Distribution of sputum glucose concentration in 117 samples.

<p>Sputum glucose (SG) was much lower than previously reported, with 34% reading < 0.01 mM, and 55% of samples reading < 1.0 mM. The distribution of SG was highly skewed: the median concentration was 0.7 mM (IQR, 0–3.5 mM) versus the mean of 4.75 mM (SD 11.4 mM).</p

Mean pulmonary function test results by glycemic control in CFRD.

<p>CFRD subjects with HbA_1c > 6.5% had significantly reduced average scores of forced expiratory volume in one second (FEV₁, left panel) and forced expiratory flow in the 25–75% of the patient’s exhaled volume (FEF25–75%, right panel) compared to CFRD subjects with HbA_1c ≤ 6.5%. Diamonds are centered on each category’s mean and the vertical distance represents the 95% confidence interval.</p

Study participant demographic information, n = 88.

<p>Study participant demographic information, n = 88.</p

Comparisons of HbA_1c and SG by glucose tolerance.

<p>CFRD subjects had significantly higher HbA_1c than subjects with impaired (IGT) or normal glucose tolerance (NGT, left panel), while NGT subjects had significantly higher average sputum glucose than IGT or CFRD subjects (right panel). Diamonds are centered on each category’s mean and the vertical distance represents the 95% confidence interval.</p

Clinical parameters of CFRD subjects.

<p>Clinical parameters of CFRD subjects.</p

Apratoxin H and Apratoxin A Sulfoxide from the Red Sea Cyanobacterium <i>Moorea producens</i>

Cultivation of the marine cyanobacterium <i>Moorea producens</i>, collected from the Nabq Mangroves in the Gulf of Aqaba (Red Sea), led to the isolation of new apratoxin analogues apratoxin H (<b>1</b>) and apratoxin A sulfoxide (<b>2</b>), together with the known apratoxins A–C, lyngbyabellin B, and hectochlorin. The absolute configuration of these new potent cytotoxins was determined by chemical degradation, MS, NMR, and CD spectroscopy. Apratoxin H (<b>1</b>) contains pipecolic acid in place of the proline residue present in apratoxin A, expanding the known suite of naturally occurring analogues that display amino acid substitutions within the final module of the apratoxin biosynthetic pathway. The oxidation site of apratoxin A sulfoxide (<b>2</b>) was deduced from MS fragmentation patterns and IR data, and <b>2</b> could not be generated experimentally by oxidation of apratoxin A. The cytotoxicity of <b>1</b> and <b>2</b> to human NCI-H460 lung cancer cells (IC₅₀ = 3.4 and 89.9 nM, respectively) provides further insight into the structure–activity relationships in the apratoxin series. Phylogenetic analysis of the apratoxin-producing cyanobacterial strains belonging to the genus <i>Moorea</i>, coupled with the recently annotated apratoxin biosynthetic pathway, supports the notion that apratoxin production and structural diversity may be specific to their geographical niche