Background Coronavirus disease 2019 (Covid-19) infection is associated with an increased risk of venous thromboembolism (VTE). However, it is unclear if mild Covid-19 infection is a significant risk factor for VTE. Our goal was to investigate the overall incidence of VTE in Covid-19 patients at our community hospital and assess its correlates. Methods We retrospectively reviewed the medical records of patients 18 years and older who tested positive for Covid-19 at our hospital between March 2020 and September 2021. Results A total of 5926 patients aged 18 to 99 years had Covid-19. Of these patients, 64 (incidence of 1.08%) had VTE; 63% were male and 58% were African Americans. The highest rate of VTE was seen in patients with cardiovascular risk factors (n=47, 73%) followed by a history of thromboembolism (n=19, 30%); patients (n=6, 9%) with mild Covid-19 also developed VTE. Conclusions In our study of a predominantly African American population, the VTE incidence (1.08%) was ten times higher than the general population’s rate of 0.1%. Covid-19 infection, even mild category, not requiring hospitalization was a risk factor for VTE. The risk was increased in men and those who have cardiovascular risk factors and/or prior history of thromboembolism.

Background  Increased mortality rates among coronavirus disease 2019 (COVID-19) positive patients admitted to intensive care units (ICUs) highlight a compelling need to establish predictive criteria for ICU admissions. The aim of our study was to identify criteria for recognizing patients with COVID-19 at elevated risk for ICU admission. Methods  We identified patients who tested positive for COVID-19 and were hospitalized between March and May 2020. Patients' data were manually abstracted through review of electronic medical records. An ICU admission prediction model was derived from a random sample of half the patients using multivariable logistic regression. The model was validated with the remaining half of the patients using c-statistic. Results  We identified 1,094 patients; 204 (18.6%) were admitted to the ICU. Correlates of ICU admission were age, body mass index (BMI), quick Sequential Organ Failure Assessment (qSOFA) score, arterial oxygen saturation to fraction of inspired oxygen ratio, platelet count, and white blood cell count. The c-statistic in the derivation subset (0.798, 95% confidence interval [CI]: 0.748, 0.848) and the validation subset (0.764, 95% CI: 0.706, 0.822) showed excellent comparability. At 22% predicted probability for ICU admission, the derivation subset estimated sensitivity was 0.721, (95% CI: 0.637, 0.804) and specificity was 0.763, (95% CI: 0.722, 0.804). Our pilot predictive model identified the combination of age, BMI, qSOFA score, and oxygenation status as significant predictors for ICU admission. Conclusion  ICU admission among patients with COVID-19 can be predicted by age, BMI, level of hypoxia, and severity of illness.

INTRODUCTION:Uncontrolled hypertension can result in severe clinical conditions such as stroke, chronic kidney disease and congestive heart failure, especially in African American populations. To the knowledge of the authors, the effect of time sequence on blood pressure (BP) using an Automated Office Blood Pressure (AOBP) device has not been documented in an African American cohort. The objective of this study was to investigate the possible influence of time sequence of measurement (pre- and post-physician visit) on BP readings in an African American cohort, in the presence or absence of a Medical Assistant (MA) via AOBP monitoring. METHODS:A two-phase, single-blinded, non-randomized trial was conducted at MI-based Ascension Providence Hospital with a convenience sample of hypertensive patients. BP readings were taken using both an Omron 907 (Omron Corp., Kyoto, Japan) and a Welch Allyn (WA) Connex Spot Monitor (Welch Allyn, Inc., Skaneateles Falls, NY) AOBP devices. Descriptive statistics were generated, and T-tests were performed. RESULTS:In Phase 1, (N = 148), the mean systolic/diastolic readings for the pre-physician visits (141/82 mmHg) were statistically significantly higher than the post-visit readings (134/80 mmHg) (p ≤ 0.02). Post-visit physician readings from either AOBP device did not differ statistically (p = 0.72). In Phase 2 (n = 50), the presence of an MA resulted in significantly higher readings than when an MA was absent, however, the results of Phase 2 also supported the trends for lower BP post-physician visit found in Phase 1. CONCLUSION:Based on the consistency of these results, a post-physician visit AOBP reading, in the presence or absence of an MA, may provide a more accurate BP measurement to determine whether or not to treat hypertension in African American patients.

[This corrects the article DOI: 10.1016/j.heliyon.2021.e08566.].

