Use of laser Doppler flowmetry for estimation of the depth of burns

The trend for treatment of deep second degree burns and third degree burns is toward early excision and skin grafting. The ability to predict burn depth accurately as early as possible is important for early excision and skin grafting. This study, prospectively evaluated the ability of laser Doppler flow measurements, obtained within 72 hours after burn injury, to predict the depth of burn wounds. A Periflux system 4001 laser Doppler flowmeter was used to measure the cutaneous microflow circulation of 100 selected points of burn wounds on 44 inpatients and of 1680 selected points on 120 volunteers from March of 1993 to February of 1994. The mean value of superficial second degree burns checked by laser Doppler was 194.6 perfusion units (PU). The value of deep second degree burns was 59.7 PU, and the value of third degree burns was 5.1 PU. The mean normal cutaneous blood flow of 120 volunteers (control group) was between 4 and 9 PU, except on the head, neck, hand, and foot. Blood flow of more than 100 PU correctly predicted (90.2 percent of cases) a superficial second degree burn. Blood flow between 100 and 10 PU correctly predicted (96.2 percent of cases) a deep second degree dermal burn. That of less than 10 PU correctly predicted (100 percent of cases) a third degree burn. There was also a significant correlation between initial flow measurements and the depth of burn wounds. We conclude that laser Doppler flow measurements performed early after burn injury are useful in predicting the depth of burn wounds. Laser Doppler flowmetry has the advantage of being easy to use and noninvasive and of providing immediate results for early determination of burn depth. Laser Doppler flowmetry is useful in selecting patients for early excision and grafting of burn wounds.     

Mother-to-infant transmission of GB virus C/hepatitis G virus: the role of high-titered maternal viremia and mode of delivery

To study mother-to-infant transmission of GB virus C/hepatitis G virus (GBV-C/HGV), blood samples of infants born to carrier mothers were collected beginning 3 months after birth and were tested for GBV-C/HGV RNA until 1 year of age. Of 2046 mothers, 2.1% were positive for GBV-C/HGV RNA, and 25 of their infants were followed for a median of 12 months. Thirteen infants (52%) were viremic, and infection became persistent in all. Maternal GBV-C/HGV RNA levels of this group were >10(7) copies/mL. Nucleotide sequence comparison in 5 viremic mother-infant pairs revealed a homology of 93%-98.2%, and none delivered by elective cesarean section. In comparison, of the 12 uninfected infants' mothers, 10 had lower GBV-C/HGV RNA levels (mean, 5 x 10(4) copies/mL), and the remaining 2 high-titered mothers had elective cesarean section. Thus, high-titered maternal viremia and mode of delivery are closely associated with the mother-to-infant transmission of GBV-C/HGV to infants, and the infection usually becomes persistent.     

Activity of growth hormone peptides bGH 96-133 and hGH 95-133 in 3T3-F442A cells

Amylin inhibits glucose-induced insulin secretion in the rat pancreas. To study the mechanism by which amylin acts on the B-cell, we have investigated, in the perfused rat pancreas, the effect of synthetic rat amylin (75 pM) on insulin release elicited by secretagogues acting on the B-cell via the adenylate cyclase/cAMP system, i.e., glucagon (10 nM), gastric inhibitory polypeptide (GIP, 1 nM), forskolin (1 microM) and isobutylmethylxanthine (IBMX, 75 microM). In addition, we examined the effect of amylin on GIP-induced insulin release in pancreata from rats pretreated with pertussis toxin, an agent which inactivates certain Gi proteins coupled to adenylate cyclase. Amylin inhibited the insulin response to glucagon (approx. 70%), GIP (approx. 90%), IBMX (approx. 75%) as well as the early phase of forskolin-induced insulin output (approx. 74%). However, amylin failed to modify GIP-induced insulin release in pancreata obtained from pertussis toxin pretreated rats. These results would indicate that the inhibitory effect of amylin on insulin secretion could be, at least in part, attributed to its interfering with the adenylate cyclase/cAMP system. Furthermore, prevention of the inhibitory effect of amylin on GIP-induced insulin output by pertussis toxin pretreatment, supports the concept that amylin can inhibit insulin release via a pertussis toxin-sensitive Gi protein coupled to the adenylate cyclase system.