Diabetes is a growing health concern in the United States and especially New York City. New York City subsequently became an epicenter for the coronavirus pandemic in the Spring of 2020. Previous ...studies suggest that diabetes is a risk factor for adverse outcomes in COVID-19.
To investigate the association between diabetes and COVID-19 outcomes as well as assess other covariates that may impact health outcomes.
Retrospective cohort study of COVID-19 hospitalized patients from March to May, 2020.
In total, 1805 patients were tested for COVID-19 and 778 tested positive for COVID-19. Patients were categorized into 2 groups: diabetes (measured by an Hba1c >6.5 or had a history of diabetes) and those without diabetes.
After controlling for other comorbidities, diabetes was associated with increased risk of mortality (aRR = 1.28, 95% CI 1.03-1.57, p = 0.0231) and discharge to tertiary care centers (aRR = 1.69, 95% CI 1.04-2.77, p = 0.036). compared to non-diabetes. Age and coronary artery disease (CAD) increased the risk of mortality among diabetic patients compared to patients with diabetes alone without CAD or advanced age. The diabetes cohort had more patients with resolving acute respiratory failure (62.2%), acute kidney injury secondary to COVID-19 (49.0%) and sepsis secondary to COVID-19 (30.1%).
This investigation found that COVID-19 patients with diabetes had increased mortality, multiple complications at discharge, and increased rates of admission to a tertiary care center than those without diabetes suggesting a more severe and complicated disease course that required additional services at time of discharge.
Universally, the volume of data has increased, with the collection rate doubling every 40 months, since the 1980s. “Big data” is a term that was introduced in the 1990s to include data sets too large ...to be used with common software. Medicine is a major field predicted to increase the use of big data in 2025. Big data in medicine may be used by commercial, academic, government, and public sectors. It includes biologic, biometric, and electronic health data. Examples of biologic data include biobanks; biometric data may have individual wellness data from devices; electronic health data include the medical record; and other data demographics and images. Big data has also contributed to the changes in the research methodology. Changes in the clinical research paradigm has been fueled by large-scale biological data harvesting (biobanks), which is developed, analyzed, and managed by cheaper computing technology (big data), supported by greater flexibility in study design (real-world data) and the relationships between industry, government regulators, and academics. Cultural changes along with easy access to information via the Internet facilitate ease of participation by more people. Current needs demand quick answers which may be supplied by big data, biobanks, and changes in flexibility in study design. Big data can reveal health patterns, and promises to provide solutions that have previously been out of society’s grasp; however, the murkiness of international laws, questions of data ownership, public ignorance, and privacy and security concerns are slowing down the progress that could otherwise be achieved by the use of big data. The goal of this descriptive review is to create awareness of the ramifications for big data and to encourage readers that this trend is positive and will likely lead to better clinical solutions, but, caution must be exercised to reduce harm.
This reference work provides comprehensive information about diabetic nephropathy. Chapters in the book introduce the reader to the link between diabetes, obesity and chronic kidney disease (CKD) and ...delve into many topics relevant to treating kidney disease in diabetic patients. These topics include CKD epidemiology, diagnosis, treatment considerations for the elderly patient, post-transplant diabetes, pathophysiology, biomarkers and much more. Special topics such as the incidence of cardiovascular disease in diabetic CKD, nutrition for obese CKD patients and the clinical use of biomarkers for evaluating cases are also included. The broad spectrum coverage of informative topics about diabetic kidney disease make this an essential reference for medical students and clinical residents/healthcare professionals in nephrology, endocrinology, geriatrics, internal medicine and general surgery. Researchers interested in the clinical biochemistry of diabetes and associated disorders will also benefit from the information presented.
Based on a single rat study by Lillemoe et al, the consensus has been formed to implicate sorbitol rather than sodium polystyrene sulfonate (SPS) as the culprit for colon necrosis in humans treated ...with SPS and sorbitol. We tested the hypothesis that colon necrosis by sorbitol in the experiment was due to the high osmolality and volume of sorbitol rather than its chemical nature.
26 rats underwent 5/6 nephrectomy. They were divided into 6 groups and given enema solutions under anesthesia (normal saline, 33% sorbitol, 33% mannitol, SPS in 33% sorbitol, SPS in normal saline, and SPS in distilled water). They were sacrificed after 48 hours of enema administration or earlier if they were very sick. The gross appearance of the colon was visually inspected, and then sliced colon tissues were examined under light microscopy.
1 rat from the sorbitol and 1 from the mannitol group had foci of ischemic colonic changes. The rats receiving SPS enema, in sorbitol, normal saline, distilled water, had crystal deposition with colonic necrosis and mucosal erosion. All the rats not given SPS survived until sacrificed at 48 h whereas 11 of 13 rats that received SPS in sorbitol, normal saline or distilled water died or were clearly dying and sacrificed sooner. There was no difference between sorbitol and mannitol when given without SPS.
In a surgical uremic rat model, SPS enema given alone or with sorbitol or mannitol seemed to cause colon necrosis and high mortality rate, whereas 33% sorbitol without SPS did not.
