fspring in their initial development and adult behavior, indicating the safety of its use during gestation and lactation. Organophosphates (OPs) are widely used as pesticides and have been employed as warfare agents. OPs inhibit acetylcholinesterase, leading to over-stimulation of cholinergic synapses and can cause status epilepticus (SE). OPs poisoning can result in irreversible brain damage and death. Despite termination of SE, recurrent seizures and abnormal brain activity remain common sequelae often associated with long-term neural damage and cognitive dysfunction. Therefore, early treatment for prevention of seizures is of high interest. Using a rat model of paraoxon poisoning, we tested the efficacy of different neuroprotective and anti-epileptic drugs (AEDs) in suppressing early seizures and preventing brain damage. Electrocorticographic recordings were performed prior, during and after injection of 4.5 LD50 paraoxon, followed by injections of atropine and toxogonin (obidoxime) to prevent death. Thirty minutes later, rats were injected with midazolam alone or in combination with different AEDs (lorazepam, valproic acid, phenytoin) or neuroprotective drugs (losartan, isoflurane). Outcome measures included SE duration, early seizures frequency and epileptiform activity duration in the first 24 -hs after poisoning. To assess delayed brain damage, we performed T2-weighted magnetic resonance imaging one month after poisoning. SE duration and the number of recurrent seizures were not affected by the addition of any of the drugs tested. Delayed brain injury was most prominent in the septum, striatum, amygdala and piriform network. Only isoflurane anesthesia significantly reduced brain damage. We show that acute treatment with isoflurane, but not AEDs, reduces brain damage following SE. This may offer a new therapeutic approach for exposed individuals. Lysophosphatidylcholine (LPC) is the main component of oxidatively damaged low-density lipoprotein (oxLDL). LPC originates from the cleavage of phosphatidylcholine by phospholipase A2 (PLA2). LPC plays a biological role by binding to G protein-coupled receptors and Toll-like receptors. LPC can induce the migration of lymphocytes and macrophages, increase the production of pro-inflammatory cytokines, induce oxidative stress, and promote apoptosis, which can aggregate inflammation and promote the development of diseases. The effects of LPC on endothelial cells, vascular smooth muscle cells and arteries play a vital role in the progression of atherosclerosis and other cardiovascular diseases. In addition, the regulation of inflammation by LPC plays different roles in inflammatory and infectious diseases. In diabetes, LPC can induce insulin resistance. On the other hand, it can decrease blood glucose. The concentration of LPC varies in different tumours. LPC plays an important role in the invasion, metastasis and prognosis of tumours.  https://www.selleckchem.com/products/gdc-0994.html  Therefore, targeting LPC and lipid metabolism might be a potential therapeutic method for inflammation-related diseases. AIMS Nonhuman primates have been used to investigate pathogenic mechanisms and evaluate immune responses following Chlamydia trachomatis inoculation. This study aimed to systemically profile antibody responses to C. trachomatis infection in nonhuman primates. MATERIALS AND METHODS Sera were obtained from 4 pig-tailed and 8 long-tailed macaques which were intravaginally or ocularly infected with live C. trachomatis organisms, and analyzed by C. trachomatis proteome array of antigens. KEY FINDINGS The sera from 12 macaques recognized total 172 C. trachomatis antigens. While 84 antigens were recognized by pig-tailed macaques intravaginally infected with serovar D strain, 125 antigens were recognized by long-tailed macaques ocularly infected with serovar A, and 37 antigens were recognized by both. Ocular inoculation with virulent A2497 strain induced antibodies to more antigens. Among the antigens uniquely recognized by A2497 strain infected macaques, outer membrane complex B antigen (OmcB) induced robust antibody response. Although macaques infected by less virulent A/HAR-13 strain failed to develop antibodies to OmcB, reinfection by A2497 strain induced high levels of antibodies to OmcB. SIGNIFICANCE Proteome array has revealed a correlation of chlamydial infection invasiveness with chlamydial antigen immunogenicity, and identified antibody responses to OmcB potentially as biomarkers for invasive infection with C. trachomatis. This review critically evaluates the sunscreen delivery and toxicity field. We chose to focus on approved sunscreens in this review. Optimal sunscreen use prevents skin cancer and photoageing but there is an important knowledge gap in sunscreen/skin interactions. Sunscreen delivery is a key for efficacy, but studying sunscreen delivery is not straightforward. We review the strengths and weaknesses of in vitro, excised skin and clinical approaches. Understanding positive and negative sunscreen effects on skin homeostasis is also challenging. The results in this field, especially in vitro testing, are controversial and experimental design varies widely which further supports disparities between some findings. We hypothesize that bias towards showing sunscreen toxicity to increase impact could be problematic. We explore that perception through a detailed review of experimental design, especially in cell culture models. Our conclusion is that emerging, non- and minimally invasive technologies are enabling new approaches to volunteer studies that could significantly improve knowledge of sunscreen delivery and interactions. V.OBJECTIVES Lipoprotein lipase (LPL) catalyzes the hydrolysis of circulating triglycerides into free fatty acids (FFA) and thereby promotes FFA uptake in peripheral tissues. LPL is negatively regulated by angiopoietin-like protein 4 (ANGPTL4) presumably by an FFA-dependent mechanism. Growth hormone (GH) suppresses LPL activity, but it is unknown whether this is mediated by FFA and ANGPTL4. Therefore, we investigated the concerted effect of GH on ANGPTL4 and LPL in the presence and absence of lipolysis in two in vivo studies in human subjects. METHODS In a randomized, placebo-controlled, cross-over study, nine obese men were examined after injection of 1) a GH bolus, and 2) a GH-receptor antagonist followed by four adipose tissue biopsies obtained over a 5-h period. In a second study, nine hypopituitary men were examined in a 2 × 2 factorial design including GH and acipimox (an anti-lipolytic agent), with biopsies from adipose tissue and skeletal muscle obtained during a basal period and a subsequent hyperinsulinemic-euglycemic clamp.