Study of domestic wastewater treatment bymacrophyte plant in Arid Region of South-east Algeria (case of el oued region)

Removal of wastewater pollution by natural treatment systems such as wetlands is achieved using filter media and macrophytes plants. The functioning of constructed wetlands relies on physical, chemical and biological processes. The aim of the present study is to evaluate the performance of the Phragmites australis for domestic wastewater  treatment under an arid climate. Experiments were conducted during three months (February, March and April). Results indicate that the variation of pH values of raw and treated wastewater is not significant. The electrical conductivity increases strongly during March and April. It was also found that dissolved oxygen in planted filter exceeds that of the unplanted one. Also, the higher performance in BOD and Ntot removal by the planted filter confirms the important role of this plant in the treatment process.Keywords: Pollution; wetlands; filter media; performance; Phragmites australis

Tribbles 2 pseudokinase confers enzalutamide resistance in prostate cancer by promoting lineage plasticity

Enzalutamide, a second-generation antiandrogen, is commonly prescribed for the therapy of advanced prostate cancer, but enzalutamide-resistant, lethal, or incurable disease invariably develops. To understand the molecular mechanism(s) behind enzalutamide resistance, here, we comprehensively analyzed a range of prostate tumors and clinically relevant models by gene expression array, immunohistochemistry, and Western blot, which revealed that enzalutamide-resistant prostate cancer cells and tumors overexpress the pseudokinase, Tribbles 2 (TRIB2). Inhibition of TRIB2 decreases the viability of enzalutamide-resistant prostate cancer cells, suggesting a critical role of TRIB2 in these cells. Moreover, the overexpression of TRIB2 confers resistance in prostate cancer cells to clinically relevant doses of enzalutamide, and this resistance is lost upon inhibition of TRIB2. Interestingly, we found that TRIB2 downregulates the luminal markers androgen receptor and cytokeratin 8 in prostate cancer cells but upregulates the neuronal transcription factor BRN2 (Brain-2) and the stemness factor SOX2 (SRY-box 2) to induce neuroendocrine characteristics. Finally, we show that inhibition of either TRIB2 or its downstream targets, BRN2 or SOX2, resensitizes resistant prostate cancer cells to enzalutamide. Thus, TRIB2 emerges as a potential new regulator of transdifferentiation that confers enzalutamide resistance in prostate cancer cells via a mechanism involving increased cellular plasticity and lineage switching

Burden, associated risk factors and adverse outcomes of gestational diabetes mellitus in twin pregnancies in Al Ain, UAE

Background: Gestational diabetes mellitus (GDM) in singleton pregnancies represent a high-risk scenario. The incidence, associated factors and outcomes of GDM in twin pregnancies is not known in the UAE. Methods: This was five years retrospective analysis of hospital records of twin pregnancies in the city of Al Ain, Abu Dhabi, UAE. Relevant data with regards to the pregnancy, maternal and birth outcomes and incidence of GDM was extracted from two major hospitals in the city. Regression models assessed the relationship between socio-demographic and pregnancy-related variables and GDM, and the associations between GDM and maternal and fetal outcomes at birth. Results: A total of 404 women and their neonates were part of this study. The study population had a mean age of 30.1 (SD: 5.3), overweight or obese (66.5%) and were majority multiparous (66.6%). High incidence of GDM in twin pregnancies (27.0%). While there were no statistical differences in outcomes of the neonates, GDM mothers were older (OR: 1.09, 95% CI: 1.06-1.4) and heavier (aOR: 1.02, 95% CI: 1.00-1.04). They were also likely to have had GDM in their previous pregnancies (aOR: 7.37, 95% CI: 2.76-19.73). The prognosis of mothers with twin pregnancies and GDM lead to an independent and increased odds of cesarean section (aOR: 2.34, 95% CI: 1.03-5.30) and hospitalization during pregnancy (aOR: 1.60, 95% CI: 1.16-2.20). Conclusion: More than a quarter of women with twin pregnancies were diagnosed with GDM. GDM was associated with some adverse pregnancy outcomes but not fetal outcomes in this population. More studies are needed to further investigate these associations and the management of GDM in twin pregnancies.</p

Burden, associated risk factors and adverse outcomes of gestational diabetes mellitus in twin pregnancies in Al Ain, UAE

