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1.
Am J Public Health ; 114(10): 1071-1080, 2024 Oct.
Article in English | MEDLINE | ID: mdl-39052959

ABSTRACT

Mortality surveillance systems can have limitations, including reporting delays, incomplete reporting, missing data, and insufficient detail on important risk or sociodemographic factors that can impact the accuracy of estimates of current trends, disease severity, and related disparities across subpopulations. The Centers for Disease Control and Prevention used multiple data systems during the COVID-19 emergency response-line-level case‒death surveillance, aggregate death surveillance, and the National Vital Statistics System-to collectively provide more comprehensive and timely information on COVID-19‒associated mortality necessary for informed decisions. This article will review in detail the line-level, aggregate, and National Vital Statistics System surveillance systems and the purpose and use of each. This retrospective review of the hybrid surveillance systems strategy may serve as an example for adaptive informational approaches needed over the course of future public health emergencies. (Am J Public Health. 2024;114(10):1071-1080. https://doi.org/10.2105/AJPH.2024.307743).


Subject(s)
COVID-19 , Centers for Disease Control and Prevention, U.S. , Humans , COVID-19/mortality , COVID-19/epidemiology , COVID-19/prevention & control , United States/epidemiology , SARS-CoV-2 , Population Surveillance/methods , Pandemics/prevention & control , Vital Statistics , Retrospective Studies
2.
BMC Med Inform Decis Mak ; 24(Suppl 2): 259, 2024 Sep 16.
Article in English | MEDLINE | ID: mdl-39285449

ABSTRACT

BACKGROUND: The population diagnosed with renal cell carcinoma, especially in Asia, represents 36.6% of global cases, with the incidence rate of renal cell carcinoma in Korea steadily increasing annually. However, treatment options for renal cell carcinoma are diverse, depending on clinical stage and histologic characteristics. Hence, this study aims to develop a machine learning based clinical decision-support system that recommends personalized treatment tailored to the individual health condition of each patient. RESULTS: We reviewed the real-world medical data of 1,867 participants diagnosed with renal cell carcinoma between November 2008 and June 2021 at the Pusan National University Yangsan Hospital in South Korea. Data were manually divided into a follow-up group where the patients did not undergo surgery or chemotherapy (Surveillance), a group where the patients underwent surgery (Surgery), and a group where the patients received chemotherapy before or after surgery (Chemotherapy). Feature selection was conducted to identify the significant clinical factors influencing renal cell carcinoma treatment decisions from 2,058 features. These features included subsets of 20, 50, 75, 100, and 150, as well as the complete set and an additional 50 expert-selected features. We applied representative machine learning algorithms, namely Decision Tree, Random Forest, and Gradient Boosting Machine (GBM). We analyzed the performance of three applied machine learning algorithms, among which the GBM algorithm achieved an accuracy score of 95% (95% CI, 92-98%) for the 100 and 150 feature sets. The GBM algorithm using 100 and 150 features achieved better performance than the algorithm using features selected by clinical experts (93%, 95% CI 89-97%). CONCLUSIONS: We developed a preliminary personalized treatment decision-support system (TDSS) called "RCC-Supporter" by applying machine learning (ML) algorithms to determine personalized treatment for the various clinical situations of RCC patients. Our results demonstrate the feasibility of using machine learning-based clinical decision support systems for treatment decisions in real clinical settings.


Subject(s)
Carcinoma, Renal Cell , Decision Support Systems, Clinical , Kidney Neoplasms , Machine Learning , Humans , Carcinoma, Renal Cell/therapy , Carcinoma, Renal Cell/drug therapy , Kidney Neoplasms/therapy , Kidney Neoplasms/drug therapy , Male , Female , Middle Aged , Republic of Korea , Clinical Decision-Making , Aged , Adult
3.
MMWR Morb Mortal Wkly Rep ; 72(32): 871-876, 2023 Aug 11.
Article in English | MEDLINE | ID: mdl-37561674

