Molecular insights into the novel aspects of diatom biology

Diatoms are unicellular photosynthetic eukaryotes that are thought to contribute as much as 25% of global primary productivity. In spite of their ecological importance in the worlds oceans, very little information is available at the molecular level about the novel aspects of their biology. Recent advances, such as the development of gene transfer protocols, are now allowing the genetic dissection of diatom biology. Notable examples are advances in understanding the genetic basis for the silica-based bioinorganic pattern formation of their cell walls and for elucidating key aspects of diatom ecophysiology. The potentiation of current research will allow an evaluation of the use of diatoms to construct submicrometre-scale silicon structures for the nanotechnology industry and will reveal the molecular secrets underlying their ecological success. Received 29 March 2001; received after revision 31 May 2001; accepted 31 May 2001     

The human selenoproteome: recent insights into functions and regulation

Selenium (Se) is a nutritional trace mineral essential for various aspects of human health that exerts its effects mainly through its incorporation into selenoproteins as the amino acid, selenocysteine. Twenty-five selenoprotein genes have been identified in humans and several selenoproteins are broadly classified as antioxidant enzymes. As progress is made on characterizing the individual members of this protein family, however, it is becoming clear that their properties and functions are quite diverse. This review summarizes recent insights into properties of individual selenoproteins such as tissue distribution, subcellular localization, and regulation of expression. Also discussed are potential roles the different selenoproteins play in human health and disease.     

Progesterone regulation of implantation-related genes: new insights into the role of oestrogen

Genomic profiling was performed on explants of late proliferative phase human endometrium after 24-h treatment with progesterone (P) or oestradiol and progesterone (17β-E₂+P) and on explants of menstrual phase endometrium treated with 17β-E₂+P. Gene expression was validated with real-time PCR in the samples used for the arrays, in endometrium collected from early and mid-secretory phase endometrium, and in additional experiments performed on new samples collected in the menstrual and late proliferative phase. The results show that late proliferative phase human endometrium is more responsive to progestins than menstrual phase endometrium, that the expression of several genes associated with embryo implantation (i.e. thrombomodulin, monoamine oxidase A, SPARC-like 1) can be induced by P in vitro, and that genes that are fully dependent on the continuous presence of 17β-E₂ during P exposure can be distinguished from those that are P-dependent to a lesser extent. Therefore, 17β-E₂ selectively primes implantation-related genes for the effects of P. H. Dassen, C. Punyadeera: These authors contributed equally. Received 18 December 2006; received after revision 6 February 2007; accepted 8 March 2007     

Splenic thymidine kinase and DNA during early postnatal development of the androgenized female rat

Administration of a pharmacologic dose of testosterone propionate to neonatal female rats had no effect on either thymidine kinase activity or DNA synthesis in the spleen during the first 3 postnatal weeks.     

The murine complement regulator Crry: new insights into the immunobiology of complement regulation

Complement has an important role in inflammation and in the normal function of the immune system. Activated complement fragments have the capacity to bind and damage self-tissues. Cells from vertebrates express on their surface regulators of complement activation that protect them from the deleterious effects of cell-bound complement fragments. Abnormalities in these regulators of complement activation may participate in the pathogenesis of autoimmune diseases and inflammatory disorders. Murine Crry is one of these regulators that inhibits the activation of the third component of complement and protects self-tissues from complement-mediated damage. Experimental work on Crry has increased our understanding of the immunobiology of complement regulation and the potential role of complement and complement inhibitors in the development and treatment of human diseases. Received 13 June 2001; received after revision 12 July 2001; accepted 9 August 2001     

Na,K ATPase activity during early postnatal development of the rat submandibular gland

Summary The activity of the ouabain-sensitive Na, K ATPase was measured in membrane fractions of the submandibular gland of 1-, 7-, 14- and 21-day-old rats. This activity increased with age and reached adult levels by 21 days.     

Na, K ATPase activity during early postnatal development of the rat submandibular gland

The activity of the ouabain-sensitive Na, K ATPase was measured in membrane fractions of the submandibular gland of 1-, 7-, 14- and 21-day-old rats. This activity increased with age and reached adult levels by 21 days.     

Incorporation of32P into renal phospholipids of mice during postnatal growth

Summary During the first 40 days of life the rate of incorporation of³²P into total phospholipids and into phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, sphingomyelin, diphosphatidylglycerol, phosphatidic acid and phosphatidylinositol of mouse kidney was by some 25–35% higher than in older animals. Results suggest a different involvement of cellular membranes during of normal and compensatory renal growth.     

