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BACKGROUND: Solid organ transplant recipients have an elevated risk of cancer following organ transplantation than the age-adjusted general population. We assessed incidence of head and neck squamous cell carcinoma (HNSCC) in heart, lung, and liver recipients. BASIC PROCEDURES/METHODS: This retrospective cohort study included 124,966 patients from the United States Scientific Registry of Transplant Recipients (SRTR) database who received heart, lung, or liver transplantation between 1991 and 2010. Follow-up data were available until 2018. Patients with prevalent HNSCC at transplantation were excluded. Incident cases of HNSCC post organ transplantation were identified, and incidence rates (per 100,000 person-years) were reported by gender, race, organ type, year and age at organ transplantation. MAIN FINDINGS: The majority of patients received liver transplantation (58.64 %), followed by heart (28.64 %), and lung (12.72 %) transplantation. During follow-up, 4.14 % patients developed HNSCC. Overall incidence rate of HNSCC was 426.76 per 100,000 person-years. Male recipients had a higher HNSCC incidence rate than female recipients (571.8 and 177.0 per 100,000 person-years, respectively). Lung recipients had the highest overall HNSCC incidence rate (1273.6 per 100,000 person-years), followed by heart (644.2 per 100,000 person-years), and liver recipients (207.1 per 100,000 person-years). Overall, an increase in HNSCC incidence rate was observed with increase in age at organ transplantation. An increase in incidence rates of HNSCC over time was observed in lung recipients; however, incidence rates decreased over time in heart recipients. CONCLUSION: Solid organ transplant recipients have a high incidence of HNSCC following organ transplantation, and the incidence varies by type of organ received.
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Vision scientists dedicated their efforts to unraveling the mechanism of filling-in at the blind-spot (BS) through numerous psychophysical experiments. The prevalent interpretation, emphasizing active filling-in, has spurred extensive research endeavors. In a parallel vein, a pertinent study highlighted the predominance of the nasal Visual Field (VF) over the temporal one and postulated the role of the Cortical Magnification Factor (CMF) in explaining the asymmetry of filling-in. In this study, we first replicated this experiment and then conducted BS-specific psychophysical experiments employing various bi-colored and bi-textured (patterned) stimuli. We observed that nasal dominance is not persistent in the context of the spread of perception for BS filling-in. We posit that the visual information processing priority index (VIPPI), comprising the CMF (an intrinsic factor unaffected by stimulus characteristics) and relative luminance (an extrinsic factor dependent on stimulus characteristics), governs the spread of perception for filling-in in case of diverse neighborhoods of the BS.
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Estimulação Luminosa , Psicofísica , Campos Visuais , Humanos , Adulto , Campos Visuais/fisiologia , Estimulação Luminosa/métodos , Masculino , Feminino , Adulto Jovem , Percepção de Cores/fisiologiaRESUMO
Introduction: The Coronavirus Disease 2019 (COVID-19) pandemic posed critical challenges in providing care to ovarian cancer (OC) patients, including delays in OC diagnosis and treatment initiation. To accommodate for delays in OC surgery, the Society of Gynecologic Oncology (SGO) recommended preferential use of neoadjuvant chemotherapy during the pandemic. The purpose of this study was to assess the association of the COVID-19 pandemic with neoadjuvant chemotherapy use in patients diagnosed with OC. Methods: This retrospective cohort study included patients diagnosed with stage II-IV ovarian cancer of epithelial subtype between 01/01/2017-06/30/2021 at Kaiser Permanente Southern California (KPSC), a large integrated healthcare system in the United States. Ovarian cancer patients diagnosed between 2017-2020 were identified from KPSC's Surveillance, Epidemiology, and End Results (SEER)-affiliated cancer registry. Patients diagnosed in 2021 were identified from the electronic medical records (EMR) using ICD-10 diagnosis codes, followed by medical chart review to validate diagnosis and extract information on histology and stage at diagnosis. March 4, 2020 was used as the cut-off to define pre-pandemic and pandemic periods. Patients diagnosed with COVID-19 between OC diagnosis and treatment completion were excluded. Data on neoadjuvant chemotherapy use were extracted from the cancer registry and EMR, supplemented by chart review. Modified Poisson regression was used to evaluate the association of the pandemic with neoadjuvant chemotherapy use. Results: Of 566 OC patients, 160 (28.3%) were diagnosed in the pandemic period. Patients diagnosed in the pandemic period were slightly younger (mean age 62.7 vs 64.9 years, p=0.07) and had a higher burden of Charlson comorbidities (p=0.05) than patients diagnosed in pre-pandemic period. No differences in time to treatment initiation were observed by pandemic periods. Neoadjuvant chemotherapy use was documented in 58.7% patients during the pandemic period compared to 47.3% in pre-pandemic period (p=0.01). After adjusting for covariates, patients diagnosed in the pandemic period were 29% more likely to receive neoadjuvant chemotherapy than patients diagnosed in pre-pandemic period [RR(95%CI): 1.29(1.12-1.49)]. Discussions: Ovarian cancer patients diagnosed in the COVID-19 pandemic were more likely to receive neoadjuvant chemotherapy than patients diagnosed before the pandemic. Future research on patient outcomes and trends in the post-pandemic period are warranted.
