[Research advances in B-type natriuretic peptide and its clinical application in the patients with cardiovascular diseases].

B-type natriuretic peptide (BNP) is a plasma marker of left ventricular dysfunction and cardiac volume overload. Currently it is mainly used in the cardiovascular field. BNP is an intrinsic regulator of the embryonic stem cell proliferation, and the reduction in BNP can increase the apoptosis rate. The epitope of N terminal pro-brain natriuretic peptide-BNP is most stable. BNP1-32 has the strongest biological activity but with lower plasma level in heart failure patients. The plasma BNP level plays an important role in the diagnosis, prognosis, hospital admission and mortality of heart failure, and can be used as a monitoring indicator in the treatment of heart failure. The deficiency of corin enzyme in patients with heart failure can cause the increase of cracking pro-BNP. BNP can also provide diagnostic and prognostic information for other populations and diseases. Genetic studies on BNP and its receptors also provide important information. Nesiritide, neutral endopeptidase inhibitors, and vasopeptidase inhibitors of the natriuretic peptide synthesis have been used for the treatment of cardiovascular disorders. However, more reliable and accurate approaches for detecting BNP and N terminal pro-brain natriuretic peptide-BNP require further investigations.

Impact of migraine attacks on the blood-brain barrier.

BACKGROUND: Cortical spreading depression can cause migraine attack, and up-regulate matrix metalloproteinase-9 (MMP-9) expression in animal. This study aimed to determine the impact on the structure and function of the blood-brain barrier by measuring plasma MMP-9 levels in patients at the acute and late stages of migraine attacks in order to elucidate the pathological mechanisms involved. METHODS: We recruited a case-control cohort of 38 adult migraine patients and 20 age- and gender-matched healthy control subjects. Five milliliter blood samples were collected at the acute and late stages of migraine (days 1 - 7), and also from the control subjects. Solid phase double antibody sandwich enzyme-linked immunosorbent assay was used to determine plasma MMP-9 levels. Statistical analysis was performed using the SAS version 9.1. RESULTS: Initial plasma MMP-9 levels of migraine patients were significantly higher than those of controls ((12.612 ± 0.016) µg/L vs. (6.069 ± 0.023) µg/L, respectively, P < 0.05). High MMP-9 expression was observed during days 1 - 6 of migraine attacks, with highest expression occurring on day 3 ((17.524 ± 0.035) µg/L). During attacks, MMP-9 levels were similar in migraine patients with and without aura (P > 0.05); in addition, levels were not correlated with degree of headache pain (P > 0.05). CONCLUSIONS: We hypothesize that migraine could lead to increased plasma MMP-9 levels resulting in blood-brain barrier damage. MMP-9 levels increase during days 1 - 6 of migraine attacks, peaking on day 3. Therefore, MMP-9 could be used as a biological marker to guide treatment of migraine attacks.

MMP-mediated cleavage of beta-dystroglycan in myelin sheath is involved in autoimmune neuritis.

Alpha-/beta-dystroglycans (DG) located at the outmost layer of myelin sheath play a critical role in its formation and stability in the peripheral nerve system. The demyelination of nerve fibers is present in autoimmune neuritis, however, it is not known about the molecular mechanisms underlying this pathological process. In an animal model of experimental autoimmune neuritis, we observed that beta-DG cleavage was associated with the demyelination of peripheral nerves. The neuritis and beta-DG cleavage were accompanied by matrix metalloproteinase (MMP)-2/-9 over-expressions and attenuated by captopril, a MMP inhibitor. The blockade of MMPs also improves clinical signs. Our results reveal a crucial role of MMP-mediated beta-DG cleavage in autoimmune neuritis, such as Guillain-Barre' syndrome, and bring insights into therapeutic strategies for autoimmune diseases.

[A multiple center study on depression and anxiety state in the department of neurology].

OBJECTIVE: Inpatients of 15 general hospitals were investigated in order to understand the incidence of depression and anxiety state and the patients'quality of life in the Department of Neurology. METHODS: We used Hospital Anxiety and Depression scale (HADS), 17-item Hamilton Rating Scale for Depression (HAMD), Hamilton Rating Scale for Anxiety (HAMA) and 36-item Short Form Health Survey (SF-36) as tools to evaluate inpatients' emotional state and health related quality of life within 48 hours after admitted and before discharge, respectively. RESULTS: 610 inpatients were finished admitted evaluation, patients showed clinical depressive symptoms and anxiety symptoms were 123 (20.2%) and 161 (26.4%) respectively, in which including 96 showed the both. 405 inpatients finished discharge evaluation, patients showed clinical depression symptoms and anxiety symptoms were 68 (16.8%) and 93 (23%) respectively, in which including 52 showed the both. Regression analysis indicated that health related quality of life was associated with gender, anxiety and depression state. Only 59 (20.8%) patients received drug treatment during they admitted. There were statistic significance decrease of the HAMA and HAMD total scores between treatment group and non-treatment group when discharged; Vitality, role of emotional and mental health were significantly increased at the time of discharge. CONCLUSION: High rate of depression and anxiety state occurred in the department of Neurology. These abnormal emotions affected the quality of life of patients. If a physician treated somatic diseases only, the depressive and anxiety disturbances could not be remission. Thus, more attention should be paid to give adequate treatment if a patient concomitant presented the emotional disturbances in the general hospital.

[rpsL gene analysis associated with Streptomycin resistance in Mycobacterium tuberculosis].

The mutation of the rpsL gene in Mycobacterium tuberculosis (M.TB) is related to Streptomycin resistance. In this experiment, 77 TB strains obtained in hospital were selected, the routine drug susceptibility test was done by using BACIEC460 system, meanwhile the TB-rspL gene was amplicated by PCR, and analyzed by SSCP, RFLP and sequence analysis. There are 20 strains sensitive to SM and 57 strains resistant to it in routine drug susceptibility test. The SSCP result displayed that 34 strains were rspL gene wild type and 43 strains were mutant type. Compared with routine drug susceptibility test, the specificity was 95% and the positive anticipate value was 98%. RFLP cut by MobII displayed that 81.4% of mutation happened in codon 43 of TB-rspL. Sequence analysis displayed that there was single base mutation in codon 43(AAG-->AGG). In conclusion, Drug resistance of TB to SM is related to rspL gene mutation and the mutation in codon 43 is the most common cause.