Induction of filopodia formation by α-Actinin-2 via RelA with a feedforward activation loop promoting overt bone marrow metastasis of gastric cancer.

BACKGROUND: Bone marrow metastasis (BMM) is underestimated in gastric cancer (GC). GC with BMM frequently complicate critical hematological abnormalities like diffused intravascular coagulation and microangiopathic hemolytic anemia, which constitute a highly aggressive GC (HAGC) subtype. HAGC present a very poor prognosis with peculiar clinical and pathological features when compared with not otherwise specified advanced GC (NAGC). But the molecular mechanisms underlying BMM from GC remain rudimentary. METHODS: The transcriptomic difference between HAGC and NAGC were analyzed. Genes that were specifically upregulated in HAGC were identified, and their effect on cell migration and invasion was studied. The function of ACTN2 gene were confirmed by GC cell lines, bone-metastatic animal model and patients' tissues. Furthermore, the molecular mechanism of ACTN2 derived-BMM was explored by multiple immunofluorescence staining, western blot, chromatin immunoprecipitation, and luciferase reporter assays. RESULTS: We elucidated the key mechanisms of BMM depending on the transcriptomic difference between HAGC and NAGC. Five genes specifically upregulated in HAGC were assessed their effect on cell migration and invasion. The ACTN2 gene encoding protein α-Actinin-2 was detected enhanced the metastatic capability and induced BMM of GC cells in mouse models. Mechanically, α-Actinin-2 was involved in filopodia formation where it promoted the Actin filament cross-linking by replacing α-Actinin-1 to form α-Actinin-2:α-Actinin-4 complexes in GC cells. Moreover, NF-κB subunit RelA and α-Actinin-2 formed heterotrimers in the nuclei of GC cells. As a direct target of RelA:α-Actinin-2 heterotrimers, the ACTN2 gene was a positive auto-regulatory loop for α-Actinin-2 expression. CONCLUSIONS: We demonstrated a link between filopodia, BMM and ACTN2 activation, where a feedforward activation loop between ACTN2 and RelA is established via actin in response to distant metastasis. Given the novel filopodia formation function and the new mechanism of BMM in GC, we propose ACTN2 as a druggable molecular vulnerability that may provide potential therapeutic benefit against BMM of GC.

A novel intergenic region (chr2: 30,193,816)-ALK fusion shows sensitivity to Alectinib in lung adenocarcinoma.

BACKGROUND: Anaplastic lymphoma kinase (ALK) rearrangement, which is mostly showed as fused with echinoderm microtubule-associated protein-like 4 gene (EML4), accounts 3-7% of all common mutations in non-small lung cancer (NSCLC). An intergenic region (chr2: 30,193,816), which located on upstream of the adjacent ALK gene, was never been reported as a ALK patterner before. CASE PRESENTATION: A 56-year-old female patient who had symptoms of persistent cough and shortness of breath visited our facility on April 24, 2022. The chest computerized tomography (CT) examination revealed a massive right hydrothorax. After draining pleural effusion, a hilar mass accompanied multiple nodules in both lungs could been seen in image. Tracheoscopy revealed neoplasm in the medial segment of the middle lobe of the right lung, and the patient was diagnosed as lung adenocarcinoma pathologically. It tested positive for cytokeratin (CK) 7, NapsinA, ALK, and thyroid transcription factor-1 (TTF-1). Next generation sequence testing confirmed the presence of the intergenic region (chr2: 30,193,816)-ALK fusion in the tumor tissue. The patient was subsequently treated with Alectinib, and her symptoms are obviously relieved, the right hilar mass and metastatic nodule were reduced in the reexamination after three months. CONCLUSIONS: The intergenic region (chr2: 30,193,816)-ALK fusion, which is firstly reported in lung adenocarcinoma, is a mutation with expression significance. It shows sensitivity to Alectinib.

Intravenous Hemostats: Foundation, Targeting, and Controlled-Release.

