New information on the ecology of nest flies in their native habitat can inform conservation efforts and allow us to make recommendations for future research.The anionic surfactant linear alkylbenzene sulfonate (LAS) is a major chemical constituent of detergent formulation. Regarding the recalcitrant nature of sulfonoaromatic compounds, discharging these substances into wastewater collection systems is a real environmental issue. A study on LAS biodegradation based on bioelectrochemical treatment and in the form of developing a single-chamber microbial fuel cell with air cathode is reported in the present work. Pretreatment study showed LAS concentration of 60 ppm resulted in the highest anaerobic LAS removal of 57%; so, this concentration was chosen to run the MFC. After the sustained anodic biofilm was formed, LAS degradation rate during 4 days in MFC was roughly 76% higher than that in the serum bottle, which indicated the role of the bioelectrochemical process in improving anaerobic LAS removal. Additionally, through 16S rRNA gene sequencing, the dominant bacterial species in the biofilm was identified as Pseudomonas zhaodongensis NEAU-ST5-21(T) with about 98.9% phylogenetic similarity and then a pathway was proposed for LAS anaerobic biodegradation. The MFC characteristics were assessed by pH monitoring as well as scanning electron microscopy and current density evolution.Microglia-mediated neuroinflammation is widely perceived as a contributor to numerous neurological diseases and mental disorders including depression. Discs large homolog 1 (Dlg1), an adaptor protein, regulates cell polarization and the function of K+ channels, which are reported to regulate the activation of microglia. However, little is known about the role of Dlg1 in microglia and the maintenance of central nervous system homeostasis. In this study, we found that Dlg1 knockdown suppressed lipopolysaccharide (LPS)-induced inflammation by down-regulating the activation of nuclear factor-κB signaling and the mitogen-activated protein kinase pathway in microglia. Moreover, using an inducible Dlg1 microglia-specific knockout (Dlg1flox/flox; CX3CR1CreER) mouse line, we found that microglial Dlg1 knockout reduced the activation of microglia and alleviated the LPS-induced depression-like behavior. In summary, our results demonstrated that Dlg1 plays a critical role in microglial activation and thus provides a potential therapeutic target for the clinical treatment of depression.

Levamisole is frequently used as a steroid-sparing agent in children with steroid-sensitive nephrotic syndrome. Side effects, such as neutropenia, gastro-intestinal upset and skin rash, have been reported. We noted an increase in creatinine in some of our patients, but literature on the effect of levamisole on kidney function is lacking.

A retrospective cohort study was conducted, including patients 1-18years of age, treated for steroid-sensitive nephrotic syndrome with levamisole at Great Ormond Street Hospital for Children between January 2010 and January 2020. Data was collected on clinical observations and serum creatinine values before, during and after treatment. eGFR was calculated using the Schwartz equation.

In total, 75 children were included in the analysis. The median duration of treatment was 19 (IQR 12-27) months. The median estimated GFR was 134 (IQR 119-160), 101 (IQR 91-113) and 116 (IQR 106-153) ml/min/1.73m

, respectively, before, during and after treatment with levamisole. The difference between eGFR before and after treatment compared with during treatment was statically significant (P < 0.0001). During the treatment period, the eGFR decrease was not progressive. The median levamisole dose was 2.5 (IQR 2.3-2.6) mg/kg on alternate days, and the dose was not correlated with the decrease in eGFR (r = 0.07, 95% CI - 0.22 to 0.35).

Levamisole significantly decreases eGFR. However, this decrease is not progressive or irreversible and would not be an indication to discontinue the treatment.

Levamisole significantly decreases eGFR. However, this decrease is not progressive or irreversible and would not be an indication to discontinue the treatment.Onco-nephrology is a recent and evolving medical subspecialty devoted to the care of patients with kidney disease and unique kidney-related complications in the context of cancer and its treatments, recognizing that management of kidney disease as well as the cancer itself will improve survival and quality of life. While this area has received much attention in the adult medicine sphere, similar emphasis in the pediatric realm has not yet been realized. As in adults, kidney involvement in children with cancer extends beyond the time of initial diagnosis and treatment. Many interventions, such as chemotherapy, stem cell transplant, radiation, and nephrectomy, have long-term kidney effects, including the development of chronic kidney disease (CKD) with subsequent need for dialysis and/or kidney transplant. Thus, with the improved survival of children with malignancy comes the need for ongoing monitoring of kidney function and early mitigation of kidney-related comorbidities. In addition, children with kidney transplant are at higher risk of developing malignancies than their age-matched peers. Pediatric nephrologists thus need to be aware of issues related to cancer and its treatments as they impact their own patients. These facts emphasize the necessity of pediatric nephrologists and oncologists working closely together in managing these children and highlight the importance of bringing the onco-nephrology field to our growing list of pediatric nephrology subspecialties.

The effectiveness of rhGH on growth and final height (FH) was determined in children with CKD and kidney failure using data linkage from two national databases.

