ELAVL4 promotes the tumorigenesis of small cell lung cancer by stabilizing LncRNA LYPLAL1-DT and enhancing profilin 2 activation.

Small cell lung cancer (SCLC) is one of the most malignant tumors that has an extremely poor prognosis. RNA-binding protein (RBP) and long noncoding RNA (lncRNA) have been shown to be key regulators during tumorigenesis as well as lung tumor progression. However, the role of RBP ELAVL4 and lncRNA LYPLAL1-DT in SCLC remains unclear. In this study, we verified that lncRNA LYPLAL1-DT acts as an SCLC oncogenic lncRNA and was confirmed in vitro and in vivo. Mechanistically, LYPLAL1-DT negatively regulates the expression of miR-204-5p, leading to the upregulation of PFN2, thus, promoting SCLC cell proliferation, migration, and invasion. ELAVL4 has been shown to enhance the stability of LYPLAL1-DT and PFN2 mRNA. Our study reveals a regulatory pathway, where ELAVL4 stabilizes PFN2 and LYPLAL1-DT with the latter further increasing PFN2 expression by blocking the action of miR-204-5p. Upregulated PFN2 ultimately promotes tumorigenesis and invasion in SCLC. These findings provide novel prognostic indicators as well as promising new therapeutic targets for SCLC.

Tight junctions and acute kidney injury.

Acute kidney injury (AKI) is characterized by a rapid reduction in kidney function caused by various etiologies. Tubular epithelial cell dysregulation plays a pivotal role in the pathogenesis of AKI. Tight junction (TJ) is the major molecular structure that connects adjacent epithelial cells and is critical in maintaining barrier function and determining the permeability of epithelia. TJ proteins are dysregulated in various types of AKI, and some reno-protective drugs can reverse TJ changes caused by insult. An in-depth understanding of TJ regulation and its causality with AKI will provide more insight to the disease pathogenesis and will shed light on the potential role of TJs to serve as novel therapeutic targets in AKI.

The removal of antibiotic resistant bacteria and antibiotic resistance genes by sulfidated nanoscale zero-valent iron activating periodate: Efficacy and mechanism.

Antibiotic resistant bacteria (ARB) and antibiotic resistance genes (ARGs) have drawn much more attention due to their high risk on human health and ecosystem. In this study, the performance of sulfidated nanoscale zero-valent iron (S-nZVI)/periodate (PI) system toward ARB inactivation and ARGs removal was systematically investigated. The S-nZVI/PI system could realize the complete inactivation of 1 × 108 CFU/mL kanamycin, ampicillin, and tetracycline-resistant E. coli HB101 within 40 min, meanwhile, possessed the ability to remove the intracellular ARGs (iARGs) (including aphA, tetA, and tnpA) carried by E. coli HB101. Specifically, the removal of aphA, tetA, and tnpA by S-nZVI/PI system after 40 min reaction was 0.31, 0.47, and 0.39 log10copies/mL, respectively. The reactive species attributed to the E. coli HB101 inactivation were HO• and O2•-, which could cause the destruction of E. coli HB101 morphology and enzyme system (such as superoxide dismutase and catalase), the loss of intracellular substances, and the damage of iARGs. Moreover, the influence of the dosage of PI and S-nZVI, the initial concentration of E. coli HB101, as well as the co-existing substance (such as HCO3-, NO3-, and humic acid (HA)) on the inactivation of E. coli HB101 and its corresponding iARGs removal was also conducted. It was found that the high dosage of PI and S-nZVI and the low concentration of E. coli HB101 could enhance the disinfection performance of S-nZVI/PI system. The presence of HCO3-, NO3-, and HA in S-nZVI/PI system showed inhibiting role on the inactivation of E. coli HB101 and its corresponding iARGs removal. Overall, this study demonstrates the superiority of S-nZVI/PI system toward ARB inactivation and ARGs removal.

Building bridges of excellence: a comprehensive competence framework for nurses in hospice and palliative care-a mixed method study.