Uncontrollable blood loss is the greatest cause of mortality in prehospital patients and the main source of disability and death in hospital care. Compared with external hemostats, intravenous hemostats are more appropriate for preventing and treating uncontrolled bleeding in vivo and large bleeding on the body surface. This Review initially establishes intravenous hemostats' response basis, including the coagulation mechanism, fibrinolytic pathway, and protein corona. Second, the study of advancement of intravenous hemostat targeting was expanded from two perspectives, cellular hemostatic agents and synthetic hemostatic agents. Meanwhile, after discussing the progress of controlled-release intravenous hemostats with platelets as the stimuli, this Review offers insight into the possibility of controlled-release intravenous hemostats with microenvironment as the stimuli, combining the studies of controlled-release targeted thrombolysis.

Practical Security of High-Dimensional Quantum Key Distribution with Intensity Modulator Extinction.

Quantum key distribution (QKD) has attracted much attention due to its unconditional security. High-dimensional quantum key distribution (HD-QKD) is a brand-new type of QKD protocol that has many excellent advantages. Nonetheless, practical imperfections in realistic devices that are not considered in the theoretical security proof may have an impact on the practical security of realistic HD-QKD systems. In this paper, we research the influence of a realistic intensity modulator on the practical security of HD-QKD systems with the decoy-state method and finite-key effects. We demonstrate that there is a certain impact in the secret key rate and the transmission distance when taking practical factors into security analysis.

S100A6 represses Calu-6 lung cancer cells growth via inhibiting cell proliferation, migration, invasion and enhancing apoptosis.

S100 calcium binding protein A6 (S100A6) has been reported to involve in many kinds of cancers through regulating intracellular calcium homeostasis. Previous studies found that S100A6 increased in lung cancer patients' plasma and pleural effusion. This study focused on its function in Calu-6 lung cancer cells. S100A6 gene was transferred into Calu-6 lung cancer cell line by lentivirus vector, the empty vector transfected cells and the blank cells were set as control groups. MTT was evaluating cell proliferation. The transwell assay was reflecting cell migration and cell invasion. The flow cytometric analysis was detecting cell apoptosis and cell cycle of three groups (Calu-6, Calu-6/neo, Calu-6/S100A6). Nude mouse tumorigenicity was then applied to evaluate S100A6's effect on cellular tumorigenicity. Compared with control groups, Calu-6/S100A6 cells showed a weakening trend in the cell behaviours of proliferation, migration and invasiveness, while had an enhancement of cell apoptosis, with all P < .05. The cell cycle of Calu-6/S100A6 cells had a reduction of S phase and an increase of G1 phase (P < .05). In animal study, after 5 weeks of cell injection, the tumour bulk of Calu-6/S100A6 group was smaller than controls, with P < .05. Our results demonstrate S100A6 inhibits the growth of Calu-6 lung cancer cells, as well as impairs Calu-6's ability in tumorigenesis. At cellular level, S100A6 is supposed to act as a tumour suppressor gene in lung cancer.

Dasatinib protects against acute respiratory distress syndrome via Nrf2-regulated M2 macrophages polarization.

Dasatinib, a tyrosine kinase inhibitor, has a protective effect on experimental acute respiratory distress syndrome (ARDS). This study investigated the effect and mechanism of dasatinib in ARDS. C57BL/6 mice were administered with dasatinib (1 and 10 mg/kg) after lipopolysaccharide (LPS) treatment to evaluate the effect of dasatinib on white blood cells (WBC), neutrophils, lymphocytes and macrophages in bronchoalveolar lavage fluid (BALF). The levels and mRNA expressions of inflammation-related cytokines in lung tissues and RAW 264.7 cells were detected by enzyme-linked immunosorbent assay and quantitative real-time PCR, respectively. The protein expressions of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase 1 (HO1) were determined by Western blot. MTT assay was performed to detect the viability of RAW 264.7 cell. Rescue experiments were used to assess the effect of Nrf2 silencing on the LPS- and dasatinib-treated mice. Under LPS treatment, levels of the WBC, neutrophils, lymphocytes and macrophages in BALF and mRNA expressions of IL-6, TNF-α and IL-10 as well as expression of iNOS were increased, but the expression of arginase-1 was inhibited, while no obvious changes of the protein expressions of Nrf2 and HO1 were observed. Dasatinib partially reversed the effects of LPS above, and further promoted the mRNA expression of IL-10 and the protein expressions of Nrf2 and HO1, while Nrf2 silencing counteracted the effect of dasatinib. Dasatinib induced the polarization of M2 subtype of macrophages and alleviated LPS-induced ARDS through activating Nrf2 signaling pathway, which may provide a new strategy for the treatment of ARDS.

