NCX1/Ca2+ promotes autophagy and decreases bortezomib activity in multiple myeloma through non-canonical NFκB signaling pathway.

Although bortezomib (BTZ) is the cornerstone of anti-multiple myeloma (MM) therapy, the inevitable primary and secondary drug resistance still seriously affects the prognosis of patients. New treatment strategies are in need. Sodium-calcium exchanger 1 (NCX1) is a calcium-permeable ion transporter on the membrane, and our previous studies showed that low NCX1 confers inferior viability in MM cells and suppressed osteoclast differentiation. However, the effect of NCX1 on BTZ sensitivity of MM and its possible mechanism remain unclear. In this study, we investigated the effect of NCX1 on BTZ sensitivity in MM, focusing on cellular processes of autophagy and cell viability. Our results provide evidence that NCX1 expression correlates with MM disease progression and low NCX1 expression increases BTZ sensitivity. NCX1/Ca2+ triggered autophagic flux through non-canonical NFκB pathway in MM cells, leading to attenuated the sensitivity of BTZ. Knockdown or inhibition of NCX1 could potentiate the anti-MM activity of BTZ in vitro and vivo, and inhibition of autophagy sensitized NCX1-overexpressing MM cells to BTZ. In general, this work implicates NCX1 as a potential therapeutic target in MM with BTZ resistance and provides novel mechanistic insights into its vital role in combating BTZ resistance.

Wearable smart contact lenses: A critical comparison of three physiological signals outputs for health monitoring.

Smart contact lenses (SCLs) have been considered as novel wearable devices for out-of-hospital and self-monitoring applications. They are capable of non-invasively and continuously monitoring physiological signals in the eyes, including vital biophysical (e.g., intraocular of pressure, temperature, and electrophysiological signal) and biochemical signals (e.g., pH, glucose, protein, nitrite, lactic acid, and ions). Recent progress mainly focuses on the rational design of wearable SCLs for physiological signal monitoring, while also facilitating the treatment of various ocular diseases. It covers contact lens materials, fabrication technologies, and integration methods. We also highlight and discuss a critical comparison of SCLs with electrical, microfluidic, and optical signal outputs in health monitoring. Their advantages and disadvantages could help researchers to make decisions when developing SCLs with desired properties for physiological signal monitoring. These unique capabilities make SCLs promising diagnostic and therapeutic tools. Despite the extensive research in SCLs, new technologies are still in their early stages of development and there are a few challenges to be addressed before these SCLs technologies can be successfully commercialized particularly in the form of rigorous clinical trials.

SSBP1 is a novel prognostic marker and promotes disease progression via p38MAPK signaling pathway in multiple myeloma.

Multiple myeloma (MM) remains an incurable disease. Identification of meaningful co-expressed gene clusters or representative biomarkers of MM may help to identify new pathological mechanisms and promote the development of new therapies. Here, we performed weighted sgene co-expression network analysis and a series of bioinformatics analysis to identify single stranded DNA binding protein 1 (SSBP1) as novel hub gene associated with MM development and prognosis. In vitro, CRISPR/cas9 mediated knockdown of SSBP1 can significantly inhibit the proliferation of MM cells through inducing apoptosis and cell cycle arrest in G0/G1 phase. We also found that decreased SSBP1 expression significantly increased mitochondrial reactive oxygen species (mtROS) generation and the level of phosphorylated p38MAPK. Furthermore, it was further verified that disruption of SSBP1 expression could inhibit the tumor growth via p38MAPK pathway in a human myeloma xenograft model. In summary, our study is the first to demonstrate that SSBP1 promotes MM development by regulating the p38MAPK pathway.

