Injury assessment of nonhuman subjects may be performed for a variety of reasons, most often in a forensic setting to prove or disprove human activity. In Adelaide, South Australia, the killing of several dolphins from nearby waterways prompted the formation of a multidisciplinary Dolphin Trauma Group, among whose aims was the performance of rapid biological and forensic assessments of dead local dolphins. Necropsy and wound evaluation by group members utilizing standard forensic techniques aimed at determining as quickly as possible causes of death, whether injuries were inflicted ante- or postmortem, whether injuries were responsible for, or had contributed to, the fatal episode, and whether human intervention was responsible for the wounds. Estimation of the type and dimensions of possible weapons was also undertaken, as well as attempts to determine possible time frames for the injuries. This information was then passed on to investigating officers. A series of necropsy findings in seven dolphins investigated by the group (four Indo-Pacific bottlenose dolphins, one southern right whale dolphin, one short-beaked common dolphin, and one common bottlenose dolphin) is described in this chapter. Two deaths were caused by exsanguination from stabbing/spearing, two to the sequelae of entanglement with fishing gear, one to blunt craniocerebral trauma from a boat propeller injury, one to probable sepsis, and one remained undetermined. All cases had extensive histological assessment of tissues with retention of blood and tissues for future toxicological screening if required. Examination of the brain is undertaken by a neuropathologist when tissues are not putrefied. Blood spots are signed and sealed and transferred to Forensic Science South Australia for storage in case comparisons are subsequently required with blood and tissue on possible weapons. In this way, each dolphin has an extensive forensic evaluation to provide as much usable information to courts and prosecutors if legal proceedings are ever undertaken.The skeletons and life history samples are held in the collections of the South Australian Museum.

Keywords Gestational diabetes.Glucokinase.MODY-2AbbreviationsHAPO Hyperglycemia Adverse Pregnancy OutcomeLGA Large for gestational ageSGA Small for gestational ageTo the Editor: We read with interest the paper by E. A. Ryan[1] concerning the new criteria suggested by the Hypergly-cemia Adverse Pregnancy Outcome (HAPO) study for thediagnosis of gestational diabetes [2]. Ryan showed thatapplying these criteria would result in a doubling of thenumber of pregnant women diagnosed with gestationaldiabetes without a clear demonstration of the benefitsderived from this new classification. As he observes,maternal obesity represents a stronger predictor of large-for-gestational-age (LGA) babies than glucose levels in allexcept the highest glucose category [1, 3]. This suggeststhat not all gestational hyperglycaemia has the sameaetiology. As was the case in paediatrics, where for manydecades we wrongly diagnosed all children with hyper-glycaemia as having type 1 diabetes [4], we risk includingin this generic categorisation of gestational diabetes theundetected monogenic forms that are often underdiagnosed[5, 6]. For example, in those patients belonging to thelowest glucose categories of HAPO those with MODY-2obtain no benefit from the treatment of their hyperglycae-mia. In the 11 patients with MODY-2 that we followed up

The LaryngoscopeVolume 116, Issue 3 p. 505-506 Article Diabetes, Sensorineural Deafness, and Mitochondrial DNA Mutation Francesco Prisco PhD, MD, Francesco Prisco PhD, MD Department of Pediatrics, Second University of Naples, ItalySearch for more papers by this authorDario Iafusco MD, Dario Iafusco MD Department of Pediatrics, Second University of Naples, ItalySearch for more papers by this author Francesco Prisco PhD, MD, Francesco Prisco PhD, MD Department of Pediatrics, Second University of Naples, ItalySearch for more papers by this authorDario Iafusco MD, Dario Iafusco MD Department of Pediatrics, Second University of Naples, ItalySearch for more papers by this author First published: 02 January 2009 https://doi.org/10.1097/01.mlg.0000200855.58539.2eRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume116, Issue3March 2006Pages 505-506 RelatedInformation

In addition to insulin therapy, diet and education, regular physical activity is usually considered to play a key role in the management of children and adolescents with type 1 diabetes mellitus (T1DM). It improves insulin sensitivity, increases glucose utilization, reduces cardiovascular risk factors, and helps to prevent obesity...

