[Compound Amino Acid Capsule (8-11) combined with L-carnitine for the treatment of asthenospermia].

OBJECTIVE: To observe the clinical effect of combined application of Compound Amino Acid Capsule (8-11) (CAAC8-11) and L-carnitine (LC) in the treatment of idiopathic asthenospermia (IAS), and to explore its possible therapeutic mechanism. METHODS: Based on the principle of double-blind and control, we selected 120 cases of IAS meeting the diagnostic criteria of asthenospermia in the WHO Manual for the Examination and Processing of Human Semen (5th Ed) and randomly divided them into three groups of an equal number: CAAC8-11 + LC, LC control and blank control, the former given CAAC8-11 in addition to LC oral liquid, and the latter two given LC oral liquid and life intervention, respectively, all for 12 weeks. We collected semen samples from all the patients before and after treatment, and examined perm motility, the contents of neutral α- glucosidase (NAG) and reactive oxygen species (ROS), sperm DNA fragmentation index (DFI), and the expression of the Nrf2 protein. RESULTS: Compared with the baseline, the total sperm motility was significantly improved in the IAS patients after treated with CAAC8-11 + LC (ï¼»27.50 ± 0.77ï¼½% vs ï¼»32.50 ± 0.74ï¼½%, P < 0.05) or LC only (ï¼»27.60 ± 0.66ï¼½% vs ï¼»30.90 ± 0.70ï¼½%, P < 0.05), dramatically higher in the CAAC8-11 + LC than in the LC and blank control groups (P < 0.01). The content of NAG in the epididymis was remarkably increased after treatment in the CAAC8-11 + LC than in the LC and blank control groups (ï¼»23.90 ± 0.56ï¼½ vs ï¼»21.20 ± 0.49ï¼½ and ï¼»16.80 ± 0.42ï¼½ mU, P < 0.05), so was the expression of Nrf2 (P < 0.05), while the ROS level was markedly decreased in the former than in the latter two groups (ï¼»81.60 ± 2.50ï¼½ vs ï¼»88.50 ± 2.50ï¼½ and ï¼»88.70 ± 2.40ï¼½ µg/ml, P < 0.05). CONCLUSION: CAAC8-11 + LC has a good clinical effect on asthenospermia, with no adverse reactions, which may be attributed to its ability to regulate the high expression of Nrf2, decrease the production of ROS and reduce the damage of oxidative stress to sperm motility.

New lymphatic cell formation is associated with damaged brain tissue clearance after penetrating traumatic brain injury.

We characterized the tissue repair response after penetrating traumatic brain injury (pTBI) in this study. Seventy specific pathogen-free Kunming mice were randomly divided into the following groups: normal control, 1, 3, 7, 15, 21, and 30 days after pTBI. Hematoxylin and eosin (H&E) staining, immunohistochemistry, and immunofluorescence were performed to examine and monitor brain tissue morphology, and the distribution and expression of lymphatic-specific markers lymphatic vessel endothelial receptor-1 (LYVE-1), hematopoietic precursor cluster of differentiation 34 (CD34) antigen, and Prospero-related homeobox-1 (PROX1) protein. H&E staining revealed that damaged and necrotic tissues observed on day 1 at and around the injury site disappeared on day 7, and there was gradual shrinkage and disappearance of the lesion on day 30, suggesting a clearance mechanism. We explored the possibility of lymphangiogenesis causing this clearance as part of the post-injury response. Notably, expression of lymphangiogenesis markers LYVE-1, CD34, and PROX1 was detected in damaged mouse brain tissue but not in normal tissue. Moreover, new lymphatic cells and colocalization of LYVE-1/CD34 and LYVE-1/PROX1 were also observed. Our findings of the formation of new lymphatic cells following pTBI provide preliminary insights into a post-injury clearance mechanism in the brain. Although we showed that lymphatic cells are implicated in brain tissue repair, further research is required to clarify the origin of these cells.

Prox1 induces new lymphatic vessel formation and promotes nerve reconstruction in a mouse model of sciatic nerve crush injury.

The peripheral nervous system lacks lymphatic vessels and is protected by the blood-nerve barrier, which prevents lymphocytes and antibodies from entering the neural parenchyma. Peripheral nerve injury results in degeneration of the distal nerve and myelin degeneration causes macrophage aggregation, T lymphocyte infiltration, major histocompatibility complex class II antigen expression, and immunoglobulin G deposition in the nerve membrane, which together result in nerve edema and therefore affect nerve regeneration. In the present paper, we show myelin expression was absent from the sciatic nerve at 7 days after injury, and the expression levels of lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) and Prospero Homeobox 1 (Prox1) were significantly increased in the sciatic nerve at 7 days after injury. The lymphatic vessels were distributed around the myelin sheath and co-localized with lymphatic endothelial cells. Prox1 induces the formation of new lymphatic vessels, which play important roles in the elimination of tissue edema as well as in morphological and functional restoration of the damaged nerve. This study provides evidence of the involvement of new lymphatic vessels in nerve repair after sciatic nerve injury.

Formation of new lymphatic vessels in glioma: An immunohistochemical analysis.