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Microtubules are nucleated by γ-tubulin ring complexes (γ-TuRCs) and are essential for neuronal development. Nevertheless, γ-TuRC depletion has been reported to perturb only higher-order branching in elaborated Drosophila larval class IV dendritic arborization (da) neurons. This relatively mild phenotype has been attributed to defects in microtubule nucleation from Golgi outposts, yet most Golgi outposts lack associated γ-TuRCs. By analyzing dendritic arbor regrowth in pupae, we show that γ-TuRCs are also required for the growth and branching of primary and secondary dendrites, as well as for higher-order branching. Moreover, we identify the augmin complex (hereafter augmin), which recruits γ-TuRCs to the sides of pre-existing microtubules, as being required predominantly for higher-order branching. Augmin strongly promotes the anterograde growth of microtubules in terminal dendrites and thus terminal dendrite stability. Consistent with a specific role in higher-order branching, we find that augmin is expressed less strongly and is largely dispensable in larval class I da neurons, which exhibit few higher-order dendrites. Thus, γ-TuRCs are essential for various aspects of complex dendritic arbor development, and they appear to function in higher-order branching via the augmin pathway, which promotes the elaboration of dendritic arbors to help define neuronal morphology.
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Dendritos , Proteínas de Drosophila , Microtúbulos , Animais , Proteínas de Drosophila/metabolismo , Proteínas de Drosophila/genética , Dendritos/metabolismo , Microtúbulos/metabolismo , Drosophila melanogaster/metabolismo , Drosophila melanogaster/crescimento & desenvolvimento , Drosophila melanogaster/genética , Tubulina (Proteína)/metabolismo , Larva/metabolismo , Larva/crescimento & desenvolvimento , Proteínas Associadas aos Microtúbulos/metabolismo , Proteínas Associadas aos Microtúbulos/genética , Drosophila/metabolismoRESUMO
Post-infectious myalgic encephalomyelitis/chronic fatigue syndrome (PI-ME/CFS) is a disabling disorder, yet the clinical phenotype is poorly defined, the pathophysiology is unknown, and no disease-modifying treatments are available. We used rigorous criteria to recruit PI-ME/CFS participants with matched controls to conduct deep phenotyping. Among the many physical and cognitive complaints, one defining feature of PI-ME/CFS was an alteration of effort preference, rather than physical or central fatigue, due to dysfunction of integrative brain regions potentially associated with central catechol pathway dysregulation, with consequences on autonomic functioning and physical conditioning. Immune profiling suggested chronic antigenic stimulation with increase in naïve and decrease in switched memory B-cells. Alterations in gene expression profiles of peripheral blood mononuclear cells and metabolic pathways were consistent with cellular phenotypic studies and demonstrated differences according to sex. Together these clinical abnormalities and biomarker differences provide unique insight into the underlying pathophysiology of PI-ME/CFS, which may guide future intervention.
