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Abstract

 

Purpose: We aimed at evaluating urinary levels of procollagen III aminoterminal propeptide (PIIINP) and β-catenin and the relationship between these markers and clinical and laboratory variables in children with a solitary functioning kidney (SFK).

 

Patients and methods: The study group consisted of 98 (M/F: 62/36) children with an SFK with a median age of 8 years. An age-matched control group contained 54 healthy peers. Urinary levels of procollagen III aminoterminal propeptide and β-catenin were measured using a commercially available immunoassay kit.

 

Results: The urinary values of PIIINP (UPIIINP) were significantly increased in patients with SFK versus controls (p?<?0.01). Our analysis revealed no significant differences in urinary β-catenin levels between the SFK patients and control subjects (p?>?0.05). Only urinary PIIINP levels were correlated to renal function tests, such as serum creatinine, urea, uric acid, and estimated glomerular filtration rate (p<0.05).

 

Conclusions: An increased urinary level of PIIINP may indicate early kidney impairment in children with SFK. Urinary β-catenin does not seem to play any important role as a marker of renal function in children with SFK. Further long-term studies are required in order to evaluate the clinical usefulness of these markers and their predictive value of chronic kidney disease (CKD) progression.

Abstract

 

Background

Breast cancer remains the most common female malignancy and metastasis is the leading cause of death in breast cancer patients. Oldenlandia diffusa has been empirically and extensively used as an adjuvant therapy for metastatic breast cancer patients in Traditional Chinese Medicine (TCM) with proven efficacy. However, its anti-metastasis mechanism has been poorly revealed.

 

Methods

Multiple molecular biology experiments as well as network pharmacology, bioinformatics analysis were conducted to investigate the anti-metastasis mechanism of Oldenlandia diffusa in breast cancer.

 

Results

We demonstrated that ethanol extract of Oldenlandia diffusa (EEOD) significantly inhibited proliferation and induced apoptosis of high-metastatic breast cancer cell lines MDA-MB-231 and MDA-MB-453, while having no obvious cytotoxic effect on multiple nonmalignant cells. Furthermore, EEOD remarkably suppressed the migration and invasion capacities of the above breast cancer cells by modulating the matrix metalloproteinases (MMPs) and the epithelial-mesenchymal transition (EMT) pathway. More importantly, EEOD also significantly inhibited breast cancer metastasis in zebrafish xenotransplantation model in vivo. Network pharmacology and bioinformatics analysis further demonstrated that EEOD yielded 12 candidate compounds and 225 potential targets, and shared 85 putative targets associated with breast cancer metastasis. Mechanistically, RNA sequencing and experimental validation results suggested that EEOD might inhibit breast cancer metastasis by attenuating the expression of caveolin-1 (Cav-1) as overexpression of Cav-1 could weaken the anti-metastasis efficacy of EEOD.

 

Conclusions

Overall, our findings proved that EEOD could inhibit breast cancer metastasis by attenuating the expression of Cav-1, highlighting the use of EEOD as an adjunctive therapy for metastatic breast cancer patients. This study also provides novel insights into network pharmacology and bioinformatics analysis as effective tools to illuminate the scientific basis of TCM.

Abstract

 

Lithium (Li+) ion due to its excellent bioactivity is one of the most well-studied element in bone-tissue engineering. In this study, we fabricated nanohydroxyapatite (nHAp) doped with Li+ ions (5?mol% Li+:nHAp) and co-doped with lanthanide ions. We investigated the effects of nHAp, 5?mol% Li+:nHAp or Li+ alone, on osteogenic differentiation of human Adipose Tissue-derived Stem Cells (hASCs), their proliferation, mitochondrial dynamics and apoptosis. Moreover, we monitored cell proliferation after treatment with samarium (III) (Sm3+) and europium (III) (Eu3+) ions co-doped 5?mol% Li+:nHAp as well as their luminescent property. The hASCs treated with 5?mol% Li+:nHAp and Li+ ions proliferated more rapidly and differentiated effectively than control cells without undergoing apoptosis. Both, 5?mol% Li+:nHAp and Li+ ions improved osteogenic differentiation of hASCs. Moreover they decreased expression of glycogen synthase kinase 3β (GSK3β) while increased β-catenin mRNA level. In addition, Li+, nHAp and 5?mol% Li+:nHAp improved mitochondrial dynamics and enhanced expression of neural differentiation marker genes. Collectively, the study indicates on pro-osteogenic and anti-apoptotic properties of nHAp doped with Li+ and Li+ alone. Moreover, unique properties of 5?mol% Li+:nHAp and 5?mol% Li+:nHAp co-doped with rare earth ions, such as Sm3+ and Eu3+ have shed a promising light on their potential application in theranostics.