Zonulin, a protein that modulates intestinal permeability, is upregulated in several autoimmune diseases and is involved in the pathogenesis of autoimmune diabetes in the BB/Wor animal model of the disease. To verify the association between serum zonulin levels and in vivo intestinal permeability in patients with type 1 diabetes, both parameters were investigated in different stages of the autoimmune process. Forty-two percent (141 of 339) of the patients had abnormal serum zonulin levels, as compared with age-matched control subjects. The increased zonulin levels correlated with increased intestinal permeability in vivo and changes in claudin-1, claudin-2, and myosin IXB genes expression, while no changes were detected in ZO1 and occludin genes expression. When tested in serum samples collected during the pre–type 1 diabetes phase, elevated serum zonulin was detected in 70% of subjects and preceded by 3.5 ± 0.9 years the onset of the disease in those patients who went on to develop type 1 diabetes. Combined, these results suggest that zonulin upregulation is associated with increased intestinal permeability in a subgroup of type 1 diabetic patients. Zonulin upregulation seems to precede the onset of the disease, providing a possible link between increased intestinal permeability, environmental exposure to non–self antigens, and the development of autoimmunity in genetically susceptible individuals.

In a previous commentary to DiMeglio et al1DiMeglio L.A. Pottorff T.M. Boyd S.R. France L. Fineberg N. Eugester E.A. A randomized, controlled study of insulin pump therapy in diabetic preschoolers.J Pediatr. 2004; 145: 380-384Abstract Full Text Full Text PDF PubMed Scopus (146) Google Scholar about factors predicting success of continuous subcutaneous insulin infusion (CSII), we reported the results of the introduction of pump therapy in two Italian Centers for Pediatric Diabetology, where patients were enrolled with somewhat different entrance criteria.2Iafusco D. Confetto S. Prisco F. Lombardo F. Salzano G. De Luca F. The egg or the chicken? Should good compliance to multi-injection insulin therapy be a criterion for insulin pump therapy, or does insulin pump therapy improve compliance.J Pediatr. 2006; 148 (reply 421-2): 421Abstract Full Text Full Text PDF PubMed Scopus (7) Google Scholar The introduction of CSII in patients with poor compliance to the multi-injection therapy and higher HbA1c levels (so called “chicken” patients from Naples, group B) was followed by a reduction of HbA1c to the same levels of the patients with previous good compliance (so called “egg” patients from Messina, group A). In their response, DiMeglio et al recommended duration of the improvement of HbA1c by pump be determined before considering CSII therapy as a standard option for adolescents in poor control. Since our first description, CSII has been implanted in the two centers in other several patients chosen with almost the same criteria (“chicken” in Naples and “egg” in Messina). At present, 139 subcutaneous insulin pumps have been implanted (48 in Naples, mean HbA1c, 9.4 ± 1.4, and 91 in Messina, mean HbA1c, 7.9 ± 1.2; P < .0001) in patients ranging between 5.9 and 33.2 years of age (average, 15.6 ± 3.9). We evaluated the prevalence of dropouts from the CSII to multi-injection therapy. Eighteen (12.9%) patients (9 males and 9 females) dropped out from CSII. There was no statistically significant difference between Naples (14.6%) and Messina (12%; P = .9). The percentage of dropouts was statistically higher in the first year than in the second year (7.3% vs 4%; P < .001) and in the first 6 months than in the following 6 months (4.6% vs 2.79%; P < .001). Our data demonstrate that the enrolment criteria on the basis of metabolic control do not predict the dropout rate. Pump therapy compliance should be assessed at least 6 months after implantation.

To the Editor, Activating missense mutations in the gene encoding potassium inwardly rectifying channel, subfamily J, member 11 (KCNJ11) represent the most common cause (40 to 64%, depending on populations) of permanent neonatal diabetes mellitus in patients diagnosed in the first 6 months of life [1, 2]. In addition, KCNJ11 activating mutations can lead to transient/relapsing neonatal diabetes [3, 4]. The KCNJ11 gene encodes the pore-forming subunit (also known as KIR6.2) of the pancreatic beta cell ATP-sensitive potassium channel (KATP), which exerts a pivotal role in glucose-regulated insulin release. In the beta cell, KIR6.2 forms a hetero-octameric complex (4:4) with the sulfonylurea receptor subtype 1 (SUR1); binding to SUR1 by sulfonylureas determines channel closure and insulin secretion [2]. In previously published cases, seven patients have been reported to respond well to the transfer from insulin to oral hypoglycaemic agents [4–8]. Here we report on the replacement of insulin with sulfonylureas in ten Italian children who have mutations in KCNJ11 (R50P, V59M [x4], K170R, R201C and R201H [x3]) and were followed in nine Diabetologia (2006) 49:2210–2213 DOI 10.1007/s00125-006-0329-x