A modified lambda-shaped LVA was performed at the left groin. In modified lambda-shaped LVA, two lymphatic vessels were transected, and both ends of the proximal and distal sides were converged respectively for an end-to-side and end-to-end anastomoses to one vein. Using modified lambda-shaped LVA, four lymph flows of two lymphatic vessels could be bypassed into a vein. Six months after the LVA surgery,

her left LEL index decreased from 261 to 247, indicating SB203580 concentration edematous volume reduction. Modified lambda-shaped LVA effectively bypasses all lymph flows from two lymphatic vessels, when only one large vein can be found in the surgical field. © 2013 Wiley Periodicals, Inc. Microsurgery 34:308–310, 2014. “
“Recalcitrant nonunions typically require vascularized bone for reconstruction. In this report, we present a case of an index finger middle phalanx nonunion that was successfully treated with a free medial femoral condyle corticocancellous flap.

Nearly 2 years after the free tissue transfer, the patient underwent debulking of the bone flap. This gave us the unique opportunity to examine the histology of the vascularized bone. © 2013 Wiley Periodicals, Inc. Microsurgery 33:567–571, 2013. “
“Big craniofacial resections for highly invasive malignant neoplasm, including skull base and maxillary bones, always represent a difficult chance for the reconstructive surgeon. In these cases it is not easy to restore anatomy and function simultaneously even adopting complex microsurgical techniques. In maxillofacial and oral surgery, simple bone homotransplantation for small bone segments

reconstruction R788 has been developing as popular technique and tissue banks offer not only bone segments but also many different tissues including complex body parts. In this paper we present, a case report Tyrosine-protein kinase BLK of a homotransplantation of a complete temporomandibular joint (TMJ) together with a portion of the medial skull base and mandibular ramus folded with an ante-brachial fascio-periosteal free flap as secondary reconstruction after nearly 5 years from the removal of a sarcoma of the TMJ involving the skull base and a follow up of more than 30 months. © 2009 Wiley-Liss, Inc. Microsurgery 2010. “
“Complex midfoot defects represent a reconstructive challenge since midfoot plays a key role in standing and gait. We report the case of a 27-year-old patient with a complex midfoot defect due to a high-energy gun shot injury. The defect included the tarsometatarsal complex, all three arches of the foot, and the overlying dorsal skin of the foot. Reconstruction was achieved in a single stage with a free fibular osteocutaneous flap. The fibula was osteotomized into three segments, which were used to reconstruct the bone defects, while the skin paddle of the flap was used for stable soft tissue coverage of the reconstructed bony skeleton. Early and late postoperative periods were uneventful.

Mice lacking IL-23 (p19−/−) have been shown to be resistant to CIA, which was correlated with an absence of IL-17-producing Th17 cells despite normal induction of collagen-specific, IFN-γ-producing Th1 cells. On the contrary, knock-out mice for the Th1 cytokine IL-12 (p35−/−) have more IL-17-producing Th17 cells and develop CIA readily [36]. The key role of Th17 in CIA was confirmed further by reports MK-2206 solubility dmso showing that CIA was suppressed in IL-17-deficient mice and that administration of neutralizing anti-IL-17 antibodies reduced significantly the severity of CIA [37,38]. IL-6 and transforming growth factor (TGF)-β are two important factors that

may be involved in the aggregation of arthritis observed in our experiment. TGF-β1 can increase buy Daporinad the IL-17+ cell fraction markedly, and is sufficient by itself to promote robust Th17 development [39–41]. Meanwhile, TGF-β1 also induces the expression of forkhead box P3 (FoxP3) (Treg), a suppressive T cell

subpopulation [42]. IL-6 can inhibit TGF-β-induced generation of FoxP3+ Treg cells and help to establish Th17 prominence [43,44]. Moreover, anti-IL-6R treatment for CIA has been confirmed to suppress the differentiation of antigen-specific Th17 and the onset of the disease [45]. In this study, we have shown in vivo that administration of Flk-1+ MSCs at day 21 increased the serum level of IL-6 (day 25) strikingly. This was confirmed in in vitro co-culture experiments. The increased IL-6 would then favour Th17 differentiation and contribute to aggravation of the disease, as discussed above. Although

