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This paper aims to develop a better understanding of what proponents of natural childbirth mean by 'natural.' Using a biosocial approach to birth that posits that all birth is both social and natural, the paper investigates how proponents represent the relationship between nature and society. The study asks about what kinds of nature-society relationships are expressed in proponents' representations of natural childbirth. The study examines how natural childbirth is represented by proponents in popular non-fictional English language books written for pregnant women. Claims in these books are not taken as reality, but are analyzed as ideas about nature-society relations. The central finding is that these authors simultaneously emphasize the naturalness of birth and showcase three types of social practices that they describe as being integral to natural childbirth: (1) activity during birth, (2) preparation before birth, and (3) social support, both in an individual and in a broader socio-cultural sense. At least for these authors, it is these social practices that allow natural childbirth to be natural. These findings on the social nature of natural childbirth challenge current social science scholarship, in which natural childbirth is characterized as an essentializing and nostalgic attempt to return to nature. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor in response to an article about the decision of the Arbitral Tribunal on the case concerning the southern bluefin tuna.

Patients with glycogen storage disease type Ia (GSD-Ia) develop renal disease of unknown etiology despite intensive dietary therapies. This renal disease shares many clinical and pathological similarities to diabetic nephropathy. We studied the expression of angiotensinogen, angiotensin type 1 receptor, transforming growth factor-β1, and connective tissue growth factor in mice with GSD-Ia and found them to be elevated compared to controls. While increased renal expression of angiotensinogen was evident in 2-week-old mice with GSD-Ia, the renal expression of transforming growth factor-β and connective tissue growth factor did not increase for another week; consistent with upregulation of these factors by angiotensin II. The expression of fibronectin and collagens I, III, and IV was also elevated in the kidneys of mice with GSD-Ia, compared to controls. Renal fibrosis was characterized by a marked increase in the synthesis and deposition of extracellular matrix proteins in the renal cortex and histological abnormalities including tubular basement membrane thickening, tubular atrophy, tubular dilation, and multifocal interstitial fibrosis. Our results suggest that activation of the angiotensin system has an important role in the pathophysiology of renal disease in patients with GSD-Ia.Kidney International (2008) 73, 716–723; doi:10.1038/sj.ki.5002718; published online 12 December 2007 [ABSTRACT FROM AUTHOR]

Glycogen storage disease type Ia (GSD-Ia) is caused by a deficiency in glucose-6-phosphatase-α (G6Pase-α), a nine-transmembrane domain, endoplasmic reticulum-associated protein expressed primarily in the liver and kidney. Previously, we showed that infusion of an adeno-associated virus (AAV) serotype 2 vector carrying murine G6Pase-α (AAV2-G6Pase-α) into neonatal GSD-Ia mice failed to sustain their life beyond weaning. We now show that neonatal infusion of GSD-Ia mice with an AAV serotype 1-G6Pase-α (AAV1-G6Pase-α) or AAV serotype 8-G6Pase-α (AAV8-G6Pase-α) results in hepatic expression of the G6Pase-α transgene and markedly improves the survival of the mice. However, only AAV1-G6Pase-α can achieve significant renal transgene expression. A more effective strategy, in which a neonatal AAV1-G6Pase-α infusion is followed by a second infusion at age one week, provides sustained expression of a complete, functional, G6Pase-α system in both the liver and kidney and corrects the metabolic abnormalities in GSD-Ia mice for the 57 week length of the study. This effective use of gene therapy to correct metabolic imbalances and disease progression in GSD-Ia mice holds promise for the future of gene therapy in humans.Gene Therapy (2006) 13, 321–329. doi:10.1038/sj.gt.3302650; published online 29 September 2005 [ABSTRACT FROM AUTHOR]