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Biomedical subjects

S Roth

Publications and source records attributed to S Roth.

414 records · Page 23Linked to original sources
PubMedDate not supplied

Drosophila development: the secrets of delayed induction.

Dorsoventral axis formation in Drosophila relies on extracellular signals which are generated only at the ventral side of the egg. This asymmetry, in turn, depends on the expression specifically in ventral follicle cells of pipe, the product of which seems likely to be a glycosaminoglycan-modifying enzyme.

Animals↗
PubMedDate not supplied

Osteoprotegerin and receptor activator of nuclear factor-kappaB ligand (RANKL) in the serum of healthy adults.

AIMS: Osteoprotegerin and the receptor activator of the nuclear factor-kappaB ligand (RANKL) are decisive factors for maintaining the balance between bone formation and bone resorption. As new, sensitive ELISAs have been developed recently, reference serum ranges should be established to use these analytes for possible diagnostic purposes. METHODS: Measurements were performed in serum samples of 142 healthy adults (82 women, 60 men) between 20 and 70 years of age (mean age: 46 years) using ELISA kits from Immundiagnostik, Bensheim, Germany. RESULTS: Serum concentrations of osteoprotegerin were age and gender independent and showed a Gaussian distribution, while RANKL concentrations were also age independent but differed between males and females, with a non-Gaussian distribution. For osteoprotegerin a gender-independent upper 97.5 percentile limit of 3.6 pmol/L was calculated while the corresponding limits for RANKL and the ratio of RANKL to osteoprotegerin amounted to 3.29 pmol/L and 2.78 in women and 1.66 pmol/L and 2.18 in men, respectively. CONCLUSIONS: Both osteoprotegerin and RANKL were quantifiable in serum of healthy adults, which means that these compounds can be used as potential diagnostic tools.

Adult↗
PubMedDate not supplied

Local cortical blood flow and oxygen consumption during isoflurane-induced hypotension. Results in patients undergoing intracranial aneurysm clipping.

Cerebral cortical blood flow (lCoBF) and metabolic rate for oxygen (lCoMRO2) were studied in eight patients undergoing intracranial aneurysm clipping. The patients were anesthetized with fentanyl 10 micrograms/kg and 70% nitrous oxide combined with 30% oxygen. Hypotension was induced with isoflurane. A thermal diffusion probe was used to measure lCoBF, and arterial and cerebral venous blood samples were obtained for measurement of arterio-cerebral venous O2 content difference. Measurements were made prior to hypotension, during hypotension (to mean arterial pressure approximately 50 mmHg), and posthypotension. Mean lCoBF decreased from 69 +/- 20 mL/100 g/min at normotension to 59 +/- 13 mL/100 g/min during hypotension (P less than .03, NS) and was 61 +/- 18 mL/100 g/min upon return to normotension (all values mean +/- 1 SD). The lCoMRO2 averaged 3.9 +/- 1.6 mL/100 g/min and 3.1 +/- 1.5 mL/100 g/min, respectively (P less than .03, NS) for normotension upsilon hypotension. Values for cerebral venous PO2 and O2 saturation also did not differ significantly between study periods. These results indicate that isoflurane-induced hypotension during fentanyl-nitrous oxide anesthesia allows maintenance of a constant lCoBF and oxygen delivery.

Adult↗
PubMedDate not supplied

Insulin-like growth factors I and II peptide and messenger RNA levels in macrosomic infants of diabetic pregnancies.

OBJECTIVE: Fetal macrosomia is a common complication of maternal diabetes mellitus and is associated with substantial morbidity, but the precise cellular and molecular mechanisms that induce fetal macrosomia are not well understood. We hypothesized that the macrosomia or accelerated fetal growth seen in infants of diabetic mothers is due to a perturbation of a putative placental-fetal growth axis involving growth hormone and insulin-like growth factors. Insulin-like growth factors I and II (IGF-I and IGF-II) are ubiquitous peptides that share structural homology with insulin and have been implicated in processes that control fetal growth. Studies of IGF levels in pregnancies complicated by diabetes and macrosomia have shown conflicting results. We set out to resolve these inconsistencies using molecular techniques to measure the placental IGF-I and IGF-II messenger RNA levels in placentas and a specific radioimmunoassay to measure IGF-I and IGF-II peptide levels in cord serum of normal and diabetic pregnancies. METHODS: Placentas and cord blood were collected immediately after delivery at term from patients from each of three study groups: 1) nonmacrosomic infants of nondiabetic mothers (controls), 2) macrosomic infants of diabetic mothers, and 3) nonmacrosomic infants of diabetic mothers. Both IGF-I and IGF-II levels were measured in cord serum and placental tissue by a specific radioimmunoassay. Total RNA was extracted and analyzed by Northern gels hybridized to IGF-I or IGF-II riboprobes. RESULTS: Levels of IGF-I in cord serum from the macrosomic diabetic group (83 +/- 4.2 ng/mL) were significantly higher than levels from either the nonmacrosomic nondiabetic group (38 +/- 1.9 ng/mL) or the nonmacrosomic diabetic group (13 +/- 3.5 ng/mL). There was a direct linear correlation between cord serum IGF-I and infant birth weight, independent of diabetes (r2 = 0.61, P < .01). On the other hand, IGF-II cord serum levels were elevated in diabetic pregnancies (337 +/- 12.2 ng/mL) compared with nondiabetic women (172 +/- 19.8 ng/mL), but there was no correlation with birth weight (r2 = 0.035, P = .52). In contrast to cord blood levels, IGF-II peptide levels were significantly decreased in the placentas from mothers with diabetes compared with nondiabetic controls (116 +/- 3.2 versus 158 +/- 5.3 ng/mL, respectively). Levels of IGF-I peptide in placentas from both nondiabetic controls and diabetic mothers were below the sensitivity of the assay. Levels of IGF-I and IGF-II mRNA did not differ in placentas from diabetic mothers versus nondiabetic controls. CONCLUSION: Cord serum IGF-II levels are elevated in diabetic pregnancies without a concomitant increase in placental IGF-II levels. This novel finding, combined with the finding that IGF-I levels are correlated with macrosomia independent of the diabetic state, contributes to our understanding of the possible mechanisms involved in fetal growth in pregnancies complicated by diabetes.

Birth Weight↗