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During the preparation of the Vascular Flora of the Marquesas Islands three new species of Cyrtandra (Gesneriaceae) have come to light and are described herein: C. uapouensis W. L. Wagner & Lorence, C. uahukaensis W. L. Wagner & Lorence, and C. kenwoodii W. L. Wagner & A. J. Wagner. Amended descriptions of the eight previously described Marquesan species are also provided as well as a key to the species. With the description of these the new species Cyrtandra in the Marquesas Islands consists of 11 species, six of which have been included in recent molecular phylogenetic studies of Pacific Cyrtandra, and appear to have arisen from one original introduction. If the other five species are members of this Marquesas clade then Cyrtandra would represent the largest lineage of Marquesas vascular plants. Psychotria is largest genus in the Marquesas Islands with 13 species, but is thought to consist of three separate lineages. [ABSTRACT FROM AUTHOR]

The reactivity of vapor-deposited Fe, Ni, Cu and Au atoms with nylon 6 ([&z.sbnd;NH(CH2)5CO&z.sbnd;]n), a nitrogen ion beam-modified polyethylene substrate (N-PE) and a nitrile-terminated self-assembled monolayer (CN-SAM) have been investigated using in situ X-ray photoelectron spectroscopy (XPS). On nylon 6, Fe deposition produced Fe&z.sbnd;O and Fe&z.sbnd;N bonded species as well as an amorphous carbonaceous film at the metal/polymer interface. Metal–nitrogen bond formation was also observed during Ni and Cu deposition on nylon 6, although the C&z.dbnd6;O functionality remained intact, and no evidence was found for the production of either Cu&z.sbnd;O or Ni&z.sbnd;O species. Deposition of Fe and Ni on N-PE and the CN-SAM also resulted in the production of metal–nitrogen bonds. In contrast, Cu exhibited little or no reactivity with N-PE and failed to activate C&z.tbnd6;N bond cleavage in the CN-SAM, while the deposition of Au produced a purely metallic overlayer on all three substrates. The relative reactivity of different polymer functional groups in the present study was found to be largely determined by their respective bond strengths, while the overall metal reactivity trend (Fe>Ni>Cu>Au) can be correlated with the strength of metal–oxygen and metal–nitrogen bonds that can potentially form during metallization. [Copyright &y& Elsevier]

By monitoring the variation in the fluorine content and the distribution of CFx (x=0–3) species in a semifluorinated self-assembled monolayer (CF-SAM) upon prolonged X-ray irradiation, the electron stimulated C–F bond breaking kinetics in fluorine-containing organic films has been determined. At short irradiation times, X-ray irradiation induced changes in the film''s chemical composition are consistent with the presence of C–F, C–C and S–Au bond cleavage events. In contrast, C–F bond breaking is identified as the dominant kinetic process for longer X-ray exposures. The kinetics of X-ray induced defluorination are consistent with a first-order decay process mediated by a series of consecutive C–F bond breaking events (e.g., CF→C) whose rate constants are in excellent agreement with a stochastic model of defluorination. [Copyright &y& Elsevier]

Presents information on a study which determined whether there is a corresponding inhibition of apical exchanger activity in proximal tubules to account for the reduced tubular reabsorption. Design and validation of fluorimetric system; Methods used in the study; Results and discussion.

Compares vasomotor responses in juxta-medullary microcirculation in Sprague-Dawley (SD) and spontaneously hypertensive rats (SHR). Description of experimental procedures; Summary of length constants, and y-intercepts for SD and SHR; Summary of conducted vascular responses in neighboring afferent arteriole (NAA) and cortical radial artery (CRA) in SD and SHR.

Tests the hypothesis that changes in endothelial cell calcium concentration in juxtamedullary afferent arterioles cause myogenic vasoconstriction. Rise in calcium with bradykinin; Indication of some other causative factors in the myogenic vasoconstriction.

Presents the findings of a study on the isolated blood-perfused juxtamedullary nephron preparation to examine conducted vasomotor responses in juxtamedullary microcirculation. Goals of the study; Interaction between adjacent nephrons; Effect of local depolarization of the distal afferent arteriole.

