Kristalloide Einschlüsse im Zytoplasma pflanzlicher Zellen

Summary In healthy as well as dahlia mosaic sick plants ofVerbesina encelioides, Sanvitalia procumbens, Zinnia elegans, Calendula spec. andDahlia hybrids, leaf cell vacuoles are found in the marginal cytoplasm which contain protein crystals. They are single membrane-limited products of the endoplasmatic reticulum. They may be found mainly in the older leaves and especially in those of virus infected plants. The crystalline structures consist of tetragonally arranged tubules of 105 Å in diameter, separated by an interspace about 35 Å wide. There are similar structures in virus infected plants ofFragaria vesca, but not inChenopodium quinoa, where the vacuoles contain no bodies. This cell organelle is compared with crystalline inclusions already described. Its significance and relations to the virus disease are discussed.     

Proton extrusion by Leaf Discs ofVicia faba L.: Influence of inhibitors and phytohormones on H+ extrusion†

The present investigations were designed to elucidate the linkage of medium acidification to metabolism and to study the influence of phytohormones (IAA, ABA) and fusieoccin (FC) on H+ extrusion from peeled leaf tissue of Vicia faba. H+ release, which was sensitive to the metabolic inhibitors sodium azide, vanadate, DCCD, and cycloheximide, was promoted by 5 to 50 μM IAA and 10 μ FC, but transiently diminished by 10 μM ABA. FC was a much more powerful inducer of H+ extrusion than IAA. Other weak acids such as acetate and citrate had no effect on H+ extruding activity of Vicia leaf tissue indicating that the IAA effect is specific. These results support the view that IAA and ABA control of cell growth can be attributed entirely to a modulation of H+ pump activity.     

Endothelin-1-induced spreading depression in rats is associated with a microarea of selective neuronal necrosis

Two different theories of migraine aura exist: In the vascular theory of Wolff, intracerebral vasoconstriction causes migraine aura via energy deficiency, whereas in the neuronal theory of Le?o and Morison, spreading depression (SD) initiates the aura. Recently, it has been shown that the cerebrovascular constrictor endothelin-1 (ET-1) elicits SD when applied to the cortical surface, a finding that could provide a bridge between the vascular and the neuronal theories of migraine aura. Several arguments support the notion that ET-1-induced SD results from local vasoconstriction, but definite proof is missing. If ET-1 induces SD via vasoconstriction/ischemia, then neuronal damage is likely to occur, contrasting with the fact that SD in the otherwise normal cortex is not associated with any lesion. To test this hypothesis, we have performed a comprehensive histologic study of the effects of ET-1 when applied topically to the cerebral cortex of halothane-anesthetized rats. Our assessment included histologic stainings and immunohistochemistry for glial fibrillary acidic protein, heat shock protein 70, and transferase dUTP nick-end labeling assay. During ET-1 application, we recorded (i) subarachnoid direct current (DC) electroencephalogram, (ii) local cerebral blood flow by laser-Doppler flowmetry, and (iii) changes of oxyhemoglobin and deoxyhemoglobin by spectroscopy. At an ET-1 concentration of 1 muM, at which only 6 of 12 animals generated SD, a microarea with selective neuronal death was found only in those animals demonstrating SD. In another five selected animals, which had not shown SD in response to ET-1, SD was triggered at a second cranial window by KCl and propagated from there to the window exposed to ET-1. This treatment also resulted in a microarea of neuronal damage. In contrast, SD invading from outside did not induce neuronal damage in the absence of ET-1 (n = 4) or in the presence of ET-1 if ET-1 was coapplied with BQ-123, an ET(A) receptor antagonist (n = 4). In conclusion, SD in presence of ET-1 induced a microarea of selective neuronal necrosis no matter where the SD originated. This effect of ET-1 appears to be mediated by the ET(A) receptor.     

Marathon related death due to brainstem herniation in rehydration-related hyponatraemia: a case report

Introduction

The natural history of patients with spontaneous parathyroid necrosis is unknown. In this case report we describe the clinical course, laboratory, radiographic, bone densitometry tests, parathyroid ultrasonography and scintigraphy examinations of a patient performed over a period of eight years after she first presented with a sudden episode of spontaneous resolution of primary hyperparathyroidism (PHPT).

Case presentation

A 24-year-old woman with a clinical history and laboratory and radiographic tests compatible with PHPT suffered a sudden episode of cervical pain and presented with clinical evidence of hypocalcemia. Biopsy of a cervical nodule revealed necrotic material compatible with ischemia of the parathyroid. The follow-up of the patient presented four distinct phases: the first, which lasted two years, was compatible with a period of bone hunger during which it was necessary to introduce calcitriol and calcium carbonate. During this period, the patient showed bone mass gain. The second phase was characterized by normalization of calcium and parathyroid hormone levels and its end was difficult to define. During the third phase there was a recurrence of hypercalcemia associated with elevated parathyroid hormone (PTH) levels and loss of bone mass. The last phase corresponded to the interval after parathyroidectomy, which was characterized by normalization of serum levels of calcium and PTH, as well as bone mass gain.

Conclusion

This case report indicates that spontaneous resolution of PHPT by adenoma necrosis is potentially temporary. Thus, in cases in which a conservative approach is chosen, clinical and laboratory follow-up is indispensable. Bone mass measurement is a useful tool in the follow-up of these cases. However, this option exposes the patient to a potential roller-coaster ride of bone mass gain and loss, whose long term consequences are still unknown.     

Nicotinamide phosphoribosyltransferase (NAMPT/PBEF/visfatin) is constitutively released from human hepatocytes

Circulating NAMPT (PBEF/visfatin) has pleiotropic functions and is secreted from adipocytes. Since it is doubtful whether serum levels can be explained by secretion from adipocytes alone, we asked whether hepatocytes are also able to liberate NAMPT. Using HepG2 cells and primary rat and human hepatocytes, release of NAMPT into the cell culture supernatant was found to occur constitutively in a time-dependent manner. In primary human hepatocytes, secretion within 24 h was far higher than the cellular content, but was neither influenced by inhibitors of secretion nor by glucose, insulin or TNFα. As determined by size exclusion chromatography, HepG2 lysates and supernatants primarily contained the dimeric form of NAMPT which exhibited similar in vitro specific enzymatic activity. In primary human hepatocytes, secreted NAMPT was less active. Our results demonstrate that human hepatocytes are a potential source of circulating NAMPT.