We investigated the distribution and formation of new lymphatic vessels in gliomas. Specimens from seven glioma cases were analyzed by immunohistochemical staining for CD34, lymphatic endothelial hyaluronic acid receptor 1 (LYVE-1), prospero-related homeobox 1 (Prox1), nestin, and hypoxia-inducible factor 1α (HIF-1α). Three types of vessels were observed in glioma specimens: LYVE-1+ lymphatic vessels, CD34+ blood vessels, and LYVE-1+ /CD34+ blood vessels. Prox1+ /LYVE-1+ cells were distributed in some lymphatic vessels as well as among vascular endothelial cells and glioma cells. Nestin+ cells were scattered throughout the gliomas, and some lymphatic cells also expressed nestin. HIF-1α+ Prox1+ cells were widely distributed within the glioma specimens. The present immunohistochemical analysis revealed upregulation of Prox1 and HIF-1α in some glioma tissues as well as the differentiation of nestin+ tumor stem cells into LYVE-1+ lymphatic vessels.

'Red - the magic color for solar salt production' - but since when?

Dense communities of carotenoid-rich members of the Halobacteria (Euryarchaeota), the bacterium Salinibacter (Bacteroidetes) and the eukaryotic alga Dunaliella color the brines of most saltern crystallizer ponds red. The first report we found from the western world mentioning these red brines dates from 1765: the Encyclopédie of Diderot and coworkers. Earlier descriptions of solar salterns since Roman times do not mention red ponds. These include the Astronomica of Manilius, Pliny's Naturalis Historia (1st century), the description of Italian salterns in De Reditu Suo by Namatianus (5th century), Agricola's De Re Metallica (1556) and an anonymous description of French salterns (1669). This suggests that in earlier times, saltern brines may not have been red. In salterns which are operated today in the traditional way as practiced in the Middle Ages, no red brines are observed. Prokaryotic densities in the salterns of Secovlje (Slovenia) and Ston (Croatia) are an order of magnitude lower than in modern saltern crystallizers. This is probably due to the much shorter residence time of the brine in the traditionally operated salterns. In China, red saltern brines were documented earlier: in Li Shizhen's compendium of Materia Medica Ben Cao Kang Mu, completed in 1578 and based on older sources.

Solubilized extracellular matrix from brain and urinary bladder elicits distinct functional and phenotypic responses in macrophages.

Extracellular matrix (ECM) derived from a variety of source tissues has been successfully used to facilitate tissue reconstruction. The recent development of solubilized forms of ECM advances the therapeutic potential of these biomaterials. Isolated, soluble components of ECM and matricryptic peptides have been shown to bias macrophages toward a regulatory and constructive (M2-like) phenotype. However, the majority of studies described thus far have utilized anatomically and morphologically similar gastrointestinal derived ECMs (small intestine, esophagus, urinary bladder, etc.) and a small subset of macrophage markers (CD206, CD86, CCR7) to describe them. The present study evaluated the effect of solubilized ECM derived from molecularly diverse source tissues (brain and urinary bladder) upon primary macrophage phenotype and function. Results showed that solubilized urinary bladder ECM (U-ECM) up-regulated macrophage PGE2 secretion and suppressed traditional pro-inflammatory factor secretion, consistent with an M2-like phenotype. The hyaluronic acid (HA) component in solubilized U-ECM played an important role in mediating this response. Brain ECM (B-ECM) elicited a pro-inflammatory (M1-like) macrophage response and contained almost no HA. These findings suggest that the molecular composition of the source tissue ECM plays an important role in influencing macrophage function and phenotype.

4-(2,3-Dimeth-oxy-phen-yl)-1H-pyrrole-3-carbonitrile.

The asymmetric unit of the title compound, C(13)H(12)N(2)O(2), obtained in a search for analogs of the fungicide fludioxonil [systematic name: 4-(2,2-difluoro-1,3-benzodioxol-4-yl)-1H-pyrrole-3-carbonitrile], contains two independent mol-ecules, A and B. The benzene and pyrrole rings are inclined to each other at 38.5 (1) and 29.3 (1)° in mol-ecules A and B, respectively. In the crystal, bifurcated N-H⋯(O,O) hydrogen bonds link A mol-ecules into chains along [001], while B mol-ecules are linked into layers parallel to the bc plane via bifurcated N-H⋯(N,N) hydrogen bonds.

4-(2,2-Difluoro-1,3-benzodioxol-4-yl)-1H-pyrrole-3-carbonitrile.

In the title compound, C(12)H(6)F(2)N(2)O(2), the 2,2-difluoro-1,3-benzodioxole ring system is approximately planar [maximum deviation = 0.012 (2) Å] and its mean plane is twisted with respect to the pyrrole ring, making a dihedral angle of 2.51 (9)°. In the crystal, N-H⋯N hydrogen bonds link the mol-ecules into chains running along the a axis. π-π stacking is also observed between parallel benzene rings of adjacent mol-ecules, the centroid-centroid distance being 3.7527 (13) Å.

Gelatinized copper-capillary alginate gel functions as an injectable tissue scaffolding system for stem cell transplants.

