• HALP score
• gastric cancer
• pathological response
• perioperative treatment

• Humans
• Stomach Neoplasms/mortality
• Stomach Neoplasms/therapy
• Retrospective Studies
• Male
• Female
• Middle Aged
• Aged
• Adult
• Aged, 80 and over
• Cohort Studies
• Prognosis
• Hemoglobins/analysis
• Neoplasm Staging
• Serum Albumin/analysis
• ROC Curve
• Predictive Value of Tests

• COVID-19
• Dexamethasone
• Inflammation
• Intranasal
• Treatment

• Humans
• COVID-19
• SARS-CoV-2
• RNA, Viral
• COVID-19 Drug Treatment
• Dexamethasone/therapeutic use

• corticosterone
• exercise training
• interleukin-6
• monocytes
• noise

• Male
• Rats
• Animals
• Interleukin-6
• Corticosterone
• Noise/adverse effects
• Rats, Wistar
• High-Intensity Interval Training

• Biomarker
• Gastric cancer
• Hemoglobin, albumin, lymphocyte, and platelet score
• Nutritional index
• Prognosis
• Survival

• Bovine alphaherpesvirus-1 (BoAHV-1)
• Bubaline alphaherpesvirus-1 (BuAHV-1)
• IBR marker vaccines
• flow cytometry
• monocyte subsets
• water buffalo

• IZSME 11/20 Ministero della Salute

• Antibodies
• Anticoagulants
• Flow Cytometry
• Humans
• Immunophenotyping
• Myeloid Cells
• Reference Values

• European Research Council
• Horizon 2020 Framework Programme
• European Federation of Pharmaceutical Industries and Associations
• Bill and Melinda Gates Foundation
• European Commission

The hospital management of patients diagnosed with COVID-19 can be hampered by heterogeneous characteristics at entry into the emergency department. We aimed to identify demographic, clinical and laboratory parameters associated with higher risks of hospitalisation, oxygen support, admission to intensive care and death, to build a risk score for clinical decision making at presentation to the emergency department.

We carried out a retrospective study using linked administrative data and laboratory parameters available in the initial phase of the pandemic at the emergency department of the regional reference hospital of Pescara, Abruzzo, Italy, March–June 2020. Logistic regression and Cox modelling were used to identify independent predictors for risk stratification. Validation was carried out collecting data from an extended timeframe covering other variants of concern, including Alpha (December 2020–January 2021) and Delta/Omicron (January–March 2022).

Several clinical and laboratory parameters were significantly associated to the outcomes of interest, independently from age and gender. The strongest predictors were: for hospitalisation, monocyte distribution width ≥ 22 (4.09; 2.21–7.72) and diabetes (OR = 3.04; 1.09–9.84); for oxygen support: saturation < 95% (OR = 11.01; 3.75–41.14), lactate dehydrogenase≥237 U/L (OR = 5.93; 2.40–15.39) and lymphocytes< 1.2 × 10³/μL (OR = 4.49; 1.84–11.53); for intensive care, end stage renal disease (OR = 59.42; 2.43–2230.60), lactate dehydrogenase≥334 U/L (OR = 5.59; 2.46–13.84), D-dimer≥2.37 mg/L (OR = 5.18; 1.14–26.36), monocyte distribution width ≥ 25 (OR = 3.32; 1.39–8.50); for death, procalcitonin≥0.2 ng/mL (HR = 2.86; 1.95–4.19) and saturation < 96% (HR = 2.74; 1.76–4.28). Risk scores derived from predictive models using optimal thresholds achieved values of the area under the curve between 81 and 91%. Validation of the scoring algorithm for the evolving virus achieved accuracy between 65 and 84%.

A set of parameters that are normally available at emergency departments of any hospital can be used to stratify patients with COVID-19 at risk of severe conditions. The method shall be calibrated to support timely clinical decision during the first hours of admission with different variants of concern.

The online version contains supplementary material available at 10.1186/s12913-022-08421-4.

• Adjuvants
• AlphaLISA
• CpG
• Cytometry
• High Throughput
• Immunoassay
• R848
• Screens
• Vaccines
• Vinblastine

• 75N93019C00044 NIAID NIH HHS
• HHSN272201400052C NIAID NIH HHS
• HHSN272201800047C NIAID NIH HHS
• R21 AI137932 NIAID NIH HHS

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by multiple organ dysfunction resulting from the production of multiple autoantibodies and adaptive immune system abnormalities involving T and B lymphocytes. In recent years, inflammasomes have been recognized as an important component of innate immunity and have attracted increasing attention because of their pathogenic role in SLE. In short, inflammasomes regulate the abnormal differentiation of immune cells, modulate pathogenic autoantibodies, and participate in organ damage. However, due to the clinical heterogeneity of SLE, the pathogenic roles of inflammasomes are variable, and thus, the efficacy of inflammasome-targeting therapies is uncertain. To provide a foundation for the development of such therapeutic strategies, in this paper, we review the role of different inflammasomes in the pathogenesis of SLE and their correlation with clinical phenotypes and propose some corresponding treatment strategies.