Compares the vasomotor responses in juxtamedullary microcirculation in normotensive Sprague-Dawley (SD) and spontaneously hypertensive rats (SHR). Decision of internephron coupling by conducted vasomotor responses; Magnitude of induced vasoconstriction in stimulation site; Response differences between SHR and SD rats.

Objective: To investigate whether leptin-induced improvements in glycemic control, hyperlipidemia, and insulin sensitivity in hypoleptinemic patients with generalized lipodystrophies are accompanied by reduction in intrahepatic and intramyocellular lipid (IMCL) accumulation.Research Design and Methods: We examined the effects 8-10 months of subcutaneous leptin replacement therapy on insulin sensitivity, IMCL, and intrahepatic lipid content in two patients with acquired generalized lipodystrophy and one patient with congenital generalized lipodystrophy. All patients had extreme lack of body fat, low plasma leptin levels, and elevated serum triglycerides, but only two had diabetes. Insulin sensitivity was measured by a high-dose (0.2 IU/kg) insulin tolerance test, as well as by hyperinsulinemic-euglycemic glucose clamp studies in two patients. IMCL and intrahepatic lipid content were measured by (1)H magnetic resonance spectroscopy. All measurements were obtained before and during 2-10 months of leptin therapy.Results: Glycemic control and lipoprotein levels markedly improved with leptin therapy in the two diabetic patients, and a slight improvement in lipoprotein levels was seen in the nondiabetic patients. Insulin stimulated glucose uptake during 60-120 min of the euglycemic clamp studies, and the rate of glucose disappearance during the insulin tolerance test nearly doubled with leptin therapy. As compared with the baseline period, after 8-10 months of leptin therapy, the mean intrahepatic lipid content was reduced by approximately 80% and the IMCL content was reduced by approximately 42%.Conclusions: Reduction in IMCL and intrahepatic lipid content may partly explain leptin-induced improvement in insulin sensitivity in patients with generalized lipodystrophy. [ABSTRACT FROM AUTHOR]

Background: The adipocyte hormone leptin is important in regulating energy homeostasis. Since severe lipodystrophy is associated with leptin deficiency, insulin resistance, hypertriglyceridemia, and hepatic steatosis, we assessed whether leptin replacement would ameliorate this condition. Methods: Nine female patients (age range, 15 to 42 years; eight with diabetes mellitus) who had lipodystrophy and serum leptin levels of less than 4 ng per milliliter (0.32 nmol per milliliter) received recombinant methionyl human leptin (recombinant leptin). Recombinant leptin was administered subcutaneously twice a day for four months at escalating doses to achieve low, intermediate, and high physiologic replacement levels of leptin. Results: During treatment with recombinant leptin, the serum leptin level increased from a mean (±SE) of 1.3±0.3 ng per milliliter to 11.1±2.5 ng per milliliter (0.1±0.02 to 0.9±0.2 nmol per milliliter). The absolute decrease in the glycosylated hemoglobin value was 1.9 percent (95 percent confidence interval, 1.1 to 2.7 percent; P=0.001) in the eight patients with diabetes. Four months of therapy decreased average triglyceride levels by 60 percent (95 percent confidence interval, 43 to 77 percent; P<0.001) and liver volume by an average of 28 percent (95 percent confidence interval, 20 to 36 percent; P=0.002) in all nine patients and led to the discontinuation of or a large reduction in antidiabetes therapy. Self-reported daily caloric intake and the measured resting metabolic rate also decreased significantly with therapy. Overall, recombinant leptin therapy was well tolerated. Conclusions: Leptin-replacement therapy improved glycemic control and decreased triglyceride levels in patients with lipodystrophy and leptin deficiency. Leptin deficiency contributes to the insulin resistance and other metabolic abnormalities associated with severe lipodystrophy. (N Engl J Med 2002;346:570-8.) [ABSTRACT FROM AUTHOR]