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The insect midgut epithelium represents an interface between the internal and the external environment and it is the almost unique epithelial tissue by which these arthropods acquire nutrients. This epithelium is indeed able to produce digestive enzymes and to support vectorial transport of small organic nutrients, ions, and water. Moreover, it plays a key role in the defense against pathogenic microorganisms and in shaping gut microbiota. Another important midgut function is the ability to produce signaling molecules that regulate its own physiology and the activity of other organs. The two main mature cell types present in the midgut of all insects, i.e., columnar and endocrine cells, are responsible for these functions. In addition, stem cells, located at the base of the midgut epithelium, ensure the growth and renewal of the midgut during development and after injury. In insects belonging to specific orders, midgut physiology is deeply conditioned by the presence of unique cell types, i.e., goblet and copper cells, which confer peculiar features to this organ. This review reports current knowledge on the cells that form the insect midgut epithelium, focusing attention on their morphological and functional features. Notwithstanding the apparent structural simplicity of this organ, the properties of the cells make the midgut a key player in insect development and homeostasis.

Insect pests negatively affect crop quality and yield; identifying new methods to protect crops against insects therefore has important agricultural applications. Our analysis of transgenic Arabidopsis thaliana plants showed that overexpression of pentacyclic triterpene synthase 1 , encoding the key biosynthetic enzyme for the natural plant product (3E)-4,8-dimethyl-1,3,7-nonatriene (DMNT), led to a significant resistance against a major insect pest, Plutella xylostella . DMNT treatment severely damaged the peritrophic matrix (PM), a physical barrier isolating food and pathogens from the midgut wall cells. DMNT repressed the expression of PxMucin in midgut cells, and knocking down PxMucin resulted in PM rupture and P. xylostella death. A 16S RNA survey revealed that DMNT significantly disrupted midgut microbiota populations and that midgut microbes were essential for DMNT-induced killing. Therefore, we propose that the midgut microbiota assists DMNT in killing P. xylostella . These findings may provide a novel approach for plant protection against P. xylostella .

[This corrects the article DOI: 10.1371/journal.ppat.1007470.].

Modulation of nutrient digestion and absorption is one of the post-ingestion mechanisms that guarantees the best exploitation of food resources, even when they are nutritionally poor or unbalanced, and plays a pivotal role in generalist feeders, which experience an extreme variability in diet composition. Among insects, the larvae of black soldier fly (BSF), Hermetia illucens, can grow on a wide range of feeding substrates with different nutrient content, suggesting that they can set in motion post-ingestion processes to match their nutritional requirements. In the present study we address this issue by investigating how the BSF larval midgut adapts to diets with different nutrient content. Two rearing substrates were compared: a nutritionally balanced diet for dipteran larvae and a nutritionally poor diet that mimics fruit and vegetable waste. Our data show that larval growth performance is only moderately affected by the nutritionally poor diet, while differences in the activity of digestive enzymes, midgut cell morphology, and accumulation of long-term storage molecules can be observed, indicating that diet-dependent adaptation processes in the midgut ensure the exploitation of poor substrates. Midgut transcriptome analysis of larvae reared on the two substrates showed that genes with important functions in digestion and absorption are differentially expressed, confirming the adaptability of this organ.

We report a case of reversed rotation (RR) of the midgut, the rarest form of intestinal malrotation (IMR), revealed by a chronic volvulus, in a 42-year-old woman presenting with episodes of abdominal pain occurring after heavy meals. The complete preoperative diagnosis was obtained by contrast-enhanced computed tomography (CT). Classical signs of volvulus were associated with typical findings of RR comprising an unusual position of the third duodenum in front of the mesenteric vessels and a very unusual location of the transverse colon behind these vessels. Complete absence of fixation of the right colon allowed secondary volvulus. A detailed reminder of the embryology of IMR and RR is presented.

Purpose & Methods Neuroendocrine neoplasms are a heterogenous group of tumours, for which nuclear medicine plays an important role in the diagnostic work-up as well as in the targeted therapeutic options. This guideline is aimed to assist nuclear medicine physicians in recommending, performing, reporting and interpreting the results of somatostatin receptor (SSTR) PET/CT imaging using Ga-68-DOTA-conjugated peptides, as well as F-18-DOPA imaging for various neuroendocrine neoplasms. Results & Conclusion The previous procedural guideline by EANM regarding the use PET/CT tumour imaging with Ga-68-conjugated peptides has been revised and updated with the relevant and recent literature in the field with contribution of distinguished experts.

