Faculty Bibliography

Background:The COVID-19 pandemic strained hospital resources in New York City, including those for providing dialysis. New York University Medical Center and affiliations, including New York City Health and Hospitals/Bellevue, developed a plan to offset the increased needs for KRT. We established acute peritoneal dialysis (PD) capability, as usual dialysis modalities were overwhelmed by COVID-19 AKI. Methods:Observational study of patients requiring KRT admitted to Bellevue Hospital during the COVID surge. Bellevue Hospital is one of the largest public hospitals in the United States, providing medical care to an underserved population. There were substantial staff, supplies, and equipment shortages. Adult patients admitted with AKI who required KRT were considered for PD. We rapidly established an acute PD program. A surgery team placed catheters at the bedside in the intensive care unit; a nephrology team delivered treatment. We provided an alternative to hemodialysis and continuous venovenous hemofiltration for treating patients in the intensive-care unit, demonstrating efficacy with outcomes comparable to standard care. Results:From April 8, 2020 to May 8, 2020, 39 catheters were placed into ten women and 29 men. By June 10, 39% of the patients started on PD recovered kidney function (average ages 56 years for men and 59.5 years for women); men and women who expired were an average 71.8 and 66.2 years old. No episodes of peritonitis were observed; there were nine incidents of minor leaking. Some patients were treated while ventilated in the prone position. Conclusions:Demand compelled us to utilize acute PD during the COVID-19 pandemic. Our experience is one of the largest recently reported in the United States of which we are aware. Acute PD provided lifesaving care to acutely ill patients when expanding current resources was impossible. Our experience may help other programs to avoid rationing dialysis treatments in health crises.

Background/Purpose: Human OA-affected cartilage does not show the cardinal signs of inflammation (redness and swelling with heat and pain- rubor et tumor cum calore et dolor) because of its unique architecture (avascular, aneural and alymphatic) of the cartilage. However, there is an upregulation of inflammatory mediators at the molecular and biochemical levels [1]. We examined if the human OA-affected cartilage [a] induced innate anti-inflammatory mediators like Lipoxin A4 [LXA4] to counter and promote inflammation resolution in OA, [b] if so, what was the range and mechanism of action of LXA4 at the genomics level in human OA-affected chondrocytes.
Method(s): Primary human OA-affected cartilage or chondrocytes were examined for spontaneous release of LXA4 [in ex-vivo ] condition using liquid chromatography-tandem mass spectrometry and LXA4-specific ELISA. Furthermore, the effects of recombinant LXA4 [rLXA4] were validated in TNFp induced primary human neutrophils in vitro. The rLXA4 and then tested in spontaneous or IL-1 induced primary human OA-affected cartilage or human or bovine chondrocytes. Gene expression arrays and bioinformatic analysis examined the total genome. Inflammatory mediators were ELISA or RIA.
Result(s): LXA4 and 15-epi-LXA4 was spontaneously released [or augmented by IL-1 ] in ex-vivo conditions in human OA-affected cartilage and chondrocytes. Exogenously added LXA4 (1nM) significantly [ p <= 0.01] inhibited 77% TNF p-induced PGE 2 production in human neutrophils. 1-100 nM of LXA4 significantly [ p <= 0.01] inhibited IL-1 induced nitric oxide (NO), and PGE 2, in human OA-affected cartilage, -chondrocytes or bovine chondrocytes. IL-1 and LXA4 exhibited an antagonistic pattern of gene expression in human chondrocytes. Specifically, LXA4 inhibited (basal and/or IL-1 -induced) gene expression of inflammatory mediators, their receptors and signaling apparatus [e.g., IL-8, CSF1, IL-1beta, IL-1R1, IL-1R2, IL-6, IL-6STP1, TNFalpha, TNFRSF1A/B, ICAM1, SELE, CD44, ITGAV, CCL-20, -2 -3, CCL4L2, CXCR- 5, -7, MMP-1, -3, -13, -14, CD-46, -55, -59, LTC4, LTB4, LTA4, PTGS2 and PTGES ]. Furthermore, LXA4 upregulated the expression of inhibitors of inflammation such as CR-1, TIMP-2 and -4, ARG-1, -2, IL-10, and IL-11. Unlike IL-1, LXA4 induced lipoxygenases [ ALOX5, ALOX5AP, ALOX15B ], phospholipases [ PLA2G1B, PLA2G7 ], and PGD synthase of the eicosanoid pathway. LXA4 significantly dampened the cycloxygenase pathway and related prostaglandins.
Conclusion(s): Human OA-affected cartilage spontaneously releases LXA4 and 15-epi-LXA4. rLXA4 inhibits gene expression of [basal and IL-1 -induced] inflammatory mediators. Furthermore, LXA4 induced lipid class switching by shifting the regulation of cyclooxygenases towards the leukotriene pathway discretely from IL-1. LXA4 exhibits multiple targets and mechanisms during anti-inflammatory, pro-resolving, and tissue repairing activity in human cartilage and chondrocytes

INTRODUCTION: Colorectal cancer (CRC) remains a leading cause of cancer-related death in the United States. While colonoscopy based screening is the most effective of all CRC prevention strategies, it is operator dependent and can result in missed lesions, which may contribute to interval cancer. Incorporation of artificial intelligence (AI) to routine colonoscopy has been investigated in several small studies. In this meta-analysis, we attempt to collate evidence from recent randomized controlled trials (RCTs) to further define the role of AI in colonoscopy based CRC screening.
METHOD(S): A comprehensive search of MEDLINE, EMBASE, CENTRAL, and ClinicalTrials.gov from inception through May 2020 was completed. Pooled statistics using bivariate random-effects, odds ratio for binary outcomes, and standardized difference in means for continuous outcomes were used. Primary outcomes were Adenoma Detection Rate (ADR) and Polyp Detection Rate (PDR). Secondary outcomes were mean adenomas and polyps/procedure, withdrawal (WT) and cecal intubation times (CIT), and adequacy of bowel preparation. Post-hoc sensitivity analysis and subgroup analyses for adenomas and polyps was completed.
RESULT(S): 6 RCTs were included. Of 4996 patients, 2487 had AI-assisted, and 2509 had routine colonoscopies. Mean age was 51.99 +/- 4.43 years, 51% of males. AI had higher ADRs (P = 0.00) and PDRs (P = 0.00) [Figure 1]. Similar findings were noted for mean number of adenomas and polyps/procedure. Mean WTs favored AI when biopsy times were included. CIT and adequacy of bowel preparation were similar in both groups [Figure 2]. On subgroup analysis, AI systems had significantly better ADRs and PDRs in the transverse colon. AI had higher detection rates for adenomas < 5 mm (P = 0.00) and polyps < 10 mm (P = 0.00). However, routine colonoscopies outperformed AI in detecting pedunculated polyps (P = 0.00). PDRs had no differences based on shape. Sensitivity analysis remained unchanged for ADR, PDR, mean adenomas or polyps detected per procedure and WTs that included biopsies. Begg's funnel plots were relatively symmetrical for ADR (P - 0.25) and PDR (P - 0.20) [Figure 3].
CONCLUSION(S): The use of AI has the potential to improve the sensitivity of colonoscopy based screening. Colonoscopies using AI algorithms demonstrated significantly improved detection rates for adenomas and polyps. However, research and advancements are needed to refine the AI systems to detect pedunculated polyps and incorporate optical diagnosis into the algorithms