T cell-derived exosomes induced macrophage inflammatory protein-1α/ß drive the trafficking of CD8+ T cells in oral lichen planus.

Oral lichen planus (OLP) is a T cell-mediated chronic inflammatory disease with uncertain aetiology. Exosomes are nanosized particles with biological capacities. Here, we aimed to study the effects of T cell-derived exosomes (T-exos) on the pathogenesis of OLP and its mechanism. T-exos were incubated with Jurkat cells for 48 hours, and 26 cytokines in the supernatant were measured by luminex assay. The expression of macrophage inflammatory protein (MIP)-1α/ß was detected using immunohistochemistry and ELISA; that of CCR1/3/5 on peripheral T cells was determined by flow cytometry. Transwell assay was performed to investigate the chemotactic effect of MIP-1α/ß, and cells in the lower chambers were examinated by flow cytometry. As a result, OLP T-exos elevated the production of MIP-1α/ß, which were highly expressed in OLP tissues and plasma. CCR1/5 were markedly expressed on OLP peripheral T cells, and the majority of CCR1/5+ T cells were CD8+ T cells. Besides, MIP-1α/ß promoted the migration of OLP mononuclear cells, while inhibiting CCR1/5 significantly decreased the trafficking of mononuclear cells, especially that of CD8+ T cells. Conclusively, OLP T-exos-induced MIP-1α/ß may drive the trafficking of CD8+ T cells after binding with CCR1/5 in OLP, contributing to the development of OLP.

TLR4-induced B7-H1 on keratinocytes negatively regulates CD4+ T cells and CD8+ T cells responses in oral lichen planus.

Oral lichen planus (OLP) is a T-cell-mediated autoimmune mucocutaneous disease affected by the interactions among the keratinocytes, CD4+ T cells and CD8+ T cells. B7-H1 induced by Toll-like receptors (TLRs) can suppress T-cell immune reaction, thereby resulting in immune tolerance. However, the role of TLR-mediated B7-H1 on keratinocytes in the immune response of OLP is still unknown. The present study showed that TLR4 could induce time-coursed B7-H1 expression on oral keratinocytes, and blocking NF-κB or PI3K/mTOR pathway downregulated B7-H1 transcriptional expression. Moreover, TLR4-stimulated oral keratinocytes inhibited the proliferation of OLP CD4+ T cells and OLP CD8+ T cells, and simultaneously prompted their apoptosis. Blockade of keratinocyte-associated B7-H1 restored the declined proliferation of OLP CD4+ T cells and OLP CD8+ T cells, and prevented their increased apoptosis. Therefore, TLR4-upregulated B7-H1 on keratinocytes could decelerate immune responses of CD4+ T cells and CD8+ T cells in OLP.

Increased circulating CXCR5+ CD4+ T follicular helper-like cells in oral lichen planus.

BACKGROUND: CD4+ T-helper cell is crucial for the inflammatory autoimmune condition of oral lichen planus (OLP). Recently, the pathogenetic functions of T follicular helper (Tfh) cells, a subtype of CD4+ T-helper cells, have been revealed in autoimmune diseases for their pivotal regulation on humoral immunity. To explore the potential pathophysiological role of Tfh cells in OLP, the expression of circulating Tfh-like cells and its correlations with IL-21 and B cells were investigated. METHODS: The frequencies of CXCR5+ CD4+ Tfh-like cells and CD19+ B cells were analyzed in peripheral blood of patients with OLP and controls by flow cytometry, respectively. Besides, the serum IL-21 concentration was measured using ELISA technology. Furthermore, the correlations of CXCR5+ CD4+ Tfh-like cells with CD19+ B cells and serum IL-21 expression levels were evaluated. RESULTS: This study showed significant increased circulating Tfh-like cells (P < 0.05) and B cells (P < 0.0001), as well as decreased serum IL-21 expression (P < 0.001) in OLP. Besides, the frequency of Tfh-like cells exhibited negative correlation with B cells in OLP (r = -0.435, P < 0.05). In particular, the proportion of CXCR5+ CD4+ Tfh-like cells in peripheral blood mononuclear cells of erosive OLP was higher than non-erosive OLP and controls (P = 0.012 and 0.021, respectively). CONCLUSIONS: Increased circulating Tfh-like cells may be involved in the pathogenesis of OLP through abnormal modulation on B-cell proliferation and IL-21 production, and associated with different clinical forms of OLP.

