1H-magnetic resonance spectroscopy-determined cerebral lactate and poor neurological outcomes in children with central nervous system disease

By using proton magnetic resonance spectroscopy ((1)H-MRS), cerebral lactate has been shown to be elevated in a wide variety of pediatric and adult neurological diseases. In this study we compared 36 newborns, infants, and children with elevated lactate peaks on (1)H-MRS with 61 patients without an identifiable lactate signal. (1)H-MRS was acquired from the occipital gray and parietal white matter (8 cm3 volume, STEAM sequence with echo time = 20 msec, repetition time = 3.0 seconds) and data were expressed as ratios of different metabolite peak areas (N-acetylaspartate [NA]/creatine [Cr], NA/choline [Ch], and Ch/Cr) and the presence of a characteristic lactate doublet peak at 1.3 ppm. Outcomes (Pediatric Cerebral Performance Category Scale score; PCPCS) were assigned 6 to 12 months after injury. Patients with lactate peaks were more likely to have suffered a cardiac arrest, were more often hyperglycemic, and had lower Glasgow Coma Scale scores on admission. They were also more likely to have abnormal metabolite ratios when compared with age-matched controls or with patients without detectable lactate. Of prognostic importance, patients with increased lactate were more likely to be severely disabled (39% vs 10%), survive in a persistent vegetative state (13% vs 2%), or have died (39% vs 7%). In contrast, patients with similar conditions without increased lactate were more likely to have had a good outcome (23% vs 3%) or recovered to a mild (38% vs 6%) or moderate disability (20% vs 0%). Our data suggest that (1)H-MRS is useful in the prediction of long-term outcomes in children with neurological disorders. Patients with elevated cerebral lactate are more likely to die acutely or are at greater risk for serious long-term disability.     

1.7 Volt, DC to 15 GHz Differential Amplifier with Constant Group Delay in InP-HBT Technology

10 dB gain–, 15 GHz-Bandwidth amplifier has been designed andfabricated in InP-HBT technology. Operation of the amplifier was achieved at1.7 V at total current consumption of 40 mA. The amplifier designed to havea Bessel-transfer-function has almost constant group delay up to 30 GHz.Pulse- and eye-diagram- measurements have been performed to verify largesignal operation. At 3.3 V, 24 dB gain and 10 GHz bandwidth was achieved.The 1dB compression point at 1.7 V supply voltage is measured at –10dBm output power.     

Bidirectional cavopulmonary shunt in patients with anomalies of systemic and pulmonary venous drainage

BACKGROUND: Bidirectional cavopulmonary shunt and Fontan repair are now commonly performed in patients with a variety of forms of complex single ventricle, including those with anomalies of systemic or pulmonary venous return. These anomalies are ideally dealt with during bidirectional cavopulmonary shunt, thereby minimizing the complexity of the eventual Fontan procedure. METHODS: Between March 1990 and December 1995, 36 patients with anomalous systemic or pulmonary venous drainage underwent bidirectional cavopulmonary shunt. A combination of anomalous systemic and pulmonary venous drainage was present in 12 patients, whereas 19 patients had anomalous drainage only from the systemic circulation and 5 patients had isolated anomalies of pulmonary venous return. Visceral heterotaxy syndrome was diagnosed in 18 patients. The median age at operation was 11 months, and bidirectional cavopulmonary shunt was the first surgical procedure performed in 10 of these patients. Techniques of repair are described. RESULTS: There were two early deaths and one bidirectional cavopulmonary shunt was taken down, for mortality and failure rates not significantly different than those for all patients undergoing bidirectional cavopulmonary shunt during this time period (n = 117). At a mean follow-up of 19.9 months, there have been three late deaths and 11 patients have undergone Fontan completion. Actuarial survival was 87% at 1 year and 81% at 3 years. Among all patients undergoing bidirectional cavopulmonary shunt during this time period, neither heterotaxy syndrome nor anomalies of systemic or pulmonary venous return were significantly associated with decreased survival or poor outcome. CONCLUSIONS: Bidirectional cavopulmonary shunt can be performed in patients with anomalous systemic or pulmonary venous drainage, including those with visceral heterotaxy syndrome, with morbidity and mortality rates that do not differ significantly from those achieved in all patients undergoing bidirectional cavopulmonary shunt. In this report, we describe our experience with this group of patients, primarily focusing on outcomes and technical issues that pertain to the use of bidirectional cavopulmonary shunt as a preparatory procedure for the extracardiac conduit Fontan operation.     