BACKGROUND: Hospice and Palliative Care (HPC) is in high demand in China; however, the country is facing the shortage of qualified HPC nurses. A well-suited competence framework is needed to promote HPC human resource development. Nevertheless, existing unstandardized single-structured frameworks may not be sufficient to meet this need. This study aimed at constructing a comprehensive multi-structured HPC competence framework for nurses. METHODS: This study employed a mixed-method approach, including a systematic review and qualitative interview for HPC competence profile extraction, a two-round Delphi survey to determine the competences for the framework, and a cross-sectional study for framework structure exploration. The competence profiles were extracted from publications from academic databases and interviews recruiting nurses working in the HPC field. The research team synthesized profiles and transferred them to competences utilizing existing competence dictionaries. These synthesized competences were then subjected to Delphi expert panels to determine the framework elements. The study analyzed theoretical structure of the framework through exploratory factor analysis (EFA) based on a cross-sectional study receiving 491 valid questionnaires. RESULTS: The systematic review involved 30 publications from 10 countries between 1995 and 2021, while 13 nurses from three hospitals were interviewed. In total, 87 and 48 competence profiles were respectively extracted from systematic review and interview and later synthesized into 32 competences. After the Delphi survey, 25 competences were incorporated into the HPC competence framework for nurses. The EFA found a two-factor structure, with factor 1 comprising 18 competences namely Basic Competences; factor 2 concluding 7 competences namely Developmental Competences. CONCLUSIONS: The two-factor HPC competence framework provided valuable insights into the need and directions of Chinese HPC nurses' development.

Detection and various environmental factors of antibiotic resistance gene horizontal transfer.

Bacterial antibiotic resistance in water environments is becoming increasingly severe, and new antibiotic resistant bacteria (ARB) and antibiotic resistance genes (ARGs) have also attracted the attention of researchers. The horizontal transfer of ARGs in water environments is considered one of the main sources of bacterial resistance in the natural environment. Horizontal gene transfer (HGT) mainly includes conjugation, natural transformation, and transduction, and conjugation has been investigated most. Several studies have shown that there are a large number of environmental factors that might affect the horizontal transfer of ARGs in water environments, such as nanomaterials, various oxidants, and light; however, there is still a lack of systematic and comprehensive reviews on the detection and the effects of the influence factors of on ARG horizontal transfer. Therefore, this study introduced three HGT modes, analysed the advantages and disadvantages of current methods for monitoring HGT, and then summarized the influence and mechanism of various factors on ARG horizontal transfer, and the possible reasons for the different effects caused by similar factors were mainly critically discussed. Finally, existing research deficiencies and future research directions of ARG horizontal transfer in water environments were discussed.

Editing out five Serpina1 paralogs to create a mouse model of genetic emphysema.

Chronic obstructive pulmonary disease affects 10% of the worldwide population, and the leading genetic cause is α-1 antitrypsin (AAT) deficiency. Due to the complexity of the murine locus, which includes up to six Serpina1 paralogs, no genetic animal model of the disease has been successfully generated until now. Here we create a quintuple Serpina1a-e knockout using CRISPR/Cas9-mediated genome editing. The phenotype recapitulates the human disease phenotype, i.e., absence of hepatic and circulating AAT translates functionally to a reduced capacity to inhibit neutrophil elastase. With age, Serpina1 null mice develop emphysema spontaneously, which can be induced in younger mice by a lipopolysaccharide challenge. This mouse models not only AAT deficiency but also emphysema and is a relevant genetic model and not one based on developmental impairment of alveolarization or elastase administration. We anticipate that this unique model will be highly relevant not only to the preclinical development of therapeutics for AAT deficiency, but also to emphysema and smoking research.

Microbial contamination in distributed drinking water purifiers induced by water stagnation.

Small-scale distributed water purifiers (SSDWPs), providing better quality drinking water, are popularly used both in homes and in the public domain. Non-continuous operation leads to water stagnation and ultimately induces microbial contamination. However, information related to such contamination in these purifiers is reported scarcely. In the present study, an SSDWP, consisting of sand filtration (SF), granular activated carbon (GAC), and ultrafiltration (UF) processes, was established to explore microbial changes induced by water stagnation, based on the aspects of bacterial count, microbial size, microbiome and pathogenic communities. Our results primary showed that: first, compared with drinking water distribution system (DWDS), bacterial counts increased more rapidly in SSDWPs, growing to > 500 cfu/mL after 2.5 h stagnation. The proportion of intact cells also increased with stagnation time. Conversely, microbial size decreased with stagnation time according to changes in forward scatter detected using flow cytometry. Second, microbiome evolution followed the isolated island model, while in stagnated DWDS, microbiome evolved according to the continent island model, and the former had higher abundance of biodiversity. Furthermore, stagnation evidently caused microbiome changes in each unit, and spatial differences contributed to microbiome dissimilarity more significantly than temporal differences. Third, Mycobacterium was the dominant pathogenic genus in the SF and GAC units while Acinetobacter was the most abundant in the UF unit. Pathogenic risks increased with water stagnation time and lower nutrients level contributed to pathogenic community richness. Therefore, terminal disinfection of SSDWPs is strongly advised.