T cells play a prominent role in the regulation and development of the autoimmune response in CIA, B cells and autoantibodies to murine Bumetanide CII appear to be the primary mechanism of immunopathogenesis in this model. It has been demonstrated previously that passive transfer of CII-specific T cells cannot induce arthritis [46,47], yet the passive transfer of immune sera from arthritic mice to naive mice induces severe inflammation [48–55], and once the transferred antibody is depleted, inflammatory responses subside. The autoantibody activates complement cascades and the inflammation that follows contributes to the development of erosive arthritis [53]. Reports from independent laboratories have demonstrated that MSCs can prolong the survival of plasma cells and stimulate antibody secretion through IL-6 and very late activation antigen-4 (VLA-4) [56,57]. IL-6/signal transducer and activator of transcription-3 (STAT3) signalling has also been reported to regulate the ability of naive T cells to acquire B cell help capacity [58]. In this study, we found that the splenocytes of Flk-1+ MSC-treated mice showed a higher proliferative capacity than those of the control CIA mice.

e. do not share a common set of characteristics identified in the model) in which

the equation was derived. A C-value of 0.75 is comparable Selleckchem AZD2014 to a model for end-stage liver disease score with C-value of 0.64, which is commonly used by many centres to prioritize patients for liver transplantation based on expected survival.38 In addition, based on DPI, the kidneys with the longest survival potential will be allocated according to the combined score of LYFT (80% of total score) and dialysis time/panel reactive antibody (PRA) (20% of total score), whereas kidneys with lower potential for long-term survival will be allocated according to dialysis time and panel reactive antibody (PRA), such that better donor kidneys are allocated to younger potential recipients, who have the longest expected LYFT. Older potential recipients (who will have a lower expected LYFT) and potential recipients with the longest dialysis time will be less likely to receive better donor kidneys but may have an advantage in being allocated shorter-lived kidneys more quickly (i.e. shorter waiting-time). Based on this allocation system using LYFT and other factors, there is a total expected increase in LYFT of 2642 years

during a single year of allocation as compared with the current allocation system in the USA. Although adoption of an allocation model based on LYFT is Y 27632 likely to increase graft longevity, this model is difficult to implement and may be perceived as being discriminatory. A perception that organ allocation is occurring in an inequitable BCKDHA manner could reduce organ

donor rates. Nevertheless, the utilization of LYFT may improve allocation based solely on age-matching, with other patient factors such as diabetes, which are known to significantly impact on graft and patient survival, are taken into account in the calculation of LYFT.39 In Australia, the initial allocation of deceased donor kidneys occurs at a national level, involving all potential recipients on the wait list. Around 20% of available deceased donor kidneys are allocated according to the Interstate Exchange Program, whereby the kidneys are shipped to potential recipients who are highly sensitized and with zero to two HLA-mismatches. However, the majority of the deceased donor kidneys are allocated locally according to primarily HLA-matching and time on dialysis. Although older donor kidneys are associated with shorter graft survival and poorer post-transplant graft function, donor issues such as age are not explicitly considered in the allocation algorithm. Some age matching still occurs, because a younger healthier potential recipient near the top of the list may decline a marginal kidney, and retain their place on the waiting list until a younger kidney becomes available.

6, PCa). Owing to the low levels of CD3+ cells in both BPH and PCa samples, it was not possible to distinguish CD4+ or CD8+ T lymphocyte populations because of the low fluorescence signal. A negative correlation between PSA value and overall percentage of P+, CD3+CD56−P+, and CD3−CD56+P+ cells was observed only in PCa samples (Fig. 7, row A–C, PCa). In contrast,

in peripheral blood, there was no correlation Daporinad mw between PSA value and overall percentage of P+, CD3+CD56−P+ and CD3−CD56+P+ cells in any of the groups investigated (data not shown). In recent decades, the incidence of BPH and PCa has augmented owing to increasing life expectancy and advanced methods of diagnosis and treatment [21]. Both conditions are related to the chronic inflammatory process and are recognized as the consequence of an altered immune response [2]. It has also been shown that different immune-competent cells infiltrate healthy, BPH, and PCa gland tissue [3], but little is known about the expression Epigenetics activator of their cytotoxic molecules. In this study, we determined

the presence and expression levels of P in different lymphocyte subsets in peripheral blood and prostate tissue to elucidate the possible mechanism responsible for BPH and PCa progression. Although total P expression in peripheral blood lymphocytes did not differ significantly between patients with BPH and patients with PCa and control group, a low P expression was observed in the BPH and PCa tissue, indicating that local microenvironment has a strong effect on cytotoxic potential. This finding is consistent with the observation of Ebelt et al. [12] who reported that P-expressing

