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To evaluate the impact of hypertension on the clinical outcome of COVID-19 patients aged 60 years old and older.This single-center retrospective cohort study enrolled consecutive COVID-19 patients aged 60 years old and older, who were admitted to Liyuan Hospital from January 1, 2020 to April 25, 2020. All included patients were divided into two groups: hypertension and nonhypertension group. The baseline demographic characteristics, laboratory test results, chest computed tomography (CT) images and clinical outcomes were collected and analyzed. The prognostic value of hypertension was determined using binary logistic regression.Among the 232 patients included in the analysis, 105 (45.3%) patients had comorbid hypertension. Compared to the nonhypertension group, patients in the hypertension group had higher neutrophil-to-lymphocyte ratios, red cell distribution widths, lactate dehydrogenase, high-sensitivity C-reactive protein, D-dimer and severity of lung lesion, and lower lymphocyte counts (all P0.05). Furthermore, the hypertension group had a higher proportion of intensive care unit admissions [24 (22.9%) vs. 14 (11.0%), P=0.02) and deaths [16 (15.2%) vs. 3 (2.4%), P0.001] and a significantly lower probability of survival (P0.001) than the nonhypertension group. Hypertension (OR: 4.540, 95% CI: 1.203-17.129, P=0.026) was independently correlated with all-cause in-hospital death in elderly patients with COVID-19.The elderly COVID-19 patients with hypertension tend to have worse conditions at baseline than those without hypertension. Hypertension may be an independent prognostic factor of poor clinical outcome in elderly COVID-19 patients.

Peripheral neuropathy, accompanied by chronic neuropathic pain, is among the frequent and debilitating complications of diabetes. Hyperglycemia is a risk factor for neuropathic pain, but the pathological mechanisms are unclear. The high mobility group box 1 (HMGB1)/toll-like receptor 4 (TLR4) inflammatory axis is strongly implicated in the pathogenesis of neuropathic pain,so we examined how hyperglycemia influences the HMGB1/TLR4 axis and behavioural manifestations of hyperalgesia in the Sprague-Dawley rat sciatic nerve chronic constriction injury (CCI) model. Short-term hyperglycemia induced by streptozotocin significantly augmented mechanical allodynia and thermal hyperalgesia in CCI model rats compared to normoglycemic CCI model rats.These augmented nociceptive behaviours were associated with increased immune cell infiltration and activation, cytokine production and expression levels of TLR4 and HMGB1, as well as with reduced Sirt1 expression in spinal cord dorsal horn and sciatic nerve. High glucose also enhanced HMGB1/TLR4 inflammatory axis activity and cytokine production in lipopolysaccharide-stimulated RAW264.7 macrophages. Our results suggest that hyperglycemia predisposes individuals with peripheral nerve injury to neuropathic pain, in part through enhancement of Sirt1/HMGB1/TLR4 signalling and ensuing neuroinflammation. &nbsp

TAMs and clinical prognosis. Patients were divided into two groups dependent on the density of Iba1 and CD163-positive cells and the percentage of CD163-postive cells in Iba1-positive TAMs. Kaplan-Myer analysis was performed and p-values by Wilcoxon test were described in the Materials and Methods section.

Recent findings have shown the significance of CD163-positive macrophages in tumor progression, yet there have been few studies on the function of CD163 in macrophages. Here, we uncover the role of CD163 in macrophage activation using CD163-deficient mice and human samples. We detected CD163 in 62 undifferentiated pleomorphic sarcoma samples, in which a high percentage of CD163-positive macrophages was associated with decreased overall survival and higher histologic grade. We observed macrophage-induced tumor cell proliferation in cocultures of human monocyte-derived macrophages and leiomyosarcoma (TYLMS-1) and myxofibrosarcoma (NMFH-1) cell lines, which was abrogated by silencing of CD163. Tumor development of sarcoma (MCA205 and LM8) cells in CD163-deficient mice was significantly abrogated in comparison with wild-type (WT) mice. Coculture with WT peritoneal macrophages significantly increased proliferation of MCA205 cells but decreased in the presence of CD163-deficient macrophages. Production of IL6 and CXCL2 in CD163-deficient macrophages was suppressed in comparison with WT macrophages, and overexpression of CD163 in CD163-deficient macrophages induced production of IL6 and CXCL2. Silencing of IL6 but not CXCL2 abrogated macrophage-induced proliferation of MCA205 cells. Taken together, our results show that CD163 is involved in protumoral activation of macrophages and subsequent development and progression of tumors in mice and humans.Significance: Macrophage CD163-mediated induction of IL6 promotes tumor development and progression in murine and human malignant tumors. Cancer Res; 78(12); 3255–66. ©2018 AACR.

Hematology analysis