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Doenças Transmissíveis , Síndrome de Fadiga Crônica , Humanos , Síndrome de Fadiga Crônica/metabolismo , Leucócitos Mononucleares/metabolismo , Doenças Transmissíveis/metabolismo , Biomarcadores/metabolismo , FenótipoRESUMO
PURPOSE: Uterine cancer risk is high in breast cancer survivors. Although breast cancer and uterine cancer share some common epidemiological risk factors, association of metabolic syndrome with incident uterine cancer in breast cancer survivors is under-studied. We evaluated the association of metabolic syndrome conditions with second primary uterine cancer in breast cancer survivors. METHODS: In this retrospective cohort study, 37,303 breast cancer patients diagnosed between 2008 and 2020 at Kaiser Permanente Southern California, an integrated healthcare system, were included. Data on cancer-related variables, sociodemographic, and clinical variables were extracted from KPSC's Surveillance, Epidemiology, and End Results (SEER)-affiliated cancer registry and electronic health records, as appropriate. Patients were followed from breast cancer diagnosis until 12/31/2021 for incident uterine cancer. Proportional hazards regression was used to report association [HR (95% CI)] between metabolic conditions and uterine cancer. RESULTS: More than half (53.1%) of the breast cancer survivors had 1-2 metabolic conditions; 19.4% had 3 + , while 27. 5% had no metabolic conditions. Median time to follow-up was 5.33 years and 185 (0.5%) patients developed second primary uterine cancer. Obesity was associated with an elevated uterine cancer risk in the adjusted model [HR (95% CI) 1.64 (1.20-2.25)]. Having 1-2 metabolic conditions (versus none) was not associated with increased uterine cancer risk [adjusted HR (95% CI) 1.24 (0.85-1.82)]; however, there was an increased uterine cancer risk with 3 + metabolic conditions [adjusted HR (95% CI) 1.82 (1.16-2.87)]. CONCLUSION: Although not statistically significant, we found a trend demonstrating greater uterine cancer risk by increasing numbers of metabolic syndrome conditions in breast cancer survivors.
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Neoplasias da Mama , Sobreviventes de Câncer , Síndrome Metabólica , Segunda Neoplasia Primária , Neoplasias Uterinas , Feminino , Humanos , Neoplasias da Mama/epidemiologia , Neoplasias da Mama/complicações , Síndrome Metabólica/complicações , Síndrome Metabólica/epidemiologia , Estudos Retrospectivos , Fatores de Risco , Neoplasias Uterinas/complicações , Neoplasias Uterinas/epidemiologia , Segunda Neoplasia Primária/epidemiologia , Segunda Neoplasia Primária/complicaçõesRESUMO
PURPOSE: The purpose of this study was to assess the association of comorbidity burden with overall survival, accounting for racial/ethnic and socioeconomic differences in patients with cancer. METHODS: In this retrospective cohort study, patients newly diagnosed with cancer between 2010 and 2018 were identified from a large health plan in southern California. Cancer registry data were linked with electronic health records (EHR). Comorbidity burden was defined by the Elixhauser comorbidity index (ECI). Patients were followed through December 2019 to assess all-cause mortality. Association of comorbidity burden with all-cause mortality was evaluated using Cox proportional hazards model. Crude and adjusted hazard ratio (HR, 95%CI) were determined. RESULTS: Of 153,270 patients included in the analysis, 29% died during the ensuing 10-year follow-up. Nearly 49% were patients of color, and 32% had an ECI > 4. After adjusting for age, sex, race/ethnicity, cancer stage, smoking status, insurance payor, medical center, year of cancer diagnosis, and cancer treatments, we observed a trend demonstrating higher mortality risk by decreasing socioeconomic status (SES) (P-trend<.05). Compared to patients in the highest SES quintile, patients in the lowest, second lowest, middle, and second highest quintiles had 25%, 21%, 18%, and 11% higher risk of mortality, respectively [(HR, 95%CI): 1.25 (1.21-1.29), 1.21 (1.18-1.25), 1.18 (1.15-1.22), and 1.11 (1.07-1.14), respectively]. When we additionally adjusted for ECI, the adjusted HRs for SES were slightly attenuated; however, the trend persisted. Patients with higher comorbidity burden had higher mortality risk compared to patients with ECI score = 0 in the adjusted model [(HR, 95%CI): 1.22 (1.17-1.28), 1.48 (1.42-1.55), 1.80 (1.72-1.89), 2.24 (2.14-2.34), and 3.39 (3.25-3.53) for ECI = 1, 2, 3, 4, and >5, respectively]. CONCLUSIONS: Comorbidity burden affects overall survival in cancer patients irrespective of racial/ethnic and SES differences. Reducing comorbidity burden can reduce some, but not all, of the mortality risk associated with lower SES.