Potential role of RhoA GTPase regulation in type interferon signaling in systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by abnormal activation of the type I interferon (IFN) pathway, which results in tissue inflammation and organ damage. We explored the role of the RhoA GTPase in the type I IFN activation pathway to provide a potential basis for targeting GTPase signaling for the treatment of SLE. METHODS: Total RNA was extracted from peripheral blood mononuclear cells (PBMCs) of SLE patients and healthy controls, and the mRNA expression levels of RhoA and IFN-stimulated genes were measured by SYBR Green quantitative reverse transcriptase-polymerase chain reaction. IFN-a-stimulated response element (ISRE)-luciferase reporter gene assays and Western blotting were conducted to assess the biologic function of RhoA. An enzyme-linked immunoassay (ELISA) measured C-X-C motif chemokine ligand 10 (CXCL10) protein expression. RESULTS: Our studies demonstrate that the expression of RhoA in the PBMCs of SLE subjects was significantly higher than in healthy controls and positively correlated with type I IFN scores and type I IFN-stimulated gene (ISGs) expression levels. SiRNA-mediated knockdown of RhoA and the RhoA/ROCK inhibitor Y27632 reduced the activity of the type I IFN-induced ISRE, the signal transducer and activator of transcription 1 (STAT-1) phosphorylation, and the expression of CXCL10 and 2'-5'-oligoadenylate synthetase 1 (OAS1). Finally, we verified that Y27632 could significantly down-regulate the OAS1 and CXCL10 expression levels in the PBMCs of SLE patients. CONCLUSION: Our study shows that RhoA positively regulates the activation of the type I IFN response pathway. Reducing the expression level of RhoA inhibits the abnormal activation of the type I IFN system, and the RhoA/ROCK inhibitor Y27632 decreases aberrant type I IFN signaling in SLE PBMCs, suggesting the possibility of targeting the RhoA GTPase for the treatment of SLE.

Risk of cancer in acromegaly patients: An updated meta-analysis and systematic review.

The incidence of cancer in acromegaly patients may be higher than that in the general population, although this has not been fully elucidated yet. This study analyzed the risk of various important types of cancer in acromegaly patients. The study was registered in INPLASY (registration number: INPLASY202340037). The PubMed, Web of Science, and EMBASE databases were searched for studies based on strict inclusion and exclusion criteria, from the time of database inception up to June 30, 2022. All observational studies of acromegaly patients with cancer were included, without language restrictions. We used the Newcastle-Ottawa scale (NOS) checklist to assess the quality of evidence. A meta-analysis revealed the relationship between acromegaly and cancer using the standardized incidence rates (SIRs) and 95% confidence intervals (CIs) retrieved from the included studies. Nineteen studies were included and analyzed. The overall incidence of cancer (SIR = 1.45, 95%CI = 1.20-1.75), as well as that of thyroid (SIR = 6.96, 95%CI = 2.51-19.33), colorectal and anal (SIR = 1.95, 95%CI = 1.32-2.87), brain and central nervous system (SIR = 6.14, 95%CI = 2.73-13.84), gastric (SIR = 3.09, 95%CI = 1.47-6.50), urinary (SIR = 2.66, 95%CI = 1.88-3.76), hematological (SIR = 1.89, 95%CI = 1.17-3.06), pancreatic and small intestine (SIR = 2.59, 95%CI = 1.58-4.24), and connective tissue (SIR = 3.15, 95%CI = 1.18-8.36) cancers, was higher among patients with acromegaly than among the general population. No association between acromegaly and hepatobiliary, respiratory, reproductive, skin, breast, or prostate cancer was observed. This study demonstrated that acromegaly patients have a modestly increased chance of cancer as compared to the general population. Risk factors for cancer need to be further explored to monitor patients with acromegaly at a high risk for cancer more carefully.

The RhoA GTPase regulates Type I Interferon Signaling in Systemic lupus erythematosus.

