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Background We compared the in-hospital complications, outcomes, cost, and length of stay (LOS) between angiography-guided percutaneous coronary intervention (PCI) and intravascular ultrasound (IVUS)-guided PCI in patients with ST-elevation myocardial infarction (STEMI) in the USA. Methods A nationwide inpatient database was queried to identify patients >18 years with STEMI who underwent angiography-guided and IVUS-guided PCI from January 2016 to December 2016. We compared the in-hospital mortality, complications, cost, and LOS between the two groups. Results We identified 100,485 patients who underwent angiography-guided PCI and 5,460 patients who underwent IVUS-guided PCI. In-hospital mortality was not statistically different (odds ratio [OR] 0.76, 95% CI 0.46 − 1.22, P = 0.24). Patients who underwent PCI with IVUS were more likely to have coronary artery dissection (OR 4.26, 95% CI 2.34 − 7.7, p =

Background: Approximately 19% of people infected with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) progress to severe or critical stages of the coronavirus disease 2019 (COVID-19) with a mortality rate exceeding 50%. We aimed to examine the characteristics, mortality rates, intubation rate, and length of stay (LOS) of patients hospitalized with COVID-19 disease with high oxygen requirements (critically ill). Methods: We conducted a retrospective analysis in a single center in Brooklyn, New York. Adult hospitalized patients with confirmed COVID-19 disease and high oxygen requirements were included. We performed multivariate logistic regression analyses for statistically significant variables to reduce any confounding. Results: A total of 398 patients were identified between March 19th and April 25th, 2020 who met the inclusion criteria, of which 247 (62.1%) required intubation. The overall mortality rate in our study was 57.3% (n = 228). The mean hospital LOS was 19.1 ± 17.4 days. Patients who survived to hospital discharge had a longer mean LOS compared to those who died during hospitalization (25.4 ± 22.03 days versus10.7 ± 1.74 days). In the multivariate analysis, increased age, intubation and increased lactate dehydrogenase (LDH) were each independently associated with increased odds of mortality. Diarrhea was associated with decreased mortality (OR 0.4; CI 0.16, 0.99). Obesity and use of vasopressors were each independently associated with increased intubation. Conclusions: In patients with COVID-19 disease and high oxygen requirements, advanced age, intubation, and higher LDH levels were associated with increased mortality, while diarrhea was associated with decreased mortality. Gender, diabetes, and hypertension did not have any association with mortality or length of hospital stay. J Clin Med Res. 2021;13(1):26-37 doi: https://doi.org/10.14740/jocmr4405

BACKGROUND Effectiveness of the immune defense formed by the genotype often determines the predisposition to cancer. Nitric oxide (NO) produced by macrophages is an important element in this defense. MATERIAL AND METHODS We hypothesized that genetic characteristics of NO generation systems can predetermine the vulnerability to tumor development. The study was conducted on mice of 2 genetic substrains - C57BL/6J and C57BL/6N - with Ehrlich ascites carcinoma (EAC). NO production in the tumor was changed using ITU, an iNOS inhibitor; c-PTIO, a NO scavenger; and SNP, a NO donor. Macrophage NO production was estimated by nitrite concentration in the culture medium. iNOS content was measured by Western blot analysis. Macrophage phenotype was determined by changes in NO production, iNOS level, and CD markers of the phenotype. RESULTS The lifespan of C57BL/6N mice (n=10) with EAC was 25% longer (p

Macrophages play a key role in immunity. In this review, we consider the traditional notion of macrophage plasticity, data that do not fit into existing concepts, and a hypothesis for existence of a new switch macrophage phenotype. Depending on the microenvironment, macrophages can reprogram their phenotype toward the proinflammatory M1 phenotype or toward the anti-inflammatory M2 phenotype. Macrophage reprogramming involves well-coordinated changes in activities of signalling and posttranslational mechanisms. Macrophage reprogramming is provided by JNK-, PI3K/Akt-, Notch-, JAK/STAT-, TGF-β-, TLR/NF-κB-, and hypoxia-dependent pathways. Posttranscriptional regulation is based on micro-mRNA. We have hypothesized that, in addition to the M1 and M2 phenotypes, an M3 switch phenotype exists. This switch phenotype responds to proinflammatory stimuli with reprogramming towards the anti-inflammatory M2 phenotype or, contrarily, it responds to anti-inflammatory stimuli with reprogramming towards the proinflammatory M1 phenotype. We have found signs of such a switch phenotype in lung diseases. Understanding the mechanisms of macrophage reprogramming will assist in the selection of new therapeutic targets for correction of impaired immunity.

