LncRNA PRNCR1 aggravates the malignancy of oral squamous cell carcinoma by regulating miR-326/FSCN1 axis.

OBJECTIVE: The important regulatory mechanism of lncRNA PRNCR1 has been emphasized in malignant tumors. However, the role of lncRNA PRNCR1 remains unclear in oral squamous cell carcinoma (OSCC). The purpose of this study is to reveal the role of lncRNA PRNCR1 in OSCC. PATIENTS AND METHODS: RT-qPCR was used to detect mRNA expression. The functional mechanism of lncRNA PRNCR1 in OSCC was investigated by CCK-8, transwell and Luciferase reporter assays. RESULTS: LncRNA PRNCR1 was upregulated in OSCC and promoted cell proliferation, migration and invasion. LncRNA PRNCR1 directly binds to miR-326. The mutual inhibition between the expressions of lncRNA PRNCR1 and miR-326 was identified in OSCC. In addition, miR-326 restrained cell proliferation, migration and invasion in OSCC. Further, miR-326 directly targets FSCN1. FSCN1 expression was positively regulated by lncRNA PRNCR1 in OSCC. And FSCN1 promoted the progression of OSCC and aggravated the carcinogenic effect of lncRNA PRNCR1 in OSCC. CONCLUSIONS: LncRNA PRNCR1 promotes the progression of OSCC by functioning as a miR-326 'sponge' to upregulate FSCN1 expression.

[Expression and significance of STOX1 in villi and placenta at different stages of normal gestation].

Objective: To investigate the expression and significance of STOX1 in different stages of gestation villi and placenta. Methods: Totally 137 cases of normal villi and placenta of pregnant women were collected from the Department of Obstetrics of Shanghai Pudong Hospital from October 1(st) 2015 to February 28(th) 2018, including 64 cases of early pregnancy (early pregnancy group) which consists of 32 cases of 5-7(+6) weeks gestation (early pregnancy group A) and 32 cases of 8-11(+3) weeks gestation (early pregnancy group B), 28 cases of 14-26 weeks gestation(middle pregnancy group) and 45 cases of 37-41 weeks gestation (late pregnancy group). The expression and localization of STOX1 mRNA and protein in placenta were evaluated by RT-qPCR, Western blotting and immunohistochemistry. Results: (1)STOX1 was positively expressed in the cytotrophoblasts and syncytiotrophoblasts as well as interstitial and vascular endothelial cells of all groups. (2)STOX1 mRNA expression in each group was significantly different (P<0.05), the lowest was in the early pregnancy group A(0.007 8±0.000 4), which increased along with the progression of gestational age(P<0.05),and reached the highest level in the third trimester(0.064 4±0.001 3). (3)The protein level of STOX1 in different stages of normal pregnancy was 0.53±0.20 in early pregnancy group A;0.62±0.37 in early pregnancy group B;0.70±0.03 in middle pregnancy group and 0.81±0.04 in late pregnancy group respectively; which was positively related with the progression of gestational age (P<0.05). Conclusion: The expressions of STOX1 is gradually increasing along with the normal pregnancy progression, suggesting that it might be involved in proliferation, differentiation and infiltration and (or) apoptosis of trophoblast cells and the development of the placenta.

Clinical analysis of 59 children with hand foot and mouth diseases due to enterovirus EV71 and concomitant viral encephalitis.

OBJECTIVE: To analyzed the clinical features of children with HFMD and viral encephalitis and to summarize some treatments. PATIENTS AND METHODS: A total of 59 children with HFMD were included in this study. All children underwent complete blood count, blood biochemical test cerebrospinal fluid examination, chest X-ray and brain MRI. RESULTS: One child died 24 hours after admission due to central respiratory failure with myocardial damage. After the treatment, 58 children had normal temperature, resolved rash, normal complete blood count, biochemical blood tests and cerebrospinal fluid test, respiratory and circulatory symptoms and signs, as well as neurological symptoms, disappeared. The hospitalization time was 12-21 days. After follow-up for 1-3 months, all children were recovered, and without any severe sequelae. CONCLUSIONS: HFMD and the complicated viral encephalitis usually occurred in the children < 3 years old. The clinical manifestations were not typical. Monitoring of the child's clinical symptoms, signs and relevant examinations was required.

Mac-1 deficiency induces respiratory failure by affecting type I alveolar epithelial cells.