ABSTRACT

Persons receiving maintenance dialysis are at increased risk for SARS-CoV-2 infection and its severe outcomes, including death. However, rates of SARS-CoV-2 infection and COVID-19-related deaths in this population are not well described. Since November 2020, CDC's National Healthcare Safety Network (NHSN) has collected weekly data monitoring incidence of SARS-CoV-2 infections (defined as a positive SARS-CoV-2 test result) and COVID-19-related deaths (defined as the death of a patient who had not fully recovered from a SARS-CoV-2 infection) among maintenance dialysis patients. This analysis used NHSN dialysis facility COVID-19 data reported during June 30, 2021-September 27, 2022, to describe rates of SARS-CoV-2 infection and COVID-19-related death among maintenance dialysis patients. The overall infection rate was 30.47 per 10,000 patient-weeks (39.64 among unvaccinated patients and 27.24 among patients who had completed a primary COVID-19 vaccination series). The overall death rate was 1.74 per 10,000 patient-weeks. Implementing recommended infection control measures in dialysis facilities and ensuring patients and staff members are up to date with recommended COVID-19 vaccination is critical to limiting COVID-19-associated morbidity and mortality.


Subject(s)
COVID-19 , Renal Insufficiency, Chronic , Humans , Centers for Disease Control and Prevention, U.S. , COVID-19/diagnosis , COVID-19/mortality , COVID-19 Vaccines , Renal Dialysis , SARS-CoV-2 , United States/epidemiology , Renal Insufficiency, Chronic/complications , Renal Insufficiency, Chronic/therapy
4.
MMWR Morb Mortal Wkly Rep ; 72(19): 523-528, 2023 May 12.
Article in English | MEDLINE | ID: mdl-37167154

ABSTRACT

On January 31, 2020, the U.S. Department of Health and Human Services (HHS) declared, under Section 319 of the Public Health Service Act, a U.S. public health emergency because of the emergence of a novel virus, SARS-CoV-2.* After 13 renewals, the public health emergency will expire on May 11, 2023. Authorizations to collect certain public health data will expire on that date as well. Monitoring the impact of COVID-19 and the effectiveness of prevention and control strategies remains a public health priority, and a number of surveillance indicators have been identified to facilitate ongoing monitoring. After expiration of the public health emergency, COVID-19-associated hospital admission levels will be the primary indicator of COVID-19 trends to help guide community and personal decisions related to risk and prevention behaviors; the percentage of COVID-19-associated deaths among all reported deaths, based on provisional death certificate data, will be the primary indicator used to monitor COVID-19 mortality. Emergency department (ED) visits with a COVID-19 diagnosis and the percentage of positive SARS-CoV-2 test results, derived from an established sentinel network, will help detect early changes in trends. National genomic surveillance will continue to be used to estimate SARS-CoV-2 variant proportions; wastewater surveillance and traveler-based genomic surveillance will also continue to be used to monitor SARS-CoV-2 variants. Disease severity and hospitalization-related outcomes are monitored via sentinel surveillance and large health care databases. Monitoring of COVID-19 vaccination coverage, vaccine effectiveness (VE), and vaccine safety will also continue. Integrated strategies for surveillance of COVID-19 and other respiratory viruses can further guide prevention efforts. COVID-19-associated hospitalizations and deaths are largely preventable through receipt of updated vaccines and timely administration of therapeutics (1-4).


Subject(s)
COVID-19 , Sentinel Surveillance , Humans , COVID-19/epidemiology , COVID-19/prevention & control , COVID-19 Testing , COVID-19 Vaccines , Public Health , SARS-CoV-2 , United States/epidemiology , Wastewater-Based Epidemiological Monitoring
5.
Sensors (Basel) ; 24(1)2023 Dec 28.
Article in English | MEDLINE | ID: mdl-38203039

