Plasma Insulin during Remission in Juvenile Diabetes Mellitus

Three juvenile diabetics in partial remission were studied before and after the recurrence of overt diabetes. The remissions were partial because glucose tolerance never returned to normal. However, it improved sufficiently to cause the discontinuance of insulin therapy for at least four months.The insulin output in response to double glucose tolerance tests was increased during remission. The degree of remission seemed to be related to the magnitude of the insulin response to glucose. In two of the patients the increase was low and the response very slight. The third patient, however, had a delayed hyper-response and his carbohydrate tolerance during the remission was much more improved than those of the other patients.     

Screening for antimicrobial resistance genes and virulence factors via genome sequencing

Second-generation genome sequencing and alignment of the resulting reads to in silico genomes containing antimicrobial resistance and virulence factor genes were used to screen for undesirable genes in 28 strains which could be used in human nutrition. No virulence factor genes were detected, while several isolates contained antimicrobial resistance genes.     

Recessive Resistance in Pisum sativum and Potyvirus Pathotype Resolved in a Gene-for-Cistron Correspondence between Host and Virus

Pea seed-borne mosaic potyvirus (PSbMV) isolates are divided into pathotypes P-1, P-2, and P-4 according to their infection profile on a panel of Pisum sativum lines. P. sativum PI 269818 is resistant to P-1 and P-2 isolates and is susceptible to P-4 isolates. Resistance to P-1 is inherited as a single recessive gene, denoted sbm-1, and the pathogenicity determinant has previously been mapped to the virus-coded protein VPg. In the cultivar Bonneville, a second recessive gene, sbm-2, confers specific resistance to P-2. By exchanging cistrons between a P-2 and a P-4 isolate, the P3-6k1 cistron was identified as the PSbMV host-specific pathogenicity determinant on Bonneville. Exchange of P3-6k1 did not affect infection on PI 269818, and infection of Bonneville was not altered by substitution of the VPg cistron, indicating that P3-6k1 and VPg are independent determinants of pathotype-specific infectivity. On PI 269818 the pathogenicity determinant of both P-1 and P-2 mapped to the N terminus of VPg. This suggests that VPg from the P-1 and P-2 isolates are functionally similar on this host and that resistance to P-1 and P-2 in PI 269818 may operate by the same mechanism. Identification of VPg-sbm-1 and P3-6k1-sbm-2 as independent pairs of genetic interactors between PSbMV and P. sativum provides a simple explanation of the three known pathotypes of PSbMV. Furthermore, analysis of beta-glucuronidase-tagged P-2 virus indicated that sbm-2 resistance affected an early step in infection, implying that the P3-6k1 region plays a critical role in potyvirus replication or cell-to-cell movement.     

Simulating transmission and control of Taenia solium infections using a Reed-Frost stochastic model

The transmission dynamics of the human-pig zoonotic cestode Taenia solium are explored with both deterministic and stochastic versions of a modified Reed-Frost model. This model, originally developed for microparasitic infections (i.e. bacteria, viruses and protozoa), assumes that random contacts occur between hosts and that hosts can be either susceptible, infected or 'recovered and presumed immune'. Transmission between humans and pigs is modelled as susceptible roaming pigs scavenging on human faeces infected with T. solium eggs. Transmission from pigs to humans is modelled as susceptible humans eating under-cooked pork meat harbouring T. solium metacestodes. Deterministic models of each scenario were first run, followed by stochastic versions of the models to assess the likelihood of infection elimination in the small population modelled. The effects of three groups of interventions were investigated using the model: (i) interventions affecting the transmission parameters such as use of latrines, meat inspection, and cooking habits; (ii) routine interventions including rapid detection and treatment of human carriers or pig vaccination; and (iii) treatment interventions of either humans or pigs. It is concluded that mass-treatment can result in a short term dramatic reduction in prevalence, whereas interventions targeting interruption of the life cycle lead to long-term reduction in prevalence.