Purified GAI, one form of glucoamylase obtained from Aspergillus niger mutant T21 contained 17.6% total carbohydrate. Analyses of amino acid composition showed that GAI contained about 25% Ser and Thr, 20.3% Asx and Glx and 6% basic amino acids. The UV absorption and fluorescence spectra of GAI were determined. The maximum absorption wavelength was at 278nm and minimum at 250nm. For fluorescent analyses the excitation and maximum emission spectra were at 284nm and 342nm respectively. The CD-spectrum determined showed two negative peaks. Its dispersion of secondary structure in solution showed 10.6% ?-helix, 16.3% ?-form and 73.1% unordered.

Objective: To determine the noninvasive imaging efficacy of 99mTc-sandostatin scintigraphy for lung cancer. Methods: 57 consecutive patients with pulmonary nodules(PN) were studied with 99mTc-sandostatin scintigraphy.Planar imaging was obtained after injection of (991.6?187.59) MBq of 99mTc-sandostatin at 1.5-4 hour with GE Dual-head gamma camera(Millennium VG, Hawkeye ;General Electric Medical Systems) . SPECT images of the chest were performed at 4-6 h post injection. All scintigraphically detected lesions were confirmed by histopathological analysis and/or by other imaging modalities.Tumor to normal tissues ratios (T/N) were calculated . Results: Out of 57 patients ,47 were malignant tumors; 12 with small cell lung cancer (SCLC), 35 with non- small cell lung cancer (NSCLC). 10 had benign lesions. The sensitivity , specificity and accuracy of 99mTc-Sandostatin in detection of lung cancer were 95.7%, 90%, 94.7%, respectively. In two patients (pts) with pulmonary squamous cell cancer 99mTc-Sandostatin imaging was false negative. In 10 pts. with benign PN, 9 pts. was true negative, but one patient with tubercolama was false positive. T/N ratio was 3.43?0.66, 2.24?0.31 in SCLC and NSCLC respectively. The T/N ratio was higher in small cell lung cancer than NSCLC(t = 4.072 ,P

Osteoarthritis (OA), in which M1 macrophage polarization in the synovium exacerbates disease progression, is a major cause of cartilage degeneration and functional disabilities. Therapeutic strategies of OA designed to interfere with the polarization of macrophages have rarely been reported. Here, we report that SHP099, as an allosteric inhibitor of src-homology 2-containing protein tyrosine phosphatase 2 (SHP2), attenuated osteoarthritis progression by inhibiting M1 macrophage polarization. We demonstrated that M1 macrophage polarization was accompanied by the overexpression of SHP2 in the synovial tissues of OA patients and OA model mice. Compared to wild-type (WT) mice, myeloid lineage conditional Shp2 knockout (cKO) mice showed decreased M1 macrophage polarization and attenuated severity of synovitis, an elevated expression of cartilage phenotype protein collagen II (COL2), and a decreased expression of cartilage degradation markers collagen X (COL10) and matrix metalloproteinase 3 (MMP3) in OA cartilage. Further mechanistic analysis showed thatSHP099 inhibited lipopolysaccharide (LPS)-induced Toll-like receptor (TLR) signaling mediated by nuclear factor kappa B (NF-κB) and PI3K-AKT signaling. Moreover, intra-articular injection of SHP099 also significantly attenuated OA progression, including joint synovitis and cartilage damage. These results indicated that allosteric inhibition of SHP2 might be a promising therapeutic strategy for the treatment of OA.