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Etnicidade , Neoplasias , Humanos , Fatores Socioeconômicos , Estudos Retrospectivos , Classe Social , Neoplasias/epidemiologia , ComorbidadeRESUMO
The eggshell that surrounds insect eggs acts as a barrier, protecting against biotic factors and desiccation. The eggshell is a multi-layered structure which is synthesised by the somatic follicle cells that surround the developing oocyte. Although the temporal order of expression of the protein eggshell components goes someway to explaining how the different layers are built up, but how the precise three-dimensional structure is achieved and how lipid components responsible for desiccation resistance are incorporated are poorly understood. In this paper, we demonstrate that wunen, which encodes a lipid phosphate phosphatase, is necessary for fertility in Drosophila females. Compared to sibling controls, females null for wunen lay fewer eggs which subsequently collapse such that no larvae emerge. We show that this is due to a requirement for wunen in the ovarian follicle cells which is needed to produce an ordered and functional eggshell. Knockdown of a septate junction component also results in collapsed eggs, supporting the idea that similar to its role in embryonic tracheal development, Wunen in follicle cells also promotes septate junction function.
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BACKGROUND: Cervical cancer oncogenesis starts with human papillomavirus (HPV) cell entry after binding to host cell surface receptors; however, the mechanism is not fully known. We examined polymorphisms in receptor genes hypothesized to be necessary for HPV cell entry and assessed their associations with clinical progression to precancer. METHODS: African American women (N = 1,728) from the MACS/WIHS Combined Cohort Study were included. Two case-control study designs were used-cases with histology-based precancer (CIN3+) and controls without; and cases with cytology-based precancer [high-grade squamous intraepithelial lesions (HSIL)] and controls without. SNPs in candidate genes (SDC1, SDC2, SDC3, SDC4, GPC1, GPC2, GPC3, GPC4, GPC5, GPC6, and ITGA6) were genotyped using an Illumina Omni2.5-quad beadchip. Logistic regression was used to assess the associations in all participants and by HPV genotypes, after adjusting for age, human immunodeficiency virus serostatus, CD4 T cells, and three principal components for ancestry. RESULTS: Minor alleles in SNPs rs77122854 (SDC3), rs73971695, rs79336862 (ITGA6), rs57528020, rs201337456, rs11987725 (SDC2), rs115880588, rs115738853, and rs9301825 (GPC5) were associated with increased odds of both CIN3+ and HSIL, whereas, rs35927186 (GPC5) was found to decrease the odds for both outcomes (P value ≤ 0.01). Among those infected with Alpha-9 HPV types, rs722377 (SDC3), rs16860468, rs2356798 (ITGA6), rs11987725 (SDC2), and rs3848051 (GPC5) were associated with increased odds of both precancer outcomes. CONCLUSIONS: Polymorphisms in genes that encode binding receptors for HPV cell entry may play a role in cervical precancer progression. IMPACT: Our findings are hypothesis generating and support further exploration of mechanisms of HPV entry genes that may help prevent progression to cervical precancer.
