With the expansion of 2019 novel coronavirus disease(COVID-19), large of suspected cases were reported. This essay compares the clinical features of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections and other viral infections among the suspected COVID-19 patients, and attempts to explore an ideal diagnostic model of COVID-19. 60 viral pneumonia patients from 86 suspected patients were enrolled and grouped into two: the COVID-19 group (19 cases) and other viral infections group (41 cases). Compare and analyze the blood test results, biochemical indicators and chest CT scan changes of patients. 60 patients were mainly young and middle-aged men, of which 60%were infected with influenza virus, and 31.6%were infected with SARS-COV-2 according to pathogenic distribution. And we found statistic differences among blood cell counts and blood biochemistry between the two groups. The COVID-19 patients' chest CT showed that the lung lesions were mainly bilateral nodule or appeared to be patchy and ground glass shadowed. While most of the lung lesions caused by other virus were mainly unilateral patchy shadow (P＜0.05). We found a new multi-marker PTG, which composed of platelet-to-neutrophil ratio(PNR), total bilirubin(TBIL) and ground-grass density, The area sunder curves(AUC)of PTG was 0.908, the sensitivity was 73.17%and the specificity was 94.44%. The ratio of blood RT to its sub-group and chest CT were considered as important reference in differential diagnosis. The PTG, with extremely high specificity and sensitivity in early differential diagnosis of COVID-19 and other viral pneumonia, had a significant clinical value.

The detection of viral nucleic acid by real time RT-PCR is the main confirmative diagnostic method for COVID-19 in clinical practice in China and worldwide. However, its sensitivity is unclear. Here we report two cases in a family in Guizhou, southwestern China. The father had a history of long stay in Wuhan. Surprisingly, although the son was diagnosed positive using the nasopharyngeal swab specimen and the rRT-PCR method, the father was diagnosed negative continuously for multiple times. Only after the alveolar lavage fluid sample was used, the father's rRT-PCR diagnosis turned positive. Their CT diagnosis and clinical symptoms did not completely align with their rRT-PCR diagnostic results. The underlying mechanisms and their implications to clinical practice are discussed.

Most of the clinical research on coronavirus disease 2019 (COVID-2019) has focused on patients in Wuhan, Hubei, China. This study describes the clinical characteristics of COVID-19 patients outside of Hubei. Eighteen confirmed COVID-19 patients at Guizhou Provincial People's Hospital were included. They were divided into nonsevere and severe groups, and their epidemiological characteristics, demographics, clinical manifestations, and laboratory results were reviewed and compared. All patients were infected through human-to-human transmission, and 9 were imported cases. The clinical features were mainly cough (16 [89%]), fever (11 [61%]), and sputum production (9 [50%]). Most patients had bilateral pneumonia. There were significant differences in the level of lactate dehydrogenase (LDH) (179 [142-193] vs 289 [260.25-368.75]), level of serum ferritin (267.2 [100.5-675.2] vs 614.85 [528.5-870.78]), lymphocyte count (1.52 [1.40-1.60] vs 0.59 [0.47-1.05]), and CD cell count (1576 [1040-1696] vs 444 [312-592] CD3+ T cells, 692 [420-708] vs 144 [128-320] CD4+ T cells, 796 [632-892] vs 228 [152-284] CD8+ T cells) between the nonsevere group and the severe group (P <0.05). As of Feb. 11th, 9 people had been discharged after treatment. This study suggests that COVID-19 cases often occur in clusters. Patients with severe COVID-19 had abnormalities in inflammation and immune indicators. Most patients outside Hubei had a good prognosis.

The coronavirus disease 2019 (COVID-19) has swept across all countries in the world within half a year, which is taking the world by surprise. We reported an elderly, severe, complicated COVID-19 case, describing the clinical manifestations, laboratory examinations, CT findings, diagnosis, treatment and dynamic disease course. 3D post-processing technique was used to reconstruct different pulmonary lesions, and it was found to be useful for highlighting and observing them, thereby helping diagnose and distinguish different diseases.

Glioblastoma Multiforme (GBM, Astrocytoma grade-IV) is the most common primary malignant brain tumour in adults and unfortunately the most deadly. Patients with GBM exhibit a deficient anti-tumor immune response. Immunotherapy is rapidly becoming one of the pillars of anti-cancer therapy. GBM has not received similar clinical successes as of yet, a fact which may be attributed to its relative inaccessibility,its poor immunogenicity, or any of the many other immune mechanisms known to be inactivated in these tumor cells. Focused Ultrasound (FUS) is emerging as a promising treatment approach. The effects of FUS on the tissue are not merely thermal. Reported FUS-induced acoustic cavitation which carries both mechanical and molecular implications as well as FUS induced immunomodulation play important roles. This is a concise research highlights on a comprehensive report by the same group. We separately discuss the different pertinent immunosuppressive mechanisms harnessed by GBM and the immunomodulatory effects of FUS. The three modes of FUS action can all be assigned a molecular final common pathway of immunomodulation. Thermal ablation induced immune effects, microbubbles effects in disrupting the BBB and introducing antigens and drugs to the tumor milieu as well as FUS induced molecular effects are discussed. The effect of FUS on the pro-inflammatory cytokines secretion profile, the stress response, the intra-tumoral immune-cellspopulations, dendritic cells activitymoderation and FUS induced increased cytotoxic cells potency are all discussed. A conceptual synopsis of the synergistic treatment of GBM utilizing FUS and immunotherapy is presented. The interaction of multiple approaches harnessing immune-components and circumventing immunosuppressing mechanisms may herald a new era in the fight against GBM.