Acute toxicity evaluation of nanoparticles mixtures using luminescent bacteria.

As the application of nanoparticles (NPs) and their release to the environment has increased, it is important to verify their toxicity, with a special emphasis on particle solubilization and the interaction of NP mixtures. In the current study, a model luminescent bacteria, Vibrio fischeri, was employed to test the acute toxicity of individual NPs and their binary mixtures, including metal NPs (ZnNPs, CuNPs) and metal oxide NPs (ZnONPs, CuONPs). The independent action model was used to reflect the synergistic, additive, or antagonistic interactions of binary mixtures of these NPs. The results showed that the median effective concentration (EC50) inhibited the luminescence of V. fischeri were 20.5, 4.1, 11.6, and 118.7 mg L-1 for ZnNPs, CuNPs, ZnONPs, and CuONPs, respectively, suggesting that the toxicity of these NPs to V. fischeri were as the following order: CuNPs > ZnONPs > ZnNPs > CuONPs. The combined effect of NPs were found to be antagonistic for CuNPs-ZnONPs and CuNPs-CuONPs, synergistic for CuONPs-ZnNPs, CuNPs-ZnNPs, and ZnONPs-CuONPs, and additive for ZnNPs-ZnONPs, revealing a complex pattern of possible interactions. The differences of dissolved metal ions partly accounted for the different combined toxicity of binary mixtures of NPs. The findings have important implications for better understanding the true environmental risk of NP mixtures.

A truncated p53 in human lung cancer cells as a critical determinant of proliferation and invasiveness.

As a transcription factor, p53 must accumulate in the nucleus to be effective. Signals related to nuclear localization are distributed mainly in the C-terminal of p53. So these nuclear location domains were reserved and the other part of the C-terminal was removed in this study. We investigated whether the truncated p53 (p53(DEL)) may affect proliferation and invasive potential of human lung cancer cells. H1299 and 801D cells expressing full-length p53 and the p53(DEL) were obtained by screening. Cell proliferation assay, cell apoptotic analysis, cell migration assay, and invasion assay were performed. Protein expression was examined by Western blotting. The data showed H1299-p53(DEL) and 801D-p53(DEL) cells grew more slowly than H1299-p53 and 801D-p53 cells, respectively. The colony formation of H1299-p53(DEL) and 801D-p53(DEL) cells reduced. The truncated p53 induced cell apoptosis. The expression levels of Bax and p53 upregulated modulator of apoptosis were increased in H1299-p53(DEL) and 801D-p53(DEL) cells. H1299-p53(DEL) and 801D-p53(DEL) cells were also characterized by decreased migration and invasion. The expression of the truncated p53 resulted in upregulation of E-cadherin and downregulation of Vimentin, Slug, Twist1, and zinc finger E-box-binding homeobox 1, which suggested the truncated p53 inhibited epithelial-mesenchymal transition occurrence. The above-mentioned characteristics were reverted by treatment of with pifithrin-a, a p53 inhibitor. These findings support the existence of a direct link between the p53(DEL), proliferation, epithelial-mesenchymal transition, and invasiveness in human lung cancer cells. So the p53(DEL) is a promising target for prevention and treatment of lung cancer.

A better experimental method to detect the sensitivity of cancer cells to anticancer drugs after adenovirus-mediated introduction of two kinds of p53 in vivo.

p53 plays an important role in drug responses by regulating cell cycle progression and inducing programmed cell death. The C-terminal of p53 self-regulates the protein negatively; however, whether it affects the sensitivity of cancer cells to anticancer drugs is unclear. In this study, two experimental methods were used to compare the sensitivity to anticancer drugs of human lung 801D cancer cells transfected with adenovirus bearing either full-length p53 or the deleted-C-terminal p53 in vivo. Adenovirus-mediated deliveries of full-length or deleted-C-terminal p53 were performed after development of tumors (the first method) or by infection into cells before xenotransplantation (the second method). The results showed that infection with the deleted-C-terminal p53 increased 801D cell sensitivity to anticancer drugs in the second, but not in the first method, as indicated by greater tumor-inhibition rates. In addition, compared with the first method, the second method resulted in viruses with more uniformly infected cells and the infection rates between groups were similar. This yielded smaller within-group variations and greater uniformity among transplanted tumors. The second method could circumvent the difficulties associated with intratumoral injection.

