Salmonella bovis morbificans in man and animal

Summary A 6 month old baby suffered from acute gastroenteritis with mucosanguinolent stools in whichSalmonella bovis morbificans could be cultivated. The child lived together with an old crippled woman who had presented earlier a long lasting enteritis with mucosanguinolent stools. It was impossible to trace the way in which infection was acquired. Experience ofS. bovis morbificans infections in animals is mentioned with a survey of literature.     

Infection withSalmonella anatum of the cow in connection with salmonellosis of ducks

Summary S. anatum was cultivated from the liver and the gall-bladder of a cow, slaughtered in emergency. Among the ducks of the same farm an infection with the sameSalmonella type was found. It is obvious that the infection of the cow was caused by the contaminated faeces of the ducks.So far as we are aware noS. anatum has previously been described from cattle.     

Three-dimensional cancer cell culture in high-yield multiscale scaffolds by shear spinning

Polymeric scaffolds comprising two size scales of microfibers and submicron fibers can better support three-dimensional (3D) cell growth in tissue engineering, making them an important class of healthcare material. However, a major manufacturing barrier hampers their translation into wider practical use: scalability. Traditional production of two-scale scaffolds by electrospinning is slow and costly. For day-to-day cell cultures, the scaffolds need to be affordable, made in high yield to drive down cost. Combining expertise from academia and industry from the United Kingdom and United States, this study uses a new series of high-yield, low-cost scaffolds made by shear spinning for tissue engineering. The scaffolds comprise interwoven submicron fibers and microfibers throughout as observed under scanning electron microscopy and demonstrate good capability to support cell culturing for tumor modeling. Three model human cancer cell lines (HEK293, A549 and MCF-7) with stable expression of GFP were cultured in the scaffolds and found to exhibit efficient cell attachment and sustained 3D growth and proliferation for 30 days. Cryosection and multiphoton fluorescence microscopy confirmed the formation of compact 3D cell clusters throughout the scaffolds. In addition, comparative growth curves of 2D and 3D cultures show significant cell-type-dependent differences. This work applies high-yield shear-spun scaffolds in mammalian tissue engineering and brings practical, affordable applications of multiscale scaffolds closer to reality. © 2018 American Institute of Chemical Engineers Biotechnol. Prog., 35: e2750, 2019.     

Centrosome defects cause microcephaly by activating the 53BP1‐USP28‐TP53 mitotic surveillance pathway

Mutations in centrosome genes deplete neural progenitor cells (NPCs) during brain development, causing microcephaly. While NPC attrition is linked to TP53‐mediated cell death in several microcephaly models, how TP53 is activated remains unclear. In cultured cells, mitotic delays resulting from centrosome loss prevent the growth of unfit daughter cells by activating a pathway involving 53BP1, USP28, and TP53, termed the mitotic surveillance pathway. Whether this pathway is active in the developing brain is unknown. Here, we show that the depletion of centrosome proteins in NPCs prolongs mitosis and increases TP53‐mediated apoptosis. Cell death after a delayed mitosis was rescued by inactivation of the mitotic surveillance pathway. Moreover, 53BP1 or USP28 deletion restored NPC proliferation and brain size without correcting the upstream centrosome defects or extended mitosis. By contrast, microcephaly caused by the loss of the non‐centrosomal protein SMC5 is also TP53‐dependent but is not rescued by loss of 53BP1 or USP28. Thus, we propose that mutations in centrosome genes cause microcephaly by delaying mitosis and pathologically activating the mitotic surveillance pathway in the developing brain.     

Self‐Euthanasia,the Dutch Experience: In Search for the Meaning of a Good Death or Eu Thanatos

My main purpose in this article is to establish the meaning of a ‘good death’ when death is self‐chosen. I will take as my point of departure the new notion of ‘self‐euthanasia’ and the corresponding practice that has evolved in the Netherlands in recent years. Both physician‐euthanasia and self‐euthanasia refer to an ideal process of a good death, the first being ultimately the physician's responsibility, while the second is definitely the responsibility of the individual choosing to die. However, if we also accept the existence of a fundamental moral difference between ending another person's life and ending your own life, and if we accept this moral difference to be also relevant to the normatively laden good death, then this difference represents a strong reason for preferring self‐euthanasia to physician‐euthanasia.     

Phospholipase C activity reduces free magnesium concentration

The events leading to decline of intracellular free magnesium concentration following traumatic brain injury are unknown. One possible mechanism that may lead to such declines is an alteration in the number and nature of magnesium binding sites within cell membranes following a traumatic event. Although both alterations in membrane structure and decrease in free magnesium concentration have been independently demonstrated to occur following brain trauma, no correlations between the two events have been shown. In the present study, rat brain phospholipids were extracted and reconstituted in MgATP containing aqueous solutions. Using 31P magnetic resonance spectroscopy to measure free magnesium concentration, enzymatic hydrolysis of the artificial membrane vesicles by phospholipase C was shown to reduce the free magnesium concentration. Since activation of phospholipase C has been demonstrated to occur following traumatic brain injury, we propose that this event may initiate decline in free magnesium levels in vivo.