Serum peptidome patterns of hepatocellular carcinoma based on magnetic bead separation and mass spectrometry analysis.

BACKGROUND/AIMS: The only hope for a cure from hepatocellular carcinoma (HCC) rests on early diagnosis. The present study aims to determine serum peptidome patterns for early diagnosis of HCC. MATERIALS AND METHODS: To identify novel peptidome patterns for diagnosing HCC, serum from31 healthy volunteers and 32 HCC patients were subjected to a comparative proteomic analysis using a ClinProt Kit combined with mass spectrometry (MS). This approach allows the determination of peptidome patterns that are able to differentiate the HCC from healthy volunteers. For further validation, the diagnostic and differential diagnostic capabilities of the peptidome patterns were verified blindly by an independent group of sera consisted of 31 HCC, 23 liver fibrosis and 33 healthy volunteers. RESULTS: A Quick Classifier Algorithm was used to construct the peptidome patterns for the identification of HCC from the control samples. One of the identified peaks at m/z 7771 was used to construct the peptidome patterns with almost 100% accuracy. Furthermore, the peptidome patterns could also differentiate the validation group with high accuracy. CONCLUSION: These results suggest that the ClinProt Kit combined with MS achieves significantly high accuracy for HCC diagnosis and differential diagnosis.

[Study on the relationship between changes of adrenomedulin in plasma and vascular resistance during traumatic shock in rats].

OBJECTIVE: To observe the changes of adrenomedulin in plasma and vascular resistance during traumatic shock in rats. METHODS: The concentration of adrenomedulin in plasma of rats after traumatic shock was detected by radio immunization. Mean arterial pressure, total peripheral vascular resistance (TPVR) and cardiac index (CI) were estimated by electrical conductance method. RESULTS: The concentration of adrenomedulin in plasma of traumatic shock without resuscitation group (68.34+/-3.71)ng/L and traumatic shock with resuscitation group (146.27+/-9.83)ng/L were higher than that of control group(32.63+/-7.55)ng/L (P<0.01 and P<0.05). TPVR of traumatic shock with resuscitation group (10.57+/-0.35) kPa.s.L-1 was lower than that of traumatic shock without resuscitation group (16.75+/-0.23) kPa.s.L-1(P<0.01) and its CI (215.59+/-1.29) ml.min-1.kg-1 was higher than that of traumatic shock without resuscitation group (143.11+/-0.86) ml.min-1.kg-1 (P<0.01). CONCLUSION: Adrenomedulin is closely correlated with changes of vascular resistance and plays an important role during pathophysiological processes in rats after traumatic shock.

[Therapeutic efficiency of nitric oxide synthase inhibitor on traumatic shock in rats].

OBJECTIVE: To evaluate the effects of aminoguanidine (AG) used as a selective inhibitor of the inducible form of nitric oxide synthase (iNOS) and N-nitro-L-arginine methyl ester (L-NAME) used as a non-selective inhibitor of nitric oxide synthase (NOS) on traumatic shock. METHODS: Thirty SD (Sprague-Dawley) rats were used to create a animal model of traumatic shock. Both shaft of femurs were crashed and bled to mean arterial pressure of 35-45 mm Hg (1 mmHg=0.133 kPa) via femoral artery. Hypotension was maintained 30 minutes, the shed blood was then returned, followed by an infusion with Ringer's solutions. Animals were randomly divided into three groups: traumatic shock group (n=10), AG group (AG 8 mg/kg was infused at resuscitation, n=10), L-NAME group (L-NAME 8 mg/kg was infused at resuscitation, n=10). Plasma levels of nitric oxide (NO) were determined before and after shock, immediately after resuscitation and 0.5, 2 and 4 hours after resuscitation. The 24 hours survival rates were recorded. Lung, liver and kidney, intestine tissues were obtained 24 hours after shock for microscopic examination. RESULTS: The plasma level of NO markedly increased after shock. The plasma level of NO markedly decreased and less tissue damages with highly survival rates in AG group. Lower plasma level of NO and survival rates and highly tissue damages were seen in L-NAME group. CONCLUSION: NO plays an important role in development of pathologically traumatic shock. AG is beneficial of treatment in traumatic shock, but L-NAME can only decrease the plasma level of NO and can not improve the outcome of shock.

Intervention with nitric oxide synthase inhibitors for traumatic shock in rats.

OBJECTIVE: To evaluate the effects of a selective inhibitor of inducible nitric oxide synthase (iNOS) aminoguanidine (AG) and a non-selective inhibitor of nitric oxide synthase (NOS) N(G)-nitro-L-arginine methylester (L-NAME) on traumatic shock in rats. METHODS: Animal models of traumatic shock were established in 44 Sprague-Dawley rats following fractures in both femur shafts and subsequent depletion until the mean arterial pressure in the femoral artery dropped to 35 to 45 mmHg(4.67-6.00 kPa). Hypotension was maintained for 30 min before the collected blood was infused back into the rats supplemented with Ringer's solution of the same volume. The rat models were then randomly divided into 3 groups, namely traumatic shock group (n=10), AG group (which was subdivided into AGI, AGII, and AGIII groups, each consisting of 8 rats and receiving 2, 8, and 60 mg/kg x b.w AG infusion respectively during resuscitation), and L-NAME group (with 8 mg/kg x b.w L-NAME infusion during resuscitation, n=10). Plasma NO levels were determined before and after shock, immediately after resuscitation and 0.5, 2, 4 h after resuscitation, and the survival rates within 24 h were recorded with tissue samples of the lung, liver, kidney and intestine obtained 24 h after shock for microscopic examination. RESULTS: Plasma NO level was seen to increase markedly after traumatic shock in the rat models. In the 3 AG groups, the elevated NO levels following the shock were obviously reduced after resuscitation with less tissue damages and higher survival rates, as compared with the other 2 groups. The best protective effect against traumatic shock was observed in AGIII group. In spite of obvious plasma NO level-lowering effect after resuscitation, L-NAME exhibited little efficacy in alleviating the tissue damages in the organs and hence failed to improve the survival rate of the rats. CONCLUSIONS: NO plays an important role in the pathological process of traumatic shock, and the application of AG may improve the condition. L-NAME can decrease plasma NO level after resuscitation, but fail to improve the outcome of traumatic shock in rats.