Systemic lupus erythematosus complicated with reversible posterior encephalopathy syndrome: a case report.

A 28-year-old female patient was hospitalized primarily because of "intermittent fever for 28 days aggravated by systemic rashes, oral ulcer, and edema in both eyelids for 5 days." During treatment, convulsions and loss of consciousness occurred. Magnetic resonance imaging (MRI) of the head revealed an abnormal signal with shadows in the bilateral frontal, parietal, temporal, and occipital lobes; cerebellar hemispheres; and basal nodes, with high signal intensity on T2 weighted imaging (T2WI), on fluid-attenuated inversion-recovery, and of the apparent diffusion coefficient and low signal intensity on T1WI and diffusion weighted imaging. Therefore, the patient was diagnosed with systemic lupus erythematosus (SLE) with reversible posterior encephalopathy syndrome (RPES). Intravenous high-dose methylprednisolone and cyclophosphamide were administered for blood pressure control, which effectively controlled the disease. Therefore, when patients with SLE and hypertension or renal insufficiency or those receiving high-dose methylprednisolone or immunosuppressants suddenly present with neurologic abnormalities, a diagnosis of RPES must be considered, and head MRI is the first choice for diagnosis of this disease. In terms of treatment, the blood pressure should be quickly controlled, and the primary disease should be aggressively treated.

Case Report: A Promising Treatment Strategy for Noninfectious Uveitis.

Background: Uveitis refers to inflammation in the uvea, retina, retinal blood vessels, and vitreous, which can lead to irreversible eye damage and permanent vision loss. Glucocorticoid drugs are the first-line treatment, but side effects, such as obesity and hyperglycemia, can occur. Therefore, biologics have become a new treatment choice. Case Presentation: A 18-year-old girl developed eye pain and was diagnosed with binocular uveitis. Prednisone 50 mg was administered once a day, and the redness and pain in both eyes improved. Later, the prednisone dose was gradually reduced, and treatment was discontinued 3 years ago. Two years ago, the patient's condition relapsed, with both eyes becoming red and painful. She was administered prednisone 20 mg once daily and adalimumab. Visual acuity in both eyes continued to progressively decrease, accompanied by cataracts. At the same time, the patient experienced complications, including obesity and hyperglycemia. Subsequently, a new treatment regimen, oral prednisone 20 mg once a day, tofacitinib 5 mg twice a day, and methotrexate 10 mg once a week, as well as the use of insulin to control blood sugar, was initiated. One month later, the patient's redness and eye pain eased, and her vision gradually improved. The dosage of prednisone was gradually reduced to 5 mg once daily. At the same time, her blood sugar returned to normal, and insulin was stopped. Outcomes: The patient was treated with tofacitinib for 10 months. Subsequently, her best-corrected visual acuity of the right eye rose from 0.06 to 0.075, and the best-corrected visual acuity of the left eye rose from CF/30 cm to CF/100 cm. Redness and eye pain were relieved, her glucocorticoid consumption reduced from 15 to 2.5 mg, and her blood sugar gradually normalized. Conclusion: This case study shows that tofacitinib relieves ocular inflammation in patients with uveitis and improves eyesight. We believe that JAK inhibitors could be another treatment option for noninfectious uveitis in patients who do not respond to conventional anti-TNF-α inhibitors (such as adalimumab).

Long non-coding RNA MALAT1 exacerbates acute respiratory distress syndrome by upregulating ICAM-1 expression via microRNA-150-5p downregulation.

Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury in which severe inflammatory responses induce cell apoptosis, necrosis, and fibrosis. This study investigated the role of lung adenocarcinoma transcript 1 (MALAT1) in ARDS and the underlying mechanism involved. The expression of MALAT1, microRNA-150-5p (miR-150-5p), and intercellular adhesion molecule-1 (ICAM-1) was determined in ARDS patients and lipopolysaccharide (LPS)-treated human pulmonary microvascular endothelial cells (HPMECs). Next, the interactions among MALAT1, miR-150-5p, and ICAM-1 were explored. Gain- or loss-of-function experiments in HPMECs were employed to determine cell apoptosis and inflammation. Furthermore, a mouse xenograft model of ARDS was established in order to verify the function of MALAT1 in vivo. MALAT1 and ICAM-1 were upregulated, while miR-150-5p was downregulated in both ARDS patients and LPS-treated HPMECs. MALAT1 upregulated ICAM-1 expression by competitively binding to miR-150-5p. MALAT1 silencing or miR-150-5p overexpression was shown to suppress HPMEC apoptosis, decrease the expressions of pro-inflammatory cytokines (IL-6, IL-1ß and TNF-α) and E-selectin in HPMECs, as well as alleviated lung injury in nude mice. These findings demonstrated that MALAT1 silencing can potentially suppress HPMEC apoptosis and alleviate lung injury in ARDS via miR-150-5p-targeted ICAM-1, suggestive of a novel therapeutic target for ARDS.

microRNA-328 in exosomes derived from M2 macrophages exerts a promotive effect on the progression of pulmonary fibrosis via FAM13A in a rat model.

