Macronutrients in the gastrointestinal (GI) lumen are able to activate "intestinal brakes", feedback mechanisms on proximal GI motility and secretion including appetite and energy intake. In this review, we provide a detailed overview of the current evidence with respect to four questions (1) are regional differences (duodenum, jejunum, ileum) present in the intestinal luminal nutrient modulation of appetite and energy intake? (2) is this "intestinal brake" effect macronutrient specific? (3) is this "intestinal brake" effect maintained during repetitive activation? (4) can the "intestinal brake" effect be activated via non-caloric tastants? Recent evidence indicates that (1) regional differences exist in the intestinal modulation of appetite and energy intake with a proximal to distal gradient for inhibition of energy intake ileum and jejunum > duodenum at low but not at high caloric infusion rates. (2) the "intestinal brake" effect on appetite and energy appears not to be macronutrient specific. At equi-caloric amounts, the inhibition on energy intake and appetite is in the same range for fat, protein and carbohydrate. (3) data on repetitive ileal brake activation are scarce because of the need for prolonged intestinal intubation. see more During repetitive activation of the ileal brake for up to 4 days, no adaptation was observed but overall the inhibitory effect on energy intake was small. (4) the concept of influencing energy intake by intra-intestinal delivery of non-caloric tastants is intriguing. Among tastants, the bitter compounds appear to be more effective in influencing energy intake. Energy intake decreases modestly after post-oral delivery of bitter tastants or a combination of tastants (bitter, sweet and umami). Intestinal brake activation provides an interesting concept for preventive and therapeutic approaches in weight management strategies.With the rise of 5G, Internet of Things (IoT), and networks operating in the mmWave frequencies, a huge growth of connected sensors will be a reality, and high gain antennas will be desired to compensate for the propagation issues, and with low cost, characteristics inherent to metallic radiating structures. 3D printing technology is a possible solution in this way, as it can print an object with high precision at a reduced cost. This paper presents different methods to fabricate typical metal antennas using 3D printing technology. These techniques were applied as an example to pyramidal horn antennas designed for a central frequency of 28 GHz. Two techniques were used to metallize a structure that was printed with polylactic acid (PLA), one with copper tape and other with a conductive spray-paint. A third method consists of printing an antenna completely using a conductive filament. All prototypes combine good results with low production cost. The antenna printed with the conductive filament achieved a better gain than the other structures and showed a larger bandwidth. The analysis recognizes the vast potential of these 3D-printed structures for IoT applications, as an alternative to producing conventional commercial antennas.Previously, DNA microarrays analysis showed that, in co-culture with Bacillus subtilis, a biosynthetic gene cluster anchored with a nonribosomal peptides synthetase of Aspergillus niger is downregulated. Based on phylogenetic and synteny analyses, we show here that this gene cluster, NRRL3_00036-NRRL3_00042, comprises genes predicted to encode a nonribosomal peptides synthetase, a FAD-binding domain-containing protein, an uncharacterized protein, a transporter, a cytochrome P450 protein, a NAD(P)-binding domain-containing protein and a transcription factor. We overexpressed the in-cluster transcription factor gene NRRL3_00042. The overexpression strain, NRRL3_00042OE, displays reduced growth rate and production of a yellow pigment, which by mass spectrometric analysis corresponds to two compounds with masses of 409.1384 and 425.1331. We deleted the gene encoding the NRRL3_00036 nonribosomal peptides synthetase in the NRRL3_00042OE strain. The resulting strain reverted to the wild-type phenotype. These results suggest that the biosynthetic gene cluster anchored by the NRRL3_00036 nonribosomal peptides synthetase gene is regulated by the in-cluster transcriptional regulator gene NRRL3_00042, and that it is involved in the production of two previously uncharacterized compounds. Silver Diammine Fluoride (SDF) is an emerging caries preventive treatment option that is inexpensive, safe, and easily accessible. The evidence is clear that the use of SDF at concentrations of 38% is effective for arresting caries in primary teeth. However, the determination of an optimal SDF application frequency for a cavitated lesion in pragmatic settings is warranted especially among high dental caries risk groups. Hence, the primary objective of this clinical trial is to compare the effectiveness of annual, bi-annual, and four times a year application of 38% SDF application in arresting active coronal dentinal carious lesions on primary teeth among tribal preschool children aged 2-6 years. Methods and Analysis This study is designed as a randomized, controlled trial consisting of three parallel arms with an allocation ratio of 111. The trial will enroll 480 preschool tribal children with a cavitated carious lesion (2-6 years) attending a primary health care Centre in Wayanad district, India. Each arm proved by Institutional Review Committee (IRB). This trial has been registered prospectively with the Clinical Trial Registry of India [Registration No CTRI/2020/03/024265].Although programmed death-ligand 1 (PD-L1) expression on tumor tissue is a validated predictive biomarker for a PD-1 pathway blockade in non-small cell lung cancer (NSCLC), longitudinal changes in its expression during treatment remains elusive. Circulating tumor cells (CTCs) are assumed to reflect the transition of characteristics of the primary tumor undergoing anticancer treatment. Here, we sequentially evaluated the PD-L1 expression on CTCs in NSCLC patients treated with nivolumab. Forty-five patients were enrolled, and CTCs were enriched from 3 mL of peripheral blood using a microcavity array system at baseline and weeks 4, 8, 12, and 24 or until progressive disease. The effective responses to therapy were compared between patients without progressive disease (PD) at week 8 (i.e., non-PD patients) and in those with PD between weeks 4 and 8 (PD patients) in terms of increased vs. decreased or equal CTC status at week 8 (for non-PD patients) or at the point of PD (for PD patients) compared to the baseline.