Charge inhomogeneity of carbon.

Charge distribution on every atom of carbon matter in four dimension forms (cluster, fullerene, atomistic carbon chain, nanotube, graphene, surface and solid) was investigated by the first-principles calculation. It is found that the charge distribution in most of these materials is inhomogeneous, even in one certain solid phase. We found that if one atom in carbon has different surrounding environment from another one nearby, they always have electron transfer, that is, they have different charge. In round C10 ring, C24 and C60 fullerenes, charge is zero, while charge is not zero in pentagon C10 ring, C30 and C70 fullerenes. At the ends of atomistic chains, nanotube or on the edges of graphenes, carbon atoms have larger positive or negative charge, while almost zero in the central parts. Charge is zero in diamond and graphite, while it is not zero in the high pressure solid phase hexagonite or on some carbon surfaces. The non-zero charge in carbon possibly means its non-zero valence.

[Outcome of kidney transplantation with graft from intracerebral hemorrhage donors].

Objective: To analyze the data of kidney transplantation with allografts from intracerebral hemorrhage donors of China donation after citizen's death (CDCD) and provide evidence to guide the clinical practice. Methods: The clinical data of CDCD donors (age ≥10 years)and corresponding kidney allograft recipients, which were done by Second Xiangya Hospital of Central South University during January 1 2013 to December 31 2017, were analyzed retrospectively. Results: 327 CDCD cases were analyzed, the number and percentage of intracerebral hemorrhage donors were gradually increasing and the percentage reached to 39.5% in 2017. The discarding rateof kidney allografts donated by intracerebral hemorrhage donors was higher than those donated by non-intracerebral hemorrhage donors, but intracerebral hemorrhage donor may not be a risk factor for DGF after the rigorous evaluation of kidney allografts. For 145 primary recipients transplanted in 2016 and had a 22±4 month follow-up, the recipients accepted the kidney from intracerebral hemorrhage donors had a higher level of serum creatinine[(130±60)µmol/L vs (111±38) µmol/L,P<0.05]and a lower eGFR[(61±23) ml·min(-1)·(1.73m(2))(-1) vs (70±23) ml·min(-1)·(1.73m(2))(-1),P<0.05] compared to the recipients accepted the kidney from non-intracerebral hemorrhage donors. Conclusion: The number and percentage of organ donation from intracerebral hemorrhage donor is increasing, but the intracerebral hemorrhage donor may be a risk factor for long-term outcome of kidney transplantation.

Regulation of NK92-MI cell cytotoxicity by substance P.

The neuropeptide substance P (SP) can regulate a number of immunological functions in vitro and in vivo and may regulate natural killer (NK) cell activity. Here, we investigated whether SP has a role in regulating NK92-MI cell function in vitro, and how it influences NK cell activity. We found that SP dose dependently increased the cytotoxicity of NK92-MI cells and had a maximal effect at a concentration of 10(-12) and 10(-10) m. Furthermore, the expression of cytotoxic-associated molecules (perforin, granzyme) and activating receptor NKp46 [a member of natural cytotoxicity receptors (NCRs)] was observed to be upregulated by SP at optimal concentration, at which SP enhanced the cytotoxicity of NK92-MI cells. Neurokinin-1 receptor (NK-1R), a functional receptor of SP, was found on NK92-MI cells, and the observed effects of SP on NK92-MI cells could be more partially blocked by an NK-1R antagonist. Our data suggest that SP induces NK92-MI cell cytotoxicity by directly increasing the expression of cytotoxic granules and upregulates NK92-MI cell receptor-mediated functions indirectly. Thus, SP may regulate NK cell function mainly through NK-1R.

The protective effect of hyperbaric oxygen on hearing during chronic noise exposure.

A series of experiments were conducted on guinea pigs to study the protective effect of hyperbaric oxygen (HBO) on hearing during chronic repeated noise exposure. A 1/3 octave band of noise centered at 1000 Hz was used (126 dB SPL, 1 h daily for 5 d; or 108 dB SPL, 1 h daily, 5 d/week for 4 weeks). Some groups of animals were treated with HBO (2-3 ATA, 1 h duration) before noise exposure. The results indicate that inhalation of HBO (every other day) can markedly reduce noise-induced threshold shift and relieve cochlear damage. The mechanism responsible for HBO protection against noise-induced hearing damage is discussed.

Noise-induced hearing loss in iron-deficient rats.

The role of iron deficiency in noise-induced hearing loss (NIHL) was evaluated in 64 rats of four different experimental groups. Iron-deficient rats (ID-rats) and normal rats (N-rats) were simultaneously exposed to a steady state white noise (20-10,000 Hz) at 110 dB SPL for 30 min. Unexposed ID- and N-rats served as controls. In N-rats the temporary threshold shifts (TTS) would have completely disappeared if the animals were allowed to survive for 72 h. No permanent threshold shift (PTS) was seen in any of the N-rats. The ultrastructural correlates in N-rats are stereocilia disarray and mitochondria swelling in outer hair cells (OHCs). The TTS in ID-rats were larger than those in the N-rats, and most ID-rats with larger threshold shifts showed varying degrees of PTSs at 11 days post-exposure. The ultrastructural correlates of NIHL in ID-rats are obvious pathology of the stereocilia, such as segmental coalescence of stereocilia of many continuous OHCs and fusion of the tips of stereocilia of OHCs, and a significant reduction of mitochondria as well as slight degeneration of nucleus in the OHCs. It is concluded that iron deficiency can provide a pathological basis for NIHL.