Wolbachia in Antarctic terrestrial invertebrates: Absent or undiscovered?

Interactions between a host organism and its associated microbiota, including symbiotic bacteria, play a crucial role in host adaptation to changing environmental conditions. Antarctica provides a unique environment for the establishment and maintenance of symbiotic relationships. One of the most extensively studied symbiotic bacteria in invertebrates is Wolbachia pipientis, which is associated with a wide variety of invertebrates.

Larval morphology of Belgica antarctica Jacobs, 1900 (Diptera, Chironomidae, Orthocladiinae) from central part of the maritime Antarctic and deformities found in the larvae.

The larval morphology of the endemic species Belgica antarctica Jacobs, collected in January and February (2022) from six sites of Antarctica, was studied. The mouth apparatus and the parapods of one hundred seventy-six larvae were analyzed. No differences were found in the morphology of these structures between individuals of different sites.

External Morphology of Larvae of Jacobs, 1900 (Diptera, Chironomidae) Obtained from Two Locations in Maritime Antarctica.

The external morphology of the fourth-instar larva of the Antarctic endemic chironomid midge is described. Larvae were collected from Jougla Point (Wiencke Island) and an un-named island close to Enterprise Island, off the coast of the western Antarctic Peninsula. Light microscopy was used to examine and document photographically the structures of the mouthparts (mandible, mentum, premandible, labrum), antennae, pecten epipharyngis, clypeus, frontal apotome and posterior parapods.

Belgica antarctica (Diptera: Chironomidae): A natural model organism for extreme environments.

Belgica antarctica (Diptera: Chironomidae), a brachypterous midge endemic to the maritime Antarctic, was first described in 1900. Over more than a century of study, a vast amount of information has been compiled on the species (3 750 000 Google search results as of January 10, 2021), encompassing its ecology and biology, life cycle and reproduction, polytene chromosomes, physiology, biochemistry and, increasingly, omics. In 2014, B.

Vitamin D Signaling Suppresses Early Prostate Carcinogenesis in TgAPT Mice.

We tested whether lifelong modification of vitamin D signaling can alter the progression of early prostate carcinogenesis in studies using mice that develop high-grade prostatic intraepithelial neoplasia that is similar to humans. Two tissue-limited models showed that prostate vitamin D receptor (VDR) loss increased prostate carcinogenesis. In another study, we fed diets with three vitamin D levels (inadequate = 25 IU/kg diet, adequate for bone health = 150 IU/kg, or high = 1,000 IU/kg) and two calcium levels (adequate for bone health = 0.

Schlafen 12 Interaction with SerpinB12 and Deubiquitylases Drives Human Enterocyte Differentiation.

Background/aims: Human enterocytic differentiation is altered during development, fasting, adaptation, and bariatric surgery, but its intracellular control remains unclear. We hypothesized that Schlafen 12 (SLFN12) regulates enterocyte differentiation.

Methods: We used laser capture dissection of epithelium, qRT-PCR, and immunohistochemistry to evaluate SLFN12 expression in biopsies of control and fasting human duodenal mucosa, and viral overexpression and siRNA to trace the SLFN12 pathway in human Caco-2 and HIEC6 intestinal epithelial cells.

Schlafen 12 expression modulates prostate cancer cell differentiation.

Background: Schlafen proteins have previously been linked to leukocyte and intestinal epithelial differentiation. We hypothesized that Schlafen 12 (SLFN12) overexpression in human prostate epithelial cells would modulate expression of prostate-specific antigen (PSA) and dipeptidyl peptidase 4 (DPP4), markers of prostatic epithelial differentiation.

Materials And Methods: Differentiation of the human prostate cancer cell lines LNCaP and PC-3 was compared after infection with an adenoviral vector coding for SLFN12 (Ad-SLFN12) or green fluorescent protein (GFP) only expressing virus (control).

Regulation of epithelial differentiation in rat intestine by intraluminal delivery of an adenoviral vector or silencing RNA coding for Schlafen 3.