Data on Australian children with CKD and kidney failure treated with rhGH were obtained by linking ANZDATA and OzGrow registries. The CKD cohort included children treated with rhGH prior to kidney replacement therapy (KRT). The KRT cohort consisted of children with kidney failure, some received rhGH, and some were untreated. Height standard deviation scores (Ht-SDS) were calculated with final height defined as last height recorded in girls > 16 years of age and boys > 17 years of age.

In the CKD group, there were 214 children treated with rhGH prior to KRT. In the KRT group, there were 1,032 children, 202 (19%) treated with rhGH and 830 (81%) untreated. Growth significantly improved in the rhGH-treated CKD group (ΔHt-SDS = +0.80 [+0.68 to +0.92]; p < 0.001) and the rhGH-treated KRT group (ΔHt-SDS = +0.38 [+0.27 to +0.50]; p < 0.001). Within the KRT cohort, final height was available for 423 patients (41%), of which 137 (32%) had been treated with rhGH. The rhGH-treated group demonstrated marginally better catch-up growth (ΔHt-SDS = +0.05 [-0.18 to 0.29]) compared to the non-rhGH-treated group (ΔHt-SDS = -0.03 [-0.16 to 0.10]; p = 0.49).

This large linkage study confirms rhGH is effective in improving height in children with CKD pre-KRT. However, rhGH appears to have a variable impact on growth once children have commenced KRT resulting in a marginal impact on final height.

This large linkage study confirms rhGH is effective in improving height in children with CKD pre-KRT. However, rhGH appears to have a variable impact on growth once children have commenced KRT resulting in a marginal impact on final height.Receptor tyrosine kinases (RTKs) are frequently dysregulated in malignancies and important for the malignant characteristics of tumor cells. RTKs are attractive structures for drug targeting of cancer. The RTK ROR1 is of significance during embryogenesis but downregulated in post-partum tissues. However, ROR1 is overexpressed in several hematological and solid tumors and important for tumor cell proliferation, survival, migration, and metastasis. WNT5a is a main ligand for ROR1. Several clinical trials are ongoing using anti-ROR1 antibody based drugs directed against the external domain (monoclonal antibodies, BiTE, CAR-T). We have produced small molecules (KAN834/1571c) fitting to the ATP pocket of the intracellular tyrosine kinase (TK) domain of ROR1 (TK inhibitor, TKI). These inhibitors of ROR1 prevented ROR1 phosphorylation and inactivated the WNT/β-catenin independent as well as WNT/β-catenin dependent pathways. ROR1-TKI induced apoptosis of ROR1 positive fresh patient derived tumor cells and appropriate cell lines and a dose and time dependent tumor reduction in animal models. In combination with other clinically relevant targeting drugs as venetoclax a synergistic apoptotic effect was seen. Two other small molecules (ARI-1 and strictinin) bound also to ROR1 and inhibited tumor growth. Development of small molecule ROR1 inhibitors is warranted to include this novel therapeutic approach for cancer therapy.The WNT/β-catenin signalling pathway is a rich and complex network of cellular proteins that orchestrates diverse short-range cell-to-cell communication in metazoans and is essential for both embryonic development and adult homeostasis. Due to its fundamental importance in controlling cell behaviour at multiple levels, its deregulation is associated with a wide range of diseases in humans and identification of drugs targeting the pathway has attracted strong interest in the pharmaceutical sector. Transduction of WNT signals across the plasma membrane of cells involves a staggering degree of complexity and variety with respect to ligand-receptor, receptor-receptor and receptor-co-receptor interactions (Niehrs, Nat Rev Mol Cell Biol 13767-779, 2012). Although the low-density-lipoprotein-receptor-related-protein (LRP) family is best known for its role in binding and endocytosis of lipoproteins, specific members appear to have additional roles in cellular communication. Indeed, for WNT/β-catenin signalling one aphanistic aspects of LRP biology is also provided, together with the implications this has for pharmacological targeting of this notoriously intractable pathway.We examine the relationship between Internet-based health information seeking and the demand for physician services, using data collected from the 28 European Union states in 2014. Unlike previous research, our analysis distinguishes seekers of health information into those who use only non-Internet sources and those who use the Internet and possibly non-Internet sources. By comparing the frequencies of physician visits among the two groups of health information seekers and non-seekers, we infer the net association between online health information and the demand for physician services while partially controlling for the effects of concurrent seeking of offline health information. The following are the two key findings (1) individuals’ health status and sociodemographic factors shape online and offline health information seeking patterns in similar ways; and (2) the demand for physician services is positively associated with offline health information seeking and not with online health information. The net association with online health information would be even smaller after controlling for the effect of concurrent offline health information seeking. These results suggest that extending the availability of online health information would potentially reinforce the unequal access to health information, which could create greater variation in individuals’ health management skills and benefits from health care in the long term. However, it would be associated with little or no increase in the demand for physician services, unlike the implications of previous research.