Currently, exosome-enclosed microRNAs (miRs) in exhaled breath have potential for biomarker discovery in patients with pulmonary diseases. This study was performed to investigate the roles of M2 macrophage-derived exosomes expressing miR-328 in pulmonary fibrosis (PF). Microarray-based analysis was used to screen differentially expressed genes (DEGs) and regulatory miRs in PF. The miR-target relationship between FAM13A and miR-328 was confirmed. The expression of FAM13A and miR-328 was measured in PF rats, and gain- and loss-of-function assays were conducted to determine the regulatory effects of FAM13A and miR-328 on PF. In addition, exosomes derived from M2 macrophages were isolated and then cocultured with pulmonary interstitial fibroblasts to identify the role of these exosomes in PF. Furthermore, the effects of M2 macrophage-derived exosomes overexpressing miR-328 on pulmonary fibroblast proliferation and the progression of PF were assessed in vivo. miR-328 might perform a vital function in PF by regulating FAM13A. FAM13A expression was downregulated while miR-328 expression was upregulated in rats with PF, and a miR-target relationship between miR-328 and FAM13A was observed. Additionally, miR-328 overexpression and FAM13A silencing each were suggested to promote pulmonary interstitial fibroblast proliferation and the expression of Collagen 1A, Collagen 3A and α-SMA. Then, in vitro experiments demonstrated that M2 macrophage-derived exosomes overexpressing miR-328 contributed to enhanced pulmonary interstitial fibroblast proliferation and promoted PF. Furthermore, in vivo experiments confirmed the promotive effects of M2 macrophage-derived exosomes overexpressing miR-328 on the progression of PF. Collectively, the results showed that M2 macrophage-derived exosomes overexpressing miR-328 aggravate PF through the regulation of FAM13A.

Pulmonary embolism, deep vein thrombosis and recurrent bone cysts in a patient with hypereosinophilic syndrome.

Herein we present a case of hypereosinophilic syndrome with a unique clinical presentation. A 32-year-old man was admitted because of fever, hemoptysis and chest pain. The main clinical features include hypereosinophilia, deep vein thrombosis, pulmonary embolism, thrombocytopenia and recurrent bone cysts. The plain film of the left foot revealed dissolvent bone destruction. The histological findings of bone cysts include eosinophilic infiltration and tissue necrosis. According to the case history and literature, it is possible that hypereosinophilia itself may be a risk for thrombogenesis and the bone destruction.

Expression of Fascin-1 on human lung cancer and paracarcinoma tissue and its relation to clinicopathological characteristics in patients with lung cancer.

BACKGROUND: Lung cancer poses a severe threat to human life. Biomarkers of cancers are helpful in the diagnosis and treatment of patients with cancers. Biomarkers of lung cancers are rare, and thus deserve further research. OBJECTIVE: The objective of the present study was to explore the expression of Fascin-1 in human lung cancer and paracarcinoma tissue, its correlation with clinicopathological characteristics in patients with lung cancer, and study the possible relationship between Fascin-1 expression and clinical-biological behavior of lung cancer. METHOD: This study used the MaxVision two-step immunohistochemical detection method to detect Fascin-1 expression in 84 of lung cancer and paracarcinoma tissues. This study set the expression of Fascin-1 in vascular endothelial cells as the positive control, and used phosphate buffered saline (replacing the primary antibodies) as negative control. RESULT: Of all the 84 lung cancer tissues and paracarcinoma tissues, positive expression of the Fascin-1 protein were detected in 78 cases (92.9%) and 27 cases (32.1%), respectively, and the difference was statistically significant (P<0.05). Differences in Fascin-1 expression between different age groups, clinical stages, and lymph node metastases were statistically significant (P<0.05), while differences in Fascin-1 expression between sexes, tumor stages, and pathological types demonstrated no statistical significance (P>0.05). The survival times of the patients with different Fascin-1 protein-positive expressions in lung cancer tissues were statistically significant (P>0.05), while the survival times of the patients with different Fascin-1 protein-positive expressions in paracarcinoma tissues were not statistically significant (P>0.05). CONCLUSION: In lung cancer, Fascin-1 expression was closely related to tumor invasion and metastasis, and the difference in expression of Fascin-1 had a significant effect on the survival time of the lung cancer patients. Therefore, Fascin-1 might be expected to serve as a possible potential biomarker of lung cancer.