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The Longmen Shan belt (eastern border of the Tibetan plateau) constitutes a tectonically active region as demonstrated by the occurrence of the unexpected 2008 Mw7.9 Wenchuan and 2013 Mw6.6 Lushan earthquakes in the central and southern parts of the belt, respectively. These events revealed the necessity of a better understanding of the long‐term geological evolution of the belt and its effect on the present dynamics and crustal structure. New structural and thermobarometric data offer a comprehensive data set of the paleotemperatures across the belt and P‐Testimates for low‐grade metamorphic domains. In the central Longmen Shan, two metamorphic jumps of 150–200 °C, 5–6 kbar and ~50 °C, 3–5 kbar acquired during the Early Mesozoic are observed across the Wenchuan and Beichuan faults, respectively, attesting to their thrusting movement and unrevealing a major decollement between the allochtonous Songpan‐Garze metasedimentary cover (at T> 500 °C) and the autochtonous units and the basement (T< 400 °C). In the southern Longmen Shan, the only greenschist facies metamorphism is observed both in the basement (360 ± 30 °C, 6 ± 2 kbar) and in the metasedimentary cover (350 ± 30 °C, 3 ± 1 kbar). Peak conditions were reached at ca. 80–60 Ma in the basement and ca. 55–33 Ma in the cover, ca. 50 Ma after the greenschist facies metamorphic overprint observed in the central Longmen Shan (ca. 150–120 Ma). This along‐strike metamorphic segmentation coincides well with the present fault segmentation and reveals that the central and southern Longmen Shan experienced different tectonometamorphic histories since the Mesozoic. Metamorphic jumps of ~150 °C, 5 kbar and ~50 °C, 3 kbar are observed across the Wenchuan and Beichuan faults, respectivelyP‐T‐tconditions for the southern Longmen Shan, lower than for central Longmen Shan, do not exceed 395 °C and 6 ± 2 kbar (at 80–33 Ma)Different segments of the Longmen Shan underwent different tectonometamorphic evolution since the Mesozoic

Background: Hematopoietic stem cell transplantation (HSCT) is used in the treatment of several hematological and non-hematological disorders. An increasing number of long-term survivors recover from their primary disease, but they are at risk of adverse late effects, including metabolic syndrome (MS), which seems to be common in long-term survivors of HSCT. Aim: To compare common metabolic parameters and adipohormone profiles in post-transplant and spontaneously occurring or “classic” MS patients. Subjects and methods: Post-transplant MS patients (15 women and 14 men; 49.8±9.3 yr) were compared to “classic” MS patients (15 women and 14 men; 52.9±8.0 yr). For each subject a record of conventional clinical parameters was made; moreover, serum leptin, insulin, quantitative C-reactive protein (CRP), tumor necrosis factor-α [TNF-α], and adiponectin concentrations were measured. Results: The patients with post-HSCT MS had significantly higher levels of leptin, CRP, and TNF-α than the patients with “classic” MS. A generalized linear model comprising serum insulin (p=0.022), body mass index (p<0.001), gender (p<0.001), and group (i.e. healthy, post-HSCT with MS, or suffering from “classic” MS; p<0.001) explained serum leptin variability (adjusted R2=0.741). Serum leptin concentrations and BMI were related in the patients with “classic” MS but not in those with post-HSCT MS. Conclusions: A possible pathogenetic mechanism in the development of MS after HSCT could be hyperleptinemia. A potential interaction among circulating leptin, components of MS, and immune function might explain the role of this adipokine in mediating cardiovascular risk after HSCT.