Background & objectives: Race plays an important role in healthcare disparities, often resulting in worse health outcomes. It is unclear if other patient factors and race interactions may influence mortality in patients with COVID-19. We aimed to evaluate how multiple determinants of all-cause in-hospital mortality from COVID-19 were linked to race. Methods: A retrospective observational study was conducted at two hospitals in metropolitan Detroit. We identified patients aged ≥18 years-old who had tested positive for COVID-19 and were admitted between March 9 through May 16, 2020. Multivariable logistic regression was performed assessing predictors of all-cause in-hospital mortality in COVID-19. Results: We identified 1064 unique patients; 74% were African Americans (AA). The all-cause in-hospital mortality was 21.7%, with the majority of deaths seen in AA (65.4%, P = 0.002) and patients 80 years or older (52%, P < 0.0001). AA women had lower all-cause mortality than AA men, white women, and white men based on race-gender interactions. In multivariable logistic regression analysis, older age (>80-year-old), dementia, and chronic kidney disease were associated with worse all-cause in-hospital mortality. Adjusted for race and body mass index (BMI), the main odds ratios (OR) and 95% confidence intervals (CI) are: Age 80 and older vs < 60 in females: OR = 7.4, 95% CI: 2.9, 18.7; in males OR = 7.3, 95% CI: 3.3, 16.2; Chronic Kidney Disease (CKD): OR = 1.7, 95% CI: 1.2, 2.6; Dementia: OR = 2.2, 95% CI: 1.5, 3.3. Conclusion: Gender significantly modified the association of race and COVID-19 mortality. African American females had the lowest all-cause in-hospital mortality risk compared to other gender-race groups.

BackgroundA multitude of chemical agents are currently used intra-articularly to decrease pain after orthopaedic procedures including total knee arthroplasty. However, the possible deleterious effects of these injectable chemicals on chondrocyte viability have not been weighed against their potential benefits. Using a human osteoarthritic chondrocyte model, the purpose of this study was to assess the potential for cartilage damage caused by bupivacaine, Toradol, Duramorph, and acetaminophen from surgical local anesthesia.MethodsHuman distal femur and proximal tibia cross sections were obtained during total knee arthroplasty and divided into control group and experimental groups treated by bupivacaine, Toradol, Duramorph, and acetaminophen respectively. Chondrocytes obtained from enzymatically digested cartilage were cultured using a 3D alginate bead culture method to ensure lower rates of dedifferentiation. Chondrocyte bead cultures were exposed to the study chemicals. The gene expression and chondrocyte viability were measured by RT-PCR and flow cytometry, respectively.ResultsCompared with untreated group bupivacaine treatment led to the greatest cellular apoptosis with 30.5 ± 11% dead cells (P = 0.000). Duramorph and acetaminophen did not result in a significant increase in cell death. Bupivacaine treatment led to an increase in Caspase 3 gene expression (P = 0.000) as well as the acetaminophen treatment (P = 0.001) when compared to control.ConclusionOur data demonstrated that Duramorph and Toradol were not cytotoxic to human chondrocytes and may be better alternatives to the frequently used and more cytotoxic bupivacaine. Acetaminophen did not result in increased cell death; however, it did show increased caspase 3 gene expression and caution should be considered.

BackgroundGenomic medicine has led to significant advancements in the prevention and treatment of cancer. The National Comprehensive Cancer Network (NCCN) guidelines recommend BRCA1/2 screening in high-risk individuals; however, the guidelines have not incorporated differences within ethnic cohorts beyond Ashkenazi Jewish ethnicity. We analyzed the prevalence of BRCA1/2 mutations in various ethnicities and identified high-risk personal characteristics and family history incorporating differences within ethnic cohorts beyond Ashkenazi Jewish ethnicity.Patients and MethodsWe reviewed data collected by a Michigan medical genetic clinic in a community-based hospital from 2008 to 2018. A retrospective chart analysis was conducted of 1090 patients who received genetic counseling regarding hereditary cancer syndromes.ResultsWe found a statistically significant higher rate of pathogenic BRCA1/2 mutation prevalence in African American patients, at 8.1%, compared to non-Ashkenazi Jewish white patients, at 3.6% (P = .02). African Americans have a mutational prevalence nearing that of the Ashkenazi Jewish population.ConclusionRevision of the NCCN guidelines regarding hereditary cancer syndrome testing in various ethnic groups is imperative and overdue. Future studies are needed to identify health care disparities in and socioeconomic barriers to genetic testing.

To examine the role of polymerization temperature on the cement porosity and antibiotic elution to optimize antibiotic release from antibiotic-laden cement (ABLC).