ABSTRACT

The presence of chironomid larvae in tap water has sparked public concern regarding the water supply system in South Korea. Despite ongoing efforts to establish a safe water supply system, entirely preventing larval occurrences remains a significant challenge. Therefore, we developed a real-time chironomid larva detection system (RT-CLAD) based on deep learning technology, which was implemented in drinking water treatment plants. The acquisition of larval images was facilitated by a multi-spectral camera with a wide spectral range, enabling the capture of unique wavelet bands associated with larvae. Three state-of-the-art deep learning algorithms, namely the convolutional neural network (CNN), you only look once (YOLO), and residual neural network (ResNet), renowned for their exceptional performance in object detection tasks, were employed. Following a comparative analysis of these algorithms, the most accurate and rapid model was selected for RT-CLAD. To achieve the efficient and accurate detection of larvae, the original images were transformed into a specific wavelet format, followed by preprocessing to minimize data size. Consequently, the CNN, YOLO, and ResNet algorithms successfully detected larvae with 100% accuracy. In comparison to YOLO and ResNet, the CNN algorithm demonstrated greater efficiency because of its faster processing and simpler architecture. We anticipate that our RT-CLAD will address larva detection challenges in water treatment plants, thereby enhancing water supply security.


Subject(s)
Chironomidae , Drinking Water , Water Purification , Animals , Artificial Intelligence , Larva
6.
Cardiovasc Diabetol ; 21(1): 82, 2022 05 23.
Article in English | MEDLINE | ID: mdl-35606846

ABSTRACT

BACKGROUND: Statin treatment increases the risk of new-onset diabetes mellitus (NODM); however, data directly comparing the risk of NODM among individual statins is limited. We compared the risk of NODM between patients using pitavastatin and atorvastatin or rosuvastatin using reliable, large-scale data. METHODS: Data of electronic health records from ten hospitals converted to the Observational Medical Outcomes Partnership Common Data Model (n = 14,605,368 patients) were used to identify new users of pitavastatin, atorvastatin, or rosuvastatin (atorvastatin + rosuvastatin) for ≥ 180 days without a previous history of diabetes or HbA1c level ≥ 5.7%. We conducted a cohort study using Cox regression analysis to examine the hazard ratio (HR) of NODM after propensity score matching (PSM) and then performed an aggregate meta-analysis of the HR. RESULTS: After 1:2 PSM, 10,238 new pitavastatin users (15,998 person-years of follow-up) and 18,605 atorvastatin + rosuvastatin users (33,477 person-years of follow-up) were pooled from 10 databases. The meta-analysis of the HRs demonstrated that pitavastatin resulted in a significantly reduced risk of NODM than atorvastatin + rosuvastatin (HR 0.72; 95% CI 0.59-0.87). In sub-analysis, pitavastatin was associated with a lower risk of NODM than atorvastatin or rosuvastatin after 1:1 PSM (HR 0.69; CI 0.54-0.88 and HR 0.74; CI 0.55-0.99, respectively). A consistently low risk of NODM in pitavastatin users was observed when compared with low-to-moderate-intensity atorvastatin + rosuvastatin users (HR 0.78; CI 0.62-0.98). CONCLUSIONS: In this retrospective, multicenter active-comparator, new-user, cohort study, pitavastatin reduced the risk of NODM compared with atorvastatin or rosuvastatin.


Subject(s)
Diabetes Mellitus , Hydroxymethylglutaryl-CoA Reductase Inhibitors , Atorvastatin/adverse effects , Cohort Studies , Diabetes Mellitus/diagnosis , Diabetes Mellitus/drug therapy , Diabetes Mellitus/epidemiology , Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Multicenter Studies as Topic , Quinolines , Retrospective Studies , Rosuvastatin Calcium/adverse effects
7.
FASEB J ; 35(5): e21467, 2021 05.
Article in English | MEDLINE | ID: mdl-33788970