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Infecções por Papillomavirus , Displasia do Colo do Útero , Neoplasias do Colo do Útero , Feminino , Humanos , Papillomavirus Humano , Estudos de Coortes , Estudos de Casos e Controles , Papillomaviridae/genética , Polimorfismo de Nucleotídeo Único , Glipicanas/genéticaRESUMO
BACKGROUND: Lower socioeconomic status (SES) affects health care delivery and is associated with worse outcomes. Integrated healthcare systems (IHS) may help reduce barriers to health care and affect outcomes. Our aim was to compare outcomes of colon cancer cases diagnosed at the largest IHS in California, Kaiser Permanente Southern California (KPSC), to other insured patients (OI) to determine how SES influences mortality. METHODS: This retrospective cohort study included insured adults in southern California diagnosed with colon cancer between 2009 and 2014, using data from the California Cancer Registry, and followed through 2017. Main outcome was all-cause mortality. Person-year mortality rates were calculated for two groups, KPSC and OI. Multivariable hazard ratios were calculated for association between SES quintiles and mortality. RESULTS: Total of 15 923 patients were diagnosed with colon cancer, 4195 patients (26.3%) within KPSC and 11 728 patients (73.7%) in OI. The overall mortality rate per 1000 person-years (PY) was lower in KPSC [103.8/1000 PY (95% CI:98.5-109.3)] compared to OI [139.3/1000 PY (95% CI:135.2-143.4)]. Compared to the highest SES group, the lowest SES group did not experience higher mortality risk in the KPSC population, after adjusting for race/ethnicity and other factors (HR, 95% CI = 1.13, .93-1.38). However, in OI patients, lowest and lower-middle SES groups had higher mortality risk compared to the highest SES group (HR, 95% CI = 1.26, 1.13-1.40 and 1.28, 1.16-1.41, respectively). DISCUSSION: Lower SES was associated with higher mortality risk within the OI group; however, within KPSC no such association was observed. Care coordination in IHS settings mitigate SES-related mortality differences.
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Neoplasias do Colo , Prestação Integrada de Cuidados de Saúde , Adulto , Humanos , Estudos Retrospectivos , Classe Social , Etnicidade , Neoplasias do Colo/terapiaRESUMO
BACKGROUND: People with mitochondrial disease (MtD) are susceptible to metabolic decompensation and neurological symptom progression in response to an infection. Increasing evidence suggests that mitochondrial dysfunction may cause chronic inflammation, which may promote hyper-responsiveness to pathogens and neurodegeneration. We sought to examine transcriptional changes between MtD patients and healthy controls to identify common gene signatures of immune dysregulation in MtD. METHODS: We collected whole blood from a cohort of MtD patients and healthy controls and performed RNAseq to examine transcriptomic differences. We performed GSEA analyses to compare our findings against existing studies to identify commonly dysregulated pathways. RESULTS: Gene sets involved in inflammatory signaling, including type I interferons, interleukin-1ß and antiviral responses, are enriched in MtD patients compared to controls. Monocyte and dendritic cell gene clusters are also enriched in MtD patients, while T cell and B cell gene sets are negatively enriched. The enrichment of antiviral response corresponds with an independent set of MELAS patients, and two mouse models of mtDNA dysfunction. CONCLUSIONS: Through the convergence of our results, we demonstrate translational evidence of systemic peripheral inflammation arising from MtD, predominantly through antiviral response gene sets. This provides key evidence linking mitochondrial dysfunction to inflammation, which may contribute to the pathogenesis of primary MtD and other chronic inflammatory disorders associated with mitochondrial dysfunction.
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Interferons , Doenças Mitocondriais , Animais , Camundongos , Interferons/genética , Transcriptoma/genética , Inflamação/genética , Inflamação/patologia , AntiviraisRESUMO
The real space decimation method has been successfully applied over the years to understand the critical phenomena as well as the nature of single particle excitations in periodic, quasiperiodic, fractal, and decorated lattices in one dimension and beyond. The power of the method is specially revealed through its application in lattice models, leading to an elegant understanding of the nature of the single-particle states and the corresponding transport properties. In this review, we discuss, using a variety of decorated lattices, how the realm of this method is extended to unravel diverse electronic phases of matter, such as the Dirac systems, or lattices exhibiting flat bands and topological phase transitions.
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Parkinson's disease (PD) is characterised by selective death of dopaminergic (DA) neurons in the midbrain and motor function impairment. Gastrointestinal issues often precede motor deficits in PD, indicating that the gut-brain axis is involved in the pathogenesis of this disease. The features of PD include both mitochondrial dysfunction and activation of the unfolded protein response (UPR) in the endoplasmic reticulum (ER). PINK1 is a mitochondrial kinase involved in the recycling of defective mitochondria, and PINK1 mutations cause early-onset PD. Like PD patients, pink1 mutant Drosophila show degeneration of DA neurons and intestinal dysfunction. These mutant flies also lack vital proteins due to sustained activation of the kinase R-like endoplasmic reticulum kinase (dPerk), a kinase that induces the UPR. Here, we investigated the role of dPerk in intestinal dysfunction. We showed that intestinal expression of dPerk impairs mitochondrial function, induces cell death, and decreases lifespan. We found that suppressing dPerk in the intestine of pink1-mutant flies rescues intestinal cell death and is neuroprotective. We conclude that in a fly model of PD, blocking gut-brain transmission of UPR-mediated toxicity, is neuroprotective.
