Clusterin expression in cutaneous CD30-positive lymphoproliferative disorders and their histologic simulants

Background:  Clusterin is a ubiquitous 80 kDa heterodimeric glycoprotein previously shown to be expressed on tumor cells of systemic and, to a lesser extent, primary cutaneous anaplastic large cell lymphoma (PC-ALCL). Lymphomatoid papulosis (LyP), an important differential diagnosis of ALCL, has been studied for clusterin expression in only a small number of cases. The aim of this study was to compare clusterin immunostaining patterns in LyP and other cutaneous histologic simulants with those of PC-ALCL.
Methods:  Formalin-fixed, paraffin-embedded sections of PC-ALCL (6), LyP (20), mycosis fungoides with large cell transformation (MF-LCT, 12), pityriasis lichenoides et varioliformis acuta (PLEVA, 12), arthropod bite reaction (ABR, 12) and lymphomatoid reactions (LR, 9) were immunostained for clusterin and evaluated for staining pattern and distribution. All diagnoses were made with clinicopathologic correlation.
Results:  Characteristic dot-like Golgi staining was identified in 10/20 LyP (50%), 4/6 PC-ALCL (67%) and 9/12 MF-LCT (75%). Two of 12 PLEVA (17%), 1 of 12 ABR (8%) and 2 of 8 LR (25%) had lymphocytes (< 25%) with diffuse cytoplasmic staining. Dermal dendritic cells stained strongly for clusterin. High background staining occurred in some cases.
Conclusion:  Clusterin immunostaining does not reliably distinguish between LyP, PC-ALCL or MF-LCT, but could distinguish LyP from its reactive histologic simulants.     

The course of schizophrenia: Some remarks on a yet unsolved problem of retrospective data collection

Summary The retrospective assessment of symptoms and syndromes is a basic measure in research of the longitudinal course of schizophrenia. In spite of its importance there have been few studies evaluating the standard of quality of instruments for retrospective data collection. Combining retrospectively and cross-sectionally collected data on schizophrenic symptomatology in a cohort study over a period of 5 years revealed a significant underestimation of symptoms when assessed in retrospect. The need for studies on the validity of instruments for the retrospective assessment of symptoms is stressed.     

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.     

Pneumatosis cystoides intestinii

Zusammenfassung Die Pneumatosis cystoides intestinii (PCI), das Auftreten submuköser oder subseröser, gasgefüllter Zysten in der Wand des Gastrointestinaltrakts, tritt als seltene Erkrankung ohne eindeutige Geschlechtspräferenz vorwiegend in der 3. bis 5. Lebensdekade auf. Atiopathogenetisch werden unterschiedliche Faktoren diskutiert, am wahrscheinlichsten ist eine bakterielle Ursache (Clostridium perfringens) in Verbindung mit einer minimalen Unterbrechung der Mukosaintegrität. Eine pathognomonische Symptomatik gibt es nicht, das klinische Bild reicht von asymptomatischen Zufallsbefunden bis zur Hämatochezie. Die Diagnose wird durch den Nachweis der Gaseinschlüsse mittels Abdomenübersichtsaufnahme und Kolonkontrasteinlauf gestellt. Als Behandlungsmethoden für symptomatische Patienten stehen Sauerstofftherapie, Antibiotikagabe (Metronidazol) und in schweren Fällen die Resektion des betroffenen Darmabschnitts zur Verfügung.

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Pneumatosis cystoides intestinalis (PCI), a condition involving submucosal or subserosal gas-containing cysts of the wall of the gastrointestinal tract, is a rare entity. It is mostly diagnosed between the third and fifth decades of life without a clear sexual predominance. Different aetiopathogenetic factors are under discussion, the most probable being a bacteriologic cause (Clostridium perfringens) in combination with minimal leaks in mucosal barrier. There are no pathognomonic symptoms; the clinical picture ranges from incidental findings to haematochezia. Diagnosis is based on plain abdominal film and X-ray following barium enema. Methods of treatment in symptomatic cases are oxygen and antibiotic (metronidazole) therapies and, in severe cases, resection of the diseased part of the intestine.

     

Carotenoids up-regulate connexin43 gene expression independent of their provitamin A or antioxidant properties.

Epidemiological evidence and studies in whole animals and cell culture have indicated that carotenoids have cancer chemopreventive action. In mouse C3H10T1/2 cells, this activity is highly correlated with the ability of carotenoids to up-regulate gap junctional intercellular communication. Here, we report that in mouse cells, carotenoids increase the expression of connexin43, a gene that encodes a major gap junction protein. This effect appears unrelated to their provitamin A or antioxidant properties, since carotenoids with and without provitamin A activity increased levels of connexin43 mRNA and protein, whereas the antioxidants methyl-bixin and alpha-tocopherol were inactive. Moreover, the active carotenoid canthaxanthin did not induce the vitamin A-inducible gene retinoic acid receptor-beta. Connexin43 is the first carotenoid-inducible gene described in mammals. By indicating an additional pathway through which carotenoids function, these data provide a mechanistic basis for cancer chemoprevention by carotenoids and may lead to a re-evaluation of carotenoid physiology.