T lymphocytes are rare in BPH and, particularly, PCa tissue. This contrasts with the significantly higher number of P-expressing cells readily detectable in healthy prostate tissue [12 and our observation]. In the peripheral blood of patients with BPH, the percentage of P+ T lymphocytes was decreased because of a significant reduction in the CD4+P+ T subset, which may be because of their recruitment to the BPH tissue. This hypothesis is consistent with the observation of diffuse accumulation of CD3+ T cells, mostly of the CD4+ phenotype, in glandular epithelium and, less frequently, in the stroma of BPH tissue [12]. Vitamin B12 Additionally, in direct contrast to the findings in the prostate tissue, the peripheral blood of patients with BPH showed significantly lower percentage of CD3+P+ lymphocytes. These T lymphocytes contained P in their cytoplasmic granules at levels comparable with that of CD3+P+ lymphocytes infiltrating healthy prostate tissue. Immunofluorescence of BPH tissue samples revealed higher levels of NK cell infiltration, predominantly in the enlarged stroma. The recruitment of NK cells (rarely P+) in the BPH tissue was probably the result of local proinflammatory factor production.

parvum infection (17,32). Recently cloned from C. parvum, P2 is one of the three acidic ribosomal proteins, including P0 and P1. These P proteins are potential vaccine targets owing to their expected surface localization and immunogenicity (19,24). The P2 antigen specifically is reactive with ∼70% of sera from adults in highly endemic countries. Strong anti-P2 antibody responses were observed in serum samples from Cryptosporidium-infected Haitian individuals that were also antibody positive for the Cp23 antigen (19). A strong and persistent cell-mediated selleck chemicals llc response is important in response and resistance to Cryptosporidium and depends,

in part, on the initial encounter between the parasite/parasitic antigens and antigen-presenting cells such as DCs. Therefore, the ability of parasite antigen to induce dendritic cells should correlate with a strong cellular response. Previously, it has been reported that Cp23 and Cp40 recombinant antigens induce a strong cellular T-cell response in mice and humans (33–35). Hence, these antigens should stimulate

DCs to produce significant levels of IL-12p70. Recombinant Cp17 did not stimulate significant cellular immune response in one study in mice (34) but Selleckchem Doxorubicin does elicit strong antibody responses, whereas the P2 antigen induces moderate levels of cellular immune responses (24). That recombinant Cp17 and P2 antigens induce modest cellular immune responses may be reflected by the ability of these antigens to activate mouse DC to produce IL-12p70 or that native antigen is necessary to induce a more optimal dendritic cell response. One human sample in the present study demonstrated significant IL-12p70 expression in response to P2, and no significant response was observed to Cp17. As noted, solubilized antigens stimulated

large amounts of IL-12p70 expression compared to excysted sporozoites in mouse BMDCs. Differences in spatial configuration, glycosylation, Amoxicillin DNA content or concentrations needed for induction may have contributed to observed differences in response. Barakat et al. (10) showed that IFN-α/β expression was detectable at sporozoite-to-DC exposure ratios higher than tested in our trials. The downstream pathway involved in the induction of immune effects by parasite proteins in the DCs appears, in part, to be mediated through TLR signalling, via the adaptor protein MyD88. However, it is unclear which specific TLR binds to the peptides, possibly by activating NF-kB signalling cascade (36). In murine toxoplasmosis, splenic DCs from MyD88−/− mice display severely impaired T. gondii-induced IL-12 responses, which, in turn, was required for promoting IFN-γ production by NK cells and subsequent activation of inflammatory monocytes and macrophages to allow them to kill the parasites (37). This is reflected in a marked reduction in serum IL-12 levels in infected MyD88 knockout animals (38).