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Proteínas de Drosophila , Doença de Parkinson , Animais , Drosophila/metabolismo , Drosophila melanogaster/genética , Drosophila melanogaster/metabolismo , Proteínas de Drosophila/genética , Proteínas de Drosophila/metabolismo , Doença de Parkinson/metabolismo , Proteínas Serina-Treonina Quinases/metabolismo , Resposta a Proteínas não DobradasRESUMO
Background: People with mitochondrial disease (MtD) are susceptible to metabolic decompensation and neurological symptom progression in response to an infection. Increasing evidence suggests that mitochondrial dysfunction may cause chronic inflammation, which may promote hyperresponsiveness to pathogens and neurodegeneration. Methods: We collected whole blood from a cohort of MtD patients and healthy controls and performed RNAseq to examine transcriptomic differences. We performed GSEA analyses to compare our findings against existing studies to identify commonly dysregulated pathways. Results: Gene sets involved in inflammatory signaling, including type I interferons, interleukin-1ß and antiviral responses, are enriched in MtD patients compared to controls. Monocyte and dendritic cell gene clusters are also enriched in MtD patients, while T cell and B cell gene sets are negatively enriched. The enrichment of antiviral response corresponds with an independent set of MELAS patients, and two mouse models of mtDNA dysfunction. Conclusions: Through the convergence of our results, we demonstrate translational evidence of systemic peripheral inflammation arising from MtD, predominantly through antiviral response gene sets. This provides key evidence linking mitochondrial dysfunction to inflammation, which may contribute to the pathogenesis of primary MtD and other chronic inflammatory disorders associated with mitochondrial dysfunction.
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Acute viral infections can have durable functional impacts on the immune system long after recovery, but how they affect homeostatic immune states and responses to future perturbations remain poorly understood1-4. Here we use systems immunology approaches, including longitudinal multimodal single-cell analysis (surface proteins, transcriptome and V(D)J sequences) to comparatively assess baseline immune statuses and responses to influenza vaccination in 33 healthy individuals after recovery from mild, non-hospitalized COVID-19 (mean, 151 days after diagnosis) and 40 age- and sex-matched control individuals who had never had COVID-19. At the baseline and independent of time after COVID-19, recoverees had elevated T cell activation signatures and lower expression of innate immune genes including Toll-like receptors in monocytes. Male individuals who had recovered from COVID-19 had coordinately higher innate, influenza-specific plasmablast, and antibody responses after vaccination compared with healthy male individuals and female individuals who had recovered from COVID-19, in part because male recoverees had monocytes with higher IL-15 responses early after vaccination coupled with elevated prevaccination frequencies of 'virtual memory'-like CD8+ T cells poised to produce more IFNγ after IL-15 stimulation. Moreover, the expression of the repressed innate immune genes in monocytes increased by day 1 to day 28 after vaccination in recoverees, therefore moving towards the prevaccination baseline of the healthy control individuals. By contrast, these genes decreased on day 1 and returned to the baseline by day 28 in the control individuals. Our study reveals sex-dimorphic effects of previous mild COVID-19 and suggests that viral infections in humans can establish new immunological set-points that affect future immune responses in an antigen-agnostic manner.
