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The Minnesota Department of Health identified an outbreak of Legionnaires' disease in a city in northern Minnesota, USA, in April 2023 that continued until chloramine disinfection of the community water system was implemented. Before chloramine disinfection was implemented, Legionella pneumophila was detected in 1 of 16 samples from the drinking water distribution system and in 5 of 10 premise plumbing samples using both cultivation-dependent (Legiolert) and cultivation-independent (digital PCR) assays in this independent investigation. Approximately 11 weeks after disinfection was implemented, all distribution system samples tested negative; however, 1 of 6 Legiolert-tested and 3 of 6 digital PCR-tested premise plumbing samples were positive. After 24 weeks of disinfection, all samples collected from the distribution system and premise plumbing tested negative. Our results show that a community water system supplied by groundwater supported substantial growth of L. pneumophila in premise plumbing and that chloramine disinfection halted the outbreak.

PurposeThis study examines the yin (promotive) and yang (prohibitive) of employee voice based on employee preference for voice channel attributes. Employee inputs may be disregarded, requiring employees to maneuver for unheeded voice and adopt alternate voice tactics. The authors emphasize the ubiquity of lurking employee silence and its affective effects on subsequent cycles of voice or silence.Design/methodology/approachQualitative design involving semi-structured interviews of employees from service sector firms in India assisted the inquiry.FindingsEmployees prefer voice channel attributes that ensure visibility and data substance for promotive voice and anonymity and confidentiality for prohibitive voice. Voice target switching and message reframing were common employee strategies. Silence on both sharing views/opinions (promotive) and voicing issues/concerns (prohibitive) weakens employee future voice incidents, besides suppressing the affect. Post-silence cognitive reappraisal increases voice incidences.Research limitations/implicationsFindings may have limited generalizability given the qualitative design of the study. Moving beyond extant episodic voice research, the authors demonstrate the recurrent nature of employee voice and silence. The study broadens perspectives on how varied voice types necessitate nuanced voice channel attributes.Originality/valuePresent work brings together organizational behavior (OB) perspective on discretionary voice through human resource (HR)-based channels, helping bridge the gap between previously disparate stands.

Purpose Intervention of artificial intelligence (AI) has brought up the issue of future job prospects in terms of the employability of the professionals and their readiness to harness the benefits of the AI. The purpose of this study is to recognize the implications of AI on employability by analyzing the issues in the health-care sector that if not addressed, can dampen the possibilities offered by AI intervention and its pervasiveness (Cornell University, INSEAD, and WIPO, 2019). Design/methodology/approach To get an insight on these concerns, an approach of total interpretive structural modelling, cross impact matrix multiplication applied to classification and path analysis have been used to understand the role of the critical factors influencing employability in the health-care sector. Findings This study primarily explores the driving-dependence power of the critical factors of the employability and displays hierarchical relationships. It also discusses measures which, if adopted, can enhance employability in the health-care sector with the intervention of AI. Research limitations/implications Employability also has an impact on the productivity of the health-care service delivery which may provide a holistic opportunity to the management in health-care organizations to forecast the allocation and training of human resources and technological resources. Originality/value The paper attempts to analyze AI intervention and other driving factors (operational changes, customized training intervention, openness to learning, attitude toward technology, job-related skills and AI knowledge) to analyze their impact on employability with the changing needs. It establishes the hierarchical relationship among the critical factors influencing employability in the health-care sector because of the intervention of AI.

Uttarakhand is recognized for its scenic beauty, fertile terrain and a rich cultural and religious heritage. Deriving a major proportion of its income from tourism and allied services, the tourism industry has become indispensable for its residents and for its government. However, the region is highly vulnerable to natural calamities like earthquakes, floods, forest fires and landslides due to its geography. Uncontrolled influx of tourists and pilgrims, unplanned construction of tourism-related infrastructure in eco-sensitive zones, massive greenhouse gas emissions, humongous waste generation and improper disposal have all added to the environmental degradation of this region. Hence, precarious condition of the terrain, rapid infrastructure development in addition to unplanned tourism and unregulated urbanisation have all led to highly volatile climatic conditions in recent decades and experts suggest that the situation will only get worse. The 2013 Kedarnath floods, the 2016 wildfires as well as the numerous reported landslides and earthquakes bear testimony to this fact. These in turn have an adverse impact on the tourism of the state. In 2016, Uttarakhand reported a sharp drop in tourist numbers after wildfires. In this paper we explore the question of sustainability of the tourism sector in Uttarakhand. We also intensively cover the various stakeholders of the tourist industry of the state, namely NGOs, Tourists, Local Communities, Local Businesses and Hotels and how losses to the same impact them. We study these impacts by using secondary data from secondary sources and primary data through interviews conducted by the authors, of locals in Rishikesh working at Tiny Lab Farm - a rural design and research studio. The authors also conducted a case study on Joshimath, which is an evident example of a tourism-dependent town in Uttarakhand, at the brink of losing its mainstay, as a result of environmental degradation. Opposing the idea of climate change being a problem of the future, the case study showcases the urgency of the situation by providing a sequential background on the course of events and its impact on tourism, as can be observed in real-time. Finally, the last section of the paper is a brief policy analysis of the current policies adopted by the government. The authors conclude that an increased community participation, usage of eco-friendly and locally sourced construction materials, promotion of tourism practices which are traditional and sustainably, a reassessment of forest laws, proper waste management, resurging indigenous practices and an increased involvement of women and elderly in the industry can pave the way for a balanced and sustained future of the tourism industry.