Objective: Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by abnormal activation of the type I interferon (IFN) pathway, which results in tissue inflammation and organ damage. We explored the role of the RhoA GTPase in the type I IFN activation pathway to provide a potential basis for targeting GTPase signaling for the treatment of SLE. Methods: Total RNA was extracted from peripheral blood mononuclear cells (PBMCs) of SLE patients and healthy controls, and the mRNA expression levels of RhoA and IFN-stimulated genes were measured by SYBR Green quantitative reverse transcriptase-polymerase chain reaction. IFN-stimulated response element (ISRE)-luciferase reporter gene assays and Western blotting were conducted to asssess the biologic function of RhoA. An Enzyme-Linked Immunoassay (ELISA) measured C-X-C motif chemokine ligand 10(CXCL10)protein expression. Results: Our studies demonstrated that the expression of RhoA in the PBMCs of SLE subjects was significantly higher than healthy controls and positively correlated with type I IFN scores and type I IFN-stimulated gene (ISGs) expression levels. SiRNA-mediated knockdown of RhoA and the RhoA/ROCK inhibitor Y27632 reduced the activity of the type I IFN-induced ISRE, the signal transducer and activator of transcription 1 (STAT-1) phosphorylation, and the expression of CXCL10 and 2'-5'-oligoadenylate synthetase 1(OAS1). Finally,we verified that Y27632 could significantly down-regulate the OAS1 and CXCL10 expression levels in PBMCs of SLE patients. Conclusion: Our study shows that RhoA positively regulates the activation of the type I IFN response pathway. Reducing the expression level of RhoA inhibits the abnormal activation of the type I IFN system, and the RhoA/ROCK inhibitor Y27632 decreases aberrant type I IFN signaling in SLE PBMCs, suggesting the possibility of targeting the RhoA GTPase for the treatment of SLE.

CD4+ T cell count in HIV/TB co-infection and co-occurrence with HL: Case report and literature review.

In the human immunodeficiency virus (HIV)-infected population, especially HIV with concomitant tuberculosis (TB) or Hodgkin's lymphoma (HL), numerous risk factors have been reported in recent years. Among them, the decreased CD4+ T cell count was recognized as the common risk factor. We report a case of a patient with HIV and TB and HL co-occurrence, in which patient's CD4+ T cell count was inconsistent with disease. A 58-year-old male presented with fever and shortness of breath that persisted for 2 months. The patient had a 4-year history of HIV infection and underwent antiretroviral therapy (ART) effectively. After blood test, computed tomography, bone biopsy, and lymphoma biopsy, the patient was diagnosed with skeletal TB and HL, underwent TB treatment and received ART, and underwent four cycles of chemotherapy. CD4+ T cell count was not decreased before diagnosed with TB/HL and increased in this case after the fourth cycle of chemotherapy. We collected and analyzed CD4+ T cell counts in our case and reviewed relevant literature. It is suggested that CD4+ T cell count may be insufficient to predict the risk of HIV-related disease, especially lymphoproliferative disorders.

BNIP3 overexpression may promote myeloma cell apoptosis by enhancing sensitivity to bortezomib via the p38 MAPK pathway.

BACKGROUND: BCL2-interacting protein 3 (BNIP3) expression varies among cancers, and its role in myeloma cells remains unknown. We investigated the role of BNIP3 overexpression in myeloma cells, and particularly its effects on apoptosis and mitochondria. METHODS: A BNIP3-overexpressing plasmid was transfected into the MM.1S and RPMI8226 myeloma cell lines. Transfected cell apoptosis rate and mitochondrial function were determined via flow cytometry and western blotting. We verified the signaling pathway underlying myeloma cell sensitivity to bortezomib (BTZ). RESULTS: Cell lines carrying the BNIP3-overexpressing plasmid exhibited higher rates of apoptosis and expression of Bax and Cleaved caspase 3 protein than the vector group, and less Bcl-2 protein expression than the control cells. Relative to the vector group, BNIP3-overexpressing strains contained more reactive oxygen species (ROS) and exhibited mitochondrial membrane potential (MMP) and dynamin-related protein 1 (Drp1) upregulation and mitofusin-1 (Mfn1) downregulation. BTZ supplementation increased BNIP3 expression. Relative to the BNIP3-OE group, the BNIP3-OE BTZ-treated group exhibited upregulated Bax and Cleaved caspase 3 protein expression, downregulated Bcl-2 protein expression, higher apoptosis rates, ROS levels, MMP, and Drp1 expression, and lower Mfn1 expression. BTZ treatment induced p38 MAPK (mitogen-activated protein kinase) signaling pathway activation in BNIP3-OE cells. Upon adding N-acetylcysteine (NAC) and the p38 MAPK inhibitor SB203580, the affected index levels returned to the baseline. CONCLUSIONS: BNIP3 overexpression induced apoptosis in myeloma cells and increased myeloma cell sensitivity to BTZ. These effects may be mediated by the ROS/p38 MAPK signaling pathway.