Effects of melengestrol acetate on onset of puberty, follicular growth, and patterns of luteinizing hormone secretion in beef heifers

Our objective was to test the hypothesis that short-term (8 days) treatment of prepubertal heifers with melengestrol acetate (MGA) and subsequent steroid withdrawal would stimulate LH secretion and follicular growth. Angus heifers were divided randomly into two groups; MGA-treated (n = 8) or control (CON; n = 9). Puberty was determined by monitoring circulating concentrations of progesterone and ovarian morphology during a 14-day period following MGA withdrawal. LH secretory patterns were assessed upon initiation of MGA (Day 0), during MGA (Day 7), and 1 day after withdrawal of MGA (Day 9). All MGA-treated heifers, versus four CON heifers, exhibited corpora lutea and luteal phase concentrations of progesterone within 10 days after treatment (p = 0.01). Mean LH and LH pulse frequency increased (p = 0.005 and 0.0001, respectively) between Days 0 and 9 in MGA-treated heifers. In CON heifers, mean LH concentrations and pulse frequencies did not change. During the same period, diameter of the largest follicle increased in MGA-treated animals (p = 0.003) but did not change in the CON heifers. On the basis of these results, we suggest that MGA withdrawal enhances onset of puberty by stimulating pulsatile LH secretion that accelerates follicle growth to the preovulatory stage.     

Heparan sulfate proteoglycan binding by herpes simplex virus type 1 glycoproteins B and C, which differ in their contributions to virus attachment, penetration, and cell-to-cell spread

Herpes simplex virus type 1 (HSV-1) mutants defective for envelope glycoprotein C (gC) and gB are highly impaired in the ability to attach to cell surface heparan sulfate (HS) moieties of proteoglycans, the initial virus receptor. Here we report studies aimed at defining the HS binding element of HSV-1 (strain KOS) gB and determining whether this structure is functionally independent of gB's role in extracellular virus penetration or intercellular virus spread. A mutant form of gB deleted for a putative HS binding lysine-rich (pK) sequence (residues 68 to 76) was transiently expressed in Vero cells and shown to be processed normally, leading to exposure on the cell surface. Solubilized gBpK- also had substantially lower affinity for heparin-acrylic beads than did wild-type gB, confirming that the HS binding domain had been inactivated. The gBpK- gene was used to rescue a KOS gB null mutant virus to produce the replication-competent mutant KgBpK-. Compared with wild-type virus, KgBpK- showed reduced binding to mouse L cells (ca. 20%), while a gC null mutant virus in which the gC coding sequence was replaced by the lacZ gene (KCZ) was substantially more impaired (ca. 65%-reduced binding), indicating that the contribution of gC to HS binding was greater than that of gB. The effect of combining both mutations into a single virus (KgBpK-gC-) was additive (ca. 80%-reduced binding to HS) and displayed a binding activity similar to that observed for KOS virus attachment to sog9 cells, a glycosaminoglycan-deficient L-cell line. Cell-adsorbed individual and double HS mutant viruses exhibited a lower rate of virus entry following attachment, suggesting that HS binding plays a role in the process of virus penetration. Moreover, the KgBpK- mutant virus produced small plaques on Vero cells in the presence of neutralizing antibody where plaque formation depended on cell-to-cell virus spread. These studies permitted the following conclusions: (i) the pK sequence is not essential for gB processing or function in virus infection, (ii) the lysine-rich sequence of gB is responsible for HS binding, and (iii) binding to HS is cooperatively linked to the process of efficient virus entry and lateral spread but is not absolutely required for virus infectivity.