As a ß2 integrin family member, Mac-1 plays an important role in the inflammatory response. Inflammation and lung injury are closely associated, but the involvement of Mac-1 in the occurrence and development of such pathologies remains poorly understood. We aimed to investigate the relationship between Mac-1 deficiency and respiratory failure in Mac-1 knockout {Mac-1-/-} mice, using C57BL/6J mice as a control. The newborn survival rate of Mac-1-/- mice was calculated, and mouse lung tissue was treated with hematoxylin and eosin and subjected to immunofluorescent staining. Moreover, western blotting and immunohistochemistry were used to detect the expression of molecules specific to type I and type II alveolar epithelial cells, as well as alveolar surfactant proteins secreted by the latter. Survival of Mac-1-/- pups was significantly lower than that of newborn C57BL/6J mice. In a float test, lung tissues from C57BL/6J mice were buoyant, whereas those of Mac-1-/- mice were not. Compared with C57BL/6J mice, expression of proSP-C {specific to type II alveolar epithelial cells} and alveolar surfactant proteins in Mac-1-/- mice was not significantly different, implying that type II cell function was unaltered. However, western blotting revealed expression of T1α, Aqp5, and Snx5 {type I alveolar epithelial cell markers} in Mac-1-/- mice to be significantly decreased {P < 0.05}. In conclusion, Mac-1 may play an important role in respiratory failure. Its absence leads to this condition not by influencing type II alveolar epithelial cells or their secreted surfactant proteins, but rather by reducing type I alveolar cell numbers.

Effects of acupotomylysis on basic fibroblast growth factor and CD34 levels in rabbits with third lumbar vertebral transverse foramen syndrome.

This study observed the local tissue homogenates in rabbits with third lumbar vertebral transverse foramen syndrome and explored the mechanism of acupotomylysis in local tissue revascularization. Thirty Japanese white rabbits were randomly divided into the following 5 groups of 6 rabbits each: normal, model, acupotomy, electroacupuncture (EA), and acupotomy-EA groups. All except the normal group were comprised of animal models of third lumbar vertebral transverse foramen syndrome prepared by embedding sponge in the left third lumbar transverse process. The rabbits in the acupotomy and EA groups underwent bilateral acupotomylysis intervention; those in the acupotomy-EA group underwent acupotomylysis and EA interventions. On the 28th day after modeling, the double-antibody ELISA was used to detect b-FGF and CD34 levels in the serum and homogenates of a muscle tissue sample from the left side of the third lumbar transverse process. The b-FGF levels in local muscle homogenates were significantly higher in the modeled rabbits than in the normal rabbits (P < 0.01), and the CD34 levels in the modeled group were significantly lower than in the normal group (P < 0.01). The b-FGF and CD34 levels in the EA, acutopomy, and acutopomy-EA groups were significantly lower than those in the modeled group (P < 0.01); the CD34 levels were significantly higher in the acupotomy-EA group than in the model group (P < 0.05); and the differences among the EA, acupotomy, and acupotomy-EA groups were not significant (P > 0.05). In conclusion, acupotomylysis regulates the levels of b-FGF and CD34 levels in serum and muscle tissue as well as local tissue revascularization.

Diagnosis of airway-invasive pulmonary aspergillosis by tree-in-bud sign in an immunocompetent patient: case report and literature review.

Invasive fungal infections are rare in immunocompetent hosts, and diagnosis may be missed or delayed due to our lack of understanding of the particular clinical signs, disease progression, and treatment outcome. Here, we present a case of pulmonary invasive aspergillosis that arose in an immunocompetent and previously healthy patient. The patient presented with a several-week history of remittent high fever, cough, and expectoration. These symptoms were unresponsive to treatments for tuberculosis and pulmonary bacterial infection. Computed tomography images revealed the characteristic bronchiolitis tree-in-bud pattern in the airways. Lung biopsy specimens were culture-positive for Aspergillus fumigatus. Treatment with voriconazole and caspofungin followed by amphotericin B cleared the infection and resolved the symptoms.

CXCL12 G801A polymorphism contributes to cancer susceptibility: a meta-analysis.