Declined hTERT expression of peripheral blood CD4(+) T cells in oral lichen planus correlated with clinical parameter.

BACKGROUND: Oral lichen planus (OLP) is a chronic, T-cell-mediated inflammatory autoimmune disease. Human telomerase reverse transcriptase (hTERT), a catalytic subunit bearing the enzymatic activity of telomerase, may have a unique function in regulating the activation, proliferation, and function of T lymphocytes. The goal of this study was to investigate the expression of hTERT in CD4(+) and CD8(+) T cells from patients with OLP and its correlation with clinical parameter. METHODS: The disease severity of OLP was assessed by RAE (reticular, atrophic, erosive) scoring system. Expressions of hTERT in CD4(+) T cells and CD8(+) T cells isolated from peripheral blood of patients with OLP were detected by real-time PCR, and their correlations with clinical features were analyzed. RESULTS: hTERT mRNA levels in CD4(+) T cells of OLP were significantly lower than that of controls, while the levels in CD8(+) T cells showed no statistical difference. The expression of hTERT in CD4(+) T cells and CD8(+) T cells was neither associated with disease severity nor gender. CD4(+) T cells of OLP patients with the age ≤50 had markedly decreased hTERT levels compared with controls, but CD8(+) T cells did not. CONCLUSIONS: A divergent hTERT pattern between CD4(+) and CD8(+) T cells was implicated in OLP. Decreased hTERT in CD4(+) T cells might be responsible for the immune dysfunction in OLP.

Altered Autophagy-Associated Genes Expression in T Cells of Oral Lichen Planus Correlated with Clinical Features.

Oral lichen planus (OLP) is a T cell-mediated inflammatory autoimmune disease. Autophagy has emerged as a fundamental trafficking event in mediating T cell response, which plays crucial roles in innate and adaptive immunity. The present study mainly investigated the mRNA expression of autophagy-associated genes in peripheral blood T cells of OLP patients and evaluated correlations between their expression and the clinical features of OLP. Five differentially expressed autophagy-associated genes were identified by autophagy array. Quantitative real-time RT-PCR results confirmed that IGF1 expression in the peripheral blood T cells of OLP patients was significantly higher than that in controls, especially in female and middle-aged (30-50 years old) OLP patients. In addition, ATG9B mRNA levels were significantly lower in nonerosive OLP patients. However, no significant differences were found in the expression of HGS, ESR1, and SNCA between OLP patients and controls. Taken together, dysregulation of T cell autophagy may be involved in immune response of OLP and may be correlated with clinical patterns.

[PTEN loss correlates withthe clinical efficacy of lapatinib in HER2 positive metastatic breast cancer with trastuzumab-resistance].

OBJECTIVE: To discuss the indexes related to the efficacy of lapatinib after failure in trastuzumab in HER2-positive metastatic breast cancer (MBC) such as the status of PTEN, p-4EBP1 and clinical features. METHODS: Sixtymatched patients were included. Immunohistochemical (IHC) test of tissue specimens of metastatic lesions were applied to determine the status of PTEN and p-4EBP1. The correlation betweenclinical efficacy andthestatus of PTEN, p-4EBP1 and clinical features were analysed by long-rank test and Cox regression. RESULTS: In all patients, themedian progression free survival (PFS), ORR and CBR was 4.6 months, 36.7% and 50.0% respectively.Univariate analysis revealed that lapatinib-treated patients with PTEN loss (P = 0.015) and liver metastasis (P = 0.02) had significantly shorter median PFS. Multivariate analysis revealed that patients with PTEN lossandliver metastasis had higher risk of diseaseprogression (P = 0.005, 0.006, respectively). CONCLUSION: HER2-positive MBC with trastuzumab-resistance could benefit from lapatinib regimen. PTEN statusand liver metastasis couldpredict theclinical efficacyof subsequent lapatinib therapy. The detection ofrelated biomarkers could provide some referenceto optimize the personal treatment with HER2-positive breast cancer.

Single-cell RNA sequencing reveals immune cell dysfunction in the peripheral blood of patients with highly aggressive gastric cancer.

