The intestinal immune system discriminates between tolerance toward the commensal microflora and robust responses to pathogens. Maintenance of this critical balance is attributed to mucosal dendritic cells (DCs) residing in organized lymphoid tissue and dispersed in the subepithelial lamina propria. In situ parameters of lamina propria DCs (lpDCs) remain poorly understood. Here, we combined conditional cell ablation and precursor-mediated in vivo reconstitution to establish that lpDC subsets have distinct origins and functions. CD103(+) CX(3)CR1(-) lpDCs arose from macrophage-DC precursors (MDPs) via DC-committed intermediates (pre-cDCs) through a Flt3L growth-factor-mediated pathway. CD11b(+) CD14(+) CX(3)CR1(+) lpDCs were derived from grafted Ly6C(hi) but not Ly6C(lo) monocytes under the control of GM-CSF. Mice reconstituted exclusively with CX(3)CR1(+) lpDCs when challenged in an innate colitis model developed severe intestinal inflammation that was driven by graft-derived TNF-alpha-secreting CX(3)CR1(+) lpDCs. Our results highlight the critical importance of the lpDC subset balance for robust gut homeostasis.

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Our data suggest a significant association between age and serum ALT activity. This association is not a simple linear correlation, but rather an inverted-U-like relation. Thus, when interpreting the laboratory results of a subject suspected of liver disease, age should probably be taken into account. Larger-scale studies are needed to better characterize this issue.

This study documents that hospitalized IBD patients with CDAD have low rate of endoscopic pseudomembranes, which is not accounted for by the use of immunosuppressant drugs. IBD patients with CDAD and discernable pseudomembranes more commonly present with fever, but their clinical outcome is similar to patients without pseudomembranes.

Leptin signaling is involved in T-cell polarization and is required for profibrotic function of hepatic stellate cells (HSCs). Leptin-deficient ob/ob mice do not develop liver fibrosis despite the presence of severe long-standing steatohepatitis. Here, we blocked leptin signaling with our recently generated mouse leptin antagonist (MLA), and examined the effects on chronic liver fibrosis in vivo using the chronic thioacetamide (TAA) fibrosis model, and in vitro using freshly-isolated primary HSCs. In the chronic TAA fibrosis model, leptin administration was associated with significantly enhanced liver disease and a 100% 5-week to 8-week mortality rate, while administration or coadministration of MLA markedly improved survival, attenuated liver fibrosis, and reduced interferon ␥ (IFN-␥)

Angiotensin converting enzyme (ACE) is a candidate gene for psychiatric disorders. We examined the frequency of a functional insertion/deletion (I/D) polymorphism in the 16th intron of the ACE gene (located on chromosome 17q23) in groups of patients with schizophrenia (n = 104 and 113), major depression (n = 55), and bipolar disorder (n = 87) compared to healthy control subjects (n = 87). There was no evidence for allelic or genotypic association of the polymorphism with any of the disorders or with tardive dyskinesia (TD) in patients with schizophrenia. In a sample of nuclear families (n = 61) made up of one or more patients with schizophrenia recruited with their parents, there was no evidence for biased transmission of ACE I/D alleles. Particularly in the case of schizophrenia, these findings do not support an association of the ACE I/D polymorphism with the phenotypes examined.

Amitraz is commonly used in agricultural industries throughout the world as a farm-animal insecticide. Despite its widespread use, amitraz intoxication is extremely rare and mainly occurs through accidental ingestion by young children. Severe, life-threatening amitraz intoxication in adults is very rarely recognized and reported. Described herein is a previously healthy 54-year-old patient who accidentally ingested a mouthful of liquid amitraz concentrate, and rapidly developed life-threatening clonidine-like overdose syndrome, manifested as nausea, vomiting, hypotension, bradycardia, bradypnoea, and deep coma. Supportive treatment, including mechanical ventilation, and atropine administration resulted in full recovery within 48 hr. Very few cases of near-fatal amitraz poisoning in adults have been described in the medical literature, leading to low awareness of physicians in general practice to the potential toxicity of amitraz. As a consequence, cases of amitraz poisoning are not recognised and therefore erroneously treated as the much more commonly recognized organophosphate and carbamate intoxication. In our discussion, we review the clinical and laboratory manifestations of amitraz poisoning, including clinical hints that aid in the recognition of this often-overlooked diagnosis. Differentiation of amitraz intoxication from the much more commonly seen pesticide-related organophosphate and carbamate intoxication is of utmost importance, in order to avoid erroneous, unnecessary, and often dangerous treatment.Amitraz is a commonly used pesticide, employed by farmers throughout the world for the treatment of insect infestation in farm animals. It is usually provided in highly concentrated liquid solutions (usually containing xylene as a solvent), while its preparation in agricultural use requires dilution in 1:500 to 1:1000 ratios. Ingestion of small quantities of amitraz is associated with self-limiting nausea and vomiting, while ingestion of larger quantities may result in clonidine-like overdose syndrome. Herein, we report a patient who, upon consumption of a small quantity of amitraz concentrate, developed a severe clonidine-like overdose syndrome associated with life-threatening coma. Materials and MethodsA 54-year-old male farmer was referred from a rural hospital to our Emergency Services, for evaluation and treatment of presumed organophosphate poisoning. The patient had ingested a mouthful (estimated 20-30 cc) of liquid pesticide, which he erroneously thought was juice. After 30 min. he developed nausea and vomiting. While being transferred to our medical center, he became progressively bradycardic, bradypnoeic, and had a declining mental status. No convulsions were noted. His medical history was unremarkable, with no medical conditions and no history of alcohol and drug abuse. The patient strongly denied consumption of any medication, including over-the-counter, natural and alternative drugs. No atherosclerotic, hypercoagulable, or bleeding tendencies were noted.On admission the patient appe...