High-flow nasal cannula therapy for pediatric obstructive sleep apnea: a systematic review and meta-analysis.

OBJECTIVE: Heated and humidified high-flow nasal cannula (HFNC) therapy has been used to manage different respiratory conditions in pediatric patients. However, no review has summarized its efficacy for the management of pediatric obstructive sleep apnea (OSA). MATERIALS AND METHODS: PubMed, Embase, CENTRAL, and Google Scholar were searched for all types of studies assessing the efficacy of HFNC for pediatric OSA. We compared pre-treatment and post-treatment obstructive apnea-hypopnea index (OAHI), obstructive hypopnea index (OHI), obstructive apnea index (OAI), SPO2 nadir and SPO2 mean values in a random-effect meta-analysis model. RESULTS: Six studies reporting data of 67 pediatric patients treated with HFNC were included. Most of the data were from one-time titration. Meta-analysis revealed a statistically significant reduction in OAHI with HFNC therapy (MD: 15.58 95% CI: 8.30, 22.86 I2=77% p=0.001). Similarly, pooled analysis revealed that both OHI (MD: 12.35 95% CI: 0.78, 23.92 I2=98% p=0.04) and OAI (MD: 7.54 95% CI: 2.10, 12.98 I2=79% p=0.007) were significantly reduced with HFNC treatment. Also, HFNC led to statistically significant improvement in SPO2 nadir values (MD: -8.17 95% CI: -10.40, -5.94 I2=21% p<0.00001) but it did not change the mean SPO2 values before and after treatment (MD: -0.85 95% CI: -1.94, 0.25 I2=52% p=0.13). CONCLUSIONS: Evidence from a limited number of heterogeneous and uncontrolled titration studies indicates that HFNC improves OAHI and minimum oxygen saturation in pediatric patients with OSA. However, further research is required on the long-term efficacy and compliance of HFNC therapy with a focus on different pediatric age groups.

MiR-98-5p regulates proliferation and metastasis of MCF-7 breast cancer cells by targeting Gab2.

The article "MiR-98-5p regulates proliferation and metastasis of MCF-7 breast cancer cells by targeting Gab2, by X.-Y. Shi, H. Wang, W. Wang, Y.-H. Gu, published in Eur Rev Med Pharmacol Sci 2019; 23 (7): 2847-2855-DOI: 10.26355/eurrev_201904_17562-PMID: 31002135" has been withdrawn from the authors. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17562.

MiR-98-5p regulates proliferation and metastasis of MCF-7 breast cancer cells by targeting Gab2.

OBJECTIVE: The aim of this study was to explore the mechanism of miR-98-5p in influencing the malignant proliferation and metastasis capacities of breast cancer cells. PATIENTS AND METHODS: Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) was used to detect the expression level of miR-98-5p and GRB2-associated-binding protein 2 (Gab2) in breast cancer samples and cells. On-line target gene prediction software and Dual-Luciferase reporter assay were used to predict and verify the target genes of miR-98-5p, respectively. Cell proliferation was measured by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay. Meanwhile, migration and invasion abilities, as well as the changes of epithelial-mesenchymal transition (EMT) after transfection were detected by transwell assay and Western blot assay, respectively. RESULTS: Compared with adjacent non-tumor tissues and MCF-10A cells, the expression level of miR-98-5p in tumor tissues and MCF-7 cells was significantly declined, whereas Gab2 was markedly up-regulated. Besides, Gab2 was predicted as a target gene of miR-98-5p. Subsequent experiments indicated that the proliferation, migration, invasion and EMT of MCF-7 cells transfected with miR-98-5p were significantly inhibited. However, up-regulation of Gab2 attenuated the biological function of miR-98-5p on malignant abilities of breast cancer cells. CONCLUSIONS: We showed that miR-98-5p served as anti-oncogene in breast cancer, which might provide a new therapeutic target for its treatment.

Long-term exposure to gaseous formaldehyde promotes allergen-specific IgE-mediated immune responses in a murine model.

It has long been questioned that whether exposure to formaldehyde in indoor environments may be a risk factor for developing allergen-specific IgE-mediated inflammatory responses, because there is limited clinical or experimental evidence that formaldehyde is involved in the cascade for IgE production. There is no known lower limit, below which there is no threat of serious allergic symptoms. The present study illustrates that the threshold limit of formaldehyde, 0.08 ppm (as defined by the World Health Organization), did not cause ovalbumin-specific IgE inflammatory immune responses, but higher than threshold concentrations of formaldehyde gas result in both enhanced allergen-specific IgE responses and NK (Natural Killer)-cell activity in peripheral blood cells in a murine model. Thus, formaldehyde gas may be involved in promoting allergic inflammatory effects in subjects primed with specific allergens by NK-cell activation. These results indicate that even threshold concentrations of formaldehyde gas may play a regulatory role for 'systemic' cell-mediated immune responses. The extensive use of adhesives for building materials has resulted in higher levels of indoor air pollutants. It is conceivable that increased time indoors may enhance pre-existing allergic symptoms by concomitant exposure to volatile organic compounds and formaldehyde. The affordable limit for formaldehyde might be much lower than currently established levels in indoor environments.

Paclitacxel and carboplatin in advanced non-small-cell lung cancer.

To evaluate the efficacy and toxicity of the combination of paclitacxel and carboplatin on advanced non-small-cell lung cancer (NSCLC). Forty-eight patients with locally advanced (stage IIIb) or metastatic (stage IV) NSCLC were enrolled into the study. The patients received paclitacxel 55-60 mg/m(2) on day 1, 8, 15, carboplatin at an AUC of 5 on day 1, administreted in 28-day cycle. An objective response was obtained in 37.5% of patients (two complete and 16 partial responses). Significant difference existed between the naive patients and pretreated patients (46.4% vs. 25.0%, P<0.05). The main toxicities were bone marrow suppression, nausea/vomiting and alopecia. The combination of paclitacxel and carboplatin is an effective, well-tolerated scheme in the treatment of advanced NSCLC. The efficacy is higher in the naive group than in the pretreated group.

