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In the title compound, C14H21N3O5, the tetra-hydro-furan ring adopts an envelope conformation with the C atom bearing the substituent as the flap. The penta-furan-ose ring adopts a twisted conformation about the C-C bond fusing the rings. The dihedral angle between these rings (all atoms), which are cis fused, is 72.89 (14)°. The cyclo-propane ring is disordered over two orientations in a 0.576 (5):0.424 (5) ratio; the dihedral angles subtended to the triazole ring are 53.3 (11) and 46.6 (9)°, respectively. In the crystal, the mol-ecules are linked by O-H⋯N and O-H⋯O hydrogen bonds, generating (001) sheets. A weak C-H⋯O inter-action also occurs.

The title compound, C(10)H(15)NO(7), consists of one methyl-enedi-oxy ring and two fused tetra-hydro-furan rings. The three fused rings exhibit cis arrangements at the ring junctions. One O atom of a tetra-hydro-furan ring and the H atoms bound to the neighboring C atoms are disordered over two orientations with site-occupancy factors of 0.69 (1) and 0.31 (1). intra-molecular O-H⋯O and C-H⋯O inter-actions stabilize the mol-ecular conformation. In the crystal structure, inter-molecular O-H⋯O and C-H⋯O inter-actions link the mol-ecules into a three-dimensional network.

The title compound, C(23)H(22)O(8), is a binary benzoyl ester whose nucleus consists of a fused system made up of a methyl-enedi-oxy ring and two tetra-hydro-furan rings. One of the benzoyl ester groups is attached at the junction of the two tetra-hydro-furan rings. The other is attached to the outer tetra-furan ring. Both the benzoyl ester groups are in an axial conformation with respect to the outer tetrhydro-furan ring. In the crystal, mol-ecules are linked by two weak C-H⋯O hydrogen bonds, forming a chain running parallel to the a axis.

The mol-ecule of the title compound, C(13)H(21)NO(8), consists of two methyl-enedi-oxy rings and one tetra-hydro-furan ring. In the crystal, inter-molecular O-H⋯O hydrogen bonds link the mol-ecules into helical chains running along the 6(1) screw axis. Weak inter-molecular C-H⋯O hydrogen bonds help to stabilize the crystal packing. Voids of 245 Å(3) per unit cell occur.

The mol-ecule of the title compound, C(22)H(27)NO(9), an azasugar derivative, consists of one benzene ring and two fused rings, which have the cis arrangement at the ring junctions, and gives a V-shaped geometry. The inter-planar angle between the five- and six-membered rings is 65.69 (11)°. The crystal structure is stablized by weak inter-molecular C-H⋯O hydrogen bonds.

Objective: To investigate the effect of chondroitinase ABC (ChABC) on the expression of growth associated protein 43 (GAP-43) and glial fibrillary acidic protein (GFAP) after spinal cord injury (SCI) in rats., Methods: A total of 150 adult female SD rats, weighing 250-300 g, were randomly divided into ChABC treatment group (group A), saline treatment group (group B), and sham operation group (group C) with 50 rats in each group. In groups A and B, the rats were made the SCI models and were treated by subarachnoid injection of ChABC and saline; in group C, the rats were not treated as a control. At 1, 3, 7, 14, and 21 days after operation, the Basso, Beattie, and Bresnahan (BBB) score system was used to evaluate the motion function, and immunofluorescent histochemical staining was used to observe the expressions of GAP-43 and GFAP., Results: At different time points, the BBB scores of groups A and B were significantly lower than those of group C (P < 0.05); there was no significant difference in BBB score between groups A and B after 1, 3, and 7 days of operation (P > 0.05), but the BBB score of group A was significantly higher than that of group B after 14 and 21 days of operation (P < 0.01). At different time points, the GAP-43 and GFAP positive neurons of groups A and B were significantly higher than those of group C (P < 0.05). After 14 and 21 days of operation, the GAP-43 positive neurons of group A were more than those of group B (P < 0.01). After 7, 14, and 21 days of operation, the GFAP positive neurons of group A were significantly less than those of group B (P < 0.01)., Conclusion: ChABC can degrade glial scar, improve the microenvironment of the injured region and enhance the expression of GAP-43, which promotes axonal growth and extension.

Objective: To explore the relationship of cathepsin L (CatL) with coronary heart disease (CHD), severity of coronary stenosis and risk factors of CHD., Methods: A total of 137 CHD patients and 48 controls were included in the study, to determined the serum levels of CatL, high sensitive C reactive protein (hs-CRP), fasting glucose (FBS), total cholesterol, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C), apolipoprotein A1(Apo-A1) and apolipoprotein B. All the subjects were invited for a coronary angiography, using the sum of the Gensini scores to assess the severity of coronary artery stenosis., Results: Serum CatL levels were significantly higher in CHD patients (5.63 +/= 0.12 microg/L) than non-CHD subjects (3.93 +/= 0.22 microg/L, P<0.01). CatL was an independent risk factor of CHD in Logistic regression analysis [Exp(B)=2.341, 95%CI 1.567 approximately 3.496, P<0.01]. Serum CatL levels were associated positively with the Gensini scores(r=0.228, P<0.01); In fact, CatL was an independent correlator of Gensini scores (P<0.05). CatL inversely associated with HDL-C (r=-0.228, P<0.01) and ApoA1(r=-0.187, P<0.05), and positively with FBS(r=0.161, P<0.05)., Conclusion: CatL is involved in the pathogenesis of CHD. Serum CatL levels could reflect the severity of coronary luminal narrowings. CatL might participate in glucose and lipid metabolic disorders.