Associations of diet with infectious diseases in UK Biobank.

This research aims to utilize multivariate logistic regression to explore associations between the frequency of 13 food groups intake (or four diet groups) and infectious diseases. 487849 participants from the UK Biobank were enrolled, and 75209 participants were diagnosed with infectious diseases. Participants reporting the highest intake frequency of processed meat [odds ratio ( OR) = 1.0964; 95% CI: 1.0622-1.1318] and red meat ( OR = 1.0895; 95% CI: 1.0563-1.1239) had a higher risk of infectious diseases compared to those with the lowest intake frequency. Consuming fish 2.0-2.9 times ( OR = 0.8221; 95% CI: 0.7955-0.8496), cheese ≥5.0 times ( OR = 0.8822; 95% CI: 0.8559-0.9092), fruit 3.0-3.9 servings ( OR = 0.8867; 95% CI: 0.8661-0.9078), and vegetables 2.0-2.9 servings ( OR = 0.9372; 95% CI: 0.9189-0.9559) per week were associated with a lower risk of infection. Low meat-eaters ( OR = 0.9404; 95% CI: 0.9243-0.9567), fish-eaters ( OR = 0.8391; 95% CI: 0.7887-0.8919), and vegetarians ( OR = 0.9154; 95% CI: 0.8561-0.9778) had a lower risk of infectious diseases compared to regular meat-eaters. Mediation analysis was performed, revealing glycosylated hemoglobin, white blood cell counts, and body mass index were mediators in the relationships between diet groups and infectious diseases. This study suggested that intake frequency of food groups is a factor in infectious diseases and fish-eaters have a lower risk of infection.

Injectable Zn2+ and Paeoniflorin Release Hydrogel for Promoting Wound Healing.

As more and more superbugs emerge, wounds are struggling to heal due to the inflammation that accompanies infection. Therefore, there is an urgent need to reduce the abuse of antibiotics and find nonantibiotic antimicrobial methods to counter infections to accelerate wound healing. In addition, common wound dressings struggle to cover irregular wounds, causing bacterial invasion or poor drug release, which reduces the wound healing rate. In this study, Chinese medicinal monomer paeoniflorin which can inhibit inflammation is loaded in mesoporous zinc oxide nanoparticles (mZnO), while Zn2+ released from mZnO degradation can kill bacteria and facilitate wound healing. The drug-loaded mZnO was encapsulated by a hydrogel formed from oxidized konjac glucomannan and carboxymethyl chitosan via rapid Schiff base reaction to obtain an injectable drug-releasing hydrogel wound dressing. The immediate-formation hydrogel allows the dressing to cover any wound shape. In vitro and in vivo studies have demonstrated that the dressing has good biocompatibility and superior antibacterial properties, which can promote wound healing and tissue regeneration by promoting angiogenesis and collagen production, providing a promising perspective for the further development of multifunctional wound dressings.

Diversity of Circulating NKT Cells in Defense against Carbapenem-Resistant Klebsiella Pneumoniae Infection.

Nosocomial infection caused by carbapenem-resistant Klebsiella pneumonia (CRKP) infection has become a global public health problem. Human NK and NKT cells in peripheral immune responses are recognized as occupying a critical role in anti-bacterial immunity. Through performed scRNA-seq on serial peripheral blood samples from 3 patients with CRKP undergoing colonization, infection, and recovery conditions, we were able to described the immune responses of NK and NKT cells during CRKP infection and identified a mechanism that could contribute to CRKP clearance. The central player of CRKP infection process appears to be the NKT subset and CD56hiNKT subset which maintained immune competence during CRKP colonization. With time, CRKP leads to the loss of NK and CD160hiNKT cells in peripheral blood, resulting in suppressed immune responses and increased susceptibility to opportunistic infection. In summary, our study identified a possible mechanism for the CRKP invasion and to decipher the clues behind the host immune response that influences CRKP infection pathogenesis.

Surgical treatment for type II macular hole retinal detachment in pathologic myopia.