Role of three commonly used scoring systems in prediction of pulmonary thromboembolism in Xining area.

OBJECTIVE: To analyze the clinical values of three commonly used scoring systems including Wells score, revised Geneva score and Pisa score in predicting pulmonary thromboembolism (PTE) in Xining area. PATIENTS AND METHODS: A total of 67 patients who had received CT pulmonary angiography (CTPA) in Qinghai Provincial People's Hospital from January 1, 2008 to July 31, 2010 due to suspected acute PTE were enrolled in this study. Among them 30 were confirmed to be with acute PTE and 37 were excluded. The risk of PTE was evaluated using the Wells score, the revised Geneva score, and Pisa score in all these patients. Clinical values of these scoring systems in diagnosis of PTE were compared using the receiver operating characteristic (ROC) curves; and CTPA values as the standard. The diagnostic accuracies were also compared. RESULTS: The probability of PTE was 33.3% (14/42) when the Wells score was <2, 89.47% (17/19) when the Wells score was 2-6, and 100% (6/6) when the Wells score was above 6. The probability of PTE was 31.71% (13/40) when the revised Geneva score was 0-3, 85.0% (17/20) when the revised Geneva score was 4-10, and 100% (7/7) when the revised Geneva score was ≥11, suggesting that PTE might be associated with the revised Geneva score (p<0.001). When Pisa score was used, the probability of PTE was 20.59% (7/34), at ≥10%, 76.92% (10/13), at 10% to 90%, and 100% (20/20) at >90% score. The AUCs for all three scoring systems showed significant differences (p<0.05). CONCLUSIONS: Thus, the Pisa score showed a relatively higher clinical value in Xining area to predict clinical probability of PTE in patients, with its overall sensitivity and specificity being higher than the Wells and revised Geneva score.

Neuroprotection of ethanol against ischemia/reperfusion-induced brain injury through decreasing c-Jun N-terminal kinase 3 (JNK3) activation by enhancing GABA release.

Our latest study indicated that ethanol could attenuate cerebral ischemia/reperfusion-induced brain injury through activating Ionotropic glutamate receptors Kainate Family (Gluk1)-kainate (KA) receptors and gamma-aminobutyric acid (GABA) receptors. However, the possible mechanism of the neuroprotective effects of ethanol remains unclear. In this study we report that ethanol shows neuroprotective effects against ischemic brain injury through enhancing GABA release and then decreasing c-Jun N-terminal kinase 3 (JNK3) activation. Electrophysiologic recording indicated that ethanol enhances GABA release from presynaptic neurons and the released GABA subsequently inhibits the KA receptor-mediated whole-cell currents. Moreover, our data show that ethanol can inhibit the increased assembly of the Gluk2-PSD-95-MLK3 (postsynaptic density protein-95, PSD-95 and mixed-lineage kinase 3, MLK3) module induced by cerebral ischemia and the activation of the MLK3-MKK4/7-JNK (mitogen-activated protein kinase kinase 4/7, MKK4/7) cascade. Pretreatment of the GABA(A) receptor antagonist bicuculline and antagonist of VGCC (a broad-spectrum blocker of the voltage-gated calcium channel [VGCC]) Chromic (CdCl(2)) can demolish the neuroprotective effects of ethanol. The results suggest that during ischemia-reperfusion, ethanol may activate presynaptic Gluk1-KA and facilitate Ca(2+)-dependent GABA release. The released GABA activates postsynaptic GABA(A) receptors, which suppress the ischemic depolarization and decrease the association of signaling module Gluk2-PSD-95-MLK3 induced by the activation of postsynaptic Gluk2-KA receptors. There is a raised possibility that ethanol inhibiting the JNK3 apoptotic pathway (MLK3/MKK4/7/JNK3/c-Jun/Fas-L) performs a neuroprotective function against ischemic brain injury.

Effect of copper and diethyldithiocarbamate combination therapy on the macular mouse, an animal model of Menkes disease.

Menkes disease (MD) is a neurodegenerative disorder characterized by a copper deficiency in the brain. It is caused by the defective intestinal absorption of copper resulting from a deficiency of a copper-transporting ATPase, ATP7A. This gives rise to an accumulation of copper in the intestine. The copper deficiency in the brain of MD patients cannot be improved by copper injections, because the administered copper accumulates at the blood-brain barrier and is not transported across to the neurons. To resolve this problem, we investigated the effect of a combination therapy of copper and sodium diethyldithiocarbamate (DEDTC), a lypophilic chelator, in an animal model of MD, the macular mouse. Four-week-old macular mice treated with 50 mug of CuCl2 on the 7th day after birth were used. Experimental mice were given a subcutaneous injection of CuCl2 (4 microg) and an intraperitoneal injection of DEDTC (0.2 mg/g body weight) twice a week for 4 weeks and then sacrificed. Copper concentrations and cytochrome-c oxidase activity in the brains of treated mice were higher than those of control macular mice, which received only copper or saline. The ratios of brain noradrenaline to dopamine and of adrenaline to dopamine were also increased by the treatment, suggesting that the activity of dopamine beta-hydroxylase, a copper-dependent enzyme, was improved by the treatment. Liver and renal function tests showed no abnormalities in the treated mice, although copper concentrations in the kidneys of treated mice were higher than those of control macular mice. These results suggest that DEDTC facilitates the passage of copper across the blood-brain barrier and that the combination therapy of copper and DEDTC may be an effective treatment for the neurological disturbances suffered by patients with MD.