Background: Limited data are available concerning patients admitted to the intensive care unit (ICU) for severe haemoptysis. We reviewed a large series of patients managed in a uniform way to describe the clinical spectrum and outcome of haemoptysis in this setting, and better define the indications for bronchial artery embolisation (BAE).
Epidemiological studies have associated environmental exposure to polychlorinated biphenyls (PCBs) with an increased risk of type 2 diabetes; however, little is known about the underlying mechanisms involved in the metabolic side-effects of PCB. Our study evaluated the transcriptional effects of a subchronic exposure (gavage at Day 0 and Day 15 with 10 or 100 μmol/Kg bw) to PCB118 (dioxin-like PCB), PCB153 (non-dioxin-like PCB), or an equimolar mixture of PCB118 and PCB153 on various tissues (liver, visceral adipose tissue, muscle, and colon) in mice. Our results showed that a short-term exposure to PCB118 and/or PCB153 enhanced circulating triglyceride levels but did not affect glycemia. Among the studied tissues, we did not observe any modification of the expression of inflammation-related genes, such as cytokines or chemokines. The main transcriptional effects were observed in visceral adipose and liver tissues. We found a downregulation of lipin1 and glut4 expression in these two target organs. In adipose tissue, we also showed a downregulation of Agpat2, Slc25a1, and Fasn. All of these genes are involved in lipid metabolism and insulin resistance. In muscles, we observed an induction of CnR1 and Foxo3 expression, which may be partly involved in PCB metabolic effects. In summary, our results suggest that lipin1 and glut4, notably in adipose tissue, are the main targeted genes in PCB-induced metabolic disorders, however, further studies are required to fully elucidate the mechanisms involved.
Cerebral malaria, a reversible encephalopathy affecting young children, is a medical emergency requiring urgent clinical assessment and treatment. We performed a whole-transcriptomic analysis of blood samples from Malian children with cerebral or uncomplicated malaria. We focused on transcripts from pathways for which dysfunction has been associated with neurodegenerative disorders. We found that SNCA, SIAH2, UBB, HSPA1A, TUBB2A, and PINK1 were upregulated (fold-increases, ≥2.6), whereas UBD and PSMC5 were downregulated (fold-decreases, ≤4.39) in children with cerebral malaria, compared with those with uncomplicated malaria. These findings provide the first evidence for pathogenic mechanisms common to human cerebral malaria and neurodegenerative disorders.
A polypeptide has been isolated from bovine adenohypopbysis which antagonizes the hypoglycemic effect of exogenous insulin and which, per se, induces loss of carbohydrate tolerance in men and dogs. Mild acid hydrolysis of the active polypeptide yields a compound which retains the same biological properties. Characteristics of the active principle and its hydrolytic product is the long duration of their activities, the greatest intensity of the effects TN RECENT COMMUNICATIONS being observed between 34 and 60 hours after a single intramuscular injection. Both substances are devoid of ACTH activity. The active polypeptide resembles closely the insulin antagonist isolated from the urine of patients with lipoatrophic diabetes previously reported from this laboratory. Details of the isolation and physiologic effects of the active substance and its hydrolytic product are described. (Metabolism 15: No. 4, April, 308-324, 1966) from this laboratory,1*2 the isolation1 of an insulin antagonist from the urine of patients with lipoatrophic diabetes has been reported. It also was demonstrated that a similar substance was present in the urine of a maturity-onset insulin-resistant diabetic without lipoatrophy. The substance was found to be a polypeptide which when administered to either dogs or man exhibited diabetogenic and anti-insulin effects. The origin of the active principle had not been determined. The present report describes a procedure for the isolation of a similar substance from the anterior lobes of bovine pituitary glands. Like the insulin antagonist from the urine, the material is also highly active both in dogs and in man.
MATERIALS AND METHODSFrozen bovine anterior pituitary glands, obtained from the Armour Pharmaceutical Company, Kankakee, Illinois, were treated according to the procedure shown in Figure 1. The
A polypeptide possessing physical and biological properties similar to that excreted in the urine by patients with lipoatrophic diabetes was previously isolated from bovine adenohypophysis. A similar principle has now been obtained from the anterior lobes of hog and sheep pituitaries by the same procedures of isolation. The material from these animals also induces hyperglycemia and insulin resistance both in humans and dogs. The substance exhibits no similarity in physicochemical properties to either growth hormone or prolactin. Its presence in the pituitary gland of all three species of animals so far studied suggests that the peptide is a naturally occurring substance but its physiological signilicante is unknown. Its physicochemical and biological similarity to the urinary polypeptide found in lipoatrophic diabetes suggests a relationship.
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