To observe the effectiveness and complications of inverted internal limiting membrane insertion through 25-G minimally invasive vitrectomy assisted with autologous blood adhesion fixation and combined with gas tamponade type-II macular hole retinal detachment in pathologic myopia.This was a retrospective study. The best-corrected visual acuity, intraocular pressure, macular hole closure, retinal reattachment, and systemic and ocular adverse events were observed.Twenty-three eyes were operated. Best-corrected visual acuity before surgery and at 3 and 6 months were 2.25 ±â€Š0.47, 1.85 ±â€Š0.32, and 1.32 ±â€Š0.36 LogMAR (P < .001). On days 2 to 5, all the retinas reattached, and the macular holes closed. On days 5 to 9, 5 eyes showed increased intraocular pressure. At 2 and 4 months, 2 eyes showed retinal detachment recurrence. No serious systemic or ocular adverse events were observed.This surgical technique showed clinical benefits and no significant complications. Clinical trials are necessary to confirm efficacy and safety.

Treatment of refractory giant macular hole by vitrectomy with internal limiting membrane transplantation and autologous blood.

AIM: To investigate the effect of internal limiting membrane transplantation and autologous blood on treating refractory giant macular hole. METHODS: Thirty-seven eyes with giant macular hole of the smallest hole diameter >700 µm, the maximum diameter of the substrate >1000 µm and hole formation factor <0.6 underwent surgical treatment. The patients were randomly divided into two groups. Nineteen eyes with surgical flip of the internal limiting membrane in group A, 18 eyes with internal limiting membrane transplantation in group B who underwent the tamponade of internal limiting membrane into the hole, autologous plasma was used to seal the hole. The patients were followed up for 3mo, optical coherence tomography and best corrected visual acuity (BCVA) were recorded before and after operation, and the results were statistically analyzed. RESULTS: At 3mo after operation, BCVA of the two groups was significantly improved compared with that before operation (tA=4.192, tB=4.374, P<0.05). But there was no significant difference in visual acuity between the two groups (χ2=0.128, P>0.05). At 3mo after operation, the closure rate of group A was 68.4%, and 100% in group B. (χ2=5.628, P<0.05). The defect diameter of inner segment/outer segment at 3mo after the operation was significantly lower than that before operation (tA=12.287, tB=15.481, P<0.05), and the difference was statistically significant (t=2.552, P<0.05). CONCLUSION: Internal limiting membrane transplantation combined with autologous whole blood can improve the postoperative closure rate of the refractory large aperture, and can effectively improve the postoperative visual acuity.

Lentivirus-mediated shRNA interference of ghrelin receptor blocks proliferation in the colorectal cancer cells.

Ghrelin, an orexigenic peptide, acts via the growth hormone secretagogue receptor (GHSR) to stimulate the release of growth hormone. Moreover, it has a range of biological actions, including the stimulation of food intake, modulation of insulin signaling and cardiovascular effects. Recently, it has been demonstrated that ghrelin has a proliferative and antiapoptotic effects in cancers, suggesting a potential role in promoting tumor growth. However, it remains unknown whether GHSR contributes to colorectal cancer proliferation. In this study, the therapeutic effect of lentivirus-mediated short hairpin RNA (shRNA) targeting ghrelin receptor 1a (GHSR1a) was analyzed in colorectal cancer cell line SW480 both in vitro and in vivo. Our study demonstrated that ghrelin and GHSR1a are significantly upregulated in cancerous colorectal tissue samples and cell lines. In vitro, human colorectal cancer cell line SW480 with downregulation of GHSR1a by shRNA showed significant inhibition of cell viability compared with blank control (BC) or scrambled control (SC) regardless of the application of exogenous ghrelin. Furthermore, GHSR1a silencing by target specific shRNA was shown capable of increasing PTEN, inhibiting AKT phosphorylation and promoting the release of p53 in SW480 cells. In addition, the effects of GHSR1a knockdown were further explored in vivo using colorectal tumor xenograft mouse model. The tumor weights were decreased markedly in GHSR1α knockdown SW480 mouse xenograft tumors compared with blank control or negative control tumors. Our results suggested that the expression of GHSR1a is significantly correlated with the growth of colorectal cancer cells, and the GHSR1a knockdown approach may be a potential therapy for the treatment of colorectal cancer.

Twist promotes angiogenesis in pancreatic cancer by targeting miR-497/VEGFA axis.