ABSTRACT

Diabetic kidney disease (DKD) and diabetic peripheral neuropathy (DPN) are two common diabetic complications. However, their pathogenesis remains elusive and current therapies are only modestly effective. We evaluated genome-wide expression to identify pathways involved in DKD and DPN progression in db/db eNOS-/- mice receiving renin-angiotensin-aldosterone system (RAS)-blocking drugs to mimic the current standard of care for DKD patients. Diabetes and eNOS deletion worsened DKD, which improved with RAS treatment. Diabetes also induced DPN, which was not affected by eNOS deletion or RAS blockade. Given the multiple factors affecting DKD and the graded differences in disease severity across mouse groups, an automatic data analysis method, SOM, or self-organizing map was used to elucidate glomerular transcriptional changes associated with DKD, whereas pairwise bioinformatic analysis was used for DPN. These analyses revealed that enhanced gene expression in several pro-inflammatory networks and reduced expression of development genes correlated with worsening DKD. Although RAS treatment ameliorated the nephropathy phenotype, it did not alter the more abnormal gene expression changes in kidney. Moreover, RAS exacerbated expression of genes related to inflammation and oxidant generation in peripheral nerves. The graded increase in inflammatory gene expression and decrease in development gene expression with DKD progression underline the potentially important role of these pathways in DKD pathogenesis. Since RAS blockers worsened this gene expression pattern in both DKD and DPN, it may partly explain the inadequate therapeutic efficacy of such blockers.


Subject(s)
Diabetes Mellitus, Experimental/complications , Diabetes Mellitus, Type 2/complications , Diabetic Nephropathies/pathology , Diabetic Neuropathies/pathology , Nitric Oxide Synthase Type III/physiology , Transcriptome , ras Proteins/antagonists & inhibitors , Animals , Diabetic Nephropathies/etiology , Diabetic Nephropathies/metabolism , Diabetic Neuropathies/etiology , Diabetic Neuropathies/metabolism , Gene Expression Regulation , Male , Mice , Mice, Inbred C57BL , Mice, Knockout
8.
MMWR Morb Mortal Wkly Rep ; 70(23): 858-864, 2021 Jun 11.
Article in English | MEDLINE | ID: mdl-34111059

ABSTRACT

Throughout the COVID-19 pandemic, older U.S. adults have been at increased risk for severe COVID-19-associated illness and death (1). On December 14, 2020, the United States began a nationwide vaccination campaign after the Food and Drug Administration's Emergency Use Authorization of Pfizer-BioNTech COVID-19 vaccine. The Advisory Committee on Immunization Practices (ACIP) recommended prioritizing health care personnel and residents of long-term care facilities, followed by essential workers and persons at risk for severe illness, including adults aged ≥65 years, in the early phases of the vaccination program (2). By May 1, 2021, 82%, 63%, and 42% of persons aged ≥65, 50-64, and 18-49 years, respectively, had received ≥1 COVID-19 vaccine dose. CDC calculated the rates of COVID-19 cases, emergency department (ED) visits, hospital admissions, and deaths by age group during November 29-December 12, 2020 (prevaccine) and April 18-May 1, 2021. The rate ratios comparing the oldest age groups (≥70 years for hospital admissions; ≥65 years for other measures) with adults aged 18-49 years were 40%, 59%, 65%, and 66% lower, respectively, in the latter period. These differential declines are likely due, in part, to higher COVID-19 vaccination coverage among older adults, highlighting the potential benefits of rapidly increasing vaccination coverage.


Subject(s)
COVID-19 Vaccines/administration & dosage , COVID-19/epidemiology , COVID-19/therapy , Emergency Service, Hospital/statistics & numerical data , Hospitalization/statistics & numerical data , Adolescent , Adult , Age Distribution , Aged , COVID-19/mortality , Humans , Incidence , Middle Aged , Mortality/trends , United States/epidemiology , Young Adult
9.
Am J Nephrol ; 51(7): 556-564, 2020.
Article in English | MEDLINE | ID: mdl-32610315

