Enterococcus gallinarum N04-0414 harbors a VanD-type vancomycin resistance operon and does not contain a D-alanine:D-alanine 2 (ddl2) gene

Enterococcus gallinarum N04-0414 (MIC for vancomycin, 256 microg/ml) harbored a vanD-type vancomycin resistance operon as well as the intrinsic vanC1 operon. The D-Ala:D-Ala ligase 2 gene (ddl2) was not present in the strain, though it is found downstream of the vanS gene from the vanC operon in E. gallinarum ATCC 49573 and 19 other E. gallinarum strains tested.     

Missed Insulin Boluses for Snacks in Youth With Type 1 Diabetes

OBJECTIVE

To evaluate the effects of missed insulin boluses for snacks in youth with type 1 diabetes.

RESEARCH DESIGN AND METHODS

Three months of simultaneous continuous subcutaneous insulin infusion and continuous glucose monitoring data from nine subjects were retrospectively evaluated. Glucose excursions between 1330 and 1700 h were defined as relating to snacks with insulin or snacks with no insulin administered. Area under the curve >180 mg/dl (AUC >180), average Δ glucose, and rate of change were analyzed and compared within and between groups.

RESULTS

A total of 94 snacks without insulin and 101 snacks with insulin were analyzed. Snacks without insulin had significantly higher log (AUC >180 + 1) (1.26 vs. 0.44 mg/dl per event; P < 0.001), Δ glucose (114 vs. 52 mg/dl; P < 0.001), and average rate of change (1.3 vs. 1.1 mg/dl per minute; P < 0.001).

CONCLUSIONS

This study shows that afternoon snacks without insulin boluses are common and result in significantly higher glucose excursions than snacks with insulin administration.Previous studies have demonstrated the deleterious effect of missed insulin doses for meals (1–4). None, however, have examined the effect of missed insulin boluses for snacks. Because youth frequently snack when unsupervised, it is likely that missed insulin boluses are even more common for snacks than for meals. The purpose of this investigation was to use data from continuous glucose monitoring (CGM) and continuous subcutaneous insulin infusion (CSII) together to evaluate the glycemic profiles of missed insulin boluses for afternoon snacks.     

In vitro effect of captopril and three captopril metabolites on neutrophilic progenitor cells from normal mice and mice given busulfan

Neutrophilic progenitor cells (CFU-NM) in mice with busulfan-induced latent bone marrow hypoplasia have been shown to be selectively suppressed by captopril in vivo. To study this further, marrow from mice given busulfan was used to test for myelotoxicity in vitro. It was found that myelotoxic agents, such as doxorubicin, cytarabine, 1,3-bis(2-chloroethyl)-1-nitrosourea, and chloramphenicol have the same suppressive effect in vitro on CFU-NM obtained from normal marrow as obtained from marrow of mice given busulfan. Our results suggest that in vitro, the CFU-NMs from mice given busulfan are not excessively sensitive to the action of at least these myelotoxic agents. It was also found that neither captopril nor three known captopril metabolites suppress CFU-NM from mice given busulfan. This result suggests either that the myelotoxicity induced in vivo by captopril is not caused by the parent compound or any of the three metabolites tested, or more likely, that the suppressive action of captopril on CFU-NM in vivo is caused by the suppression of an earlier myeloid progenitor cell.     

Cyanovirin-N, a potent human immunodeficiency virus-inactivating protein, blocks both CD4-dependent and CD4-independent binding of soluble gp120 (sgp120) to target cells, inhibits sCD4-induced binding of sgp120 to cell-associated CXCR4, and dissociates bound sgp120 from target cells

Cyanovirin-N (CV-N), an 11-kDa protein originally isolated from the cyanobacterium Nostoc ellipsosporum, potently inactivates diverse strains of human immunodeficiency virus type 1 (HIV-1), HIV-2, simian immunodeficiency virus, and feline immunodeficiency virus. It has been well established that the HIV surface envelope glycoprotein gp120 is a molecular target of CV-N. We recently reported that CV-N impaired the binding of virion-associated gp120 to cell-associated CD4 and that CV-N preferentially inhibited binding of the glycosylation-dependent neutralizing monoclonal antibody 2G12 to gp120. However, CV-N did not interfere with the interactions of soluble CD4 (sCD4) with either soluble gp120 (sgp120) or virion-associated gp120. In the present study, we have evaluated the effects of CV-N on the binding of sgp120 to cell-associated CD4 to clarify the experimental basis of the previous binding results, and we further address the detailed mechanism of action of CV-N. Here we present evidence that (i) CV-N impairs both CD4-dependent and CD4-independent binding of sgp120 to the target cells, (ii) CV-N blocks the sCD4-induced binding of sgp120 with cell-associated coreceptor CXCR4, and (iii) CV-N dissociates bound sgp120 from target cells. The results illustrate that the measured effects of CV-N on gp120-CD4 binding interactions depend upon the type of CD4 (soluble or cell associated), but not upon the type of gp120 (soluble or virion associated), employed in the experimental protocol. In addition, this study reinforces that CV-N acts uniquely to prevent essential interactions between the envelope glycoprotein and target cell receptors and further supports the potential broad utility of CV-N as a microbicide to prevent the transmission of HIV and AIDS.     

The Relationship Between Respite Care and Child Abuse Potential in Parents of Children with Developmental Disabilities: A Preliminary Report

This study longitudinally examined the impact of respite care services on child abuse potential and family relations in a sample of parents (N = 14) whose children were admitted for respite care to a center for developmental disability. A sample of parents (N = 18) whose children were admitted for short-term hospitalization (STH) was used as a contrast group. In addition, we examined the interrelationships between child abuse potential, family relations, and parenting stress at 3 time points. Parents completed measures of child abuse potential, family relations, and parenting stress at time of admission, discharge, and at a 2-month follow-up. Results indicated that neither respite care nor STH resulted in significant effects on child abuse potential or family relations although trends were found in the expected direction. Strong interrelationships were found between child abuse potential, family relations, and parenting stress at each of the 3 time points. These preliminary results suggest that respite care may be insufficient to directly impact child abuse potential; however, interventions that target variables related to abuse (e.g., quality of family relations, parenting stress) might be beneficial.     

Incidence and follow-up of inflammatory cardiac complications after smallpox vaccination

OBJECTIVES: The purpose of this study was to assess the follow-up of patients with vaccinia-associated myocarditis. BACKGROUND: With the threat of biological warfare, the U.S. Department of Defense resumed a program for widespread smallpox vaccinations on December 13, 2002. One-year afterwards, there has been a significant increase in the occurrence of myocarditis and pericarditis among those vaccinated. METHODS: Cases were identified through sentinel reporting to military headquarters, systematic surveillance, and spontaneous reports. RESULTS: A total of 540,824 military personnel were vaccinated with a New York City Board of Health strain of vaccinia from December 2002 through December 2003. Of these, 67 developed myopericarditis at 10.4 +/- 3.6 days after vaccination. The ST-segment elevation was noted in 57%, mean troponin on admission was 11.3+/- 22.7 ng/dl, and peak cardiac enzymes were noted within 8 h of presentation. On follow-up of 64 patients (96%) at a mean of 32 +/- 16 weeks, all patients had objective normalization of echocardiography, electrocardiography, laboratory testing, graded exercise testing, and functional status; 8 (13%) reported atypical, non-limiting persistent chest discomfort. CONCLUSIONS: Post-vaccinial myopericarditis should be considered in patients with chest pain within 30 days after smallpox vaccination. Normalization of echocardiography, electrocardiography, and treadmill testing is expected, and nearly all patients have resolution of chest pain on follow-up.