The purpose of this study was to compare blood leukocyte profiles and metal ion concentrations between hip resurfacing arthroplasty (articular surface replacement) patients with and without revision. A total of 25 articular surface replacement patients were recruited (10 with stable implants and 15 undergoing revision). Blood concentrations of chromium (Cr) and cobalt (Co) were measured. Flow cytometry was used to quantify the subpopulations of leukocytes, including CD14+ monocytes, CD16+ monocytes, CD3+ T-lymphocytes, CD19+ B-lymphocytes, CD4+ helper T-cells, and CD45+RA memory vs naïve T-cells. Patients undergoing revision had higher blood Co (mean, 10.85 µg/L) and Cr (mean, 3.19 µg/L) levels than patients with stable implants (mean Co, 3.06 µg/L; mean Cr, 1.07 µg/L) (P<.05). The number of CD4+ helper T-cells was higher in patients with stable implants (mean, 842±311 cells/µL) than in patients undergoing revision (mean, 591±208 cells/µL) (P<.05). There was a significant association between total metal ion levels (Co+Cr) and the number of CD14+ monocytes (P=.045) and inflammatory CD16+ monocytes (P=.046). The authors observed that the increase in blood metal ions was associated with an increase in CD16+ monocytes. They believe that continued analysis of blood leukocyte profiles may be helpful in defining differences among failed articular surface replacement, stable articular surface replacement, and failed metal-on-polyethylene implants. [Orthopedics. 2018; 41(3):e424-e431.].

Objective: There are two monocyte populations in human blood: CD14CD16 classical monocytes and CD14CD16 inflammatory monocytes. CD14CD16 inflammatory monocytes, account for approximately 10% of the total monocytes, may be expanded in various types of inflammatory conditions. The purpose of this study was to investigate whether the expansion of the CD14CD16 monocyte population represents a risk factor of aseptic loosening (AL). Methods: Peripheral monocytes subsets were measured in revision patients with AL (n = 35) and in patients with stable implants (SI, n = 56). The gene profiles of TNFα, IL-1β, CD16, CD68 and TRAP5B from collected loosening periprosthetic tissues were analyzed. Results: There were no significant differences in the CD14CD16 monocyte populations between the SI and AL patients. The CD14CD16 monocytes were marginally higher in revision patients with osteolysis (n = 30), compared to patients without osteolysis (n = 5) though no statistically difference was found. There was an association between the CD14CD16 monocyte subpopulation and the tissue gene profiles, including IL-1β (p = 0.063), CD68 (p = 0.036), and TRAP5B (p = 0.073). Conclusion: It was demonstrated that the expansion of CD14CD16 monocytes reflects, to some extent, the inflammatory status of the loosening periprosthetic tissues. It is unclear if some of those SI patients (no pain and negative radiograph) who have a higher frequency of CD14CD16 monocytes may be at the early stage of AL. Further evaluation of CD14CD16 monocyte population, independently or combined with other factors, will be useful to design a risk profile for AL incidence and progression.

Background: Monofilament and barbed monofilament sutures have been shown in in vitro models to have less bacterial adherence than braided suture. This study evaluates bacterial adherence to suture materials and tissue reactivity with an in vivo contaminated wound mouse model.Methods: Staphylococcus aureus was used to create an in vivo contaminated wound model at 2 amounts (106 colony-forming units [CFU] and 10(8) CFU) using a mouse air pouch. Three types of commonly used absorbable suture were evaluated: braided, monofilament, and barbed monofilament. Bacterial suture adherence was evaluated with suture culture, a photon-capturing camera system, and scanning electron microscopy. Tissue reactivity was assessed through histology and protein expression.Results: The braided suture group with the high amount of S aureus exhibited frank purulence and air pouch hypertrophy in all 8 mice. A significant difference was found between suture groups inoculated with 108 CFU (P < .05) as measured by bacterial culture concentration using the optical density method. The braided suture hosted more bacteria than either monofilament (P < .005) or barbed monofilament suture (P < .005). No difference was appreciated between the monofilament and barbed monofilament groups. Kruskal-Wallis test demonstrated a significant difference between groups in regard to levels of tumor necrosis factor-alpha (P < .05) and interleukin-1 (P < .05).Conclusion: Our in vivo contaminated wound model demonstrated that barbed monofilament suture performed similarly to monofilament suture and better than braided suture in terms of bacterial adherence, biofilm formation, and tissue reactivity. (C) 2016 Elsevier Inc. All rights reserved.

