Gripping and holding of objects are key tasks for robotic manipulators. The development of universal grippers able to pick up unfamiliar objects of widely varying shape and surface properties remains, however, challenging. Most current designs are based on the multifingered hand, but this approach introduces hardware and software complexities. These include large numbers of controllable joints, the need for force sensing if objects are to be handled securely without crushing them, and the computational overhead to decide how much stress each finger should apply and where. Here we demonstrate a completely different approach to a universal gripper. Individual fingers are replaced by a single mass of granular material that, when pressed onto a target object, flows around it and conforms to its shape. Upon application of a vacuum the granular material contracts and hardens quickly to pinch and hold the object without requiring sensory feedback. We find that volume changes of less than 0.5% suffice to grip objects reliably and hold them with forces exceeding many times their weight. We show that the operating principle is the ability of granular materials to transition between an unjammed, deformable state and a jammed state with solid-like rigidity. We delineate three separate mechanisms, friction, suction, and interlocking, that contribute to the gripping force. Using a simple model we relate each of them to the mechanical strength of the jammed state. This advance opens up new possibilities for the design of simple, yet highly adaptive systems that excel at fast gripping of complex objects.stress-strain | packing density | friction | suction | interlocking

Human microbial colonization begins at birth and continues to develop and modulate in species abundance for about 3 years, until the microbiota becomes adult-like. During the same time period, children experience significant developmental changes that influence their health status as well as their immune system. An ever-expanding number of articles associate several diseases with early-life imbalances of the gut microbiota, also referred to as gut microbial dysbiosis. Whether early-life dysbiosis precedes and plays a role in disease pathogenesis, or simply originates from the disease process itself is a question that is beginning to be answered in a few diseases, including IBD, obesity, and asthma. This review describes the gut microbiome structure and function during the formative first years of life, as well as the environmental factors that determine its composition. It also aims to discuss the recent advances in understanding the role of the early-life gut microbiota in the development of immune-mediated, metabolic, and neurological diseases. A greater understanding of how the early-life gut microbiota impacts our immune development could potentially lead to novel microbial-derived therapies that target disease prevention at an early age.

SUMMARY Mucus production by goblet cells of the large intestine serves as a crucial anti microbial protective mechanism at the interface between the eukaryotic and prokaryotic cells of the mammalian intestinal ecosystem. However, the regulatory pathways involved in goblet cell-induced mucus secretion remain largely unknown. Here we demonstrate that the NLRP6 inflammasome, a recently described regulator of colonic microbiota composition and bio-geographical distribution, is a critical orchestrator of goblet cell mucin granule exocytosis. NLRP6 deficiency leads to defective autophagy in goblet cells and abrogated mucin secretion into the large intestinal lumen. Consequently, NLRP6 inflammasome-deficient mice are unable to clear enteric pathogens from the mucosal surface, rendering them highly susceptible to persistent infection. This study identifies the first innate immune regulatory pathway governing goblet cell mucus secretion, linking non-hematopoietic inflammasome signaling to autophagy and highlighting the goblet cell as a critical innate immune player in the control of intestinal host-microbial mutualism.

BackgroundFecal bacteriotherapy (‘stool transplant’) can be effective in treating recurrent Clostridium difficile infection, but concerns of donor infection transmission and patient acceptance limit its use. Here we describe the use of a stool substitute preparation, made from purified intestinal bacterial cultures derived from a single healthy donor, to treat recurrent C. difficile infection that had failed repeated standard antibiotics. Thirty-three isolates were recovered from a healthy donor stool sample. Two patients who had failed at least three courses of metronidazole or vancomycin underwent colonoscopy and the mixture was infused throughout the right and mid colon. Pre-treatment and post-treatment stool samples were analyzed by 16 S rRNA gene sequencing using the Ion Torrent platform.ResultsBoth patients were infected with the hyper virulent C. difficile strain, ribotype 078. Following stool substitute treatment, each patient reverted to their normal bowel pattern within 2 to 3 days and remained symptom-free at 6 months. The analysis demonstrated that rRNA sequences found in the stool substitute were rare in the pre-treatment stool samples but constituted over 25% of the sequences up to 6 months after treatment.ConclusionThis proof-of-principle study demonstrates that a stool substitute mixture comprising a multi-species community of bacteria is capable of curing antibiotic-resistant C. difficile colitis. This benefit correlates with major changes in stool microbial profile and these changes reflect isolates from the synthetic mixture.Trial registrationClinical trial registration number: CinicalTrials.gov NCT01372943