, Staphylococcus aureus. To enable wider use of our methodology, we provide detailed protocols herein for the synthesis of FSPMs, labeling of live bacteria, and evaluation of crosslinking by flow cytometry and super-resolution microscopy. We believe that FSPMs, together with complementary biosynthetic probes and traditional bacteriologic methods, will help to advance our understanding of peptidoglycan biology and accelerate the search for new antibiotics.

© 2020 Institution of Engineering and Technology. All rights reserved. With the increasing integration of photovoltaic power generation in the low-voltage distribution network, the grid voltage regulation becomes critical, which demands support from different resources. This study presents the feasibility study of home appliance to be applied for appliance to grid mode of operation. The analysis includes the amendments in topology and control to support the concept of supportive platform provided by smart home and smart grid. Home appliances are then proposed as new distributed reactive sources, which are utilised to resolve the issue of voltage regulation, as well as produce reactive power locally for voltage stability. This study discusses the technical transitions in current home appliance to accommodate auxiliary functionality of grid reactive power support (RPS) and how it can fit in the home energy management system architecture to provide the required RPS.

Understanding the mechanisms of bacterial cell wall synthesis is essential for microbiology and medicine alike. A key step in this process is peptidoglycan crosslinking, which confers mechanical strength to the cell wall and represents a target for numerous classes of antibiotics. However, the biology of crosslinking remains poorly understood due to a lack of tools for studying the reaction in vivo. Recently, we developed a class of synthetic probes called fluorescent stem peptide mimics (FSPMs) that meet this need, allowing quantification and localization of crosslinking activity in live bacteria. We have utilized FSPMs to describe novel aspects of peptidoglycan synthesis in the human pathogen, Staphylococcus aureus. To enable wider use of our methodology, we provide detailed protocols herein for the synthesis of FSPMs, labeling of live bacteria, and evaluation of crosslinking by flow cytometry and super-resolution microscopy. We believe that FSPMs, together with complementary biosynthetic probes and traditional bacteriologic methods, will help to advance our understanding of peptidoglycan biology and accelerate the search for new antibiotics.

Chitinases are the enzymes that cleave chitin. Even in the absence of chitin, mammalians have significant amounts of chitinases present in the body including at baseline. The precise role of chitinase is not known, however it was believed to play important role in digestion and host defense against chitin-containing food and pathogens, respectively. Recent work, including ours, has shown an important role of chitinase and chitinase-like proteins in host immunity and allergic diseases. Importantly, chitinase activities serve as important biomarkers of disease severity in a wide-range of diseases including type 2 inflammatory diseases such as asthma and pulmonary fibrosis. Similarly, patients with genetic disorders like Gaucher disease have significantly elevated chitinase levels, which not only correlate with disease severity but also serve as a reliable biomarker for therapeutic effectiveness. The protocol outlined here describes a simple, quick, and straightforward way to measure chitinase activity in BAL or serum samples of mice and can be widely adapted to human subjects and other model organisms due to the highly conserved nature of the enzymes.

Tracheoesophageal fistula is an abnormal communication between trachea and esophagus. Benign acquired types are rare with the incidence of less than 1%. Prolonged endotracheal intubation remains the most common cause. We are reporting a 28 years old female patient presented with chief complaint of a cough after each meal intake in the outpatient clinic. She had a recent history of admission in the intensive care unit with prolonged intubation (11 days). Her general physical examination, laboratory examination, and chest x-ray were normal. Esophagogastroscopy was performed and revealed communication between upper esophagus and trachea approximately at 14-17cm embedded in longitudinal mucosal folds of the esophagus. She was referred to the higher center for surgical repair. Though, a rare complication, high suspicion is necessary to accurately diagnose the disease in a patient with the history of prolonged intubation. Keywords: case report; endotracheal intubation; mechanical ventilation; tracheoesophageal fistula.