31–33 Interestingly, ICCs in the lamina propria respond to ATP but not to muscarinic agonist carbachol, MAPK Inhibitor Library while ICCs in the detrusor respond to carbachol via M3 receptor, indicating a parasympathetic control of ICCs in the detrusor.34 This implies the two types of ICCs have different functional

roles in the bladder physiology. Spontaneous electrical activity and Ca2+-transients in the ICCs and close structural connections with nerves and SMCs26,35 have suggested that the ICCs may be pacemaking cells of SCs in the bladder. Indeed, the c-Kit tyrosine kinase inhibitor imatinib mesylate inhibited SCs.36,37 However, the frequency of spontaneous Ca2+-transients differed between the ICCs and neighboring SMCs.38 This evidence contradicts the notion that ICCs in the bladder function as pacemakers. ICCs in the detrusor are positive for cyclooxygenase Selleckchem CP 673451 related to prostaglandins synthesis,39,40 and a recent study showed that ICCs in the detrusor have numerous vesicles, indicating a secretory function.41 Therefore, ICCs

may control the SMC activity by releasing a modulator. This is an attractive hypothesis. There are at least three factors that may contribute to changes in the SCs due to SCI or BOO: myogenic alterations, local mediators in the detrusor and urotheliogenic modulation (Table 1). SMCs have spontaneous electrical and contractile activity. However, electrical coupling is normally limited to some neighboring cells, and action potentials may spread through gap junctional intercellular communication.42 In BOO, cell-to-cell communication between primary cultured SMCs of bladders stained with a fluorescent dye was enhanced in SMCs from rats with BOO compared with those from control rats.43 This enhancement was inhibited by a gap-junction inhibitor. Enhanced cell-to-cell communication may, therefore, contribute to the enhanced SCs associated with BOO. The expression of

connexin 43 gap junctions between SMCs is increased in the human bladder with DO mainly due to SCI.44 This implies that intercellular communication between SMCs is enhanced and may result in enhanced SCs in SCI. Alterations in ion channel activity may be involved in the generation of enhanced SCs Etomidate in BOO. Downregulation of large and small conductance calcium-activated potassium channels and the TREK-1 potassium channel, and upregulation of calcium-activated chloride channels may cause enhanced SCs.45–47 However, there have been contradictory findings, namely, upregulated expression of potassium channels has also been identified in bladders with BOO.22 The reason for this contradiction is unknown. Further studies of alterations to potassium channels are required. There is an intracellular signal transduction mechanism that can increase the contractile ability of SMCs, that is, calcium sensitization that involves the rhoA/rho-kinase pathway.48 The expression of rhoA and rho-kinase was upregulated in obstructed rat bladders.

CD40L is a potent activator of B cells and is able to induce proliferation and, in combination with cytokines, isotype switching and differentiation of B cells.29,67,68 The importance of this molecule for B cell responses is demonstrated by mice lacking CD40 or CD40L, which display abortive B cell responses and a failure to generate GCs and long-term memory.29,69–71 Similarly,

in humans, mutations in CD40LG or CD40 result in the primary immunodeficiency hyper-immunoglobulin M syndrome, which is characterized by recurrent bacterial infections, an inability to respond to vaccinations and a lack of serum IgG, IgA and IgE.72 Although PD-1 is highly expressed on Tfh cells, little is LDK378 supplier known about the role of PD-1 in Tfh cell development or function. The ligands for PD-1, namely PD-L1 and PD-L2, are expressed on multiple cells including B cells. Studies in mice deficient in PD-1 or its ligands PD-L1 and PD-L2 suggest that these may regulate GC cells and long-lived plasma cells either positively73,74 or negatively.75 It is likely, however, that this is not a direct effect HIF inhibitor of signalling to the B cell but, rather, reflects a role of B cell expressed PD-L1 and/or PD-L2 in regulating the number and function of the Tfh cells via PD-1, as

all three papers reported increased numbers of Tfh cells when PD-1/PD-L1 interactions were ablated.73–75 Another important mechanism by which Tfh cells regulate B cell responses is through the secretion of cytokines. Tfh cells are characterized by expression of IL-21, a cytokine capable of modulating B cell differentiation and proliferation.76–78 Addition of IL-21 to CD40L-stimulated human B cells is able to induce switching to IgG Megestrol Acetate and IgE and the formation of antibody-secreting cells.76,77 In addition, it has been demonstrated that ablation of IL-21:IL-21R signalling in vivo in mice can affect

multiple aspects of the B cell response, including formation of GCs, antibody production and the generation and/or function of memory B cells.59,60,62,78–80 The nature and severity of these effects varied widely, however, depending on the immunization or infectious challenge used. This suggests that, as for the generation of Tfh cells, there may be other signals that can compensate for IL-21 under certain circumstances. None the less, it is clear that IL-21 produced by Tfh cells is able to modulate B cell responses. While IL-21 is the cytokine associated primarily with Tfh cells, there have been increasing reports of Tfh cells producing other cytokines, including IL-4,8,20,25,36,81,82 IL-10,1,8 IL-1725,40,83,84 and IFN-γ.16,20,25,40,81 This is consistent with the ability of these cytokines to modulate B cell behaviour such as isotype switching and antibody production.85–89 This raises questions, however, about the status of Tfh cells as a distinct lineage.