Background: Gestational diabetes mellitus (GDM) in singleton pregnancies represent a high-risk scenario. The incidence, associated factors and outcomes of GDM in twin pregnancies is not known in the UAE. Methods: This was five years retrospective analysis of hospital records of twin pregnancies in the city of Al Ain, Abu Dhabi, UAE. Relevant data with regards to the pregnancy, maternal and birth outcomes and incidence of GDM was extracted from two major hospitals in the city. Regression models assessed the relationship between socio-demographic and pregnancy-related variables and GDM, and the associations between GDM and maternal and fetal outcomes at birth. Results: A total of 404 women and their neonates were part of this study. The study population had a mean age of 30.1 (SD: 5.3), overweight or obese (66.5%) and were majority multiparous (66.6%). High incidence of GDM in twin pregnancies (27.0%). While there were no statistical differences in outcomes of the neonates, GDM mothers were older (OR: 1.09, 95% CI: 1.06-1.4) and heavier (aOR: 1.02, 95% CI: 1.00-1.04). They were also likely to have had GDM in their previous pregnancies (aOR: 7.37, 95% CI: 2.76-19.73). The prognosis of mothers with twin pregnancies and GDM lead to an independent and increased odds of cesarean section (aOR: 2.34, 95% CI: 1.03-5.30) and hospitalization during pregnancy (aOR: 1.60, 95% CI: 1.16-2.20). Conclusion: More than a quarter of women with twin pregnancies were diagnosed with GDM. GDM was associated with some adverse pregnancy outcomes but not fetal outcomes in this population. More studies are needed to further investigate these associations and the management of GDM in twin pregnancies.</p

Indoor Air Pollutants and Health in the United Arab Emirates

Background: Comprehensive global data on the health effects of indoor air pollutants are lacking. There are few large population-based multi–air pollutant health assessments. Further, little is known about indoor air health risks in the Middle East, especially in countries undergoing rapid economic development

Androgen deprivation upregulates SPINK1 expression and potentiates cellular plasticity in prostate cancer

Emergence of an aggressive androgen receptor (AR)-independent neuroendocrine prostate cancer (NEPC) after androgen-deprivation therapy (ADT) is well-known. Nevertheless, the majority of advanced-stage prostate cancer patients, including those with SPINK1-positive subtype, are treated with AR-antagonists. Here, we show AR and its corepressor, REST, function as transcriptional-repressors of SPINK1, and AR-antagonists alleviate this repression leading to SPINK1 upregulation. Increased SOX2 expression during NE-transdifferentiation transactivates SPINK1, a critical-player for maintenance of NE-phenotype. SPINK1 elicits epithelial-mesenchymal-transition, stemness and cellular-plasticity. Conversely, pharmacological Casein Kinase-1 inhibition stabilizes REST, which in cooperation with AR causes SPINK1 transcriptional-repression and impedes SPINK1-mediated oncogenesis. Elevated levels of SPINK1 and NEPC markers are observed in the tumors of AR-antagonists treated mice, and in a subset of NEPC patients, implicating a plausible role of SPINK1 in treatment-related NEPC. Collectively, our findings provide an explanation for the paradoxical clinical-outcomes after ADT, possibly due to SPINK1 upregulation, and offers a strategy for adjuvant therapies

Trop-2 is up-regulated in invasive prostate cancer and displaces FAK from focal contacts

In this study, we show that the transmembrane glycoprotein Trop-2 is up-regulated in human prostate cancer (PCa) with extracapsular extension (stages pT3/pT4) as compared to organ-confined (stage pT2) PCa. Consistent with this evidence, Trop-2 expression is found to be increased in metastatic prostate tumors of Transgenic Adenocarcinoma of Mouse Prostate mice and to strongly correlate with α5β1 integrin levels. Using PCa cells, we show that Trop-2 specifically associates with the α5 integrin subunit, as binding to α3 is not observed, and that Trop-2 displaces focal adhesion kinase from focal contacts. In support of the role of Trop-2 as a promoter of PCa metastatic phenotype, we observe high expression of this molecule in exosomes purified from Trop-2-positive PCa cells. These vesicles are then found to promote migration of Trop-2-negative PCa cells on fibronectin, an α5β1 integrin/focal adhesion kinase substrate, thus suggesting that the biological function of Trop-2 may be propagated to recipient cells. In summary, our findings show that Trop-2 promotes an α5β1 integrin-dependent pro-metastatic signaling pathway in PCa cells and that the altered expression of Trop-2 may be utilized for early identification of capsule-invading PCa