Highly aggressive gastric cancer (HAGC) is a gastric cancer characterized by bone marrow metastasis and disseminated intravascular coagulation (DIC). Information about the disease is limited. Here we employed single-cell RNA sequencing to investigate peripheral blood mononuclear cells (PBMCs), aiming to unravel the immune response of patients toward HAGC. PBMCs from seven HAGC patients, six normal advanced gastric cancer (NAGC) patients, and five healthy individuals were analysed by single-cell RNA sequencing. The expression of genes of interest was validated by bulk RNA-sequencing and ELISA. We found a massive expansion of neutrophils in PBMCs of HAGC. These neutrophils are activated, but immature. Besides, mononuclear phagocytes exhibited an M2-like signature and T cells were suppressed and reduced in number. Analysis of cell-cell crosstalk revealed that several signalling pathways involved in neutrophil to T-cell suppression including APP-CD74, MIF-(CD74+CXCR2), and MIF-(CD74+CD44) pathways were increased in HAGC. NETosis-associated genes S100A8 and S100A9 as well as VEGF, PDGF, FGF, and NOTCH signalling that contribute to DIC development were upregulated in HAGC too. This study reveals significant changes in the distribution and interactions of the PBMC subsets and provides valuable insight into the immune response in patients with HAGC. S100A8 and S100A9 are highly expressed in HAGC neutrophils, suggesting their potential to be used as novel diagnostic and therapeutic targets for HAGC.

Increasing CCL5/CCR5 on CD4+ T cells in peripheral blood of oral lichen planus.

Oral lichen planus (OLP) is a T cell-mediated autoimmune disease of oral mucosa, in which T helper 1 (Th1) cells are greatly involved. Chemokine CCL5 is required for T cells infiltration and activation. CCR5, one of its receptors, specifically expressed on Th1 cells among CD4(+) T cells, can be up-regulated by Th1 cytokines like interleukin2 (IL-2) and interferon-gamma (IFN-γ), and down-regulated by Th2 cytokines like IL-4. The present study aimed to determine whether CCL5 and CCR5 had effects on the immune response of OLP. We analyzed the proportion of CCR5(+)CD4(+) T cells in CD4(+) T cells using flow cytometry and the serum levels of CCL5, IL-2, IFN-γ, and IL-4 with ELISA. MicroRNA-125a (miR-125a), a blocker of CCL5, was examined with RT-PCR. The results showed both the serum CCL5 and the percentage of CCR5(+)CD4(+) T cells elevated in OLP patients. Serum IL-2 and IFN-γ increased in OLP patients, but IL-4 decreased. MiR-125a was down-regulated in OLP patients, and there was a negative correlation between miR-125a content and the OLP severity which was measured with a RAE (reticular, atrophic and erosive lesion) scoring system. In conclusion, increasing CCl5/CCR5 might participate in the immune response of OLP. Th1-type cytokines environment presented in OLP probably performed as a magnifier for the CCR5. Moreover, miR-125a might be a candidate biomarker to estimate the severity of OLP.

Effect of electroacupuncture at "Neiguan" (PC 6) and "Zusanli" (ST 36) on gastrointestinal hormone in the antral tissue of rats with functional dyspepsia. / 电针"å† å ³""足三里"å¯¹åŠŸèƒ½æ€§æ¶ˆåŒ–ä¸è‰¯å¤§é¼ èƒƒçª¦ç»„ç»‡èƒƒè‚ æ¿€ç´ çš„å½±å“.