Autophagy-dependent cell death can be defined as cell demise that has a strict requirement of autophagy. Although autophagy often accompanies cell death following many toxic insults, the requirement of autophagic machinery for cell death execution, as established through specific genetic or chemical inhibition of the process, is highly contextual. During animal development, perhaps the best validated model of autophagy-dependent cell death is the degradation of the larval midgut during larval–pupal metamorphosis, where a number of key autophagy genes are required for the removal of the tissues. Surprisingly though, even in the midgut, not all of the ‘canonical’ autophagic machinery appears to be required. In other organisms and cancer cells many variations of autophagy-dependent cell death are apparent, pointing to the lack of a unifying cell death pathway. It is thus possible that components of the autophagy machinery are selectively utilised or repurposed for this type of cell death. In this review, we discuss examples of cell death that utilise autophagy machinery (or part thereof), the current knowledge of the complexity of autophagy-dependent cellular demise and the potential mechanisms and regulatory pathways involved in such cell death.

In patients with midgut neuroendocrine tumors that progressed during octreotide analogue therapy, the addition of 177 Lu-Dotatate to octreotide resulted in an 18% response rate and a significantly higher rate of progression-free survival at 20 months than high-dose octreotide alone. Neuroendocrine tumors of the midgut (which is defined as the jejunoileum and the proximal colon) commonly metastasize to the mesentery, peritoneum, and liver and are frequently associated with the carcinoid syndrome. 1 , 2 Neuroendocrine tumors of the midgut represent the most common type of malignant gastrointestinal neuroendocrine tumors and are associated with 5-year survival rates of less than 50% among persons with metastatic disease. 3 , 4 First-line systemic therapy usually consists of a somatostatin analogue for control of both hormonal secretion and tumor growth. 5 – 7 With the exception of everolimus for the treatment of nonfunctional neuroendocrine tumors, 8 no standard second-line systemic treatment . . .

The gastrointestinal tract has recently come to the forefront of multiple research fields. It is now recognized as a major source of signals modulating food intake, insulin secretion and energy balance. It is also a key player in immunity and, through its interaction with microbiota, can shape our physiology and behavior in complex and sometimes unexpected ways. The insect intestine had remained, by comparison, relatively unexplored until the identification of adult somatic stem cells in the Drosophila intestine over a decade ago. Since then, a growing scientific community has exploited the genetic amenability of this insect organ in powerful and creative ways. By doing so, we have shed light on a broad range of biological questions revolving around stem cells and their niches, interorgan signaling and immunity. Despite their relatively recent discovery, some of the mechanisms active in the intestine of flies have already been shown to be more widely applicable to other gastrointestinal systems, and may therefore become relevant in the context of human pathologies such as gastrointestinal cancers, aging, or obesity. This review summarizes our current knowledge of both the formation and function of the Drosophila melanogaster digestive tract, with a major focus on its main digestive/absorptive portion: the strikingly adaptable adult midgut.

The yellow fever mosquito, Aedes aegypti, is distributed worldwide and transmits viruses that cause many diseases, including dengue, yellow fever, chikungunya, and zika. Epigenetic modifications such as acetylation of histones regulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs) control insect development. We recently reported that the Creb-binding protein (a HAT) regulates the metamorphosis of A. aegypti. However, the function of HDACs in A. aegypti is not known. In this study, we identified 10 genes coding for HDACs in A. aegypti and determined their function in larval development using RNA interference (RNAi). Knockdown of each HDAC has a distinct effect on the growth, development, and metamorphosis of A. aegypti. Knockdown of HDAC3 severely affected the larval survival, indicating its indispensable role in larval development. HDAC3 is highly expressed during the larval stages, and its messenger RNA (mRNA) levels correlate with the juvenile hormone (JH) titers. JH induces the expression of HDAC3 through its receptor, methoprenetolerant (Met). Knockdown of HDAC3 resulted in increased expression of proapoptotic genes involved in apoptosis of larval midgut cells. This consequently decreased midgut size and led to larval death. HDAC3 deacetylates histone H4 localized at the promoters of proapoptotic genes and suppresses their expression. In addition, a corepressor, SMRTER, is required for HDAC3-mediated suppression of proapoptotic genes. Interestingly, ecdysone attenuates HDAC3-mediated repression of proapoptotic genes. These data demonstrate that JH-induced HDAC3 is a key player in JH suppression of precocious larval cell death and metamorphosis in A. aegypti.