CXCL12 is an important alpha-chemokine that regulates many essential biological processes including tumor development and metastasis. The CXCL12 G801A polymorphism is associated with multiple kinds of malignant cancer, but the associations are inconsistent. To derive a more precise estimation of the relationship, we conducted a meta-analysis of 16 publications with 2,888 cases and 3,611 controls. We used the odds ratio (OR) corresponding to 95% confidence interval (CI) to estimate the strength of association. The increased risk of overall cancer was found in the homozygote comparison (AA vs. GG, OR=1.43, 95℅CI=1.07-1.91), the recessive model (AA vs. GG+GA, OR=1.26, 95℅CI=1.03-1.54), and the dominant model (GA+AA vs. GG, OR=1.35, 95℅CI=1.15-1.58). In the stratified analyses, the associations were significant in breast cancer, Asians and hospital-based controls. In conclusion, this meta-analysis suggests that the CXCL12 G801A polymorphism may be a risk factor of cancer, especially in the subgroups of breast cancer, Asians and hospital-based controls.

Dectin-1 is inducible and plays a crucial role in Aspergillus-induced innate immune responses in human bronchial epithelial cells.

Airway epithelial cells are the first cells to be challenged upon contact with the conidia of Aspergillus. In response, they express pattern-recognition receptors that play fundamental roles as sentinels and mediators of pulmonary innate immunity. The C-type lectin Dectin-1 is expressed predominantly on the surface of myeloid lineage cells. We examined the induction, regulation, and functions of Dectin-1 in pulmonary epithelial cells by challenging human bronchial epithelial (HBE) cells with A. fumigatus. Inflammatory, antimicrobial peptide genes and reactive oxygen species (ROS) were quantified, with and without knockdown of Dectin-1. We found that A. fumigatus induced the expression of Dectin-1 mRNA and protein in HBE cells in a toll-like receptor (TLR) 2-dependent manner. In addition, A. fumigatus-mediated generation of ROS was dependent on the upregulation of Dectin-1. Moreover, A. fumigatus actively induced the expression of TNFα, GM-CSF, IL8, HBD2, and HBD9. Knockdown of Dectin-1 inhibited TNFα, IL8, HBD2, and HBD9 expression. Hence, Dectin-1 was required for the upregulation of pro-inflammatory cytokines and antimicrobial peptides. Finally, knockdown of TLR2 significantly inhibited Dectin-1 upregulation. Our results demonstrate the novel induction of Dectin-1 in human bronchial epithelial cells and its critical role in the innate immune response against A. fumigatus in non-phagocytic cells.

Extracellular matrix production of lens epithelial cells.

PURPOSE: To examine extracellular matrix (ECM) production of lens epithelial cells (LECs) and their regulation by cytokines. SETTING: Research Laboratory, International Intraocular Implant Training Center, Tianjin Medical University, People's Republic of China. METHODS: Bovine LECs were cultured with or without tumor necrosis factor alpha (TNF-alpha) and transforming growth factor beta2 (TGF-beta2). Immunohistochemistry and in situ hybridization were used to detect the expression of ECM. The slides were quantified by computer analysis. RESULTS: Laminin expression was increased by both TNF-alpha and TGF-beta2. The expression of type IV collagen at the mRNA level was upregulated by TNF-alpha and TGF-beta2. Its protein expression was promoted by only TNF-alpha. CONCLUSIONS: Type IV collagen and laminin are the main components of the lens capsule. Their production of LECs could be increased by cytokines derived from the aqueous humor or LECs. This may lead to ECM deposition and capsule fibrosis during the development of posterior capsule opacification.

Detection of integrins in cataract lens epithelial cells.

PURPOSE: To detect the expression of integrin subunits in lens epithelial cells (LECs) of human cataracts. SETTING: Research Laboratory, International Intraocular Implant Training Centre, Tianjin Medical University, China. METHODS: The circular sections of the anterior capsules with attached LECs were obtained during cataract surgery from 100 patients. The LECs were stained with an avidin-biotin-complex immunohistochemical technique using 5 monoclonal antibodies specific for alpha subunits 2, 3, 5 and beta subunits 1, 2. RESULTS: All integrin subunits studied were found to varying degrees in specimens. The positive percentages were 70%, 65%, 75%, 70%, and 80%, respectively. CONCLUSION: Integrin subunits were present in LECs of human cataracts. These molecules may serve in the adhesion of LECs to the lens capsule and play a role in cell-posterior capsule interaction after cataract surgery.