We analyzed the biological performance of spinodally and droplet-type phase-separated 45S5 Bioglass generated by quenching the melt from different equilibrium temperatures. MC3T3-E1 pre-osteoblast cells attached more efficiently to 45S5 Bioglass® with spinodal than to the one with droplet morphology, providing the first demonstration of the role of micro-/nano-scale on the bioactivity of Bioglass®. Upon exposure to biological solutions, phosphate buffered saline (PBS) and cell culture medium (α-MEM), a layer of hydroxyapatite (HA) formed on both glass morphologies. Although both Bioglass® varieties were incubated under identical conditions, and physico-chemical characteristics of the HA layers were similar, the adsorption magnitude of a model protein, bovine serum albumin (BSA, an abundant blood serum component) and its β-sheet/β-turn ratio and α-helix content were significantly higher on spinodal than droplet type Bioglass®. These results indicate that: (i) a protein layer quickly adsorbs on the surface of 45S5 Bioglass® varieties (with or without HA layer), (ii) the amount and the conformation of adsorbed proteins are guided by the glass micro-/nano-structure, and (iii) cell attachment and proliferation are influenced by the concentration and the conformation of attached proteins with a significantly better cell adhesion to spinodal type 45S5 Bioglass® substrate. Taken together, our results indicate that the biological performance of 45S5 Bioglass® can be improved further with a relatively simple, inexpensive fabrication procedure that provides a superior glass micro-/nano-structure. A simple modification to the fabrication procedure of classic 45S5 Bioglass® generates spinodal (A(a)) and droplet (A(b)) varieties and has a significant impact on protein adsorption (B) and cell adhesion (C).

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Background: Coronavirus disease-19 (COVID-19) is associated with acute kidney injury (AKI) and acute respiratory distress syndrome (ARDS) with high mortality rates. In African American (AA) populations, COVID-19 presentations and outcomes are more severe. NIH and Interim WHO guidelines had suggested against the use of corticosteroids unless in clinical trials until the recent publication of the RECOVERY trial. Here, we analyzed the treatment effect of methylprednisolone on patients with AKI and ARDS during the initial 2 months of COVID-19 and detail the learning effect within our institution. Methods: Between March 1 and April 30, 2020, 75 AA patients met our inclusion criteria for ARDS and AKI, of which 37 had received corticosteroids. Twenty-eight-day mortality, improvement in PaO2/FiO2 ratio, and renal function were analyzed. The impact of methylprednisolone treatment was assessed with multivariable methods. Results: Survival in the methylprednisolone group reached 51% at 21 days compared to 29% in the non-corticosteroid group ( P < .001). Methylprednisolone improved the likelihood of renal function improvement. PaO2/FiO2 ratio in the methylprednisolone group improved by 73% compared to 45% in the non-corticosteroid group ( P = .01). Age, gender, BMI, preexisting conditions, and other treatment factors did not show any impact on renal or PaO2/FiO2 ratio improvement. The use of anticoagulants, the month of treatment, and AKI during hospitalization also influenced outcomes. Conclusion: In AA COVID-19 positive patients with ARDS and AKI, IV methylprednisolone lowered the incidence of mortality and improved the likelihood of renal and lung function recovery. Further investigation with a randomized control trial of corticosteroids is warranted.

INTRODUCTION: Accumulating evidence indicates an association between CD4 count and Ulcerative colitis (UC) flares in patients with Human Immunodeficiency Virus (HIV)[1,4], whereby patients who have low CD4 counts are less likely to experience UC flares compared to those who have normal CD4 counts. While the exact mechanism is unknown, it is hypothesized that an immunosuppressed state allows for the remission of UC; this idea has been deemed the “Remission Hypothesis” [1]. CASE DESCRIPTION/METHODS: Objective: To present a case series of 3 patients with concomitant HIV and Ulcerative Colitis (UC) and examine the association between UC flares, CD4 counts and viral load over time. METHODS: Patient records at two urban university-affiliated medical centers were queried for patients with concomitant HIV and UC. ICD 9 and ICD 10 diagnostic codes for HIV and UC were used to identify patients. Inclusion criteria were confirmed UC via endoscopy, outpatient follow up, viral load and CD4 count documentation. CD4 counts and viral loads levels were compared during hospitalizations and outpatient follow-ups. RESULTS: 7 patients with UC and HIV were identified; 3 of these 7 patients had sufficient data available for further analysis. Our three patients lived with HIV for an average of 10 years. Patient 1 experienced 4 UC flares requiring inpatient hospitalizations while maintaining CD4 counts above 250 cells/µL and undetectable viral loads (Table 1). Patient 2 had five UC flares with CD4 counts above 250 cells/µL; an undetectable viral load was noted during 4 of the UC flares (Table 2). Patient 1 had two flares with CD4 counts above 250 cells/µL; the viral load was undetectable during flares (Table 3). DISCUSSION: The remission hypothesis suggests that patients who have concomitant HIV and UC can experience remission of their inflammatory bowel disease as their CD4 count declines [1]. HIV viral load is a more accurate and more important marker of HIV disease progression, and therefore, a relationship between viral load and UC flares need to be further studied. Our patients continued to experience flares despite suppressed viral load, and CD4 counts above 250 cells/µL. This case series is the first study that considers viral load and CD4 counts when considering IBD flares and disease progression. These findings raise the question of whether IBD flares occurs as a consequence of CD4 count above 250 or low viral load. Further studies with larger populations are needed to elucidate the pathophysiology of IBD and HIV coexistence.