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COVID-19 , Imunidade Inata , Memória Imunológica , Vacinas contra Influenza , Caracteres Sexuais , Linfócitos T , Vacinação , Feminino , Humanos , Masculino , Linfócitos T CD8-Positivos/imunologia , COVID-19/imunologia , Vacinas contra Influenza/imunologia , Influenza Humana/imunologia , Influenza Humana/prevenção & controle , Interleucina-15/imunologia , Receptores Toll-Like/imunologia , Linfócitos T/citologia , Linfócitos T/imunologia , Monócitos , Imunidade Inata/genética , Imunidade Inata/imunologia , Análise de Célula Única , Voluntários SaudáveisRESUMO
OBJECTIVES: Qualitative studies of the relationship between acquired invisible disability (AcqID) and posttraumatic growth (PTG) are scant, especially in the context of healthcare professionals. This study aimed to explore in-depth accounts of the lived experience of PTG in doctors with AcqID arising from physical illness with cognitive dysfunction. DESIGN: Five doctors who had been diagnosed in the last decade with a physical illness with cognitive dysfunction resulting in an AcqID, and who self-reported at least one feature of PTG participated in this qualitative research study. METHODS: Semi-structured interviews were used to collect data, which were analysed using interpretative phenomenological analysis. RESULTS: This study recognized that AcqID supported a process of PTG for participants. Three superordinate themes were apparent across the sample: identity (The human left behind), self (Acceptance of the disabled self), and rebirth (The phoenix rises from the ashes). Human connection, service as a value, and the role of the body were found to be key facilitators of PTG in these participants. This study offers new perspectives on cognitive-embodied appreciation in facilitating PTG in doctors with AcqID. CONCLUSIONS: While the participants perceived AcqID with cognitive dysfunction to be a trauma, they also experienced PTG, Corporeal PTG and a new considered domain, Cognitive-Embodied PTG. The unrealised potential of PTG can be harnessed if doctors with disability are viewed as assets to the medical profession, and diversity is promoted through the provision of appropriate support. Thus, there is potential to cultivate a flourishing, inclusive, and compassionate culture within medicine.
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Pessoas com Deficiência , Crescimento Psicológico Pós-Traumático , Transtornos de Estresse Pós-Traumáticos , Humanos , Adaptação Psicológica , Pesquisa Qualitativa , Pessoal de Saúde , Transtornos de Estresse Pós-Traumáticos/psicologiaRESUMO
INTRODUCTION: Neonatal sepsis is a major cause of morbidity and mortality with a higher burden from the low- and middle-income countries. The coronavirus disease 2019 (Covid 19) pandemic has impacted healthcare in various ways including healthcare-associated infections (HAI). The objective of the present study was to determine changes in organism profile and incidence rates of HAI in neonates admitted to the index hospital during the pandemic and compared it with the data from the pre-pandemic period. MATERIALS AND METHODS: The study design was a retrospective, observational analysis of data from neonates with culture-positive sepsis, in a tertiary care children's hospital, between January 2018 and December 2021. Pre-Covid (January 2018 to December 2019) and Covid period data (January 2020 to December 2021) were analyzed for the significance of change. RESULTS: The prevalence of culture-positive sepsis, in pre-Covid and Covid periods, was 19.55% [95% confidence interval (95% CI) 17.13-21.52)] and 18.36% (CI 16.05-20.74), respectively. HAI rates/1000 patient days increased slightly during the Covid pandemic [7.2% (95% CI 6.98-10.08) to 9.8% (95% CI 9.78-13.67)] mainly due to an increase in fungal HAI (26% pre- vs. 41.5% Covid period). However, the proportion of Gram-negative (GN) infections fell significantly (70.5% vs. 48.6%) during the same period. In the pre-Covid period, Klebsiella followed by Burkholderia cepacia, Acinetobacter spp and Pseudomonas, were the major HAI isolates. During the Covid period, there was a decline in these isolates and Burkholderia spp was not detected. All fungal isolates were Candida species. The case fatality ratio (CFR) from HAI decreased significantly from 38% to 15.45%, mainly due to a decrease in GN HAI. CONCLUSION: During Covid pandemic, there was a significant decline in GN HAI and CFR from HAI, due to improved compliance with infection control measures in the neonatal intensive care unit (NICU). At the same time, there was a rise in the fungal HAI, possibly because of a higher proportion of premature, and sick neonates with longer hospital stay and more invasive procedures. Consolidations of gains in infection control and restriction of invasive procedures could help to minimize HAI in NICUs.
