Finding the optimal dose of vitamin K1 to treat vitamin K deficiency and to avoid anaphylactoid reactions.

Vitamin K1 injection induces severe dose-related anaphylactoid reactions and overdose for the treatment of vitamin K deficiency. We aimed to find an optimal and small dose of vitamin K1 injection to treat vitamin K deficiency and avoid anaphylactoid reactions in animal. Rats were administered a vitamin K-deficient diet and gentamicin to establish vitamin K deficiency model. Behaviour tests were performed in beagle dogs to observe anaphylactoid reactions. The results showed an increased protein induced by vitamin K absence or antagonist II (PIVKA-II) levels, a prolonging of prothrombin time (PT) and activated partial thromboplastin time (APTT) and a decrease in vitamin K-dependent coagulation factor (F) II, VII, IX and X activities in the model group. In vitamin K1 0.01 mg/kg group, the liver vitamin K1 levels increased fivefold and the liver vitamin K2 levels increased to the normal amount. Coagulation markers PT, APTT, FVII and FIX activities returned to normal. Both in the 0.1 and 1.0 mg/kg vitamin K1 groups, coagulation functions completely returned to normal. Moreover, the amount of liver vitamin K1 was 40 (0.1 mg/kg) or 100 (1.0 mg/kg) times as in normal. Vitamin K2 was about 4 (0.1 mg/kg) or 5 (1.0 mg/kg) times as the normal amount. There was no obvious anaphylactoid symptom in dogs with the dose of 0.03 mg/kg, which is equivalent to the dose of 0.01 mg/kg in rats. These results demonstrated that a small dose of vitamin K1 is effective to improve vitamin K deficiency and to prevent anaphylactoid reactions, simultaneously.

[Pathogenic significance and possible pathogenic mechanism of human endogenous viruses in development of schizophrenia].

The association between psychogenic illness and human endogenous viruses (HEVs), including human endogenous retrovirus and Borna disease virus, remains unclear. As the component of human genome, HEVs may become the joint of various pathogenic factors of schizophrenia (SZ), such as heredity, environment, and immunity. In this review, we strive to uncover the clinical and laboratory evidence for the roles and possible pathogenic mechanism of HEVs in the development of SZ.

Expression pattern of the ASPP family members in endometrial endometrioid adenocarcinoma.

BACKGROUND: Apoptosis-stimulating protein of p53 (ASPP) family members can stimulate the apoptotic function of p53 but have no impact on its cell cycle arrest function. MATERIAL AND METHODS: The expression pattern of the ASPP family consisting of ASPP1, ASPP2, and iASPP was examined by immunohistochemistry in 45 formalin-fixed and paraffin-embedded endometrial endometrioid adenocarcinoma (EEA) specimens and 26 normal endometrial tissue (NET) samples. RESULTS: The expression rates of ASPP1 and ASPP2 in EEA were significantly lower than those in NET (p < 0.05). However, the iASPP expression rate in EEA was statistically higher in contrast to NET (p < 0.05). Expression of ASPP1 and iASPP in EEA had no correlation with any clinicopathological features (p > 0.05). iASPP was associated with grade, invasion, and lymph node metastasis (p < 0.05). CONCLUSIONS: It is a novel finding that the expression pattern of the ASPP family members has respective pathological and clinical implications in EEA, and iASPP might be a candidate target for EEA therapy.

[Surveillance of antimicrobial resistance among nosocomial gram-negative pathogens from 15 teaching hospitals in China in 2005].

OBJECTIVE: To investigate the antimicrobial resistance among the nosocomial gram-negative pathogens from 15 teaching hospitals located in different areas in China in 2005. METHODS: A total of 1927 non-repetitive nosocomial gram-negative pathogens were collected from 15 teaching hospitals in different areas in China and sent to the central lab for reidentification and susceptibility testing. The levels of minimal inhibitory concentration (MIC) of 18 antimicrobial agents were determined by agar dilution method. WHONET 5.4 software was used to analyze the data. RESULTS: The strains of Escherichia coli, Klebsiella pneumoniae, and Proteous mirabilis isolates that did not produce extended spectrum beta lactamases (ESBLs) showed high sensitivity to beta-lactams. The antibiotics with a susceptibility rates over 80% against the strains of Entorobacter cloacae, Enterobacter aerogene, Citrobacter spp, Serratia spp, and Proteous vulgaris producing AmpC enzyme included meropenem, imipenem, and piperacillin-tazobactam, and these 3 drugs showed a susceptibility rate of more than 80% against the ESBL-producing strains of Escherichia coli and Klebsiella pneumoniae. Other antimicrobial agents showing a relatively high activity against Enterobacter spp, Citrobacter spp, Serratia spp and Proteous vulgaris included cefepime (67.3% - 100%), amikacin (67.3% - 95.2%), ceftazidime (52.9% - 100%) and cefoperazone-sulbactam (51.9% - 100%). The susceptibility rate of fluoroquinolones was 34.8% - 36.1% against non-ESBL-producing Escherichia coli and was 13.4% - 17.1% against ESBL-producing isolates. The most active agent against Pseudomonas aeruginosa was polymyxin B (95.6%). The agents with the activity rates of 70% - 80% included meropenem, imipenem, amikacin, and piperacillin-tazobactam. The antibiotic with a high susceptible rate against Acinetobacter baumannii was polymyxin B (98.3%), followed by imipenem (80.8%), meropenem (76.2%), and minocycline (67.4%). The susceptible rates of other agents were all below 60%. The agents with relatively high activity against Stenotrophomonas maltophilia included minocycline (85%), levofloxacin (82.5%), and trimethoprim-sulfamethoxazole (77.5%). The agents with a relatively high activity against Burkholderia cepacia included minocycline (77.2%) and meropenem (61.4%). CONCLUSION: Carbapenem, piperacillin-tazobactam, amikacin and cefepime remained relatively high activity against nosocomial Enterobacteriaceae, Non-fermenting pathogens have lower susceptibility to the antimicrobial agents than before.

[Biological activities of the coagulation factor VIII, IX in platelet concentrates collected by platelet apheresis during preservation].

The study was to explore the change of coagulation factor VIII and IX activities in the platelet suspension collected by platelet apheresis during storage at 22 degrees C. 18 samples of platelet concentrates were collected by the cs-3000 plus and stored at 22 degrees C and then FVIII: C, FIX: C activities were detected at 0, 12, 24, 48, 72, 96, 120 hours respectively by SYSMEX CA-1500. The results showed that FVIII: C activity was (100.51 + 44.02)% at 0 hour, and then decreased dramatically to 10% - 40% of primary level from 12 to 120 hours, while FIX: C activity was (120.93 +/- 20.50)% at 0 hour and decreased to 10% - 35% of primary level from 24 to 120 hours. In conclusion, FVIII and FIX in the platelet concentrates stored at 22 degrees C could keep their biological activities at physiologically high levels.