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Objective To assess hypoxic right heart remodeling after acclimatization at high altitude area. Methods One hundred volunteers who came to Tibet from the low-altitude areas by plane were randomly selected to serve as control group, and another 100 servicemen, who were dispatched from low altitude area to a station in Tibet area 3000m above sea level and got acclimatized to serve as altitude group. The altitude group was divided into altitude group 1 (3000-4000m above sea level, n=67) and altitude group 2 (4000-5500m above sea level, n=33) according to the altitude of the campsite, and also into migration-time group 1 (entered and stationed in Xizang for 1-2 years, n=72) and migration-time group 2 (entered and stationed in Xizang for over 2 years, n=28). The structure and function of the right heart were measured using a portable multi-functional composite echocardiography in a quiescent state, and hypoxic right heart remodeling after high-altitude acclimatization was comprehensively analyzed and assessed. Results Compared with control group, the main manifestations of the subjects in the altitude group were right ventricular and right atrial enlargement, right ventricular wall thickening, aggravation of tricuspid regurgitation, and broadening of pulmonary trunk and branch (P < 0.01). As the altitude increased, the right heart remodeling became more obvious, and the right heart remodeling was significantly more obvious in the subjects who svere stationed in the place > 4000m above sea level than in those who were in the area < 4000m (P < 0.01). The longer the time the subjects stationed in the high-altitude area, the more obvious the right heart remodeling. The right heart remodeling was significantly more obvious in those who lived in high-altitude area for > 2 years, particularly in those for > 5 years, than those who lived there for < 2 years (P < 0.01). Conclusions The altitude and living time in high-altitude are main factors for hypoxic right heart remodeling. Altitude acclimatization is only the adjustment of human body to hypoxic environment. A portable multi-functional composite echocardiography can early and timely assess hypoxic right heart remodeling and it is of important significance for ensuring the health of the serviceman in high-altitude area.

Objective To examine atrial natriuretic peptide(ANP) and endothelin-1(ET-1) and ultrastructural pathologic changes in myocardial tissues in rabbits after severe crush injury and to investigate the secondary damage to myocardial tissues after severe injury and its mechanism.Methods A crush injury model was established in rabbits.Forty-two rabbits were randomly assigned into one control group(n=6) and one crush injury group(n=36).The crush injury group was further divided to six subgroups based on the time after crush release,i.e.,immediately after release and at 6,12,24,48,and 72h after release;each subgroup has six rabbits.The level of blood urea nitrogen,Cr,K+,and CK in serum is detected with an automatic biochemical analyzer.Myoglobin(MYO),cardiac troponin I(c-TnI),and CK-MB in the serum were measured using the chemiluminescence method.The myocardial tissues were collected from the same part of rabbit in each group and the content of ANP and ET-1 was determined by radio-immunoassay and the morphologic changes(at different times after the injury) in hematoxylin and eosin-stained myocardial tissue samples were observed under light microscopy and electron microscopy.Results The levels of CK,CK-MB and c-TnI in serum 12-24h after crush are apparently higher than that before crush(P < 0.05),whereas the content of ANP and ET-1 in the myocardial tissue drops(P < 0.05).Observation under light microscopy and electron microscopy revealed progressive pathologic changes in the myocytes,with the most severe myocardial damage observed within 12-24h after crush injury.The damage subsequently decreased and eventually disappears.Conclusions Severe crush injury may induce secondary damage to myocardial tissues and cardiac function.The changing trend in the cardiac markers ANP and ET-1 is consistent with the pathologic changes in myocytes during crush injury.

A simple, sensitive and selective fluorimetric determination for trace nitrites was developed using an unsymmetrical rhodamine with a high fluorescence quantum yield and large Stokes shift. The method is based on the reaction of the unsymmetrical rhodamine with nitrite in an acidic medium to form a nitroso product, which has much lower fluorescence because the electron-withdrawing effect of the nitroso group influences the system of p-π conjugation between N atom and benzene ring. Under optimum conditions, the fluorescence quenching intensity is linear over a nitrite concentration range of 1.0 × 10 −8 to 3.5 × 10 −7 M. The detection limit is 2.0 × 10 −10 M (S/N = 3). The method was applied to the determination of nitrite in tap water and lake water with satisfactory results. The mechanism for the reaction is also reported.

Objective To explore the mechanism of myocardial secondary injury and cardiac dysfunction after crush injury in rabbits. Methods Forty-two New Zealand rabbits were randomly divided into control group (6 rabbits) and crush injury group (36 rabbits that received pressure of 20kg for 6h), and crush injury group were subdivided into instant group, 6, 12, 24, 48 and 72h group after pressure relief with 6 rabbits in each group according to pressure relief time. The cardiac function changes in different time periods were detected by the multi-functional composite echocardiography, and the myocardial ultrastructural changes in different time periods were observed under electron microscope. Results The systolic indexes such as left ventricular ejection fraction (EF), left ventricular circumference shortening (CS), ventricular wall thickening and cardiac output per minute and diastolic function indexes such as peak flow velocity during rapid filling phase, peak flow velocity during slow filling phase, E/A ratio and diastolic filling rate were progressively reduced at respective time points after pressure relief, especially EF and CS. All the indexes for cardiac function were reduced to negative peak level 12-24h after pressure relief (P < 0.01); the myocardial ultrastructural changes were obvious, particularly 24h after injury. Conclusions Crush injury may result in secondary injury to the myocardium and cardiac dysfunction, and the peak phase of cardiac injury was during 12-24h after pressure relief. Multi-functional composite cardiac echocardiography can accurately, objectively and rapidly assess the myocardium damage after crush injury.

In the title compound, C16H15NO4·CH4O, the dihedral angle between the benzene rings is 75.21 (5)°. The structure is stabilized by an intramolecular O—H...O interaction [O...O = 2.589 (2) Å]. The solvent molecule links symmetry-related molecules of the complex via hydrogen bonds with O...O separations of 2.631 (2) and 2.815 (2) Å. C—H...O hydrogen bonds are also present.

Five fluorescent labels were synthesized and used in the preparation of polystyrene fluorescent microspheres by the dispersion copolymerization and absorption method. Spectral properties of copolymerization fluorescent microspheres in tetrahydrofuran indicated these individual characteristics of labels should be maintained in the fluorescent microspheres. The differences of the fluorescent spectra between five fluorescent microspheres and their corresponding parent labels in ethanol have been investigated. These fluorescent microspheres were characterized by environmental scanning electron microscopy, laser scanning confocal microscopy and fluorescence spectrophotometry. They exhibited good dispersion and stable and high fluorescence intensity. Furthermore, copolymerization fluorescent microspheres were functionalized with amino groups. This means that a method for the preparation of copolymerization fluorescent microspheres was developed as a platform for the generation of functional fluorescent microspheres for diverse applications.