Two-phase anaerobic co-digestion of food waste and sewage sludge.

The feasibility and performance of food waste and sewage sludge co-digestion were investigated to gain insight into their resource utilization. In this study, two-phase anaerobic digestion (TPAD) was operated under a total solids mixing ratio of 1:1 and different sludge retention times (SRTs). Results show that an acidogenic reactor with a 5-day SRT obtained the highest acidification efficiency, and its acetic acid content was dominant. The organic removal rate of a methanogenic reactor (MR) with a 20-day SRT and its corresponding TPAD system with a 25-day SRT were both the highest among the MRs and TPAD systems. Volatile solids and total chemical oxygen demand average removal efficiencies of the TPAD system with a 25-day SRT reached 64.7 and 60.8%, respectively. The MR with a 30-day SRT obtained the minimum ratio of volatile fatty acid to alkalinity (0.12). The methane content generated from the different MRs fluctuated at around 70%. All of the above results can provide reference for future research.

Changes Due to Patient Deaths: Medical Students' Expectations vs. Health Professionals' Experiences.

CONTEXT: Preparing healthcare professionals for inevitable encounters with patient deaths is crucial to preventing maladaptive professional bereavement outcomes. OBJECTIVES: This study aimed to explore the discrepancies between medical students' pre-patient death expectations and healthcare professionals' post-patient death experiences regarding accumulated global changes due to patient deaths (AGC), identify heterogeneous expectation patterns among students, and reveal risk factors for worthy-of-concern expectation patterns. METHODS: Cross-sectional survey data from 231 professional caregivers and 405 medical and nursing students were used. Independent t tests and analyses of covariance were run for staff-student AGC comparisons. Latent profile analysis (LPA) among students was followed by logistic regression. RESULTS: The students scored higher than did the staff in two AGC factors: more acceptance of limitations and more death-related anxiety. LPA identified four latent expectation patterns, with the "overoptimistic" (27.8%) group being worthy of concern, as students overestimated positive changes and underestimated negative changes. The overoptimistic pattern was predicted by students' motivations to study medicine, which were driven by "interests," "career opportunities," and "improving medical services in the hometown," rather than "by chance," and higher scores on the death attitude of "neutral acceptance." CONCLUSION: In general, students tend to overestimate the long-term impacts of patient deaths. However, approximately 1/4 of students hold overly optimistic expectations, which are predicted by motivations to study medicine and death attitudes.

Cancer-associated fibroblasts: heterogeneity and their role in the tumor immune response.

In recent decades, many reports have been published on the composition and function of the tumor microenvironment (TME), among which cancer-associated fibroblasts (CAFs) have received much attention. CAFs have different degrees of heterogeneity in terms of their origin, phenotype, and function and can be divided into different subpopulations. These subgroups may play different roles in the occurrence and development of tumors. In addition, CAFs are closely associated with tumor immunity and have been found to regulate immune cell activity and to suppress the tumor immune response. In this review, we systematize the heterogeneity and characteristics of CAFs, discuss how specific CAF subgroups contribute to cancer progression by inducing an immunosuppressive microenvironment, and finally, we examine the future clinical applications of CAF subgroups.

Clinical significance of miR-9-5p in NSCLC and its relationship with smoking.

Purpose: Dysregulated expression of microRNA (miRNAs) in lung cancer has been wildly reported. The clinicopathologic significance of miR-9-5p in non-small-cell lung cancer (NSCLC) patients and its effect on NSCLC progression were explored in this study. Patients and methods: A total of 76 NSCLC patients were included. miR-9-5p expression was evaluated by real-time quantitative polymerase chain reaction (RT-qPCR). Then, in vitro experiments including cell growth curve assays, colony formation assays, and transwell migration assays were performed. Further clinicopathological and prognostic values were explored using bioinformatics analysis of the TCGA database. Results: miR-9-5p expression was significantly increased in tumor tissues (both P < 0.0001). miR-9-5p expression was relatively higher in larger tumors (P = 0.0327) and in lung squamous carcinoma (LUSC) (P = 0. 0143). In addition, miR-9-5p was significantly upregulated in the normal lung tissues of cigarette smokers (P = 0.0099). In vitro, miR-9-5p was correlated with cell proliferation and migration. After that, bioinformatics analysis of the TCGA database indicated that miR-9-5p was correlated with tumor size (P = 0.0022), lymphatic metastasis (P = 0.0141), LUSC (P < 0.0001), and smoking history (P < 0.0001). Finally, a prognostic study indicated high miR-9-5p expression was correlated with poor prognosis in LUAD (P = 0.0121). Conclusion: Upregulation of miR-9-5p may have an oncogenic effect in NSCLC and may be related to smoking. The conclusion of this study may help find new prognostic and therapeutic targets for NSCLC and the exploration of the relationship between smoking and lung cancer.