Efficacy and safety of azathioprine plus prednisone versus prednisone alone as first-line treatment for antinuclear antibody-positive immune thrombocytopenia: a retrospective cohort study.

OBJECTIVE: Antinuclear antibody (ANA)-positive immune thrombocytopenia (ITP) patients have an unsatisfactory prognosis due to the more severe conditions of these patients and poor response to first-line glucocorticoids (GCs). The current study intended to compare the efficacy and safety of AZA plus prednisone and prednisone alone as first-line treatment in ANA-positive ITP patients. METHODS: Fifteen ANA-positive ITP patients receiving AZA plus prednisone (AZA + GC group) and eighteen ANA-positive ITP patients receiving prednisone alone (GC group) as first-line treatment were retrospectively enrolled. RESULTS: The complete response (CR) rate (60.0% versus 22.2%) (P = 0.038) was increased in the AZA + GC group versus the GC group, while the overall response rate (86.7% versus 55.6%) (P = 0.070) only showed an increasing trend that did not achieve statistical significance. In addition, multivariate analysis revealed that AZA + GC (versus GC) (odds ratio = 31.331, P = 0.018) was independently associated with a higher possibility of achieving CR. Additionally, accumulating relapse-free duration was prolonged in the AZA + GC group versus the GC group (median: 7.8 months versus 3.4 months) (P = 0.038). Additionally, the multivariate analysis suggested that AZA + GC (versus GC) (hazard ratio = 0.306, P = 0.007) was independently correlated with longer accumulating relapse-free duration. The incidence of adverse events did not differ between the two groups (all P > 0.05), and the common adverse events in the AZA + GC group were pneumonia (13.3%), anemia (13.3%), cough (13.3%), nausea (6.7%), and granulocytopenia (6.7%), which were all tolerable and manageable. CONCLUSION: First-line AZA plus prednisone realizes a better hematological response and relapse-free duration with acceptable adverse events compared to prednisone alone in ANA-positive ITP patients.

Clinical features and high-risk indicators of central nervous system involvement in primary Sjögren's syndrome.