Effects of Diabetes Prevention Education Program for Overweight and Obese Subjects with a Family History of Type 2 Diabetes Mellitus: A Pilot Study from the United Arab Emirates

Objectives: The association of obesity and family history of type 2 diabetes mellitus (T2DM) provides an opportunity for risk stratification and prevention, as these two conditions are the most well-known risk factors for T2DM. We aimed to test the feasibility and effects of a diabetes mellitus prevention education program designed for overweight and obese Emirati people with at least one parent with T2DM. Methods: We conducted a pilot study using a pre-post design without a control arm at the Diabetes Center at Tawam Hospital in Al Ain, UAE. Overweight and obese subjects with at least one parent with T2DM were invited to participate. Three study assessments were conducted at baseline, three months, and six months including a questionnaire, anthropometry, and laboratory assessments. Interventions included three individualized or family-engaged counseling sessions based on the DiAlert protocol. The study outcomes included awareness of risks and prevention opportunities to T2DM, behavior changes in nutrition and exercise, decreased waist-circumference, and clinical/metabolic/inflammatory markers. Pre-post changes were analyzed using repeated-measures analysis of variance. Results: One hundred twenty-two overweight or obese individuals were approached. Forty-four individuals met the eligibility criteria, and 32 individuals (35.0±9.0 years; 75.0% female) completed the study. At six months, there were significant improvements in the glycated hemoglobin levels (p = 0.007), high-density lipoprotein (p < 0.049), serum creatinine (p < 0.025), estimated glomerular filtration rate (p = 0.009), and adiponectin levels (p < 0.024). Sixteen of 32 participants had ≥ 2 cm reduction in waist circumference. They demonstrated notable physical and laboratory improvements in moderate-vigorous activity, average activity counts per day, tumor necrosis factor-alpha, and interleukin-6 total cholesterol, triglyceride, and low-density lipoprotein. Conclusions: Offering family-oriented diabetes education to people at risk for T2DM is well received and has favorable effects on relevant risk factors. Better testing with large-scale randomized controlled studies is needed, and implementing similar educational programs for the Emirati population seems warranted

UCHL1 Is a Potential Molecular Indicator and Therapeutic Target for Neuroendocrine Carcinomas

Neuroendocrine carcinomas, such as neuroendocrine prostate cancer and small-cell lung cancer, commonly have a poor prognosis and limited therapeutic options. We report that ubiquitin carboxy-terminal hydrolase L1 (UCHL1), a deubiquitinating enzyme, is elevated in tissues and plasma from patients with neuroendocrine carcinomas. Loss of UCHL1 decreases tumor growth and inhibits metastasis of these malignancies. UCHL1 maintains neuroendocrine differentiation and promotes cancer progression by regulating nucleoporin, POM121, and p53. UCHL1 binds, deubiquitinates, and stabilizes POM121 to regulate POM121-associated nuclear transport of E2F1 and c-MYC. Treatment with the UCHL1 inhibitor LDN-57444 slows tumor growth and metastasis across neuroendocrine carcinomas. The combination of UCHL1 inhibitors with cisplatin, the standard of care used for neuroendocrine carcinomas, significantly delays tumor growth in pre-clinical settings. Our study reveals mechanisms of UCHL1 function in regulating the progression of neuroendocrine carcinomas and identifies UCHL1 as a therapeutic target and potential molecular indicator for diagnosing and monitoring treatment responses in these malignancies

Opposing transcriptional programs of KLF5 and AR emerge during therapy for advanced prostate cancer.

Endocrine therapies for prostate cancer inhibit the androgen receptor (AR) transcription factor. In most cases, AR activity resumes during therapy and drives progression to castration-resistant prostate cancer (CRPC). However, therapy can also promote lineage plasticity and select for AR-independent phenotypes that are uniformly lethal. Here, we demonstrate the stem cell transcription factor Krüppel-like factor 5 (KLF5) is low or absent in prostate cancers prior to endocrine therapy, but induced in a subset of CRPC, including CRPC displaying lineage plasticity. KLF5 and AR physically interact on chromatin and drive opposing transcriptional programs, with KLF5 promoting cellular migration, anchorage-independent growth, and basal epithelial cell phenotypes. We identify ERBB2 as a point of transcriptional convergence displaying activation by KLF5 and repression by AR. ERBB2 inhibitors preferentially block KLF5-driven oncogenic phenotypes. These findings implicate KLF5 as an oncogene that can be upregulated in CRPC to oppose AR activities and promote lineage plasticity