Summary
We showed in the present study that, not unlike in adult patients with sickle cell disease (SCD), Townes mice exhibit increases in serum intestinal fatty acid binding proteins and ...lipopolysaccharides (LPS), together with a breach in the intestinal barrier. These abnormalities increased rapidly after the induction of vaso‐occlusive crisis (VOC). We also confirmed higher intestinal microbial density in SCD. These findings support the concept that SCD and/or its complications, and not hospitalisation or medications, are responsible for the intestinal pathophysiological changes. The present results provide the basis for use of Townes mice to further elucidate the mechanistic relationship between intestinal pathophysiology and VOC.
What Do We Know about Opioids and the Kidney? Mallappallil, Mary; Sabu, Jacob; Friedman, Eli A ...
International journal of molecular sciences,
01/2017, Letnik:
18, Številka:
1
Journal Article
Recenzirano
Odprti dostop
Evidence suggests a link between opioid use and kidney disease. This review summarizes the known renal manifestations of opioid use including its role in acute and chronic kidney injury. Both the ...direct and indirect effects of the drug, and the context which leads to the development of renal failure, are explored. While commonly used safely for pain control and anesthesia in those with kidney disease, the concerns with respect to side effects and toxicity of opioids are addressed. This is especially relevant with the worldwide increase in the use of opioids for medical and recreational use.
Focal segmental glomerulosclerosis (FSGS) is a cause of proteinuric kidney disease, compromising both native and transplanted kidneys. Treatment is limited because of a complex pathogenesis, ...including unknown serum factors. Here we report that serum soluble urokinase receptor (suPAR) is elevated in two-thirds of subjects with primary FSGS, but not in people with other glomerular diseases. We further find that a higher concentration of suPAR before transplantation underlies an increased risk for recurrence of FSGS after transplantation. Using three mouse models, we explore the effects of suPAR on kidney function and morphology. We show that circulating suPAR activates podocyte β(3) integrin in both native and grafted kidneys, causing foot process effacement, proteinuria and FSGS-like glomerulopathy. Our findings suggest that the renal disease only develops when suPAR sufficiently activates podocyte β(3) integrin. Thus, the disease can be abrogated by lowering serum suPAR concentrations through plasmapheresis, or by interfering with the suPAR-β(3) integrin interaction through antibodies and small molecules targeting either uPAR or β(3) integrin. Our study identifies serum suPAR as a circulating factor that may cause FSGS.
Purpose
To examine the involvement of the F11R/JAM-A protein in breast cancer metastasis, we utilized the F11R/JAM-A antagonistic peptide 4D (P4D) in experiments of transendothelial migration (TEM) ...of breast cancer cells.
Methods
Experiments were conducted in the mouse 4T1 breast cancer model utilizing the human mammary epithelial cell and endothelial cell lines. The levels of soluble F11R/JAM-A (sJAM-A) in the murine plasmas were measured by ELISA. Levels of F11R/JAM-A mRNA and protein in cell lines were assessed by qRT-PCR and Western blot, respectively. Cell surface expression of F11R/JAM-A was demonstrated by flow cytometry. Functional tests included the TEM of breast cancer cells and adhesion of breast cancer cells to the endothelium. The endothelial permeability was studied by fluorescent tracer assay and by the Real-Time Cell Analysis (RTCA).
Results
The tumor inducers Tβ4 and TGF-β1 reduced the levels of sJAM-A in murine plasma, and reduced the F11R/JAM-A protein levels in the human microvascular endothelial cell line HMEC-1. The adhesion and TEM measured between breast cancer cells and inflamed or Tβ4-treated endothelium were inhibited by P4D. The presence of P4D did not destabilize the pre-existing tight junctions in the endothelial monolayer. The barrier-protecting effect of P4D was stronger than that of forskolin, when a booster dose of P4D was applied to the inflamed endothelium.
Conclusions
F11R/JAM-A protein can be considered as a novel target in the treatment of breast cancer metastasis. In vivo and clinical studies are needed to further investigate the effectiveness of F11R/JAM-A-derived peptide as a possible anti-metastatic drug.
To determine whether inhibition of the F11 receptor/JAM-A (F11R) using F11R-specific antagonist peptide 4D results in inhibition of smooth muscle cell (SMC) proliferation and migration in vivo, known ...as neointimal hyperplasia (NIH), using a mouse focal carotid artery stenosis model (FCASM).
The mouse FCASM was chosen to test the hypothesis because the dominant cell type at the site of stenosis is SMC, similar to that in vascular access stenosis. Fourteen C57BL/6 mice underwent left carotid artery (LCA) partial ligation to induce stenosis, followed by daily injection of peptide 4D in 7 mice and saline in the remaining 7 mice, and these mice were observed for 21 days and then euthanized. Bilateral carotid arteries were excised for histologic analysis of the intima and media areas.
The mean intimal area was significantly larger in control mice compared with peptide 4D-treated mice (0.031 mm
SD ± 0.024 vs 0.0082 mm
SD ± 0.0103; P = .011). The mean intima-to-intima + media area ratio was significantly larger in control mice compared with peptide 4D-treated mice (0.27 SD ± 0.13 vs 0.089 SD ± 0.081; P = .0079). NIH was not observed in the right carotid arteries in both groups.
Peptide 4D, an F11R antagonist, significantly inhibited NIH in C57BL/6 mice in a FCASM.
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