9 Unfortunately, the measurement of UPC cannot be standardized because urine protein is composed of variable proportions of albumin and other proteins.18 Dip-stick proteinuria correlates poorly with ACR,22,23 while PCR correlates reasonably well with ACR.24 Proteinuria of 0.5 g/day or more usually signifies macroalbuminuria.1,4 However, there have been no studies on the direct comparison between proteinuria and albuminuria in CKD in terms of utilities (biomarker, surrogate end-point and cost-effectiveness). Thus, any comparison between proteinuria and albuminuria in CKD is subject to problems inherent in indirect comparisons.25 Proteinuria and

albuminuria are good biomarkers (Table 1) because they predict clinical end-points (CV events, renal events or mortality) Hydroxychloroquine in both diabetic and non-diabetic patients.2,3 However, there must be three general lines of evidence to support the acceptance of a biomarker to be a surrogate end-point: biological plausibility, epidemiological data and RCT.3 Despite ample evidence in biological plausibility and epidemiological data, there are limitations in RCT regarding the validity of proteinuria or albuminuria as a surrogate end-point.3 For example, a secondary analysis (but not a primary analysis) of

the Modification of Diet in Renal Disease (MDRD) study indicated that a low BP target slows the GFR decline only in patients with proteinuria of 3 g/day or more.26 Similarly, a secondary analysis of the Prevention Palbociclib molecular weight of Renal and Vascular End-stage Disease Intervention Trial (PREVEND-IT) found that BP lowering decreases CV events only

in patients with higher albuminuria levels.27 The Ongoing Telmisartan Alone and in Combination with Ramipril Global End-point Trial (ONTARGET) study even found that combined ACEI and ARB therapies decrease ACR while increasing renal outcome.3 Moreover, there has only been one renoprotective RCT with proteinuria as a treatment target to show that a reduction in proteinuria by titrated ACEI decreases Cediranib (AZD2171) renal end-points.28 Unfortunately, there have been no RCT with head-to-head comparisons between proteinuria and albuminuria.2 However, a change between normoalbuminuria and macroalbuminuria may be a surrogate for the development or remission of early diabetic nephropathy (Table 1).3 The remission of nephrotic proteinuria is a surrogate for the remission of GFR decline (Table 1).3 Moreover, ACEI- or ARB-induced change in proteinuria or albuminuria is a surrogate for changes in CKD progression in patients with mild to moderate proteinuria (Table 1).3 A randomized trial comparing screening for proteinuria and albuminuria is the best evidence of cost-effectiveness, but modelling is an alternative.29 However, most modelling approaches estimate effectiveness from traditional RCT, which are designed for testing efficacy and are not suitable for cost-effectiveness studies.

5A–E). Because CD8 alone had a negligible binding propensity to pMHC compared to any of these TCRs, the increased /mpMHC at the second stage can only be explained by cooperation or synergy between TCR and CD8 for pMHC binding, or cooperative TCR–pMHC–CD8 trimolecular interaction. We quantify this synergy using Δ(/mpMHC), the difference between the normalized adhesion bonds of the dual-receptor Regorafenib molecular weight curve and the sum of the normalized adhesion

bonds of the two single-receptor curves. The synergy indices Δ(/mpMHC) were zero at contact times smaller than the transition point (∼1 s). Beyond the transition from the first to the second stage, the values (at 2 s contact time) for the TCR panel are shown in Figure 6A together with the /mpMHC values for the two TCR–pMHC and pMHC–CD8 bimolecular interactions. These data show that the cooperative TCR–pMHC–CD8 trimolecular interaction dominates the dual-receptor this website interaction in the second stage. The exception in the preceding paragraph is W2C8, the TCR with lowest affinity for gp209–2M:HLA-A2, even lower than that of CD8. Its binding curve measured with the TCR+CD8+ cells shows a single plateau instead of the two-stage

pattern (Supporting Information Fig. 5F) with the /mpMHC values indistinguishable from those for the pMHC–CD8 bimolecular interaction but much higher than those for the TCR–pMHC bimolecular interaction (Fig. 5F). The affinity calculated from the plateau

