Resveratrol attenuates neurological deficit and neuroinflammation following intracerebral hemorrhage.

Resveratrol (RESV) improves histopathological and behavioral outcomes in diseases of the central nervous system. However, to the best of our knowledge, there have been no studies investigating its neuroprotective effects on secondary brain injury following intracerebral hemorrhage (ICH). The aim of the present study was to evaluate the neuroprotective function of resveratrol following ICH. Male Sprague-Dawley rats were randomly divided into 3 groups: Sham, ICH and ICH+RESV groups. Rats underwent ICH and received an intraperitoneal injection of RESV daily. Rotarod and open field tests were performed to evaluate improvements in motor disturbance pre- and post-surgery. Rats were sacrificed following the final behavioral test; subsequently, neuron injury and cell death in the hippocampus and microglia activation in the cortex were determined using Nissl staining and ionized calcium binding adaptor molecule 1 immunofluorescence staining, respectively. Compared with the ICH group, rats treated with resveratrol for 2 weeks performed significantly better in behavioral tests. Furthermore, less neural damage in the hippocampus and decreased activation of microglia was observed in the ICH+RESV group. The results of the present study therefore indicate that resveratrol may alleviate secondary brain injury following ICH.

Dual In-Tether Chiral Centers Modulate Peptide Helicity.

The facile chemical modification on the peptide cross-linking moiety is an important strategy for improving the physicochemical properties of a peptide. Herein, peptides were constrained into helical conformations via the synergistic effects of dual in-tether chiral centers. A pentapeptide minimalistic model was used to determine the correlation between the absolute configurations of the dual in-tether chiral centers and the secondary structures of the peptides. This strategy provides an on-tether modification site that does not interrupt the secondary structure of the peptide.

Improved cellular immune response elicited by a ubiquitin-fused DNA vaccine against Mycobacterium tuberculosis.

This study evaluated the immune response elicited by a ubiquitin (Ub)-fused MPT64 DNA vaccine against Mycobacterium tuberculosis. BALB/c mice were vaccinated with plasmid DNA encoding MPT64 protein, Ub-fused MPT64 DNA vaccine (UbGR-MPT64), and negative DNA vaccines, respectively. MPT64 DNA vaccine immunization induced a Thl-polarized immune response. The production of Thl-type cytokine (interferon-gamma [IFN-γ]) and proliferative T cell responses were enhanced significantly in mice immunized with UbGR-MPT64 fusion DNA vaccine, compared with nonfusion DNA vaccine. Moreover, this fusion DNA vaccine also resulted in an increased relative ratio of IgG2a to IgGl and the cytotoxicity of T cells. IFN-γ intracellular staining of splenocytes indicated that UbGR-mpt64 fusion DNA vaccine activated CD4+ and CD8+ T cells, particularly CD8+ T cells. Thus, this study demonstrated that the UbGR-MPT64 fusion DNA vaccine inoculation could improve antigen-specific cellular immune responses, which is helpful for protection against TB.

[Experimental study on mechanism of recompression therapy of decompression sickness].

OBJECTIVE: To elucidate that recompression is the most efficient measure in removing the pathogenic factors. METHOD: When rabbits were suffering from severe DCS, their pressure were immediately compressed to 0.5 Mpa. Precordial region was monitored continuously with a Doppler flow meter, micrography of the bulbar conjunctiva was done intermittently and the behaviors of the animals were recorded. RESULT: Effects of therapeutic recompression and elimination of circulating bubbles were correlated to rate and extent of recovery of microvascular function. The animals' DCS with severe dysfunction or failure of blood vessels, DCS became worse owing to progressive impairment of microvascular function during recompression and decompression. CONCLUSION: The pressure could only cancel the tension provoked by supersaturated gas in the blood so as to relieve the spasm of the compensatory blood vessels, which can restore the blood circulation and reverse the developing course of the DCS. The pressure, however, couldn't recover the function of the blood vessels with severe dysfunction or failure, or repair the injured tissues, or eliminate the circulating bubbles directly.

[A study on etiology and pathogenic mechanism of decompression sickness].

OBJECTIVE: To explain the etiology of decompression sickness (DCS) and to elucidate its pathogenic mechanism. METHOD: Tunica conjunctiva was examined by microscopy and blood pressure was measured at the exposed femoral arteries in inadequately decompressed animals after hyperbaric exposure. Then pathological examinations were done. RESULT: Animals with vascular spasm and dysfunction after decompression showed DCS symptoms. Severe DCS was found in the period of increasing of blood pressure swelling. Appeared in endothelial cells, fracted, hemorrhages were also formed in the body of DCS animals. CONCLUSION: DCS is a disease with vascular spasm and dysfunction caused by decompression. It's resulted from anoxia or pathological change caused by vascular spasm, dysfunction or even failure of blood vessels due to the gas tension (etiology) provoked by supersaturated gas in the blood during descending of ambient pressure. Vascular spasm and dysfunction impede the elimination of gas from the blood, and once the gas amount is sufficient to cause severe ischemia of the circulation system, the state of disease would be severe.

Characterization of a novel plasmid pXZ608 from Corynebacterium glutamicum.

The complete nucleotide sequence of a novel cryptic plasmid pXZ608 from Corynebacterium glutamicum 227 was determined. pXZ608 was 5949 bp with six open reading frames (ORF1-6). The predicted ORF1 gene product was homologous to replication proteins of rolling circle replication plasmids. The conserved single- and double-stranded origins of rolling circle replication were found, and interestingly, the two origins were both located on ORF1, which indicated that the Rep protein encoded by ORF1 could bind to its own gene region. Deletion analysis revealed that the minimal replicon was located on the 2.14-kb SacI-BstEII fragment.

Sequence analysis and characterization of plasmid pSFD10 from Salmonella choleraesuis.

The nucleotide sequence of a small plasmid, designated pSFD10, is isolated from the vaccine strain Salmonella choleraesuis C500 in China, has been determined. This plasmid is 4091 bp long with a total G+C content of 51.4%, which is in the range of Salmonella genomic DNA. Analysis of the complete nucleotide sequence reveals that pSFD10 has a high degree of similarity to ColE1-type plasmid, having the possible cer and rom genes, and a putative mobilization origin of ColE1-type. Plasmid pSFD10 possesses six main open reading frames (ORFs), five of which have a very high degree of amino acid identity to ColE1-type plasmid gene products involved in mobilization and copy number control. The other ORF (ORF6) encodes a putative protein, which has 49% homology to the invasion plasmid antigen J protein (IpaJ) secreted by the type III secretion apparatus of Shigella flexneri. In addition, pSFD10 belongs to a different incompatibility group than ColE1-type and pMB1-type to which it is related. Plasmid pSFD10 can be mobilized by the plasmid RP4 in E. coli.