OBJECTIVES: To observe the effects of electroacupuncture (EA) at "Neiguan" (PC 6) and "Zusanli"(ST 36) on the gastric emptying rate, the level of serotonin (5-HT) and the protein expression of motilin (MTL), ghrelin, substance P (SP) and vasoactive intestinal peptide (VIP) in the antral tissue of the rats with functional dyspepsia (FD) and explore the effect mechanism of EA in treatment of FD. METHODS: A total of 21 SPF male SD rat pups were randomly divided into a normal group, a model group and an EA group, with 7 rats in each group. In the model group and the EA group, FD model was prepared by the gavage with 0.1% sucrose iodoacetamide solution combined with the modified small platform method. After the successful modeling, EA was applied to "Neiguan" (PC 6) and "Zusanli"(ST 36) in the rats of the EA group, with disperse-dense wave, 20 Hz/100 Hz in frequency, stimulated for 30 min, once daily, for 7 days consecutively. Before and after intervention, the general condition of the rats was observed in each group. After the completion of intervention, the gastric emptying rate was measured, the morphological changes of gastric antral tissue were observed using HE staining, the level of 5-HT was detected with ELISA method, and the protein expression of MTL, ghrelin, SP, and VIP was determined with Western blot method in the antral tissue of rats. RESULTS: In the normal group, the rats were in a good mental state, with lustrous fur, flexible movement and the increase of food intake and body mass. In the model group, the rats were poor in mental state, lack of lustre in fur, preference for the body curled up, reduced activity and response; and a part of rats had loose stool, obviously enlarged gastric body and gastric food retention. In the EA group, the general condition of rats, e.g. the mental state, food intake and activity, were improved, the gastric body got smaller obviously and the gastric food retention was reduced when compared with the model group. The antral structure was intact, the glands were rich and no injury of the gastric mucosa was found, e.g. inflammatory reaction and edema in the rats of each group. Compared with the normal group, the gastric emptying rate was decreased (P<0.01), 5-HT level was increased (P<0.01), the protein expression of MTL and ghrelin was reduced (P<0.01) and that of VIP was elevated (P<0.01) in the rats of the model group. The gastric emptying rate was increased (P<0.01), 5-HT level was decreased (P<0.01), and the protein expression of MTL and ghrelin was elevated (P<0.05, P<0.01) in the rats of the EA group when compared with those in the model group. CONCLUSIONS: Electroacupuncture at "Neiguan" (PC 6) and "Zusanli"(ST 36) may effectively relieve gastric dysfunction, strengthen gastric motility and promote gastric emptying so as to alleviate the symptoms of dyspepsia in FD rats, and its mechanism may be related to the regulation of gastrointestinal hormones in the antral tissue.

Increased B7-H1 expression on peripheral blood T cells in oral lichen planus correlated with disease severity.

BACKGROUND: Oral lichen planus (OLP) is a chronic and T cell-mediated autoimmune disease whose immunopathogenesis may involve antigen-presentation, T cells activation and migration as well as keratinocytes apoptosis. PD-1/B7-H1 pathway may have a unique function in regulating self-reactive T cells associated with inflammatory response and maintaining tolerance in peripheral tissues. In this study, we aimed to explore the contribution of PD-1/B7-H1 pathway to OLP. METHODS: We determined the expression of PD-1 and B7-H1 on peripheral blood T cells from OLP cases and analyzed their association with disease severity assessed by RAE (reticular, atrophic and erosive lesion) scoring system. In addition, interferon-γ, interleukin (IL)-2, IL-4, IL-10 and soluble PD-1 concentrations in serum were measured using ELISA. Then, we explored the regulation of PD-1/B7-H1 pathway on T cells immune response in OLP by blockade of PD-1 or B7-H1. RESULTS: We found that PD-1 and B7-H1 were up-regulated on peripheral blood T cells from OLP patients and B7-H1 expression positively correlated with disease severity of OLP. It is suggested that Th1 dominant inflammatory situation might contribute to the high expression of PD-1 and B7-H1 in OLP. Blockade of PD-1/B7-H1 pathway significantly increased the proliferation, and IFN-γ and IL-2 production of T cells. CONCLUSIONS: PD-1/B7-H1 pathway may play an important role in negatively modulating T cell-mediated immune response in OLP, and provide the rationale to employ B7-H1 expression on peripheral blood T cells as a marker of severity of OLP and to develop agonists targeting PD-1/B7-H1 pathway as a promising immunotherapeutic strategy for OLP.

Value of ultrasonography in determining the nature of pleural effusion: Analysis of 582 cases.