Interlocking nails coated with antibiotic-supplemented cement provide effective treatment of infected long bone nonunion, but the thicker coating on guidewires may provide greater antibacterial activity. This study compared the properties of cement cured on each construct by evaluating 2-cm segments of 8-mm interlocking nails and 3.5-mm guidewires coated with antibiotic-supplemented cement. Each construct (n=7 for each group) was coated with polymethylmethacrylate cement (Simplex; Stryker Orthopaedics, Mahwah, New Jersey) containing either 1 g tobramycin or 1 g vancomycin powder plus 2.2 g tobramycin powder. A No. 40 French polyvinyl chloride chest tube was used as a mold for all constructs. Segments were soaked in sterile phosphate-buffered saline, and entire aliquots were exchanged at various intervals over a 6-week period. Antibiotic concentration, antibacterial activity, cement curing temperature, and porosity were measured. At least half of the total elution of antibiotics occurred within the first 24 hours for all constructs. For the tobramycin-only cement, no differences between constructs were observed. For constructs containing both antibiotics, interlocking nails showed more antibiotic release than guidewires at most time points (P<.05-P<.001). Antibiotics were released for 6 weeks and continued to inhibit Staphylococcus aureus growth. Cement curing temperatures for interlocking nails were lower than those for guidewires (P<.05). Guidewires coated with cement containing tobramycin and vancomycin showed significantly greater porosity compared with the other 3 groups (P<.05), but the amount of antibiotic released did not directly relate to porosity for any construct type. Interlocking nails coated with antibiotic-supplemented cement may provide greater antibiotic delivery to infected long bone nonunion compared with guidewires. A thin mantle of cement may allow greater elution, possibly as a result of cooler exothermic reactions. [Orthopedics. 2017; 40(3):e436-e442.].

Background:Statins (HMG-CoA Reductase inhibitors) reduce the incidence and progression of osteoarthritis of the knee. Nitrogen-containing bisphosphonates (N-BPs) and statins have similar mechanisms of action, but the effects of N-BPs on articular cartilage in osteoarthritis are not understood. We sought to determine if the bisphosphonate alendronate (ALN) has anti-inflammatory effects on articular chondrocytes in vitro.Methods:An in vitro model was developed for sustaining harvested rat chondrocytes in an alginate gel matrix. Using this model with human chondrocytes, osteoarthritis was simulated using interleukin- 1 beta (IL-1 beta) stimulation. Cells were treated with ALN (10100 mM) and IL-1 beta (0.01 and 0.1 ng/mL) for 24 and 48 h. RNA was isolated to quantify the effects of IL-1 beta and ALN on chondrocyte gene expression for cartilage matrix synthesis (aggrecan, collagen type I and II) and degradation (MMP13, ADAMTS4, ADAMTS5).Results:Collagen type I, collagen type II, and aggrecan expression decreased with IL-1 beta stimulation in human chondrocytes, which was not reversed by ALN treatments. MMP13, ADAMTS4, and ADAMTS5 expression increased with IL-1 beta stimulation, and the increases in MMP13 and ADAMTS5 were reduced by ALN treatments after 24 h.Conclusions:ALN reversed increases in chondrocyte MMP13 and ADAMTS5 expression due to IL-1 beta stimulation in vitro, and ALN may play a role in preventing cartilage matrix degradation in osteoarthritis.

ABSTRACT Wear debris‐induced monocyte recruitment plays a key role in the formation of chronic periprosthetic tissue inflammation associated with aseptic loosening. The purpose of this study was to investigate the role(s) of chemokine receptor CX3CR1 in ultra high molecular weight polyethylene (UHMWPE) particle‐induced tissue inflammation using a murine air pouch model developed in CX3CR1 knockout (CX3CR1 −/− ) mice. UHMWPE debris or saline were introduced into established air pouches on CX3CR1 −/− and CX3CR1 +/+ mice. Pouch tissues were collected 7 days after UHMWPE inoculation. Results showed that UHMWPE stimulation induced strong pouch tissue inflammation in CX3CR1 +/+ mice, as manifested by inflammatory cellular infiltration (mainly macrophages), pouch tissue proliferation, and increased gene expression of IL‐1ß and TNFα. UHMWPE‐induced inflammation was significantly mitigated in CX3CR1 −/− mice, as manifested by reduction of tissue inflammation (pouch thickness and cell density), inflammatory cytokine production (IL‐1ß and TNFα) and macrophage accumulation. The observations support the hypothesis that the activation of the CX3CR1 chemokine pathway contributes to the severity of UHMWPE particle‐induced tissue inflammation, and suggests that CX3CR1 signaling is involved in the recruitment of monocytes to the wear debris‐containing inflammatory tissues. Blocking of CX3CR1 pathway may represent a viable therapeutic approach to the prevention and treatment of patients with aseptic loosening. © 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:1037–1043, 2014.