Although we stimulate enterocytic proliferation to ameliorate short gut syndrome or mucosal atrophy, less effort has been directed at enterocytic differentiation. Schlafen 3 (Slfn3) is a poorly understood protein induced during IEC-6 enterocytic differentiation. We hypothesized that exogenous manipulation of Slfn3 would regulate enterocytic differentiation in vivo.

The correlation between the expression of differentiation markers in rat small intestinal mucosa and the transcript levels of schlafen 3.

Importance: The normal absorptive function and structural maintenance of the intestinal mucosa depend on a constant process of proliferation of enterocytic stem cells followed by progressive differentiation toward a mature phenotype. The mechanisms that govern enterocytic differentiation in the mucosa of the small intestine are poorly understood.

Objective: To determine whether schlafen 3 (but not other schlafen proteins) act in vivo and whether its effects are limited to the small intestine.

Influence of defunctionalization and mechanical forces on intestinal epithelial wound healing.

The influence on mucosal healing of luminal nutrient flow and the forces it creates are poorly understood. We hypothesized that altered deformation and extracellular pressure mediate, in part, the effects of defunctionalization on mucosal healing. We created patent or partially obstructing defunctionalizing jejunal Roux-en-Y anastomoses in rats to investigate mucosal healing in the absence or presence of luminal nutrient flow and measured luminal pressures to document partial obstruction.

Loss of MLK3 signaling impedes ulcer healing by modulating MAPK signaling in mouse intestinal mucosa.

Mixed-lineage kinase 3 (MLK3) activates multiple MAPK pathways and can initiate apoptosis, proliferation, migration, or differentiation in different cell types. However, whether MLK3 signaling regulates intestinal epithelial cell sheet migration in vivo is not known. We sought to investigate whether MLK3 signaling is important in intestinal mucosal healing and epithelial cell motility in vivo and in vitro.

Changes in morphology and function in small intestinal mucosa after Roux-en-Y surgery in a rat model.

Background: Currently there is no an appropriate model to study intestinal mucosal atrophy in vivo that preserves the nutritional status of the organism.

Materials And Methods: We created a defunctionalized segment of jejunum via a dead-end Roux-en-Y anastomosis in rats. We compared tissue morphometric parameters in the intestinal mucosa of the defunctionalized bowel with that of the mucosa proximal and distal to the anastomosis.

Dietary vitamin D and vitamin D receptor level modulate epithelial cell proliferation and apoptosis in the prostate.

Low vitamin D (VD) status may increase prostate cancer risk but experimental evidence for this relationship is modest. We tested whether low VD status or VD receptor (VDR) deletion influences prostate epithelial cell (PEC) biology using intact mice, castrated mice, or castrated mice treated with testosterone propionate (TP, 2.5 mg/kg BW).

Constitutive activation of the mitogen-activated protein kinase pathway impairs vitamin D signaling in human prostate epithelial cells.

We studied the effect of prolonged activation of mitogen-activated protein kinase (MAPK) signaling on 1,25 dihydroxyvitamin D (1,25(OH)(2)D(3)) action in the immortalized human prostate epithelial cell line RWPE1 and its Ki-Ras transformed clone RWPE2. 1,25(OH)(2)D(3)-treatment caused growth arrest and induced gene expression in both cell lines but the response was blunted in RWPE2 cells. Vitamin D receptor (VDR) levels were lower in RWPE2 cells but VDR over-expression did not increase vitamin-D-mediated gene transcription in either cell line.

1,25 dihydroxyvitamin D-mediated orchestration of anticancer, transcript-level effects in the immortalized, non-transformed prostate epithelial cell line, RWPE1.

Background: Prostate cancer is the second leading cause of cancer mortality among US men. Epidemiological evidence suggests that high vitamin D status protects men from prostate cancer and the active form of vitamin D, 1alpha,25 dihydroxyvitamin D3 (1,25(OH)2D) has anti-cancer effects in cultured prostate cells. Still, the molecular mechanisms and the gene targets for vitamin D-mediated prostate cancer prevention are unknown.