Incorporation of 32P into renal phospholipids of mice during postnatal growth

During the first 40 days of life the rate of incorporation of 32P into total phospholipids and into phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, sphingomyelin, diphosphatidylglycerol, phosphatidic acid and phosphatidylinositol of mouse kidney was by some 25-35% higher than in older animals. Results suggest a different involvement of cellular membranes during of normal and compensatory renal growth.     

On temperature regulation and metabolism in the swift,Micropus aapus L., during fasting

Zusammenfassung Durch vollständiges Fasten können junge und erwachsene Mauersegler in eine Art von Erstarrungszustand versetzt werden. Hierbei sinkt ihre Körpertemperatur nach 24stündigem Schlaf beinahe bis auf die Temperatur der Umgebung). So wurde zum Beispiel am 7. Fasttag bei 19°C eine Körpertemperatur von 21°C gemessen. Während des Tages wurde die Temperatur wieder annähernd normal. Der Erstarrungszustand ist bei Jungtieren am deutlichsten. Bei den erwachsenen Mauerseglern gibt es Störungen der Temperaturregulation; der Tod tritt schneller ein als bei den jungen Individuen. Die Jungtiere können bedeutend länger fasten als die ausgewachsenen Mauersegler, da sie reichlich Reservestoffe besitzen (das durchschnittliche Gewicht der Jungen ist etwa siebenmal größer als das der Erwachsenen). Überdies ist der Stoffwechsel im Erstarrungszustand verlangsamt. In der Natur dürfte diese vom Verfasser festgestellte Hungerstarre während der Zeit des schlechten Wetters eine große Bedeutung besitzen, wenn die Mauersegler — und zwar vor allem ihre Jungen — kein Futter bekommen können.     

Novel insights into the biology of interleukin-32

Interleukin (IL)-32 is known as a proinflammatory cytokine that is likely involved in several diseases, including infections, chronic inflammation, and cancer. Since the first report in 2005, IL-32 has been the subject of numerous studies to unravel the biological function of this molecule. For example, silencing of endogenous IL-32 in primary or cell lines of human origin consistently suppressed responses to Toll-like receptors. The protein folding structure of the six isoforms of IL-32 does not resemble that of any classical cytokine and as of this writing, a specific IL-32 receptor has not been identified. Instead, we propose a mechanism by which exposure to extracellular IL-32 or overexpression of the molecule results in binding to intracellular partners that influences functions such as gene expression, cell death, or survival. As such, this review offers insights into the role of IL-32 in several diseases, host defense, inflammation, immune function, and cancer. Finally, possibilities to target IL-32 in several diseases are proposed.     

New insights into the molecular mechanisms of sperm-egg interaction

At the moment of insemination millions of mammalian sperm cells are released into the female reproductive tract in order to find a single cell – the oocyte. The spermatozoa subsequently ignore the thousands of cells they make contact with during their journey to the site of fertilisation, until they reach the surface of the oocyte. At this point, they bind tenaciously to the acellular coat, known as the zona pellucida, that surrounds the oocyte and initiate the chain of cellular interactions that will culminate in fertilization. These exquisitely cell- and species-specific recognition events are among the most strategically important cellular interactions in biology. Understanding the cellular and molecular mechanisms that underpin them has implications for diagnosis of the aetiology of human infertility and the development of novel targets for fertility regulation. Herein, we describe two models indicating the plethora of highly orchestrated molecular interactions underlying successful sperm zona binding and sperm oocyte fusion. Received 17 December 2006; received after revision 31 January 2007; accepted 16 March 2007     

New insights into the metabolic and molecular basis for diabetic neuropathy

Diabetic polyneuropathy is the most common complication of diabetes mellitus. Several interactive pathogenetic mechanisms have been identified mainly in streptozotocin-induced diabetes in rats and have been ascribed to hyperglycemia. Over the last number of years it is becoming increasingly clear that diabetic neuropathy differs in type 1 and type 2 diabetes in humans and in murine models that more accurately mimic the human disorders. Beside hyperglycemia, attention is increasingly being paid to the pathogenetic roles of insulin and C-peptide deficiencies, particularly in type 1 diabetic neuropathy. There is now evidence to suggest that insulin and C-peptide deficiencies are mainly responsible for perturbations of neurotrophic factors and contribute to oxidative stress in diabetic nerve. This may also be true for apoptotic phenomena afflicting both the peripheral and central nervous systems in diabetes. The new data have lead to re-evaluations of pathogenetic components in this complex disorder, and their further exploration is likely to form a more refined basis for future therapeutic and preventive measures.Received 25 February 2003; received after revision 12 May 2003; accepted 19 May 2003