Study on the preparation of ascorbic acid reduced ultrafine copper powders in the presence of different protectants and the properties of copper powders based on methionine protection.

High-purity, monodisperse, and low-oxygen submicron copper powder particles with particle sizes in the range of 100-600 nm were synthesized under alkaline conditions using ascorbic acid (C6H8O6) as a reductant and copper chloride (CuCl2·2H2O) as a copper source. The redox potential of the Cu-Cl-H2O system was obtained by calculations and plotted on pH-E diagrams, and a one-step secondary reduction process (Cu(ii) → CuCl(i) → Cu2O(i) → Cu(0)) was proposed to slow down the reaction rate. The commonalities and differences in the nucleation and growth process of copper powders under methionine (Met), hexadecyl trimethyl ammonium bromide (CTAB), and sodium citrate dihydrate (SSC) as protectants and without the addition of protectants are compared, and the reaction mechanism is discussed. Among them, methionine (Met) showed excellent properties and the Cu2O(i) → Cu(0) process was further observed by in situ XRD. The synthesized copper powder particles have higher particle size controllability, dispersibility, antioxidant properties, and stability, and can be decomposed at lower temperatures (<280 °C). The resistivity can reach 21.4 µΩ cm when sintered at a temperature of 325 °C for 30 min. This green and simple synthesis process facilitates industrialization and storage, and the performance meets the requirements of electronic pastes.

The Ribonuclease ZC3H12A is required for self-inflicted DNA breaks after DNA damage in small cell lung cancer cells.

Radiotherapy is the first line treatment for small cell lung cancer (SCLC); However, radio-resistance accompanies with the treatment and hampers the prognosis for SCLC patients. The underlying mechanisms remains elusive. Here we discovered that self-inflicted DNA breaks exist in SCLC cells after radiation. Moreover, using nuclease siRNA screening combined with high-content ArrayScan™ cell analyzer, we identified that Ribonuclease ZC3H12A is required for the self-inflicted DNA breaks after radiation and for SCLC cell survival after DNA damage. ZC3H12A expression was increased in response to DNA damage and when ZC3H12A was knocked down, the DNA repair ability of the cells was impaired, as evidenced by decreased expression of the DNA damage repair protein BRCA1, and increased γH2AX at DNA damage sites. Colony formation assay demonstrates that ZC3H12A knocked down sensitized small cell lung cancer radiotherapy. Therefore, the Ribonuclease ZC3H12A regulates endogenous secondary breaks in small cell lung cancer and affects DNA damage repair. ZC3H12A may act as an important radiotherapy target in small cell lung cancer.

Combined toxicity of pesticide mixtures on green algae and photobacteria.

Different organisms have diverse responses to the same chemicals or mixtures. In this paper, we selected the green algae Chlorella pyrenoidosa (C. pyrenoidosa) and photobacteria Vibrio qinghaiensis sp.-Q67 (V. qinghaiensis) as target organisms and determined the toxicities of six pesticides, including three herbicides (simetryn, bromacil and hexazinone), two fungicides (dodine and metalaxyl) and one insecticide (propoxur), and their mixtures by using the microplate toxicity analysis. The toxicities of three herbicides to C. pyrenoidosa are much higher than those to V. qinghaiensis, and the toxicities of metalaxyl and propoxur to V. qinghaiensis are higher than those to C. pyrenoidosa, while the toxicity of dodine to C. pyrenoidosa is similar to those to V. qinghaiensis. Using the concentration addition as an additive reference model, the binary pesticide mixtures exhibited different toxicity interactions, i.e., displayed antagonism to C. pyrenoidosa but synergism to V. qinghaiensis. However, the toxicities of the multi-component mixtures of more than two components are additive and can be predicted by the concentration addition model.

Behaviors and mechanisms of microbially-induced corrosion in metal-based water supply pipelines: A review.