BACKGROUND: Evidence for central nervous system involvement in primary Sjögren's syndrome (pSS) patients is controversial and extremely limited. We aimed to describe the clinical profiles and high-risk indicators of primary Sjögren's syndrome (pSS) patients with central nervous system (CNS) involvement (pSS-CNS). METHODS: A total of 412 participants with pSS from a hospital in China from January 2012 to December 2019 were enrolled in the retrospective study. 42 pSS-CNS patients were compared with 370 pSS patients without CNS involvement. The clinical features, laboratory examinations, imaging characteristics, and treatment of the pSS-CNS cases were systematically analyzed. Potential risk factors related to pSS-CNS patients were identified by multivariate logistic regression analysis. RESULTS: The prevalence of central nervous system involvement in the studied pSS patients was 10.2% (42/412), with 31.3% (14/42) of pSS patients having neurological manifestations as the initial symptom. The manifestations of hemiparesis (35.7%, 15/42), paraparesis (28.6%, 12/42), dysphonia (31.0%, 13/42), blurred vision (21.4%, 9/42), and dysfunctional proprioception (23.8%, 10/42) were more common in the pSS-CNS patients. Cerebral infarction (57.1%, 24/42), demyelination (31.0%, 13/42), myelitis (23.8%, 11/42), and angiostenosis (21.4%, 9/42) were most often found on MRI or CT scan imaging in the pSS-CNS patients. Intrathecal IgG level and total protein of cerebrospinal fluid were increased in 50% (8/16) of the pSS-CNS group. In comparison with patients without CNS involvement, the pSS-CNS patients were found to also have kidney and lung involvement, hematologic abnormalities, positive ANA and anti-SSA antibody tests, and reduced complement 3 (C3) and complement 4 (C4) levels (all p < 0.05). The prevalence of lung involvement, immune thrombocytopenia, and high-titer ANA (1:1000) were significantly higher in pSS-CNS disease activity compared to those in the moderately active group. Multivariate analysis identified lung involvement, anti-SSA positivity, and low C3 levels as prognostic factors for pSS-CNS. After high-dose glucocorticoids and immunosuppressive therapy, 60.5% (26/38) of pSS-CNS patients improved, 36.8% (14/38) were unresponsive to treatment, and 2.6% (1/38) died. CONCLUSION: Clinical features are diverse in pSS-CNS patients, and the morbidity rate is low. CNS involvement was the initial presentation in state percentage here pSS patients. Pulmonary involvement, a positive anti-SSA antibody test, and reduced C3 levels are potential risk factors for CNS involvement in pSS. Treatment with high-dose glucocorticoids and immunosuppressive therapy appeared effective in 60% of pSS-CNS patients. Key Points • The CNS manifestations of pSS are diverse, and CNS imaging and CSF analysis are important for the diagnosis. • Pulmonary involvement, positive anti-SSA, and reduced C3 levels are potential risk factors of pSS-CNS. • About 60% of pSS-CNS patients were responsive to high-dose glucocorticoid administration and immunosuppressive therapy.

Simultaneous Presentation of Multiple Myeloma and Lung Cancer: Case Report and Gene Bioinformatics Analysis.

Patients diagnosed with more than one cancer generally develop the individual tumors sequentially. There are a few cases of co-occurring multiple myeloma and lung cancer reported in the literature. Here, we report two cases of co-occurring multiple myeloma and lung cancer in patients who presented with the chief complaint of pain. The diagnoses of multiple myeloma and lung cancer were supported by hematologic and biochemical investigations, as well as bone marrow and lung histopathologic examination. We provided suitable interventions for both two patients. The patients are still currently undergoing treatment and followed up closely. We first performed a bioinformatic analysis to determine commonly shared genes and pathways in the two types of cancer types. Fortunately, we identified the hub gene mitochondrial trans-2-enoyl-CoA reductase (MECR), which was overexpressed in both tumors. Survival analysis correlated higher MECR expression with poorer overall survival. Signaling pathway analysis suggested possible transduction pathways implicated in the co-occurrence of both tumors. The clinical cases combined with bioinformatic analysis may provide insight for the pathogenesis of synchronous tumors.

TTP protects against acute liver failure by regulating CCL2 and CCL5 through m6A RNA methylation.

Tristetraprolin (TTP), an important immunosuppressive protein regulating mRNA decay through recognition of the AU-rich elements (AREs) within the 3'-UTRs of mRNAs, participates in the pathogenesis of liver diseases. However, whether TTP regulates mRNA stability through other mechanisms remains poorly understood. Here, we report that TTP was upregulated in acute liver failure (ALF), resulting in decreased mRNA stabilities of CCL2 and CCL5 through promotion of N6-methyladenosine (m6A) mRNA methylation. Overexpression of TTP could markedly ameliorate hepatic injury in vivo. TTP regulated the mRNA stabilization of CCL2 and CCL5. Interestingly, increased m6A methylation in CCL2 and CCL5 mRNAs promoted TTP-mediated RNA destabilization. Moreover, induction of TTP upregulated expression levels of WT1 associated protein, methyltransferase like 14, and YT521-B homology N6-methyladenosine RNA binding protein 2, which encode enzymes regulating m6A methylation, resulting in a global increase of m6A methylation and amelioration of liver injury due to enhanced degradation of CCL2 and CCL5. These findings suggest a potentially novel mechanism by which TTP modulates mRNA stabilities of CCL2 and CCL5 through m6A RNA methylation, which is involved in the pathogenesis of ALF.

