The Mesozoic along-strike tectono-metamorphic segmentation of Longmen Shan (eastern Tibetan plateau)

The Longmen Shan belt (eastern border of the Tibetan plateau) constitutes a tectonically active region as demonstrated by the occurrence of the unexpected 2008 Mw 7.9 Wenchuan and 2013 Mw 6.6 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 dataset of the paleo‐temperatures across the belt and P‐T estimates 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 c. 80‐60 Ma in the basement and c. 55‐33 Ma in the cover, c. 50 Ma after the greenschist‐facies metamorphic overprint observed in the central Longmen Shan (c. 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 tectono‐metamorphic histories since the Mesozoic

SORVEGLIANZA DI UNA EPIDEMIA DA E. FAECIUMVANCOMICINA RESISTENTE (VRE) IN SETTE REPARTI DELL'OSPEDALE DI LEGNANO.

n/

Successful desensitization with human insulin in a patient with an insulin allergy and hypersensitivity to protamine: a case report

<p>Abstract</p> <p>Introduction</p> <p>Insulin allergy may occur in patients treated with subcutaneous applications of insulin preparations. Besides additives in the insulin preparation such as protamine, cresol, and phenol, the insulin molecule itself may be the cause of the allergy. In the latter case, therapeutic options are rare.</p> <p>Case presentation</p> <p>A 68-year-old man with poorly controlled type 2 diabetes mellitus received different insulin preparations subcutaneously while on oral medication. Six to eight hours after each subcutaneous application, he developed pruritic plaques with a diameter of >15 cm at the injection sites that persisted for several days. Allergologic testing revealed positive reactions against every insulin preparation and against protamine. Investigation of serum samples demonstrated IgG antibodies against human and porcine insulin. We treated the patient with human insulin using an ultra-rush protocol beginning with 0.004 IU and a rapid augmentation in dose up to 5 IU. Therapy was accompanied by antihistamine therapy. Subsequent conversion to therapy with glargine insulin (6 IE twice daily) was well-tolerated.</p> <p>Conclusion</p> <p>As reported in this case, desensitization with subcutaneously administered human insulin using an ultra-rush protocol in patients with an insulin allergy may present an easy form of therapy that is successful within a few days.</p

Cell Type-Specific Neuroprotective Activity of Untranslocated Prion Protein

Background: A key pathogenic role in prion diseases was proposed for a cytosolic form of the prion protein (PrP). However, it is not clear how cytosolic PrP localization influences neuronal viability, with either cytotoxic or anti-apoptotic effects reported in different studies. The cellular mechanism by which PrP is delivered to the cytosol of neurons is also debated, and either retrograde transport from the endoplasmic reticulum or inefficient translocation during biosynthesis has been proposed. We investigated cytosolic PrP biogenesis and effect on cell viability in primary neuronal cultures from different mouse brain regions. Principal Findings: Mild proteasome inhibition induced accumulation of an untranslocated form of cytosolic PrP in cortical and hippocampal cells, but not in cerebellar granules. A cyclopeptolide that interferes with the correct insertion of the PrP signal sequence into the translocon increased the amount of untranslocated PrP in cortical and hippocampal cells, and induced its synthesis in cerebellar neurons. Untranslocated PrP boosted the resistance of cortical and hippocampal neurons to apoptotic insults but had no effect on cerebellar cells. Significance: These results indicate cell type-dependent differences in the efficiency of PrP translocation, and argue that cytosolic PrP targeting might serve a physiological neuroprotective function

Central hyperthermia, brain hyperthermia and low hypothalamus temperature

Introduction, Patients and Methods: We measured brain temperature in a case of central hyperthermia. Results Brain temperature was increased except for hypothalamus that was colder. Conclusion: We suppose that central hyperthermia is driven by cold hypothalamus

Extrapulmonary tuberculosis : an unusual presentation in an immunocompetent patient

A 50-year-old Brazilian woman was admitted to our department because of pelvic pain irradiated to the lower left limb, ipsilateral ankle swelling and progressive weight loss. Doppler ultrasound demonstrated deep venous femoropopliteal thrombosis, while a thorax-abdomen CT scan showed multiple solid hypodense pulmonary lesions, a large hypodense lesion in the iliopsoas muscles bilaterally and a complex cystoid lesion at the hepatic hilum. These findings were better characterised as active in flammatory colliquated lymph nodes by positron emission tomography and echo-guided percutaneous fine-needle aspiration of the left iliopsoas abscessual lesion finally allowed the diagnosis of tubercular infection with positive cultures for Mycobacterium tuberculosis complex

Effect of chronic clonidine administration on GH secretion in adult human subjects

It is well known that the acute administration of clonidine, an alpha 2-adrenergic agonist commonly used as an antihypertensive drug, stimulates GH secretion, likely via hypothalamic growth hormone releasing hormone (GHRH) release. Conversely, evidences of a hyperactivity of GHRH-GH-somatomedin C (SMC) axis during chronical administration of clonidine are controversial. In this study, GH and SMC levels have been evaluated in 16 hypertensive patients chronically treated with clonidine. The subjects were randomized to receive either TRH or saline with the aim of evaluating the non specific GH response to TRH as compared to spontaneous fluctuations during a control test. In basal conditions, GH and SMC concentrations in clonidine treated patients were similar to those observed in an age and sex matched group of normal untreated subjects. An abnormal increase in plasma GH occurred in 5 out of the 10 patients who received TRH, while plasma GH did not show significant variations during testing in the subjects who received saline. It is suggested that chronical administration of clonidine does not induce an hyperactivity of GHRH-GH-SMC axis as estimated by plasma GH and SMC concentrations, but may induce a disorder in hypothalamic control of GH secretion, possibly implicated in the abnormal GH responsivity to TRH

Idiopathic pulmonary hemosiderosis in an adult. Favourable response to azathioprine

Idiopathic pulmonary hemosiderosis (IPH) is a rare disorder characterised by intermittent, diffuse alveolar hemorrhage (DAH). Although an inflammatory pulmonary capillaritis can be evidenced in most patients with DAH, IPH is a distinct entity in which pulmonary inflammatory alterations are lacking. Most cases occur in children, although the disease has been exceptionally reported in adults too. Here, we, describe a case of IPH in a 30-year-old woman who was admitted to our hospital because of recurrent episodes of hemoptysis since the age of 21. IPH was diagnosed on the basis of: 1) an open lung biopsy showing focal alveolar edema and hemorrhage without parenchymal inflammatory alterations, 2) a bronchoalveolar lavage showing hemosiderin-laden macrophages, and 3) exclusion of infectious or immunologic causes of hemoptysis. Prednisone administration could control the disease, but every attempt to lower the dose to less than 25 mg per day was followed by recurrence of hemoptysis. Then, azathioprine was started, and after three months prednisone was gradually tapered to the dose of 10 mg per day, without any relapse of the disease. These findings indicate that azathioprine, in combination with prednisone, may be an effective therapy for IPH and suggest that an immunologic mechanism could be involved in the pulmonary capillary damage underlying alveolar bleeding