Pa agrees with the CD8–pMHC affinity measured using TCR−CD8+ cells but is much higher than the TCR–pMHC affinity measured using TCR+CD8− cells, indicating the dominant CD8 contribution to binding of these TCR+CD8+ cells to RBCs bearing gp209–2M:HLA-A2 (Supporting Information Fig. 5G). Because of the lack of TCR–pMHC binding, the synergy index is negligibly small for the W2C8 TCR (Fig. 6A). Similar to our previous finding [34], the synergy index Δ(/mpMHC) increased with the 2D affinity for the TCR–pMHC interaction (Fig. 6B). Indeed, the linear regression OSBPL9 of the Δ(/mpMHC) versus AcKa log-log plot resulted in an R2 = 0.98 (p = 0.0001), showing a strong correlation between these parameters. Having characterized the 2D interactions on hybridoma cells, we next determined the correlation of the 2D kinetic parameters with T-cell function to evaluate whether 2D parameters perform better than their 3D counterparts. The 2D kinetic parameters (affinity, on-rate, off-rate, and /mpMHC; Fig. 7) all showed better correlation with IL-2 secretion than 3D parameters (Fig. 2A and D and Supporting Information Fig. 1B and F and Table 1). Importantly, affinity, on-rate, and /mpMHC all had statistically significant correlation with IL-2 secretion (p values < 0.05) while none of the 3D parameters did.

Further studies, including molecular and genetic analyses, will provide insight into the histogenesis of astroblastoma. “
“K. Aquilina, E. Chakkarapani, S. Love and M. Thoresen (2011) Neuropathology and Applied Neurobiology37, 156–165 Neonatal rat model of intraventricular haemorrhage and post-haemorrhagic ventricular dilatation with long-term survival into adulthood Aims: Post-haemorrhagic ventricular dilatation (PHVD) is a significant problem in neonatal care, with sequelae extending beyond childhood. Its management is important in determining outcome. Although rodent hydrocephalus models have been developed, PHVD, as a specific entity with a distinct pathophysiology, has not been studied

in a small animal model surviving to adulthood. ICG-001 clinical trial Our objective is to evaluate survival, to adulthood, in our immature (7-day-old, P7) neonatal rat model, and to analyse early motor reflexes and fine motor and cognitive Gefitinib function, and neuropathology, at 8–12 weeks. Methods: Sixty-six rats underwent sequential bilateral stereotactic

intraventricular haemorrhage (IVH); 36 more acted as controls. Staircase and radial maze evaluations were carried out at 7–11 weeks; animals were sacrificed at 12 weeks. Post mortem ventricular size and corpus callosum thickness were determined. Results: Seventy-six per cent of IVH animals developed PHVD; median (interquartile range) composite ventricular area was 3.46 mm2 (2.32–5.24). Sixteen (24%) animals demonstrated severe ventricular dilatation (area >5 mm2). IVH animals failed to improve

on the negative geotaxis test at 2 weeks. The staircase test did not identify any significant difference. On the radial maze, animals with severe PHVD made more reference errors. Histopathology confirmed PHVD, ependymal disruption and periventricular white matter injury. Median anterior corpus callosum thickness was significantly Metformin nmr lower in IVH animals (0.35 mm) than in those not undergoing IVH (0.43 mm). Conclusion: Our P7 neonatal rat IVH model is suitable for long-term survival and replicates many of the morphological and some of the behavioural features seen in human PHVD. “
“Brain edema is a major contributing factor to the morbidity and mortality of a variety of brain disorders. Although there has been considerable progress in our understanding of pathophysiological and molecular mechanisms associated with brain edema so far, more effective treatment is required and is still awaited. Here we intended to study the effects of low intensity ultrasound (LIUS) on brain edema. We prepared the rat hippocampal slice in vitro and acute water intoxication model in vivo models of brain edema. We applied LIUS stimulation in these models and studied the molecular mechanisms of LIUS action on brain edema. We found that LIUS stimulation markedly inhibited the edema formation in both of these models. LIUS stimulation significantly reduced brain water content and intracranial pressure resulting in increased survival of the rats.