Therapeutic potential of endothelial progenitor cells in a rat model of epilepsy: Role of autophagy

Posted by N N. Shahin, M M. Safar, S M. Rizk, et al. on 2019-02-28 10:16:00

Abstract

 

Epilepsy is one of the most well-known neurological conditions worldwide. One-third of adult epileptic patients do not respond to antiepileptic drugs or surgical treatment and therefore suffer from the resistant type of epilepsy. Stem cells have been given substantial consideration in the field of epilepsy therapeutics. The implication of pathologic vascular response in sustained seizures and the eminent role of endothelial progenitor cells (EPCs) in maintaining vascular integrity tempted us to investigate the potential therapeutic effects of EPCs in a pentylenetetrazole (PTZ)-induced rat model of epilepsy. Modulation of autophagy, a process that enables neurons to maintain an equilibrium of synthesis, degradation and subsequent reprocessing of cellular components, has been targeted. Intravenously administered EPCs homed into the hippocampus and amended the deficits in memory and locomotor activity. The cells mitigated neurological damage and the associated histopathological alterations and boosted the expression of brain-derived neurotrophic factor. EPCs corrected the perturbations in neurotransmitter activity and enhanced the expression of the downregulated autophagy proteins light chain protein-3 (LC-3), beclin-1, and autophagy-related gene-7 (ATG-7). Generally, these effects were comparable to those achieved by the reference antiepileptic drug, valproic acid. In conclusion, EPCs may confer therapeutic effects against epilepsy and its associated behavioural and biochemical abnormalities at least in part via the upregulation of autophagy. The study warrants further research in experimental and clinical settings to verify the prospect of using EPCs as a valid therapeutic strategy in patients with epilepsy.


Abstract

Background
Major symptoms of chronic obstructive pulmonary disease (COPD) are chronic bronchitis and emphysema leading from lung tissue destruction, that is an effect of an imbalance between metalloproteinases (MMPs) and their tissue inhibitors activity. As potential factor involved in this COPD pathogenesis, MMP-12 is considered. We investigated the role of genetic polymorphism and protein level of MMP-12 in the COPD development among Poles.

Methods
We analyzed ??82 A?>?G SNP in the promoter region of MMP-12 gene (rs2276109) among 335 smoked COPD patients and 309 healthy individuals, including 110 smokers. Additionally, 60 COPD patients and 61 controls (23 smokers) were tested for serum levels of MMP-12 using ELISA. All subjects were analyzed for lung function using spirometry (FEV1% and FEV1/FVC parameters).

Results
We observed that -82G allele and -82GG homozygous genotype frequencies of the SNP rs2276109 were significantly lower in COPD patients than in controls (12.5% vs 16.9%, respectively; X2?=?4.742, p?=?0.02 for allele and 0.5% vs 3.9%, respectively; X2?=?9.0331, p?=?0.01 for genotype). Moreover, -82G allele was more frequent in controls smokers than in non-smokers (22.3% vs 14.1%, X2?=?6.7588, p?=?0.01). Serum level of MMP-12 was significantly higher in COPD patients than in controls groups (6.8?ng/ml vs 3.3?ng/ml, respectively; F?=?7.433, p?<?0.0001), although independently of analyzed gene polymorphisms. Additionally, no correlation between parameters of lung function (FEV1% and FEV1/FVC) and protein level was found.

Conclusions
We found that -82G allele of SNP rs2276109 was associated with reduced risk of COPD, and COPD patients released more MMP-12 than healthy individuals, but independently on this SNP.

Keywords
COPD Metalloproteinase 12 Genetics SNP ELISA

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