CC chemokines, a subfamily of 27 chemotactic cytokines, are a component of intercellular communication, which is crucial for the functioning of the tumor microenvironment. Although many individual chemokines have been well researched, there has been no comprehensive review presenting the role of all known human CC chemokines in the hallmarks of cancer, and this paper aims at filling this gap. The first part of this review discusses the importance of CCL1, CCL3, CCL4, CCL5, CCL18, CCL19, CCL20, CCL21, CCL25, CCL27, and CCL28 in cancer. Here, we discuss the significance of CCL2 (MCP-1), CCL7, CCL8, CCL11, CCL13, CCL14, CCL15, CCL16, CCL17, CCL22, CCL23, CCL24, and CCL26. The presentation of each chemokine includes its physiological function and then the role in tumor, including proliferation, drug resistance, migration, invasion, and organ-specific metastasis of tumor cells, as well as the effects on angiogenesis and lymphangiogenesis. We also discuss the effects of each CC chemokine on the recruitment of cancer-associated cells to the tumor niche (eosinophils, myeloid-derived suppressor cells (MDSC), tumor-associated macrophages (TAM), tumor-associated neutrophils (TAN), regulatory T cells (Treg)). On the other hand, we also present the anti-cancer properties of CC chemokines, consisting in the recruitment of tumor-infiltrating lymphocytes (TIL).

Background In the diagnosis of brain death (BD), computed tomography angiography (CTA) results in some cases show intracranial filling, leading to diagnostic confusion. Because cerebral circulatory arrest commences at the capillary level, we hypothesized that computed tomography perfusion (CTP) would be a more sensitive approach than CTA; therefore, the aim of the study was to compare the sensitivities of CTP and CTA in the diagnosis of BD. Material and Methods Whole brain CTP was performed in patients in the intensive care unit diagnosed with BD and CTA was derived from CTP datasets. Cerebral blood flow (CBF) and volume (CBV) were calculated in all brain regions. The CTP findings were interpreted as being consistent with a diagnosis of BD (positive) when CBF and CBV in all regions of interest (ROIs) were below 10 ml/100 g/min and 1.0 ml/100 g, respectively. The CTA findings were interpreted using a 4-point grading system. Results A total of 50 patients were included in the study. The CTP results revealed CBF from 0.00 to 9.98 ml/100 g/min (mean, 1.98 ± 1.68 ml/100 g/min) and CBV from 0.00 to 0.99 ml/100 g (mean, 0.14 ± 0.12 ml/100 g) and were thus interpreted as positive in all 50 patients. In contrast, the CTA results suggested 7 negative cases,

Introduction: Neutrophil-lymphocyte count ratio (NLCR) is a simple and low-cost marker of inflammatory response. NLCR has shown to be a sensitive marker of clinical severity in inflammatory-related tissue injury, and high value of NLCR is associated with poor outcome in traumatic brain injured (TBI) patients. The purpose of this study was to retrospectively analyze NLCR and its association with outcome in a cohort of TBI patients in relation to the type of brain injury. Methods: Adult patients admitted for isolated TBI with Glasgow Coma Score lower than eight were included in the study. NLCR was calculated as the ratio between the absolute neutrophil and lymphocyte count immediately after admission to the hospital, and for six consecutive days after admission to the intensive care unit (ICU). Brain injuries were classified according to neuroradiological findings at the admission computed tomography (CT) as DAI—patients with severe diffuse axonal injury; CE—patients with hemispheric or focal cerebral edema; ICH—patients with intracerebral hemorrhage; S-EH/SAH—patients with subdural and/or epidural hematoma/subarachnoid hemorrhage. Results: NLCR was calculated in 144 patients. Admission NLCR was significantly higher in the non-survivors than in those who survived at 28 days (p < 0.05) from admission. Persisting high NLCR value was associated with poor outcome, and admission NLCR higher than 15.63 was a predictor of 28-day mortality. The highest NLCR value at admission was observed in patients with DAI compared with other brain injuries (p < 0.001). Concussions: NLCR can be a useful marker for predicting outcome in TBI patients. Further studies are warranted to confirm these results.

IntroductionThe standardized diagnostic criteria for computed tomographic angiography (CTA) in diagnosis of brain death (BD) are not yet established. The aim of the study was to compare the sensitivity and interobserver agreement of the three previously used scales of CTA for the diagnosis of BD.MethodsEighty-two clinically brain-dead patients underwent CTA with a delay of 40 s after contrast injection. Catheter angiography was used as the reference standard. CTA results were assessed by two radiologists, and the diagnosis of BD was established according to 10-, 7-, and 4-point scales.ResultsCatheter angiography confirmed the diagnosis of BD in all cases. Opacification of certain cerebral vessels as indicator of BD was highly sensitive: cortical segments of the middle cerebral artery (96.3 %), the internal cerebral vein (98.8 %), and the great cerebral vein (98.8 %). Other vessels were less sensitive: the pericallosal artery (74.4 %), cortical segments of the posterior cerebral artery (79.3 %), and the basilar artery (82.9 %). The sensitivities of the 10-, 7-, and 4-point scales were 67.1, 74.4, and 96.3 %, respectively (p < 0.001). Percentage interobserver agreement in diagnosis of BD reached 93 % for the 10-point scale, 89 % for the 7-point scale, and 95 % for the 4-point scale (p = 0.37).ConclusionsIn the application of CTA to the diagnosis of BD, reducing the assessment of vascular opacification scale from a 10- to a 4-point scale significantly increases the sensitivity and maintains high interobserver reliability.

IntroductionStasis filling, defined as delayed, weak, and persistent opacification of proximal segments of the cerebral arteries, is frequently found in brain dead patients. This phenomenon causes a major problem in the development of reliable computed tomographic angiography (CTA) protocol in the diagnosis of brain death (BD). The aim of our study was to characterize stasis filling in the diagnosis of BD. To achieve this, we performed a dynamic evaluation of contrast enhancement of the cerebral and extracranial arteries in patients with BD and controls.MethodsStudy population included 30 BD patients, who showed stasis filling in computed tomographic perfusion (CTP) series. Thirty patients, after clipping of an intracranial aneurysm, constituted the control group. The study protocol consisted of CTA, CTP, and angiography. Time–density curves (TDCs) of cerebral and extracranial arteries were generated using 40-s series of CTP.ResultsCerebral TDCs in BD patients represented flat curves in contrast to TDCs in controls, which formed steep and narrow Gaussian curves. We found longer time to peak enhancement in BD patients than in controls (32 vs. 21 s; p < 0.0001). In BD patients, peak enhancement in the cerebral arteries occurred with a median delay of 14.5 s to peak in extracranial arteries, while no delay was noted in controls (p < 0.0001). Cerebral arteries in BD patients showed lower peak enhancement than controls (34.5 vs. 81.5 HU; p < 0.0001). In all BD patients, CTP revealed zero values of cerebral blood flow and volume. Angiography showed stasis filling in 14 (46.7 %) and non-filling in 16 (53.3 %) cases.ConclusionA confrontation of stasis filling with CTP results showed that stasis filling is not consistent with preserved cerebral perfusion, thus does not preclude diagnosis of BD.