It has been postulated that obstructive sleep apnea (OSA) induces atherosclerosis through direct and indirect atherogenic mechanisms. However, OSA patients carry a higher burden of conventional cardiovascular (CV) risk factors. Therefore, whether OSA is uniquely associated with atherosclerosis or it

This study examined the timing of counterarguing effects in resistance. Specifically, it investigated the persistence of counterarguing output in resistance across time and explored inoculation message strategies designed to boost the persistence of counterarguing. Results indicated that contrary to what one might expect, the counterarguing output elicited by inoculation treatments was stable across time. The counterarguing output did not increase in the days following treatment, suggesting that inoculation messages require a minimal delay following recipient exposure to elicit counterarguing output, and it proved to be surprisingly robust across time, sustaining itself for much longer periods than early inoculation research had intimated. Also, the results revealed that inoculation-different treatments and reinforcement (booster) messages boost the persistence of the counterarguing output over time. Inoculation-same treatments were initially best in generating counterarguing output, but their effects det...

This investigation compared the traditional explanation for the way inoculation confers resistance to influence with an alternative rationale for resistance based on attitude accessibility. Four hundred forty-three participants took part in the investigation in four phases spanning 54 days. The combined multiple regression and structural equation modeling results suggest that the traditional and alternative explanations for the way that inoculation confers resistance involve separate processes; counterarguing and accessibility appear to be distinct tracks en route to resistance, but the two explanations also are overlapping processes in which elicited threat plays an integral role.

It is accepted that the immune system responds to pathogens with activation of antigen-independent innate and antigen-dependent adaptive immunity. However many immune events do not fit or are even inconsistent with this notion. We developed a new homeostatic model of the immune response. This model consists of four units: a sensor, a regulator, an effector and a rehabilitator. The sensor, macrophages or lymphocytes, recognize pathogenic cells and generate alarm signals. The regulator, antigen-presenting cells, Тregs and myeloid-derived suppressor cells, evaluate the signals and together with sensor cells program the effector. The effector, programmed macrophages and lymphocytes, eliminate the pathogenic cells. The rehabilitator, M2 macrophages, restrict inflammation, provide angiogenesis and reparation of tissue damage, and restore the homeostasis. We suggest the terms “immune matrix” for a biological template of immune responses to pathogens and “matrix reprogramming” for the interdependent reprogramming of different cells in the matrix. In an adequate immune response, the matrix forms a negative feedback mechanism to support the homeostasis. We defined the cellular and phenotypic composition of a tumor immune matrix. A tumor reprograms the homeostatic negative feedback mechanism of matrix into a pathogenic positive feedback mechanism. M2 macrophages play a key role in this transformation. Therefore, macrophages are an attractive target for biotechnology. Based on our hypotheses, we are developing a cell biotechnology method for creation of macrophages with a stable antitumor phenotype. We have shown that such macrophages almost doubled the survival time of mice with tumor.

BACKGROUND M1 macrophages target tumor cells. However, many tumors produce anti-inflammatory cytokines, which reprogram the anti-tumor M1 macrophages into the pro-tumor M2 macrophages. We have hypothesized that the problem of pro-tumor macrophage reprogramming could be solved by using a special M3 switch phenotype. The M3 macrophages, in contrast to the M1 macrophages, should respond to anti-inflammatory cytokines by increasing production of pro-inflammatory cytokines to retain its anti-tumor properties. Objectives of the study were to form an M3 switch phenotype in vitro and to evaluate the effect of M3 macrophages on growth of Ehrlich ascites carcinoma (EAC) in vitro and in vivo. MATERIAL AND METHODS Tumor growth was initiated by an intraperitoneal injection of EAC cells into C57BL/6J mice. RESULTS 1) The M3 switch phenotype can be programed by activation of M1-reprogramming pathways with simultaneous inhibition of the M2 phenotype transcription factors, STAT3, STAT6, and/or SMAD3. 2) M3 macrophages exerted an anti-tumor effect both in vitro and in vivo, which was superior to anti-tumor effects of cisplatin or M1 macrophages. 3) The anti-tumor effect of M3 macrophages was due to their anti-proliferative effect. CONCLUSIONS Development of new biotechnologies for restriction of tumor growth using in vitro reprogrammed M3 macrophages is very promising.