Blood stream infections in children less than 4 weeks old are known as neonatal sepsis. Several predisposing factors can make a neonate (less than 4 weeks) more prone to sepsis, such as prematurity, male gender, cultural practices, presence of underlying medical or surgical conditions, hospitalization, antibiotic use and invasive treatment. Neonatal sepsis in a hospitalized child can be eitherpre-harbored infection (PHI), which means infection acquired prior to hospital admission or it could be healthcare-associated infection (HAI), where the infection is acquired during the hospital stay. Organisms causing neonatal sepsis in hospitalized neonates include bacteria and fungi. The coronavirus disease 2019 (Covid 19) pandemic impacted all aspects of life including healthcare. The investigators conducted the present study to look into the changes in the incidence rate as well as in the type of organisms causing healthcare-associated blood stream infections in neonates in the pre-Covid and during the Covid period.
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COVID-19 , Infecção Hospitalar , Sepse Neonatal , Sepse , Criança , Humanos , Recém-Nascido , Antibacterianos/uso terapêutico , COVID-19/epidemiologia , Infecção Hospitalar/microbiologia , Bactérias Gram-Negativas , Índia/epidemiologia , Unidades de Terapia Intensiva Neonatal , Sepse Neonatal/tratamento farmacológico , Estudos Retrospectivos , Sepse/epidemiologia , Sepse/tratamento farmacológicoRESUMO
Mastering manual small-incision cataract surgery (MSICS) for beginner surgeons is difficult. In the initial days of residency or training, surgeons struggle to make a proper scleral tunnel and keratome entry. It commonly results in premature entry and iris prolapse. Most of the literature has shed light on premature entry during tunnel construction by a crescent blade, whereas a significant majority of iris prolapse happens due to improper keratome entry. This novel trypan blue dye-assisted tunnel staining (TBTS) technique helps in proper tunnel demarcation which can reduce the incidence of premature entry with a keratome.
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Extração de Catarata , Catarata , Cristalino , Ferida Cirúrgica , Humanos , Extração de Catarata/métodos , Prolapso , Coloração e RotulagemRESUMO
Learning manual small-incision cataract surgery (SICS) is essential for ophthalmic surgeons as it provides an alternative to phaco-emulsification in complicated cases. Nearly 10% of ophthalmic surgeons are left-handed. Left-handed surgeons do face more difficulties because of their laterality, which have been highlighted in various surveys even in other surgical specialities. Surgical training programs, residency programs, and fellowships have traditionally been designed considering the right hand as the dominant hand. Left-handed surgeons (LHSs) are at disadvantage as they are trained by right-handed surgeons (RHSs), which may result in more initial intra-operative errors. Intra-ocular lenses are also designed such that dialing into the bag is relatively difficult for LHSs. Developing customized training modules for LHSs can help them overcome the laterality challenges and enhance their surgical capabilities. In this article, we herein present a brief description of the SICS technique for LHSs, elaborating the crucial steps and customized maneuvers that, if performed differently, may make surgeries easier for them.
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Extração de Catarata , Catarata , Oftalmologia , Cirurgiões , Ferida Cirúrgica , Humanos , Oftalmologia/educação , Implante de Lente IntraocularRESUMO
Indian mustard (Brassica juncea) faces significant yield loss due to the 'Black Spot Disease,' caused by a fungus Alternaria brassicicola. In plants, NAC transcription factors (NAC TFs) are known for their roles in development and stress tolerance. One such NAC TF, NAC 62, was induced during A. brassicicola challenge in Sinapis alba, a non-host resistant plant against this fungus. Sequence analyses of BjuNAC62 from B. juncea showed that it belonged to the membrane-bound class of transcription factors. Gene expression study revealed differential protein processing of NAC62 between B. juncea and S. alba on pathogen challenge. Furthermore, NAC62 processing to 25 kDa protein was found to be unique to the resistant plant during pathogenesis. Conditional expression of BjuNAC62ΔC, which lacks its transmembrane domain, in B. juncea showed improved tolerance to A. brassicicola. BjuNAC62ΔC processing to 25 kDa product was also observed in tolerant transgenic plants. Additionally, transgenic plants showed induced expression of genes associated with defense-related phytohormone signaling pathways on pathogen challenge. Again, altered phenotypes suggest a possible developmental effect of BjuNAC62∆C in transgenic plants. The overall results suggest that the processing of BjuNAC62 might be playing a crucial role in resistance response against Black Spot disease by modulating defense-associated genes.