Labile Soil Carbon Inputs Mediate the Soil Microbial Community Composition and Plant Residue Decomposition Rates

• Root carbon (C) inputs may regulate decomposition rates in soil, and in this study we ask: how do labile C inputs regulate decomposition of plant residues, and soil microbial communities? • In a 14 d laboratory incubation, we added C compounds often found in root exudates in seven different concentrations (0, 0.7, 1.4, 3.6, 7.2, 14.4 and 21.7 mg C g soil) to soils amended with and without 13C-labeled plant residue. We measured CO2 respiration and shifts in relative fungal and bacterial rRNA gene copy numbers using quantitative polymerase chain reaction (qPCR). • Increased labile C input enhanced total C respiration, but only addition of C at low concentrations (0.7 mg C g-1) stimulated plant residue decomposition (+2%). Intermediate concentrations (1.4, 3.6 mg C g-1) had no impact on plant residue decomposition, while greater concentrations of C (\u3e 7.2 mg C g-1) reduced decomposition -50%). Concurrently, high exudate concentrations (\u3e 3.6 mg C g-1) increased fungal and bacterial gene copy numbers, whereas low exudate concentrations (\u3c 3.6 mg C g-1) increased metabolic activity rather than gene copy numbers. • These results underscore that labile soil C inputs can regulate decomposition of more recalcitrant soil C by controlling the activity and relative abundance of fungi and bacteria

Iodine and goiter involution.

Iodine administration, although efficient in goiter treatment or prevention, is also responsible for adverse effects such as cell necrosis or thyroiditis. These two effects were reproduced in iodide-treated goitrous mice. Morphological observations strongly suggest that thyroid cell death results from an excessive production of free radicals, which initiates lipid peroxidation. This hypothesis is strengthened by the facts that the thyroidal concentration of malonic dialdehyde, a stable product of lipid peroxidation, is increased, and that necrosis is partially prevented by free radicals scavengers. Epithelial necrosis is associated to an inflammatory reaction. The infiltrate is mainly made of cells expressing class II molecules of major histocompatibility complex (macrophages and dendritic cells), but also of T lymphocytes. However, this inflammation, which varies among mouse strains, is transient and it is not amplified or maintained by administration of cytokines, IFN gamma or TNF alpha, known to induce class II expression on thyrocytes

Chronic pelvic pain and the role of exploratory laparoscopy as diagnostic and therapeutic tool: a retrospective observational study

Background: Forty percent of exploratory laparoscopies are performed for chronic pelvic pain (CPP). However, a final diagnosis is still unreported in 35% of the patients. We decided to evaluate the identification of pathological lesions and the improvement of painful symptoms in patients with CPP and normal physical examination and imaging and who are scheduled for exploratory laparoscopy. The prospective study was designed in a tertiary referral center for endometriosis. Forty-eight patients complaining of CPP and scheduled for exploratory laparoscopy were included. Pelvic pain intensity was assessed using the visual analogue pain scale (VAS), and at inclusion, negative clinical and imaging assessments were required. During exploratory laparoscopy, the recognized lesions were reported and different surgical treatment options were performed depending on the location of the lesion. Results: In 98% of the cases, exploratory laparoscopy demonstrated the presence of pelvic anomalies that had not been diagnosed at the time of clinical and imaging examination. After surgery, a significant improvement of CPP has been demonstrated in 24 (59%) patients with VAS < 5 postoperatively. Conclusions: Exploratory laparoscopy is reasonable in patients complaining of CPP, allowing a final diagnosis in a high percentage of patients and a significant improvement in pain symptom in 59% of the cases. This study was retrospectively registered by our local Ethics Committee on February 7, 2018 (B412201835729)

La goitrigenèse expérimentale.

Various modern aspects of experimental goitrogenesis are reviewed and discussed. Regulation of follicular cell proliferation clearly involves several stimulatory but also inhibitory mechanisms. Furthermore, different stimuli are probably involved. Growth of the vascular and connective interstitial tissue probably involves paracrine factors and that of the follicles maybe autocrine factors; indeed, several growth factors are secreted by stimulated follicular cells. The formation of nodules is still poorly understood. They could derive from different cell populations or from cells being in different reactivity status with respect to the variations of the iodine fluxes in the gland. Finally, the relationship between iodine toxicity, nodularity and autoimmunity are discussed

The non-obese diabetic (NOD) mouse: an animal model for autoimmune thyroiditis.

The NOD mouse, an ideal model for insulin-dependent diabetes mellitus, is also useful to study the pathogenesis of autoimmune thyroiditis. Spontaneous thyroiditis greatly varies in frequency among NOD colonies, but Hashimoto-like thyroiditis can be induced in two experimental models: goiter involution after iodide administration and immunization by TSH receptor, described hereunder

Precocity of the endothelial proliferation during a course of rapid goitrogenesis.

Thyroid hyperplasia was induced in C3H mice by a low iodine diet feeding supplemented with propylthiouracil. The morphological modifications associated to the development of hyperplasia were analyzed at light microscopical level and the cellular proliferation was studied by autoradiography after a pulse labelling with [3H]thymidine. The initial modification during the course of hyperplasia is the development of the vascularization. It includes the dilatation of the capillaries, which occurs before any extended modification of the follicular cells and any change of the thyroid weight, and the proliferation of endothelial cells which starts earlier than that of follicular cells