ABSTRACT

BACKGROUND: Polycystic kidney disease (PKD) is a hereditary disease characterized by cyst formation in the kidneys bilaterally. It has been observed that semaphorin-3C (SEMA3C) is overexpressed in polycystic kidney epithelial cells. It is hypothesized that upregulated SEMA3C would contribute to survival of polycystic kidney epithelial cells. Furthermore, as the kidney is a highly vascularized organ, the secreted SEMA3C from PKD epithelial cells will affect glomerular endothelial cells (GECs) in a paracrine manner. METHODS: To evaluate the effect of SEMA3C on renal cells, siSEMA3C-treated PKD epithelial cells were used for further analysis, and GECs were exposed to recombinant SEMA3C (rSEMA3C). Also, co-culture and treatment of conditioned media were employed to confirm whether PKD epithelial cells could influence on GECs via SEMA3C secretion. RESULTS: SEMA3C knockdown reduced proliferation of PKD epithelial cells. In case of GECs, exposure to rSEMA3C decreased angiogenesis, which resulted from suppressed migratory ability not cell proliferation. CONCLUSIONS: This study indicates that SEMA3C is the aggravating factor in PKD. Thus, it is proposed that targeting SEMA3C can be effective to mitigate PKD.


Subject(s)
Endothelial Cells/metabolism , Kidney Glomerulus/pathology , Neovascularization, Physiologic , Polycystic Kidney Diseases/pathology , Semaphorins/metabolism , Cell Culture Techniques/methods , Cell Line , Cell Movement , Cell Proliferation , Cells, Cultured , Culture Media/metabolism , Endothelial Cells/pathology , Gene Knockdown Techniques , Humans , Kidney Glomerulus/blood supply , Kidney Glomerulus/cytology , Polycystic Kidney Diseases/drug therapy , Recombinant Proteins/metabolism , Semaphorins/antagonists & inhibitors , Semaphorins/genetics , Signal Transduction , Up-Regulation
10.
BMC Nephrol ; 21(Suppl 1): 398, 2020 09 25.
Article in English | MEDLINE | ID: mdl-32977749

ABSTRACT

BACKGROUND: Acute kidney injury (AKI) is defined as a sudden event of kidney failure or kidney damage within a short period. Ischemia-reperfusion injury (IRI) is a critical factor associated with severe AKI and end-stage kidney disease (ESKD). However, the biological mechanisms underlying ischemia and reperfusion are incompletely understood, owing to the complexity of these pathophysiological processes. We aimed to investigate the key biological pathways individually affected by ischemia and reperfusion at the transcriptome level. RESULTS: We analyzed the steady-state gene expression pattern of human kidney tissues from normal (pre-ischemia), ischemia, and reperfusion conditions using RNA-sequencing. Conventional differential expression and self-organizing map (SOM) clustering analyses followed by pathway analysis were performed. Differential expression analysis revealed the metabolic pathways dysregulated in ischemia. Cellular assembly, development and migration, and immune response-related pathways were dysregulated in reperfusion. SOM clustering analysis highlighted the ischemia-mediated significant dysregulation in metabolism, apoptosis, and fibrosis-related pathways, while cell growth, migration, and immune response-related pathways were highly dysregulated by reperfusion after ischemia. The expression of pro-apoptotic genes and death receptors was downregulated during ischemia, indicating the existence of a protective mechanism against ischemic injury. Reperfusion induced alterations in the expression of the genes associated with immune response such as inflammasome and antigen representing genes. Further, the genes related to cell growth and migration, such as AKT, KRAS, and those related to Rho signaling, were downregulated, suggestive of injury responses during reperfusion. Semaphorin 4D and plexin B1 levels were also downregulated. CONCLUSIONS: We show that specific biological pathways were distinctively involved in ischemia and reperfusion during IRI, indicating that condition-specific therapeutic strategies may be imperative to prevent severe kidney damage after IRI in the clinical setting.


Subject(s)
Acute Kidney Injury/genetics , Gene Expression , Kidney/metabolism , RNA-Seq , Reperfusion Injury/genetics , Signal Transduction/physiology , Acute Kidney Injury/metabolism , Gene Expression Profiling , Humans , Kidney/pathology , Male , Reperfusion Injury/metabolism
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