Angiogenesis is a critical step in the growth and dissemination of malignant diseases, including pancreatic cancer. Twist has been shown to stimulate angiogenesis in the tumor site. However, whether Twist contributes to angiogenesis in pancreatic cancer remains unknown. In this paper, we found that the expression of Twist was significantly increased in human pancreatic cancer cell lines and pancreatic cancer specimens. It is also closely engaged to adverse clinical feature, diminished survival and angiogenesis in pancreatic cancer patients. The up-regulation of Twist was found to be promoting cell growth, invasion and tubule formation of human umbilical vein endothelial cells (HUVECs) in vitro. By contrast, the silencing of Twist inhibited orthotopic xenograft tumor growth, metastasis and angiogenesis. Subsequent investigations disclosed that Twist was regulated by miR-497 directly, leading to the increased level of Vascular Endothelial Growth Factor-A (VEGFA). Moreover, gain-of-function and loss-of-function studies demonstrated that miR-497 could suppress the pro-proliferative, angiogenic and metastatic ability of pancreatic cancer cells. The ectopic expression of VEGFA obviously abrogated the anti-angiogenic effect induced by Twist knockdown, whereas the silencing of VEGFA markedly rescued the pro-angiogenic effect of Twist. By analyzing the expression levels of miR-497, Twist was found inversely correlated with miR-497 in pancreatic cancer tissues, and a positive correlation was found between Twist and VEGFA levels in pancreatic cancer specimens. In conclusion, our results suggested that the Twist/miR-497/VEGFA axis is significantly correlated with metastasis and angiogenesis in pancreatic cancer.

miR-497 suppresses angiogenesis in breast carcinoma by targeting HIF-1α.

Angiogenesis is a key factor in the growth and dissemination of malignant diseases, including breast cancer, with significant implications for its clinical management. It is known that microRNAs (miRNAs) play important roles in regulating tumor properties in cancers. However, whether miR-497 contributes to breast cancer angiogenesis remains unknown. Our study demonstrated that miR-497 was significantly downregulated in breast cancer tissue samples and cell lines. Conditioned medium obtained from breast cancer cell line MCF-7, treated with miR-497 mimics, suppressed the proliferation and tube formation of human umbilical vein endothelial cells in vitro, in comparison with the untransfected cells or cells transfected with the control vector alone. Furthermore, western blot assay confirmed that the overexpression of miR-497 reduced VEGF and HIF-1α protein levels. In addition, stable transfection of miR-497 inhibited tumorigenicity and angiogenesis in vivo. Moreover, HIF-1α was also increased in the breast cancer cells under a hypoxic condition, while the ectopic expression of miR-497 partially restored its level. Taken together, our findings indicate that miR-497 is a potential target for the biological therapy of breast cancer. Moreover, miR-497 inhibited the growth of tumors and reduced angiogenesis in a nude mouse xenograft tumor model, which was probably caused by the downregulation of pro-angiogenic molecules, such as VEGF and HIF-1α.

miR-497 inhibits epithelial mesenchymal transition in breast carcinoma by targeting Slug.

Epithelial to mesenchymal transition (EMT) is a critical step in the growth and dissemination of malignant diseases, including breast cancer. It is known that microRNAs (miRNAs) play important roles in the regulation of tumor properties in cancers. However, whether miR-497 contributes to EMT in breast cancer cells remains unknown. Our study demonstrated that the expression of miR-497 was significantly decreased in human breast cancer cell lines and breast cancer specimens. In breast cancer cells, EMT was inhibited and promoted by the over-expression as well as depletion of miR-497, respectively. Dual-Luciferase ReporterAassay confirmed that Slug was a direct target of miR-497. The upregulation of miR-497 in breast cancer cells suppressed cell proliferation and induced apoptosis both in vitro and in vivo. Correlation analysis indicated that miR-497 was highly negatively correlated with Slug expression in breast cancer specimens. The knockdown of Slug expression in breast cancer cells significantly suppressed cell proliferation and promoted apoptosis. Our results suggested that the expression of miR-497 is significantly correlated with EMT in breast cancer cells by regulating Slug at the transcriptional as well as translational levels. Therefore, targeting miR-497 may provide a novel strategy for the treatment of breast cancer.