Local tissue reactivity to intra-articular injections of hyaluronic acid hylan G-F 20 (Synvisc) has been described. We used a murine biocompatibility model to study the inflammatory response to Synvisc after a single bolus injection versus the traditional three shot series of injections. Air pouches were established subcutaneously in BALB/c mice, which were injected with phosphate-buffered saline (PBS), 5 mg ultra-high molecular weight polyethylene particles (to simulate synthetic joint wear debris, positive control), 0.5 mL Synvisc (one injection/week for three weeks, harvested 14 days after last injection), or 1.5 mL Synvisc bolus (harvested either 14 or 28 days after last injection). Inflammatory gene expression and inflammation of air pouch tissue, and serum antibody titers to Synvisc were determined. Inflammation was observed with all Synvisc treatments relative to PBS (p < 0.01). However, the three injection series of Synvisc resulted in significantly (p < 0.05) greater tumor necrosis factor-alpha gene expression compared to both PBS and bolus single shot Synvisc harvested after 14 or 28 days. While all Synvisc treatments resulted in serum antibodies to Synvisc (p < 0.02 compared to PBS control group), mice that received three injections of Synvisc had higher levels than mice receiving a single injection (p < 0.01). These results demonstrate that a single bolus injection of Synvisc led to less inflammation and a lower antibody response when compared to the three-shot series of injections, supporting the current change in treatment from multiple injections to a single injection of Synvisc .

We previously showed that strontium-doped calcium polyphosphate (SCPP) scaffold with poly(vinyl alcohol) (PVA) coating extended the impregnated erythromycin (EM) release. In this study, we examined the bactericidal effect of EM-doped SCPP (SCPP(EM) ) scaffolds with PVA coating in a Staphylococcus aureus (S. aureus) infected mouse pouch. SCPP scaffolds with or without 5% EM, and SCPP(EM) scaffolds coated with PVA (with or without 5% EM) were prepared. Scaffolds were implanted in the pouch of BALB/c mice, followed by inoculation of 1 × 10(3) colony-forming units of S. aureus. Mice were sacrificed 14 days after surgery. Pouch tissues and scaffolds were collected for histology, scanning electron microscopy, and microbiological analysis. In the absence of SCPP scaffolds, the pouch infection was eliminated by the host immune surveillance. In the presence of SCPP scaffolds, both the pouch tissues and scaffolds were infected, but SCPP(EM) scaffolds successfully inhibited bacterial growth. Although PVA coating of SCPP(EM) scaffolds enhanced bacterial growth, incorporation of EM into PVA coating inhibited growth. In conclusion, BALB/c mice were capable of eradicating a low grade S. aureus infection. SCPP protected S. aureus growth from host immune surveillance. Though PVA coating sustained EM release in vitro, it was unable to inhibit bacterial growth because PVA gel matrix provided a temporary shelter for bacteria to grow and slowed the EM release from SCPP scaffold. To guarantee a sufficient inhibition of bacterial growth at the initial stage, embedding EM or other antibiotics in the PVA coating is also essential.

Purpose This study aims to determine the value of PET with C-11-isoquinoline carboxamide (C-11-PK11195) and F-18-fluorodeoxyglucose (F-18-FDG) in assisting the differentiation of aseptic loosening (AL) from septic loosening (SL) in rat models.Procedures Initially, the histological profiles of SL and AL (cellular infiltration and the number of CD68(+) macrophage and PBR+ cells) were compared. Subsequently, we investigated whether C-11-PK11195 alone and also in combination with F-18-FDG increases the sensitivity and specificity of PET imaging for distinguishing SL from AL.Results There were distinguishable features between the histological profiles of the SL and AL rat groups. The number of CD68(+)/PBR+ cells in AL rats was significantly higher than that seen in SL rats (P<0.05). The uptake of C-11-PK1195 was higher in AL and lower in SL rats. The uptake of F-18-FDG was higher in SL and lower in AL rats.Conclusion PET with a C-11-PK11195 and F-18-FDG imaging protocol is helpful in the clinical differential diagnosis of AL from SL. Nucl Med Commun 33:747-756 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.