In severe hypoxic-ischemic brain injury, cellular components such as neurons and astrocytes are injured or destroyed along with the supporting extracellular matrix. This presents a challenge to the field of regenerative medicine since the lack of extracellular matrix and supporting structures makes the transplant milieu inhospitable to the transplanted cells. A potential solution to this problem is the use of a biomaterial to provide the extracellular components needed to keep cells localized in cystic brain regions, allowing the cells to form connections and repair lost brain tissue. Ideally, this biomaterial would be combined with stem cells, which have been proven to have therapeutic potentials, and could be delivered via an injection. To study this approach, we derived a hydrogel biomaterial tissue scaffold from oligomeric gelatin and copper-capillary alginate gel (GCCAG). We then demonstrated that our multipotent astrocytic stem cells (MASCs) could be maintained in GCCAG scaffolds for up to 2 weeks in vitro and that the cells retained their multipotency. We next performed a pilot transplant study in which GCCAG was mixed with MASCs and injected into the brain of a neonatal rat pup. After a week in vivo, our results showed that: the GCCAG biomaterial did not cause a significant reactive gliosis; viable cells were retained within the injected scaffolds; and some delivered cells migrated into the surrounding brain tissue. Therefore, GCCAG tissue scaffolds are a promising, novel injectable system for transplantation of stem cells to the brain.

Reconstruction of central lacteals in the murine jejunum following ischemia-reperfusion injury.

The intestinal mucosa is vulnerable to an ischemia-reperfusion (I/R) attendant on some bowel diseases and surgery; thus, the restoration of the mucosal integrity is critical to achieving functional recovery of the intestine injured by I/R. In this histochemical study, we investigated the alteration of the central lacteals--which are essential for the transport of fat, tissue fluid, and immune cells in the intestinal mucosa--in the murine jejunum after I/R. The intestine inflicted with I/R demonstrated mucosal injury involving the inflammatory response, with interstitial edema, disruption of the villous tissue, and subsequent tissue regeneration of the villi. The regenerative villous tissue revealed lymphatic regrowth showing proliferative activity from the residual mucosal lymphatics behind the regenerated blood vasculature. During the regenerative phase, the blood vascular pericytes expressed an intense immunoreaction for VEGF-A, an inducer for monocyte/macrophage recruitment as well as angiogenesis. Also, the F4/80-immunopositive macrophages significantly increased in number in the regenerating villous stroma. Furthermore, the macrophages recruited around the regrowing lacteals expressed the immunoreactivity for VEGF-C, which is a highly specific lymphangiogenic factor. The present study is first to delineate alterations in the central lacteals in the small intestine following I/R, thereby suggesting that the recruitment of the macrophages induced by upregulation of VEGF-A in the pericytes of regenerative blood vessels might promote reconstruction of the central lacteals through their release of VEGF-C.

Self-assembled copper-capillary alginate gel scaffolds with oligochitosan support embryonic stem cell growth.

Biomaterial scaffolds are fundamental components of strategies aimed at engineering a wide range of tissues. Scaffolds possessing uniform, oriented microtubular architectures could be ideal for multiple tissues, but are challenging to produce. Therefore, we developed hydrogel scaffolds possessing regular, tubular microstructures from self-assembled copper-capillary alginate gel (CCAG). To abrogate the rapid dissolution of CCAG in cell culture media, we treated it with oligochitosan and created a stable oligochitosan-CCAG (OCCAG) polyelectrolyte complex. Fourier transform infrared spectroscopy confirmed polyelectrolyte complexation between alginate and oligochitosan. OCCAG retained capillary morphology, shrank anisotropically in bulk, lost Cu(2+) ions, and maintained (71.9 +/- 5.65)% of its mass in cell culture media. Next, we seeded mouse embryonic stem (ES) cells within OCCAG scaffolds, and examined cell morphology and quantified cell growth and viability over four days. ES cells were guided to form cylindrical structures of staggered cells within scaffold capillaries. Analysis of the total cells recovered from the scaffolds revealed exponential cell growth (normalized to day 0) that was statistically similar to gelatinized-plate controls. OCCAG-cultured ES cell viability was also not significantly different from controls at day 4. CCAG-derived scaffolds can therefore serve as a unique platform for stem cell-based tissue engineering.

[Identification of interaction and interaction domains between neuroglobin and Na(+), K(+)-ATPase beta2 subunit].

The pre-transformed human fetal brain cDNA library was used to screen the protein interacting with neuroglobin by using yeast two hybrid system III from ClonTech Inc. The protein encoded by one of the clones interacting with neuroglobin (NGB) was confirmed to be the C terminus of the Na(+), K(+)-ATPase beta2 subunit (NKA1b2) based on amino acid sequences. Then the full-length coding region cDNA sequence of NKA1b2 was obtained from human fetal brain cDNA library by PCR. A set of experiments were designed to test the interaction between NGB and NKA1b2. Interaction between NGB and NKA1b2 was confirmed by binding assay in vitro. Furthermore, the interaction was also proved by co-immunoprecipitation test in vivo. Moreover, the structure integrity of neuroglobin was found to be essential for the interaction between NGB and NKA1b2 by yeast two hybrid method with a series of neuroglobin truncated mutants.