Microbially-induced corrosion (MIC) is unstoppable and extensively spread throughout drinking water distribution systems (DWDSs) as the cause of pipe leakage and deteriorating water quality. For maintaining drinking water safety and reducing capital inputs in pipe usage, the possible consequences from MIC in DWDSs is still a research hotspot. Although most studies have investigated the effects of changing environmental factors on MIC corrosion, the occurrence of MIC in DWDSs has not been discussed sufficiently. This review aims to fill this gap by proposing that the formation of deposits with microbial capture may be a source of MIC in newly constructed DWDSs. The microbes early attaching to the rough pipe surface, followed by chemically and microbially-induced mineral deposits which confers resistance to disinfectants is ascribed as the first step of MIC occurrence. MIC is then activated in the newly-built, viable, and accessible microenvironment while producing extracellular polymers. With longer pipe service, oligotrophic microbes slowly grow, and metal pipe materials gradually dissolve synchronously with electron release to microbes, resulting in pipe-wall damage. Different corrosive microorganisms using pipe material as a reaction substrate would directly or indirectly cause different types of corrosion. Correspondingly, the formation of scale layers may reflect the distribution of microbial species and possibly biogenic products. It is therefore assumed that the porous and loose layer is an ideal microbial-survival environment, capable of providing diverse and sufficient ecological niches. The usage and chelation of metabolic activities and metabolites, such as acetic, oxalic, citric and glutaric acids, may lead to the formation of a porous scale layer. Therefore, the microbial interactions within the pipe scale reinforce the stability of microbial communities and accelerate MIC. Finally, a schematic model of the MIC process is presented to interpret MIC from its onset to completion.

Giant Cellulitis-Like Sweet Syndrome Masquerading As Cellulitis and Shingles: A Case Report and Literature Review.

Sweet syndrome (SS) is also known as acute febrile neutrophilic dermatoses. Clinically, SS features fever, arthralgias, and the sudden onset of an erythematous rash. The morphologies of skin lesions in SS are heterogenous, varying from papules, plaques, and nodules to hemorrhagic bullae, which sometimes makes the diagnosis of SS more challenging. We report a 62-year-old obese male with a history of chronic myeloid leukemia in remission for 10 years who presented with a rash for five days. The patient reported prodromal flu-like symptoms with subjective fever, malaise, cough, and nasal congestion followed by a sudden onset, painful, non-pruritic rash. The rash was associated with bilateral hip arthralgias and abdominal pain. The patient denied any recent travel, exposure to sick contacts, or the use of any new medications. Physical examination showed a well-demarcated, non-blanching, confluent, erythematous plaque involving the bilateral buttocks and extending to the lower back and flanks with coalescent "juicy"-appearing plaques and flaccid bullae. No oral or mucosal involvement was noted. Laboratory investigations revealed mild leukocytosis, elevated inflammatory markers, and acute kidney injury. The patient was started on antibiotics given the cellulitis-like skin lesions, leukocytosis with neutrophilia, and elevated inflammatory markers. Dermatology was consulted, who attributed the patient's rash to shingles and recommended initiating acyclovir and obtaining a skin biopsy. However, the patient's rash and arthralgias worsened with anti-viral treatment while awaiting pathology results. Antinuclear antibodies, complement, human immunodeficiency virus, hepatitis panel, blood cultures, and tumor markers were all negative. Flow cytometry showed no evidence of hematopoietic neoplasms. The skin punch biopsy revealed dense neutrophilic infiltration in the dermis with no evidence of leukocytoclastic vasculitis, consistent with acute neutrophilic dermatoses. The diagnosis of giant cellulitis-like Sweet syndrome was established, and the patient was started on prednisone 60 milligrams daily. His symptoms improved promptly with steroid treatment. Our case suggests that SS can camouflage a wide spectrum of diseases, including cellulitis, shingles, vasculitis, drug eruptions, leukemia cutis, and sarcoidosis, which emphasizes the importance of keeping a high index of suspicion for SS when assessing the clinical constellations of fever, neutrophilia, and erythematous plaques suggesting atypical cellulitis. Approximately 21% of Sweet syndrome is associated with malignancy. Sweet syndrome can precede, concur with, or follow the onset of malignancy. Due to the lack of a systematic approach to patients with SS, under-investigation and diagnostic delays are common. Therefore, further screening and continuous monitoring in patients with SS becomes especially important in facilitating the early detection of a potential underlying malignancy and assists in initiating adequate therapy.