• inflammasome
• strategy
• systemic lupus erythematosus (SLE)
• target
• treatment

• MSCs
• adult stem cells
• cellular therapy
• clinical trials
• cytokines
• immunotherapy
• lymphocytes
• monocyte

• Non-small cell lung cancer (NSCLC)
• hemoglobin, albumin, lymphocytes, platelet score (HALP score)
• lymphocyte-to-monocyte ratio (LMR)
• nomogram
• overall survival (OS)
• prognosis
• risk factors

• Antiplatelet drug
• CD36
• Impaired glucose tolerance
• Inflammation
• Monocytes
• Prediabetes
• T2DM

• Crohn’s disease
• Inflammatory bowel disease
• JAK/STAT inhibition
• JAK/STAT pathway
• Janus kinase
• Signal transducer and activator of transcription
• Tofacitinib
• Ulcerative colitis

• Colitis, Ulcerative/drug therapy
• Crohn Disease/drug therapy
• Humans
• Janus Kinase Inhibitors/pharmacology
• Janus Kinase Inhibitors/therapeutic use
• Janus Kinases
• Transducers

• Acoustic overstimulation
• Cochlea
• Immune cells
• Inflammation
• Macrophages
• Noise-induced hearing loss

Small cell lung cancer (SCLC) is a special type of lung cancer and it is responsive to chemotherapy. Blood parameters have been proved to be associated with survival for many types of malignancies. This study aimed to investigate the prognostic significance of platelet-to-lymphocyte ratio (PLR) and mean platelet volume (MPV) for SCLC patients with etoposide-based first-line treatment.

We retrospectively identified 138 patients diagnosed as SCLC who underwent etoposide-based first-line chemotherapy. The patients’ baseline clinical characteristics and blood parameters were collected. Kaplan–Meier analysis and Cox regression methods were used to determine the factors associated with progression-free survival (PFS).

The optimal cut-off value of diagnosis was depended on the ROC curve, the cut-off value of pretreatment PLR was 190 (sensitivity 39.0%, specificity 88.5%), and the cut-off value of pretreatment MPV was 10.0 (sensitivity 60.7%, specificity 61%). Kaplan–Meier analysis showed patients with high PLR levels in baseline had worse PFS than those with low PLR levels (P <0.001). Multivariate analysis revealed pretreatment MPV was an independent prognostic factor for PFS (HR: 0.815, 95% CI: 0.711–0.933, P =0.003). Further research suggested continuous high PLR indicated a poor therapy outcome (P =0.002).

Pretreatment MPV can be an independent predictor for first-line treatment outcome and a continuously high level of PLR suggested inferior PFS in etoposide-treated SCLC patients.

• MPV
• PLR
• SCLC
• first-line chemotherapy
• mean platelet volume
• platelet-to-lymphocyte ratio
• prediction
• small cell lung cancer

• Diabetic ischemic limb
• Glutamine
• Immune cell polarization
• Muscle regeneration

Parkinson’s disease (PD) is a neurodegenerative disorder with progressive loss of dopaminergic (DA) neurons. Systemic inflammation is shown to initiate and exacerbate DA neuronal degeneration in the substantia nigra. The infiltration and transformation of immune cells from the peripheral tissues are detected in and around the affected brain regions of PD patients. Our previous studies demonstrated the crucial role that microglial Nod-like receptor protein (NLRP) 3 inflammasome plays in the pathogenesis of PD. Nevertheless, the direct linkage between peripheral inflammation and DA neuron death remains obscure.

In the present study, we detected the NLRP3 expressions in the midbrain, liver, and bone marrow-derived macrophages in response to 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) acute and chronic challenge. We then used a tail vein injection of Nlrp3-siRNA wrapped with lentivirus to explore the potential influence of hepatic NLRP3 inflammasome-mediated inflammation on neuronal injury in a mouse model of PD via immunohistochemistry, ELISA, and Western blotting analysis.

We showed that siNlrp3 downregulated the NLRP3 protein expression and inhibited the activation of NLRP3 inflammasomes in mice livers. The tail vein injection of LV3-siNlrp3 reduced the liver pro-inflammatory cytokine production, which subsequently alleviated MPTP-triggered microglial activation and DA neuron loss in the midbrain. These findings indicated that inhibition of hepatic NLRP3 inflammasome weakens inflammatory cytokines spreading into the brain and delays the progress of neuroinflammation and DA neuronal degeneration.

This study gives us an insight into the direct linkage between liver inflammation and DA neuron damage in the pathogenesis of PD and provides the potential target of NLRP3 for developing novel drugs for PD therapy.

The online version of this article (10.1186/s12974-018-1236-z) contains supplementary material, which is available to authorized users.

• IL-1β
• NLRP3 inflammasome
• Neurodegeneration
• Parkinson’s disease
• Systemic inflammation