To explore the value of ultrasonography in the auxiliary diagnosis of pleural effusion, we retrospectively analyzed the ultrasonographic findings of 275 exudates and 307 transudates and summarized the ultrasonographic image features of pleural effusion according to patients' primary diseases. The findings of thoracic ultrasonography performed before the initial thoracentesis in 582 patients with subsequently confirmed exudative/transudative pleural effusion were analyzed with regard to the sonographic features of pleural effusion. In 275 cases with exudates, thoracic ultrasonography showed a complex septate appearance in 19 cases (6.9%), complex nonseptate appearance in 100 cases (36.4%), complex homogenous sign in 46 cases (16.7%), and pleural thickness > 3 mm in 105 cases. In contrast, in 307 patients with transudates, most patients (97.1%) had bilateral pleural effusion. Ultrasonographic images displayed anechoic appearance and absence of pleural thickening in a vast majority of cases (306, 99.7%; 301, 98%). These positive findings in the exudate were statistically higher than those in their counterparts (P < .05). In the empyema subgroup, the proportion of complex septate appearance, complex nonseptate appearance, complex homogenous sign, and pleural thickening was the highest, at 19/41, 12/41, 10/41, and 30/41, respectively. Ultrasonography is valuable in defining the nature of pleural effusion. Some sonographic features of pleural effusion, such as echogenicity, septation, and pleural thickening, may indicate a high risk of exudative pleural effusion.

Comparison Between Percutaneous Endoscopic Gastrostomy and Nasogastric Feeding in 160 Patients with Swallowing Disturbances: A Two-Year Follow-Up Study.

Purpose: We retrospectively compared the complications, blood biochemical indexes and outcomes in patients with swallowing disturbances receiving nasogastric tube (NGT) feeding and percutaneous endoscopy gastrostomy (PEG). Methods: Among 160 patients, 72 cases received PEG and 88 cases received NGT. All patients were followed up for two years. We collected their clinical data from the medical records. Indicators, such as body mass index (BMI), white blood cell (WBC), hemoglobin (HGB), complications, including recurrent aspiration pneumonia, gastrointestinal bleeding, reflux esophagitis, and outcomes (survival or death) were compared between the two groups semi-annually. Results: SAt both six months and one year after receiving treatment, there was no statistical difference between the two groups in indicators, complications and outcomes, with all P >0.05. It can be seen that, when the patients were followed up for one and a half years18 months, ALB was lower in the NGT group (33.81±0.46) compared with the PEG group (36.14±0.50) (P <0.05). After two years of follow-up, differences between the NGT and PEG group could be seen in a variety of indicators, including BMI (20.08±0.27 vs 21.03±0.25), WBC (9.12±0.56 vs 7.08±0.29), ALB (33.11±0.43 vs 35.75±0.49), creatinine (55.07±1.83 vs 63.21±2.94), and the complications, such as aspiration pneumonia, gastrointestinal bleeding, reflux esophagitis, and electrolyte disorder, in the PEG group were significantly reduced compared to the NGT groupthan that in its counterpart, P <0.05. In the two-year follow-up period, there were 13 and 22 patients died in the PEG group and NGT group, respectively. Conclusion: Both techniques are safe and effective in the short term. However, on a longer-term basis, PEG is shown to be superior to NGT feeding in improving nutrition and preventing common complications for patients with swallowing disturbances.

Biologics, an alternative therapeutic approach for oral lichen planus.

Oral lichen planus (OLP) is generally accepted as a chronic and T-cell-mediated autoimmune disease, whose immunopathogenesis may involve antigen presentation, T-cell activation and migration as well as, possibly, tumor necrosis factor-alpha (TNF-α)-induced keratinocytes apoptosis. However, present treatment options for OLP are far from being satisfactory. Recent advances in understanding the pathogenesis of OLP, progress in biologics, and the success of biologic therapies in OLP indicate that biologic agents are facing expanding indications in OLP. In this review, we mainly discuss the role of T cells in the pathogenesis of OLP and several biologic therapies that directly and/or indirectly target T cells to treat OLP.

The S100 protein family in lung cancer.

The S100 protein family is involved in the pathogenesis of several malignancies including lung cancer. Recent studies have shown that one member, S100A2, was over-expressed in advanced stage non-small cell lung cancer (NSCLC). Another, S100A6, demonstrated variable expression in different lung cancer subtypes. Research using NSCLC cell lines reported that SIX3 inhibited cell metastasis and proliferation via S100P down-regulation. This review represents an update on S100 proteins in lung cancer from 2017 to 2021 and includes the aforementioned as well as S100A4, S100A7, and S100B. Inconsistencies in mechanisms of action for S100A8/S100A9 are highlighted and a comprehensive evaluation of the most recent evidence for the S100 proteins in lung cancer is presented.