Background. Clinical and/or laboratory signs of systemic inflammation occur frequently in patients undergoing long-term haemodialysis. It is likely, therefore, that a compensatory release of endogenous anti-inflammatory molecules occurs to limit host reactions. The aim of the present research was to determine if the potent anti-inflammatory peptide α-melanocyte-stimulating hormone (α-MSH), a pro-opiomelanocortin derivative, is increased in plasma of haemodialysis patients. Because endotoxin and cytokines induce α-MSH in vivo and in vitro, we also measured plasma concentrations of endotoxin, interleukin-6 (IL-6), and tumour necrosis factor α (TNF-α), and the two circulating products of activated monocytes, nitric oxide (NO) and neopterin.
Methods. Thirty-five chronic haemodialysis patients, 20 patients with chronic renal failure not yet on dialysis, and 35 normal controls were included in the study. In the haemodialysis group, blood samples were obtained before and at the end of a dialysis session. Plasma α-MSH was measured using a double antibody radioimmunoassay, and IL-6, TNF-α, and neopterin using specific enzyme-linked immunosorbent assays. Plasma nitrites were determined by a colorimetric method, and endotoxin with the quantitative chromogenic LAL (limulus amoebocyte lysate) method.
Results. Mean plasma α-MSH was higher in haemodialysis patients than in control subjects, with the peptide concentrations being particularly elevated in dialysed patients with detectable endotoxin. High α-MSH concentrations were observed in the pre-dialysis samples, with no substantial change at the end of the dialysis session. Plasma concentrations of IL-6, TNF-α, neopterin, and NO were generally elevated in chronic haemodialysis patients and there was a negative correlation between circulating α-MSH and IL-6. In patients with renal failure not yet on dialysis, mean plasma α-MSH was similar to that of normal subjects.
Conclusions. α-MSH is increased in the circulation of chronic haemodialysis patients and particularly so in case of detectable endotoxaemia. Reduction of renal clearance is unlikely to contribute to the observed rise of the peptide because α-MSH concentration is not increased in patients with chronic renal failure who are not yet on dialysis. It is likely that dialysis-associated endotoxaemia, directly and/or through cytokine release, enhances the production of the anti-inflammatory mediator α-MSH that limits host reactions.

Clinical and/or laboratory signs of systemic inflammation occur frequently in patients undergoing long-term haemodialysis. It is likely, therefore, that a compensatory release of endogenous anti-inflammatory molecules occurs to limit host reactions. The aim of the present research was to determine if the potent anti-inflammatory peptide alpha-melanocyte-stimulating hormone (alpha-MSH), a pro-opiomelanocortin derivative, is increased in plasma of haemodialysis patients. Because endotoxin and cytokines induce alpha-MSH in vivo and in vitro, we also measured plasma concentrations of endotoxin, interleukin-6 (IL-6), and tumour necrosis factor alpha (TNF-alpha), and the two circulating products of activated monocytes, nitric oxide (NO) and neopterin.

Abstract. To evaluate whether HLA-B14 positive individuals are at increased risk for non-classic 21-hydroxylase deficiency, the response of progesterone and 17-hydroxyprogesterone to ACTH stimulation test was studied in a group of 27 apparently normal, HLA-B14 positive, blood donors. Four of these subjects showed a response typical of 21-hydroxylase defect. In the present series, the enzymatic defect was found to have a considerably lower prevalence than in a previous study of smaller size (15% vs 66%); however, considering the low frequency of the gene coding for the defect in the general population (0.015–0.057), the present results confirm an increased risk for non-classic 21-hydroxylase deficiency in HLA-B14 positive individuals. Therefore, in these subjects, a screening for 21-hydroxylase deficiency may be indicated.

The response of plasma 17-hydroxyprogesterone (17-OHP) to exogenous ACTH was investigated in 85 consecutive women referred for postmenarchal hirsutism, in order to assess the prevalence of late-onset adrenal hyperplasia due to 21 -hydroxylase deficiency and its relevance to the clinical practice. An exaggerated response of plasma 17-OHP to ACTH, indicating 21-hydroxylase deficiency, was found in only one patient with a prevalence of 1.1 %. The patient with late-onset adrenal hyperplasia presented signs of virilism and had high basal levels of 17-OHP. On the basis of our results, late-onset adrenal hyperplasia accounts for a very small proportion of cases of hirsutism; moreover, from this and previous studies it is apparent that the determination of basal plasma 17-OHP may be sufficient to discover late-onset 21-hydroxylase deficiency. Therefore, we do not consider ACTH testing an advisable step in the routine screening for hirsutism.

The response of plasma beta-endorphin (beta-EP) to dexamethasone suppression was studied in 14 patients with Alzheimer's disease (AD), 14 patients with Parkinson's disease (PD), and 13 age-matched controls in order to evaluate whether an impairment of the opiate system is present in these neurodegenerative disorders. Basal circulating beta-EP was in normal range in all subjects, although the mean concentration was slightly reduced in the patients compared to controls. After 1 mg dexamethasone given at 11:00p.m. the night before, plasma beta-EP concentration measured at 08:00 a.m. and 04:00 p.m. was not inhibited in AD and PD patients while it was significantly reduced in controls. Circulating ACTH and Cortisol were similar in patients and controls and a normal inhibition of plasma Cortisol after dexamethasone was observed in 13/14 AD and 12/14PD patients. The resistance of beta-EP to dexamethasone inhibition is consistent with previous clinical and experimental data indicating a disorder of the opiate system in brain degenerative diseases.