Treatment for CD57-negative γδ T-cell large granular lymphocytic leukemia with pure red cell aplasia: A case report.

BACKGROUND: T-cell large granular lymphocytic leukemia (T-LGLL) is a rare type of aplastic anemia with diverse clinical manifestations. Concomitant diseases are often present at the first manifestation. We describe the treatment of a patient with CD57-negative γδT-LGLL with pure red cell aplasia (PRCA). CASE SUMMARY: A 34-year-old woman with a 20-year history of anemia visited our hospital owing to severe dizziness and was admitted. Her condition was diagnosed as CD57-negative γδT-LGLL with PRCA through bone marrow cytology, bone marrow pathology, bone marrow flow cytometry, bone marrow multiplex polymerase chain reaction combined with fluorescent fragment analysis, and other tests. Treatment with prednisone, methotrexate, and subcutaneous erythropoietin did not significantly change her hemoglobin level. After treatment with oral cyclophosphamide for 3 mo, her hemoglobin level increased to approximately 100 g/L. After 5 mo of treatment, the patient could perform activities of daily living independently. CONCLUSION: The treatment of CD57-negative γδT-LGLL with PRCA with cyclophosphamide helps to improve prognosis.

An NF-κB-responsive long noncoding RNA, PINT, regulates TNF-α gene transcription by scaffolding p65 and EZH2.

Long noncoding RNAs (lncRNAs) are central regulators of the inflammatory response and play an important role in inflammatory diseases. PINT has been reported to be involved in embryonic development and tumorigenesis. However, the potential functions of PINT in the innate immune system are largely unknown. Here, we revealed the transcriptional regulation of inflammatory genes by PINT, whose expression is primarily dependent on the NF-κB signaling pathway in human and mouse macrophage and intestinal epithelial cell lines. Functionally, PINT selectively regulates the expression of TNF-α in basal and LPS-stimulated cells. Mechanistically, PINT acts as a modular scaffold of p65 and EZH2 to coordinate their localization and specify their binding to the target genes. Further, a high expression level of PINT was detected in intestinal mucosal tissues from patients with ulcerative colitis (UC). Together, these findings demonstrate that PINT acts as an activator of inflammatory responses, highlighting the importance of this lncRNA as a potential therapeutic target in infectious diseases and inflammatory diseases.

Influence of NQO1 Polymorphisms on Warfarin Maintenance Dose: A Systematic Review and Meta-Analysis (rs1800566 and rs10517).

This meta-analysis was conducted to analyze the effect of NQO1 polymorphism on the warfarin maintenance dosage. Using strict inclusion and exclusion criteria, we searched PubMed, EMBASE, and the Cochrane Library for eligible studies published prior to July 7, 2021. The required data were extracted, and experts were consulted when necessary. Review Manager Version 5.4 software was used to analyze the relationship between NQO1 polymorphisms and the warfarin maintenance dosage. Four articles involving 757 patients were included in the meta-analysis. Patients who were NQO1 rs10517 G carriers (AG carriers or GG carriers) required a 48% higher warfarin maintenance dose than those who were AA carriers. Patients with NQO1 rs1800566 CT carriers required a 13% higher warfarin dose than those who were CC carriers, with no associations observed with the other comparisons of the NQO1 rs1800566 genotypes. However, the results obtained by comparing the NQO1 rs1800566 genotypes require confirmation, as significant changes in the results were found in sensitivity analyses. Our meta-analysis suggests that the NQO1 rs10517and NQO1 rs1800566 variant statuses affect the required warfarin maintenance dose.