Glucocorticoid (GC) hormone exerts numerous physiological roles that include modulation of immune, nervous, cardiovascular and metabolic systems. Synthetic GCs such as dexamethasone and prednisone/prednisolone are widely prescribed in the clinical context to the treatment of inflammatory-related diseases. In spite of its positive therapeutic effect, GC-based therapies may cause several adverse effects including glucose intolerance and peripheral insulin resistance. Reduction of insulin sensitivity in the adipocytes and adipose tissue caused by GC treatment is associated with increased lipolysis and abnormal Ser phosphorylation of insulin substrate receptor (IRS)-1 and protein kinase B (PKB). However, there is no consensus about the precise mechanisms whereby GC treatment promotes such attenuation in the insulin signaling pathway. In this paper, we will briefly discuss and present some molecular evidences that might be involved with this negative impact of GC in the insulin signaling in the adipose tissue.

Invariant natural killer T (iNKT) cells are a distinct lineage of αβ T lymphocytes with the capacity to recognize glycolipid antigens in the context of the atypical major histocompatibility complex (MHC) class I molecule CD1d. In response to engagement of the T cell receptor (TCR), iNKT cells efficiently and rapidly produce a broad range of cytokines and several chemokines. iNKT cells participate in a variety of immune responses through cross-talk with many other innate and adaptive immune cells, including dendritic cells (DCs), natural killer (NK) cells, conventional CD4+ T cells, CD8+ T cells, B cells, neutrophils and regulatory T cells. Despite a relatively restrictive diversity in their TCR, these cells respond to vastly diverse microbial pathogens. The mechanisms underlying activation of iNKT cells at the maternal-fetal interface in inflammation-induced preterm delivery is not fully understood. In a recent study, we investigated which specific pathways were involved in decidual iNKT cell activation in a model for lipopolysaccharide (LPS)-stimulated preterm delivery. To do this, we employed an adoptive transfer system in combination with a diverse array of neutralizing antibodies (Abs) and inhibitors. We demonstrated that the activation of decidual iNKT cells requires TLR4-mediated nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK) p38 and extracellular signal-regulated kinase (ERK) pathways, the proinflammatory cytokines IL-12 and IL-18, and endogenous glycolipid antigens presented by CD1d. Our findings give new insights into the molecular mechanisms underlying iNKT cell activation during microbial infection as well as the role of iNKT cells in preterm delivery induced by inflammation. These findings underscore the promise that iNKT cell-based immunotherapies that target specific pathways utilized during iNKT cell activation could advance our ability to treat iNKT cell-associated inflammatory diseases, including preterm delivery.

Release of glutamate during inflammation and injury changes sensitivity and transmission efficiency of noxious sensory information via glutamate receptors. We found that activation of metabotropic glutamate receptor type 5 (mGluR5) transiently increased, and then subsequently decreased, noxious heat sensitivity. Similarly, mGluR5 activation in cultured sensory neurons potentiated intracellular calcium elevation mediated by transient receptor potential channel, subfamily V, member 1 (TRPV1), a noxious heat receptor; subsequent cessation of mGluR5 activation depressed intracellular calcium levels. The underlying mechanisms were potentiation of TRPV1 current in the presence of mGluR5 ligands and persistent inhibition of voltage-gated calcium channels (VGCC), even after mGluR5 ligand washout. Thus, mGluR5 biphasically modulates TRPV1-mediated cellular responses in sensory neurons, which contributes to heat hyper- and hypoalgesia. These phenomena may contribute to changes in noxious heat sensitivity during inflammation and healing.

In the clinical setting may be difficult the discrimination of patients with inflammatory bowel diseases from those with functional intestinal disorders due to the overlapping and non-specific symptoms, such as abdominal pain and altered bowel habit. Several blood markers currently help clinicians in the management of these patients, but the low specificity makes them unreliable for the detection and monitoring of the disease activity. The gold standard to establish a diagnosis of organic bowel disease is colonoscopy with multiple biopsies, but is an invasive and costly procedure. In the last decade, fecal calprotectin (FC), a cytosolic protein mainly found in neutrophil granulocytes, has been proposed as a surrogate marker of intestinal mucosa inflammation and has been associated with several gastrointestinal disorders. We recently addressed FC ability in distinguish inflammatory from functional disorders, taking into consideration different pathological intestinal conditions. In this research highlight we provide a brief review on FC role as a biomarker of intestinal inflammation discussing the clinical applications.

Chronic kidney disease (CKD), especially end-stage renal disease (ESRD), is associated with high morbidity and mortality due to cardiovascular disease (CVD) and infection, two common complications of ESRD that may be related, in part, to chronic inflammation and protein-energy wasting (PEW). Recently, in a Japanese prospective cohort study, we reported that there was significantly higher risk for CVD-related events in CKD patients with an increased neutrophil/lymphocyte ratio (NLR) at the start of their dialysis therapy. Because higher neutrophil count reflects inflammation and lower lymphocyte count may reflect malnutrition, NLR is hypothesized to be a more sensitive index than other existing inflammatory markers for detecting those at high risk for CVD-related events. This research highlight describes the potentials of NLR as a prognostic marker in patients with CKD. Although further studies are required to better understand its value as prognostic tool in clinical practice, current data suggest that NLR may be a useful and inexpensive marker for identifying CKD patients at high risk for CVD-related complications.