Effect of plasma TNF-alpha on filgrastim-stimulated hematopoiesis in mice and humans

Marshall syndrome is a rare, autosomal dominant skeletal dysplasia that is phenotypically similar to the more common disorder Stickler syndrome. For a large kindred with Marshall syndrome, we demonstrate a splice-donor-site mutation in the COL11A1 gene that cosegregates with the phenotype. The G+1-->A transition causes in-frame skipping of a 54-bp exon and deletes amino acids 726-743 from the major triple-helical domain of the alpha1(XI) collagen polypeptide. The data support the hypothesis that the alpha1(XI) collagen polypeptide has an important role in skeletal morphogenesis that extends beyond its contribution to structural integrity of the cartilage extracellular matrix. Our results also demonstrate allelism of Marshall syndrome with the subset of Stickler syndrome families associated with COL11A1 mutations.     

Antinociception produced by microinjection of morphine in the rat periaqueductal gray is enhanced in the foot, but not the tail, by intrathecal injection of alpha1-adrenoceptor antagonists

Antinociception produced by microinjection of morphine in the ventrolateral periaqueductal gray is mediated in part by alpha2-adrenoceptors in the spinal cord dorsal horn. However, several recent reports demonstrate that microinjection of morphine in the ventrolateral periaqueductal gray inhibits nociceptive responses to noxious heating of the tail by activating descending neuronal systems that are different from those that inhibit the nociceptive responses to noxious heating of the feet. More specifically, alpha2-adrenoceptors appear to mediate the antinociception produced by morphine using the tail-flick test, but not that using the foot-withdrawal or hot-plate tests. The present study extended these findings and determined the role of alpha1-adrenoceptors in mediating the antinociceptive effects of morphine microinjected into the ventrolateral periaqueductal gray using both the foot-withdrawal and the tail-flick responses to noxious radiant heating in lightly anesthetized rats. Intrathecal injection of selective antagonists was used to determine whether the antinociceptive effects of morphine were modulated by alpha1-adrenoceptors. Injection of the selective alpha1-adrenoceptor antagonists prazosin or WB4101 potentiated the increase in the foot-withdrawal response latency produced by microinjection of morphine in the ventrolateral periaqueductal gray. In contrast, either prazosin or WB4101 partially reversed the increase in the tail-flick response latency produced by morphine. These results indicate that microinjection of morphine in the ventrolateral periaqueductal gray modulates nociceptive responses to noxious heating of the feet by activating descending neuronal systems that are different from those that inhibit the nociceptive responses to noxious heating of the tail. More specifically, alpha1-adrenoceptors mediate a pro-nociceptive action of morphine using the foot-withdrawal response, but in contrast, alpha1-adrenoceptors appear to mediate part of the antinociceptive effect of morphine determined using the tail-flick test.     

Synthesis and antidiuretic activities of novel glycoconjugates of arginine-vasopressin

Arginine-vasopressin (AVP) was acylated with various acyl azides (2a-j) in pH 9.1 buffer to give AVP derivatives (11a-j) modified at the tyrosine side chain with a carbohydrate via a spacer arm. Glycoconjugates of AVP modified at the N-terminal amide (12a-e) were also synthesized from AVP and carboxylic acids (3a-e) using dicyclohexylcarbodiimide and 1-hydroxybenzotriazole as coupling agent. Analogues (11a-j) exhibited greater in vivo antidiuretic activity than AVP. AVP and glycoconjugates (12a-e) were stable in rat plasma. On the other hand, glycoconjugates (11a-i) were found to readily convert to AVP according to first order kinetics. Hence, 11a-j are considered to be prodrugs of AVP.     

Surgical treatment of the massively dilated ureter in children. Part II. Management by primary reconstruction

Bypass of the left ventricle was accomplished in dogs and the entire circulation was supported temporarily by only the right ventricle. The atrial septum was excised, and the atrium was repartitioned so that the pulmonary veins were in continuity with the right ventricle and the venae cavae were connected through the atrium. Anastomosis of the superior vena cava to the right pulmonary artery brought systemic venous return directly to the lungs. The main pulmonary artery was ligated proximal to the bifurcation, preserving distal confluence of right and left pulmonary arteries. A tubular prosthesis between the proximal pulmonary artery and the aorta connected the right ventricle to the systemic circuit. This procedure, or some modification of the principle, may have clinical feasibility in the treatment of patients with hypoplastic left heart syndrome.     

Saturated spectroscopy applied to Xenon at 3.5 µm

We report the observation of the xenon isotope spectrum using saturation spectroscopy on a gain cell external to a He-Xe laser. Six resonances centered about 3.508μm are observed over the limited tuning range of the laser. These resonances are assigned to the Xe¹²⁸Xe¹³⁰Xe¹³¹Xe¹³²Xe¹³⁴and Xe¹³⁶isotopes. The observed homogeneous linewidth is 9 ± 1 MHz, and the pressure broadening of the homogeneous linewidth is experimentally determined to be 71 ± 20 MHz/ torr.