A High-Sensitivity Method Based on Advanced Optical Waveguide Technology to Detect HBsAg.

A novel method for the detection of the hepatitis B surface antigen (HBsAg) at low concentrations, using the ultrahigh-order guided mode acting as the probe excited by a symmetrical metal-cladding waveguide, is proposed. The method using the fact of the minimum value of the absorption peaks is proportional to the concentration of the sample to be detected to realize the detection of the hepatitis B virus at extremely low concentrations. It is realized that the low concentration of the HBsAg measurement relied on the principle of the minimum value of the absorption peak and the concentration having a good linear relationship. The measurement results indicate that this new method can precisely detect HBsAg at the concentrations in the lower region of the clinical gray area (i.e., below 20 ng/mL), the lower region of the current clinical gray area of HBsAg (below 20 ng/ml) can be measured, and the resolution can be reached (2 ng/mL).

Peptide Nucleic Acid-Functionalized Nanochannel Biosensor for the Highly Sensitive Detection of Tumor Exosomal MicroRNA.

Compared with free miRNAs in blood, miRNAs in exosomes have higher abundance and stability. Therefore, miRNAs in exosomes can be regarded as an ideal tumor marker for early cancer diagnosis. Here, a peptide nucleic acid (PNA)-functionalized nanochannel biosensor for the ultrasensitive and specific detection of tumor exosomal miRNAs is proposed. After PNA was covalently bound to the inner surface of the nanochannels, the detection of tumor exosomal miRNAs was achieved by the charge changes on the surface of nanochannels before and after hybridization (PNA-miRNA). Due to the neutral characteristics of PNA, the efficiency of PNA-miRNA hybridization was improved by significantly reducing the background signal. This biosensor could not only specifically distinguish target miRNA-10b from single-base mismatched miRNA but also achieve a detection limit as low as 75 aM. Moreover, the biosensor was further used to detect exosomal miRNA-10b derived from pancreatic cancer cells and normal pancreatic cells. The results indicate that this biosensor could effectively distinguish pancreatic cancer tumor-derived exosomes from the normal control group, and the detection results show good consistency with those of the quantitative reverse-transcription polymerase chain reaction method. In addition, the biosensor was used to detect exosomal miRNA-10b in clinical plasma samples, and it was found that the content of exosomal miRNA-10b in cancer patients was generally higher than that of healthy individuals, proving that the method is expected to be applied for the early diagnosis of cancer.

ASC Performance Prediction for Medical IoT Communication Networks.

Wearable devices are gradually entering the medical health field. Medical Internet of Things (IoT) has been widely used in all walks of medical health. With the complexity of medical health application scenarios, the medical IoT communication networks face complex environments. The secure communication issue is very important for medical IoT communication networks. This paper investigates the secrecy performance of medical IoT communication networks. To improve the secrecy performance, we adopt a cooperative communication strategy. We also use the average secrecy capacity (ASC) as a metric, and the expressions are first derived. Then, a secrecy performance intelligent prediction algorithm is proposed. The extensive simulations are used to verify the proposed method. Compared with other methods, the proposed algorithm realizes a better prediction precision.

Brucellosis of unknown origin with haemophagocytic syndrome: A case report.

BACKGROUND: Brucellosis is a contagious bacterial disease caused by Brucella species, which is a leading zoonotic disease worldwide. Most patients with brucellosis have a clear infection source; however, our case had a rare presentation of secondary haemophagocytic lymphohistiocytosis without any epidemiological history. CASE SUMMARY: A 50-year-old man was admitted to our hospital with a fever of unknown origin. After laboratory examinations, such as blood culture and bone marrow biopsy, the patient was diagnosed with brucellosis and secondary haemophagocytic lymphohistiocytosis. After antibiotic therapy, the patient was afebrile, and his haemogram recovered to normal, after which he was discharged. CONCLUSION: Brucellosis cannot be excluded in patients with clinically unexplained fever, even in those without epidemiologic history.