Sheath blight disease of rice caused by the fungal pathogen R. solani AG1‐IA remains a big threat to rice production worldwide. A limited genetic variation in rice for tolerance to this pathogen and little success in understanding how it defeats host defence are major reasons behind it. In this study, we attempted to decode the virulence spectrum of R. solani AG1‐IA in rice using time‐course transcriptome analysis and functional genomics tools. Several stage‐specific and commonly expressed genes were identified. Notably, the shikimate pathway emerged as an important pathway and was implicated in the virulence of R. solani AG1‐IA. Inhibition of the shikimate pathway by glyphosate, a known inhibitor of 5‐enolpyruvylshikimate‐3‐phosphate (EPSP) synthase, reduced the vegetative growth of R. solani AG1‐IA and several other phytopathogens. Our results were complemented by in vitro inhibition studies of RsEPSP synthase using a recombinantly expressed protein. Comparative sequence analysis of RsEPSP synthase with plants and known major phytopathogens revealed a distinct region in RsEPSP synthase. Using Nicothaiana benthamiana as a model system and stable rice transgenic lines, we demonstrated that targeting this distinct region through host‐induced gene silencing (HIGS) compromises the growth and virulence of R. solani AG1‐IA. The study lays a foundation for a deeper understanding of the identified virulence genes and establishes the shikimate pathway as a central target to control phytopathogens.

Burkholderia pseudomallei causes a fatal and infectious disease, melioidosis or Whitmore’s disease in humans and animals. Melioidosis is present in different parts of the world and is endemic in Southeast Asia and Northern Australia. Accurate diagnosis of melioidosis is difficult due to its common flu-like symptoms, potentially long incubation period and erroneous identification as culture contaminant. Early diagnosis of the disease is essentially required for administration of suitable antibiotics and disease containment. The present study reports a rapid, specific and sensitive recombinase polymerase amplification lateral flow assay for detection of B. pseudomallei. Specific primers and probe were designed and the assay was performed at 41 °C for 20 min in a portable incubator. End products were detected using ready-to-use lateral flow strips. RPA lateral flow assay could detect ≥ 250 fg genomic DNA of B. pseudomallei and ≥ 50 copies of recombinant plasmid harbouring the target DNA sequence. The assay was found to be highly specific and did not cross-react with other bacterial strains. In artificially spiked human blood and urine samples, the detection limit of the assay was 4.8 × 10 4 and 4.95 × 10 4  CFU/mL of B. pseudomallei , respectively. The detection limit of assay after 6 h of enrichment of artificially spiked urine samples was found to be 4.95 × 10 3  CFU/mL of B. pseudomallei . Detection limit in artificially spiked tap water and soil samples was determined to be 7.5 × 10 2  CFU/mL and 3.3 × 10 4  CFU per 5 g of B. pseudomallei , respectively.

Lymphangioleiomyomatosis (LAM) is a progressive cystic lung disease caused by tuberous sclerosis complex 1/2 (TSC1/2) gene mutations in pulmonary mesenchymal cells, resulting in activation of the mechanistic target of rapamycin complex 1 (mTORC1). A subset of patients with LAM develop pulmonary vascular remodeling and pulmonary hypertension. Little, however, is known regarding how LAM cells communicate with endothelial cells (ECs) to trigger vascular remodeling. In end-stage LAM lung explants, we identified EC dysfunction characterized by increased EC proliferation and migration, defective angiogenesis, and dysmorphic endothelial tube network formation. To model LAM disease, we used an mTORC1 gain-of-function mouse model with a Tsc2 KO (Tsc2KO) specific to lung mesenchyme (Tbx4LME-Cre Tsc2fl/fl), similar to the mesenchyme-specific genetic alterations seen in human disease. As early as 8 weeks of age, ECs from mice exhibited marked transcriptomic changes despite an absence of morphological changes to the distal lung microvasculature. In contrast, 1-year-old Tbx4LME-Cre Tsc2fl/fl mice spontaneously developed pulmonary vascular remodeling with increased medial thickness. Single-cell RNA-Seq of 1-year-old mouse lung cells identified paracrine ligands originating from Tsc2KO mesenchyme, which can signal through receptors in arterial ECs. These ECs had transcriptionally altered genes including those in pathways associated with blood vessel remodeling. The proposed pathophysiologic mesenchymal ligand-EC receptor crosstalk highlights the importance of an altered mesenchymal cell/EC axis in LAM and other hyperactive mTORC1-driven diseases. Since ECs in patients with LAM and in Tbx4LME-Cre Tsc2fl/fl mice did not harbor TSC2 mutations, our study demonstrates that constitutively active mTORC1 lung mesenchymal cells orchestrated dysfunctional EC responses that contributed to pulmonary vascular remodeling.

