Serum IGFBP-2 levels are uniquely elevated in active prostate carcinoma but not. In benign prostatic hyperplasia. In prostate carcinoma, serum IGFBP-2 levels closely parallel those of prostate-specific antigen and probably reflect tumour burden. The relationship between prostatic-specific antigen and IGFBP-2 is partially independent of their individual relationships with age. Although serum IGFBP-2 is less sensitive than prostate-specific antigen in prostate carcinoma it may have adjunctive value in its management.

Hypoglycemia in patients with nonislet cell tumors is often secondary to overexpression of tumor insulin-like growth factor (IGF) II. In these patients the formation of serum complexes between IGFs, IGF binding protein-3 (IGFBP-3), and the acid-labile subunit (ALS) is impaired. An 87-yr-old woman with nonislet cell tumor hypoglycemia resulting from a localized fibrous tumor of the pleura was treated for 97 days with graded doses of prednisolone (30, 10, and 5 mg/day) followed by GH (1, 4, 8, 4, and 2 U/day). Both prednisolone and GH alleviated the hypoglycemia, concomitantly with increases in IGF-I, IGFBP-3, and ALS levels. Pretreatment serum IGFBP-2 and IGFBP-6 levels were greatly elevated, but as glucose normalized with treatment, only IGFBP-2 decreased, showing an inverse correlation with glucose (r = 0.716). IGFBP-1 gave a variable pattern not clearly related to blood glucose. Both treatments caused a redistribution of serum IGFBP-3 from binary- to ternary-complexed forms. However, only prednisolone improved the ability of IGFBP-3 to bind ALS in vitro. Prednisolone also suppressed IGF-II, the effect being confined to pro-IGF-II forms. Compared with normal IGF-II, pro-IGF-II inhibited ALS binding to IGFBP-3 in vitro. Although prednisolone and GH reverse hypoglycemia by different mechanisms, with only prednisolone suppressing tumor IGF-II secretion, both increase the formation of ternary IGF-IGFBP-3 complexes. We conclude that the failure of serum IGFBP-3 and tumor IGF-II to complex with ALS is a primary cause of hypoglycemia in nonislet cell tumor hypoglycemia.

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A voltage-tunable multicolor triple-coupled quantum-well infrared photodetector (TC-QWIP) has been developed for 8–12 μm detection. The TC-QWIP consists of three coupled quantum wells formed by an enlarged Si-doped InxGa1−xAs quantum well and two undoped GaAs quantum wells separated by two thin AlyGa1−yAs barriers. Two TC-QWIP structures with varying indium and aluminum compositions were designed and demonstrated. Due to the strong coupling effect of the asymmetrical quantum wells, three bound states (E1, E2, E3) are formed inside the quantum wells of the TC-QWIP. The main detection peak wavelength is due to E1→E3 bound states transition for both devices, while two secondary detection peaks due to E1→E2 and E1→Ec continuum states transitions under different biases were also observed. In addition, a strong quantum-confined Stark shift effect for the E1→E3 transition was observed in the wavelength range of 8.2–9.1 and 10.8–11.5 μm for QWIP-A and QWIP-B, respectively; both devices exhibit a linear dependence of detection peak wavelength on the applied bias voltage. A spectral responsivity of Ri=0.05 A/W and background limited performance (BLIP) detectivity DBLIP*=6.1×109 cm√Hz/W were obtained at Vb=5 V, λp=8.6 μm, and TBLIP=66 K for QWIP-A, while Ri=0.33 A/W and DBLIP* =1.63×1010 cm√Hz/W at Vb=4 V, λp=11.2 μm, and TBLIP=50 K were obtained for QWIP-B.

We treated seven GH-deficient children with 3-hourly 1 microgram/kg sc pulses of GHRH-(1-44) for 6 months and 2 micrograms/kg.pulse for another 6 months. Four patients had a serum GH response to iv GHRH before treatment, and an additional patient responded to iv GHRH after 1 month of pulsatile sc GHRH administration. The mean cumulative growth velocity increased from a pretreatment mean of 2.7 +/- 0.2 (+/- SE) to 8.4 +/- 2.5 and 5.4 +/- 0.7 cm/yr after 2 months and 1 yr of treatment, respectively. Low dose pulsatile GHRH therapy was effective in promoting growth in five of seven children, with height gain ranging from 4.4-7.5 cm at the end of 1 yr's therapy. Only one of the two patients who did not respond to GHRH had an improvement in linear growth when they were subsequently treated with synthetic GH. The other patient, a 16.5-yr-old pubertal girl who had both satisfactory GH and somatomedin-C responses during GHRH therapy, did not respond to either GHRH or, later, synthetic GH. The pretreatment serum GH response to iv GHRH, the serum somatomedin-C concentrations, and the peak serum GH response during sc GHRH therapy were not reliable predictors of clinical response.

Bolus injection of the synthetic hexapeptide GH-releasing peptide-6 (GHRP-6) reliably promotes GH secretion. However, desensitization to the GH-releasing effects of GHRP has been shown to occur during short term iv infusion. To determine whether humans would remain responsive to prolonged exposure to GHRP and to study the mechanism of action of GHRP, we compared the effects of a 34-h iv infusion of either GHRP or normal saline on parameters of pulsatile GH concentration in nine healthy young men. Each infusion was administered from 0800 h on day 1 to 1800 h on day 2. GHRP was given as a 1 microgram/kg loading bolus, then at the rate of 1 microgram/kg.h. A 50-microgram iv bolus of TRH was given at 0800 h on day 2, followed by iv boluses of GH-releasing hormone (GHRH; 1 microgram/kg, iv, at 1000, 1200, and 1400 h) and then a bolus of GHRP (1 microgram/kg at 1600 h). The integrated GH concentration (IGHC) and parameters of pulsatile GH concentration were calculated for the period between 1400 h on day 1 to 0800 h on day 2, and IGHC was calculated for 2 h after each bolus of GHRP or GHRH. During GHRP infusion, there was a significant increase in IGHC (2908 +/- 450 vs. 1374 +/- 160 micrograms x min/L), maximum pulse amplitude (15.2 +/- 2.8 vs. 8.4 +/- 1.7 micrograms/L), and mean pulse amplitude (7.0 +/- 1.1 vs. 3.8 +/- 1.5 micrograms/L). Plasma insulin-like growth factor-I increased from 252 +/- 23 to 312 +/- 23 micrograms/L. There was no change in either GH pulse frequency or interpulse GH concentration. During GHRP infusion, the GH responses to the GHRH boluses were augmented; however, baseline TSH was lower, and the GH and TSH/PRL responses to GHRP and TRH, respectively, were smaller. We conclude that the pituitary remains sensitive to GHRP during a prolonged GHRP infusion. The mechanisms of the GHRP effect on GH secretion are uncertain, and the possibility that GHRP acts as a functional somatostatin antagonist is discussed. The contrasting effects of GHRP on GH and TSH/PRL secretion could be due to differential effects of GHRP on the pituitary and hypothalamus.

We report the successful growth of high quality molecular beam epitaxy (MBE) GaAs, AlGaAs, AlGaAs/GaAs modulation doped heterostructures and a GaAs/InGaAs/GaAs quantum well on GaAs (111)B substrates. Modulation doped heterostructures show a 77 K mobility of 145 500 cm2/V s with a sheet density of 5.0×1011 cm−2. Photoluminescence of (111)B GaAs indicates a lower carbon incorporation than achieved on (100) substrates. The low growth temperature and high material quality obtainable in (111)B growth will provide advantages for laser diodes and heterostructure field effect transistors.