AMPK在妊娠期糖尿病发病机制中的作用

腺苷酸活化蛋白激酶是一种重要的蛋白激酶,主要作用是协调代谢和能量平衡.腺苷酸活化蛋白激酶被激活后,在增加骨骼肌对葡萄糖摄取、增强胰岛素敏感性、增加脂肪酸氧化以及调节基因转录等方面发挥重要作用.已经证实脂联素有调节糖脂代谢的作用,但其作用机制尚不十分清楚,很可能是通过腺苷酸活化蛋白激酶介导,对脂联素信号转导通路的研究将成为进一步理解脂联素作用的关键所在.而脂联素又是妊娠期糖尿病的预测因子,所以腺苷酸活化蛋白激酶逐渐成为对妊娠期糖尿病研究中的焦点.     

The use of computed tomography-guided stereotactic techniques in the treatment of brain stem abscesses

A case of a brain stem abscess that was successfully treated using CT guided stereotaxy together with antibiotic therapy is presented. The literature is reviewed and the role of stereotaxy in the treatment of brain stem abscess is discussed.     

The autonomic dysfunction syndrome: aetiology and treatment

Nine patients with autonomic dysfunction syndrome (ADS) characterised by sympathetic discharge and extensor posturing are presented. Morphine was given to three patients and in all cases consistently stopped the episodes. Dantrolene was given to one patient and reduced the severity of the extensor posturing without affecting the other components of the ADS. Bromocriptine was given to three patients and appeared to have both short- and long-term effects. Acutely, the drug partially corrected the hyperthermia and diaphoresis associated with these episodes. Two patients were given bromocriptine long-term. In one patient, the ADS was completely controlled and in the other, the frequency of the episodes decreased. The autonomic dysfunction syndrome appears to be related to both severe closed head injury and acute hydrocephalus. The clinical similarity of the two diverse etiologic groups and the absence of precipitating increased ICP in the former suggests the common theme is a release of the brain stem from higher control. The responses to morphine and bromocriptine suggest that the opiate and dopaminergic pathways play roles in the entity.     

A hyperthermic syndrome in two subjects with acute hydrocephalus

Although intracranial hypertension may cause autonomic disturbances, as well as alterations in the regulation of body temperature, an acute hyperthermic syndrome with autonomic disturbance as a consequence of hydrocephalus has not been described previously. Two subjects presented with such a syndrome, with each of several episodes of acute shunt failure and hydrocephalus. With correction of the hydrocephalus, the autonomic disturbances and fever immediately cleared. Observations from human and experimental studies suggest some potential mechanisms for the development of the syndrome. One of the subjects of this report was being treated with neuroleptics at the time of hospitalization; in him, and potentially in other similar patients, the syndrome could easily be confused with the neuroleptic malignant syndrome. The need for prompt appreciation of the correct diagnosis was emphasized by the rapid clearing of all neurological signs after correction of the shunt malfunction in both of these patients.     

Diencephalic seizures: responsiveness to bromocriptine and morphine

Two patients with posttraumatic diencephalic seizures, characterized by autonomic dysfunction and extensor posturing, had partial responses to bromocriptine and complete responses to morphine. Probable synergism between the two agents was noted. These 2 cases suggest the potential effectiveness of this regimen for the treatment of diencephalic seizures, raise questions regarding the role of the dopaminergic and opioid systems in this disease entity, and support the hypothesis that diencephalic seizures represent a release phenomenon in the brain.     

Further experience utilizing the Gildenberg technique for computed tomography-guided stereotactic biopsies

Initial experience using the Gildenberg technique for computed tomography-guided stereotactic biopsies is reviewed. Of 50 patients, adequate tissue was obtained in 49. In one patient, the stereotactic frame was unable to reach the selected biopsy site. In 32 of 49 patients, the diagnosis was obtained with one biopsy; in the remainder, two to five samples were required. In 4 cases, a subsequent craniotomy was performed; these provided similar histopathological tissue and in no case was the diagnosis altered. The lesions were categorized by CT as ring-enhancing lesions (REL), enhancing lesions with surrounding low density (ELLD), and low density lesions with and without peripheral areas of enhancement. Of the REL, 21 of 23 were primary tumors. Of the ELLD, 5 of 13 were primary tumors; the remainder had a wide spectrum of disease. Of the low density lesions without enhancement, 6 were primary tumors and 1 was an inflammatory process. Three patients had low density lesions with peripheral areas of enhancement and proved to have malignant primary tumors. The remaining patients had multiple lesions with both primary and metastatic disease. Twelve RELs were biopsied in multiple sites. An accurate diagnosis was best obtained by performing the first biopsy in the enhancing rim with additional biopsies as needed in the low density center. Homogeneous lesions could be biospied with target selection based upon a primary regard for safety rather than imaging characteristics. Three patients had transiently increased hemiparesis and one had a transient decrease in level of consciousness after biopsy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Loss of LFA-1, but not Mac-1, protects MRL/MpJ-Fas(lpr) mice from autoimmune disease

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune complex-mediated tissue injury. Many different adhesion molecules are thought to participate in the development of SLE; however, few studies have directly examined the contributions of these proteins. Here we demonstrate that LFA-1 plays an essential role in the development of lupus in MRL/MpJ-Fas(lpr) mice. Mice deficient in LFA-1, but not Mac-1, showed significantly increased survival, decreased anti-DNA autoantibody formation, and reduced glomerulonephritis. The phenotype of the LFA-1-deficient mice was similar to that observed in beta(2) integrin-deficient (CD18-null) MRL/MpJ-Fas(lpr) mice, suggesting a lack of redundancy among the beta(2) integrin family members and other adhesion molecules. These studies identify LFA-1 as a key contributor in the pathogenesis of autoimmune disease in this model, and further suggest that therapeutic strategies targeting this adhesion molecule may be beneficial for the treatment of SLE.