Background & objectives: Studies have shown that apart from hereditary breast carcinomas, breast cancer susceptibility gene 1 (BRCA1) mutations conferring to its loss are seen in sporadic breast carcinomas (SBC) as well. The aim of the present study was to assess BRCA1 methylation in females presenting at King George's Medical University, Lucknow, with SBC by both immunohistochemistry (IHC) and methylation PCR with respect to hormonal profile and various morphological prognostic parameters. The primary objective was to look for the association between BRCA1 protein expression and DNA promoter methylation. Methods: 81 mastectomy specimens from SBC of invasive breast carcinoma (no special type) were included in this study. After a detailed morphological assessment, formalin fixed paraffin embedded tissue from a representative tumour area was selected for BRCA1 IHC by heat-mediated antigen retrieval under high pH and DNA extraction and further bisulphate treatment. BRCA1 was studied for methylation by methylated and unmethylated PCR-specific primers. Results: BRCA1 promoter methylation was present in 42/81 (51.9%) participants, with significant BRCA1 protein loss (72.7%; P=0.002). A significant association between BRCA1 loss and hormonal profile was found (P=0.001); maximum in triple negative breast carcinoma (TNBC) (72%; 18/25). Most of the TNBC also harboured methylation (68%). Although not significant grade II and III tumours, lymph vascular invasion, ductal carcinoma in situ, and nodal metastasis (≥3) were seen in a higher percentage in methylated tumours. Mortality in SBC was significantly associated with BRCA1 loss (30.3%; P=0.024). Interpretation & conclusions: Study results highlight the concept of “BRCAness” in SBC as well. Hence, we can confer that identification of BRCA1 loss in SBC can make it a perfect candidate for poly ADP-ribose polymerase inhibitors or cisplatin-based therapy like hereditary ones.

Lymphangioleiomyomatosis (LAM) is a progressive cystic lung disease caused by tuberous sclerosis complex 1/2 (TSC1/2) gene mutations in pulmonary mesenchymal cells, resulting in activation of the mechanistic target of rapamycin complex 1 (mTORC1). A subset of patients with LAM develop pulmonary vascular remodeling and pulmonary hypertension. Little, however, is known regarding how LAM cells communicate with endothelial cells (ECs) to trigger vascular remodeling. In endstage LAM lung explants, we identified EC dysfunction characterized by increased EC proliferation and migration, defective angiogenesis, and dysmorphic endothelial tube network formation. To model LAM disease, we used an mTORC1 gain-offunction mouse model with a Tsc2 KO ([Tsc2.sup.KO]) specific to lung mesenchyme ([Tbx4.sup.LME-Cre] [Tsc2.sup.fl/fl]), similar to the mesenchymespecific genetic alterations seen in human disease. As early as 8 weeks of age, ECs from mice exhibited marked transcriptomic changes despite an absence of morphological changes to the distal lung microvasculature. In contrast, 1-year-old [Tbx4.sup.LME-Cre] [Tsc2.sup.fl/fl] mice spontaneously developed pulmonary vascular remodeling with increased medial thickness. Single-cell RNA- Seq of 1-year-old mouse lung cells identified paracrine ligands originating from [Tsc2.sup.KO] mesenchyme, which can signal through receptors in arterial ECs. These ECs had transcriptionally altered genes including those in pathways associated with blood vessel remodeling. The proposed pathophysiologic mesenchymal ligand-EC receptor crosstalk highlights the importance of an altered mesenchymal cell/EC axis in LAM and other hyperactive mTORC1-driven diseases. Since ECs in patients with LAM and in [Tbx4.sup.LME-Cre] [Tsc2.sup.fl/fl] mice did not harbor TSC2 mutations, our study demonstrates that constitutively active mTORC1 lung mesenchymal cells orchestrated dysfunctional EC responses that contributed to pulmonary vascular remodeling.