Jordan's derivation of blackbody fluctuations

The celebrated Dreimännerarbeit by Born, Heisenberg and Jordan contains a matrix-mechanical derivation by Jordan of Einstein's formula for blackbody fluctuations. Jordan appears to have considered this to be one of his finest contributions to quantum theory, but the status of his derivation is puzzling. In our Dreimenschenarbeit, we show how to understand what Jordan was doing in the double context of a Boltzmannian approach to statistical mechanics and of the early ‘statistical interpretation’ of matrix mechanics.     

Mitochondrial swelling induced by diphtheria toxin in vivo: A comparison with the action of some other bacterial toxins

Riassunto In precedenti lavori è stato studiato il rigonfiamento causato dalla tossina difterica nei mitocondri di cellule coltivate in vitro. Si è fatto un confronto fra l'azione della tossina difterica e quella di altre tossine batteriche come la O-streptolisina, la-stafilotossina e la tossina tetanica sui mitocondri di cellule di cuore di embrione di pollo coltivate in vitro. Solo la tossina difterica ha manifestato capacità rigonfianti mentre le altre tossine, alle dosi usate e con questo tipo di cellule, sono apparse sprovviste di questa proprietà.     

Demonstration of dopaminergic receptors in human pituitary adenomas secreting prolactin]

3H Domperidone binding on cellular membranes from human prolactin adenomas demonstrates the presence of two dopaminergic binding sites. The mean value of the dissociation constant (Kd) for five adenomas is of 0.29 +/- 0.14 nM for the first site and of 4.19 +/- 1.56 nM for the second site. The maximal number of binding sites (Bmax) varies from one adenoma to another. The binding is completely displaced at 30 nM of tritiated Domperidone by apomorohine, a specific dopaminergic agonist.     

Mitochondrial dynamics in cell death and neurodegeneration

Mitochondria are highly dynamic organelles that continuously undergo two opposite processes, fission and fusion. Mitochondrial dynamics influence not only mitochondrial morphology, but also mitochondrial biogenesis, mitochondrial distribution within the cell, cell bioenergetics, and cell injury or death. Drp1 mediates mitochondrial fission, whereas Mfn1/2 and Opa1 control mitochondrial fusion. Neurons require large amounts of energy to carry out their highly specialized functions. Thus, mitochondrial dysfunction is a prominent feature in a variety of neurodegenerative diseases. Mutations of Mfn2 and Opa1 lead to neuropathies such as Charcot-Marie-Tooth disease type 2A and autosomal dominant optic atrophy. Moreover, both Aβ peptide and mutant huntingtin protein induce mitochondrial fragmentation and neuronal cell death. In addition, mutants of Parkinson’s disease-related genes also show abnormal mitochondrial morphology. This review highlights our current understanding of abnormal mitochondrial dynamics relevant to neuronal synaptic loss and cell death in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and Huntington’s disease.     

Daily rhythms in the endocrine glands of drosophila larvae

Zusammenfassung Neurosekretorische Zellen, Corpus allatum, Prothoraxdrüsen- und Fettkörperzellen in Drosophilalarven zeigen tägliche, zweigipflige Schwankungen der Zellkerngrösse. Ein ähnliches Muster konnte auch in den Nucleoli der Prothoraxdrüsen beobachtet werden.     

Minimal assumption derivation of a weak Clauser–Horne inequality

According to Bell's theorem a large class of hidden-variable models obeying Bell's notion of local causality (LC) conflict with the predictions of quantum mechanics. Recently, a Bell-type theorem has been proven using a weaker notion of LC, yet assuming the existence of perfectly correlated event types. Here we present a similar Bell-type theorem without this latter assumption. The derived inequality differs from the Clauser–Horne inequality by some small correction terms, which render it less constraining.     

Mitochondrial swelling induced by unconjugated bilirubin in vitro

Riassunto Gli Autori hanno studiato, per mezzo del microscopio in contrasto di fase e del microscopio a contrasto di fase interferenziale, le modificazioni della morfologìa dei mitocondri di cellule coltivate in vitro e sottoposte all'azione della bilirubina non coniugata. Questo pigmento biliare induce, dopo 15 min di contatto con le cellule, la perdita della motilità mitocondriale e dopo 30 min un evidente rigonfiamento dei mitocondri. Viene discussa l'interpretazione dei risultati sulla base dei dati morfològici e biochimici ottenuti da altri Autori su mitocondri isolati.     

重症急性胰腺炎病人外周血单个核细胞线粒体DNA拷贝数的意义

目的探讨重症急性胰腺炎患者外周血单个核细胞线粒体DNA拷贝数与患者病情严重程度、预后的相关性。方法分离研究对象（重症急性胰腺炎患者34名,健康对照组17名）外周血单个核细胞,采用荧光实时定量PCR检测各组PBMC线粒体DNA相对舍量,其与严重程度、预后的相关性。结果重症急性胰腺炎患者线粒体DNA含量较健康对照组明显降低（P〈0．05）。患者单个核细胞线粒体DNA拷贝教与APACHEⅡ评分呈负相关（r=-0．425）其中并发症组mtDNA拷贝数显著低于无并发症组（P〈0．05）。结论重症急性胰腺炎患者外周血单个核细胞中线粒体DNA含量显著下降,与患者APACHEⅡ评分呈负相关,且低水平的线粒体DNA拷贝数提示并发症发生率的升高,因此,线粒体DNA拷贝数可作为潜在评估患者病情危重程度及预后的指标,这一发现值得进一步大型,前瞻性的研究。     

Behavior and endocrine effects of 3,4,5-trimethoxyamphetamine in male mice

Summary Effects of single doses of 50 and 100 mg/kg of TMA given i.p. were noted in male albino mice after 40 min and 2 1/2 h. Locomotor activity was significantly altered and biochemical tests indicated stimulatory effects on adrenocortical and adrenomedullary functions due to TMA.     

Mitochondrial bioenergetics decay in aging: beneficial effect of melatonin

Aging is a biological process characterized by progressive decline in physiological functions, increased oxidative stress, reduced capacity to respond to stresses, and increased risk of contracting age-associated disorders. Mitochondria are referred to as the powerhouse of the cell through their role in the oxidative phosphorylation to generate ATP. These organelles contribute to the aging process, mainly through impairment of electron transport chain activity, opening of the mitochondrial permeability transition pore and increased oxidative stress. These events lead to damage to proteins, lipids and mitochondrial DNA. Cardiolipin, a phospholipid of the inner mitochondrial membrane, plays a pivotal role in several mitochondrial bioenergetic processes as well as in mitochondrial-dependent steps of apoptosis and in mitochondrial membrane stability and dynamics. Cardiolipin alterations are associated with mitochondrial bienergetics decline in multiple tissues in a variety of physiopathological conditions, as well as in the aging process. Melatonin, the major product of the pineal gland, is considered an effective protector of mitochondrial bioenergetic function. Melatonin preserves mitochondrial function by preventing cardiolipin oxidation and this may explain, at least in part, the protective role of this compound in mitochondrial physiopathology and aging. Here, mechanisms through which melatonin exerts its protective role against mitochondrial dysfunction associated with aging and age-associated disorders are discussed.