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Human gingival fibroblasts (HGF) play a vital role in wound healing, oral cancer, and are among the first cells being exposed to e-cigarette vapor (eCV) or cigarette smoke (CS) during inhalation. Although the cell-damaging effect of CS has been well studied, the effects of eCV on gingival cells are still unclear. The aim of this in vitro study was to compare the effects of eCV and CS on HGF in terms of proliferation, metabolic activity, cell death, and formation of reactive oxygen species (ROS). After 24 h cell numbers in CS-exposed cells in contrast to eCV-exposed cells were significantly decreased compared to the control. At later points in time, such differences could no longer be observed. Compared to the control, HGF stimulated with eCV showed a significantly higher metabolic activity 1 h, 24 h, and 48 h after exposure. 24 h after exposure, the metabolic activity was increased in both test groups. learn more No caspase 3/7 activation nor significant differences in the amount of apoptosis/necrosis among the groups were seen. Only in CS-exposed cells ROS formation was increased at 1 h, 3 h, and 6 h after exposition. In conclusion, when compared to conventional CS, a less harmful effect of eCV on HGF can be assumed.A preterm child, born at 24 weeks’ postmenstrual age (PMA), suffered a traumatic nasotracheal intubation at birth, with exteriorization of the tube through the right orbit. Delayed routine screening for retinopathy of prematurity (ROP) at 34 weeks’ PMA revealed a right ischemic retinopathy. Right eye fundus examination at 39 weeks’ PMA showed a neovascularized ridge delimiting the vascular retina from an avascular zone over 360°, with localized fibrosis and traction in the right eye, mimicking a zone II stage 3-4 ROP. The left fundus was normal. We suggest that the traumatic ocular contusion stunned the physiological vascularization process of the premature eye leading to permanent retinal sequalae.

Acupuncture has been used to treat a wide variety of diseases, disorders, and conditions for more than 2500years. While the anatomical structures of acupuncture points (or acupoints) are largely unknown, our previous studies have suggested that many acupoints can be identified as cutaneous neurogenic inflammatory spots (neurogenic spots or Neuro-Sps), arising from the release of neuropeptides from activated small diameter sensory afferents at topographically distinct body surfaces due to the convergence of visceral and somatic afferents. In turn, the neuropeptides released during neurogenic inflammation may play important roles in the effects of acupuncture as well as the formation of active acupoints. Thus, the present study has focused on the role of substance P (SP) in acupuncture signal transduction and effects.

Neuro-Sps were detected by using in vivo fluorescence imaging after intravenous injection of Evans blue dye (EBD) and compared with traditional acupoints. Stimulatory effects of the Neuro-Sps response (WDR) neurons significantly increased following SP or acupuncture treatment in Neuro-Sps in normal rats, but decreased following the injection of CP-99994 into Neuro-Sps in IMH rats.

Our findings suggest that SP released during neurogenic inflammation enhances the responses of sensory afferents to the needling of acupoints and triggers acupuncture signaling to generate acupuncture effects.

Our findings suggest that SP released during neurogenic inflammation enhances the responses of sensory afferents to the needling of acupoints and triggers acupuncture signaling to generate acupuncture effects.Up to 30% of stroke patients experience cognitive decline within one year of their stroke. There are currently no FDA-approved drugs that can prevent post-stroke cognitive decline, in part due to a poor understanding of the mechanisms involved. We have previously demonstrated that a B-lymphocyte response to stroke, marked by IgA + cells, can cause delayed cognitive dysfunction in mice and that a similar adaptive immune response occurs in the brains of some human stroke patients that suffer from vascular dementia. The stimuli which trigger B-lymphocyte activation following stroke, and their target antigens, are still unknown. Therefore, to learn more about the mechanisms by which B-lymphocytes become activated following stroke we first characterized the temporal kinetics of the B-lymphocyte, T-lymphocyte, and plasma cell (PC) response to stroke in the brain by immunohistochemistry (IHC). We discovered that B-lymphocyte, T-lymphocyte, and plasma cell infiltration within the infarct progressively increases between 2 and 7 weeks after stroke. We then compared the B-lymphocyte response to stroke in WT, MHCII-/-, CD4-/-, and MyD88-/- mice to determine if B-lymphocytes mature into IgA + PCs through a T-lymphocyte and MyD88 dependent mechanism. Our data from a combination of IHC and flow cytometry indicate that following stroke, a population of IgA + PCs develops independently of CD4 + helper T-lymphocytes and MyD88 signaling. Subsequent sequencing of immunoglobulin genes of individual IgA + PCs present within the infarct identified a novel population of natural antibodies with few somatic mutations in complementarity-determining regions. These findings indicate that a population of IgA + PCs develops in the infarct following stroke by B-lymphocytes interacting with one or more thymus independent type 2 (TI-2) antigens, and that they produce IgA natural antibodies.Immune dysfunction is implicated in Alzheimer’s disease (AD), whereas systemic immune modulation may be neuroprotective. Our previous results have indicated immune challenge with Bacillus Calmette-Guerin attenuates AD pathology in animal models by boosting the systemic immune system. Similarly, independent studies have shown that boosting systemic immune system, by blocking PD-1 checkpoint pathway, modifies AD. Here we hypothesized that influenza vaccine would potentiate function of moderate dose anti-PD-1 and therefore combining them might allow reducing the dose of PD-1 antibody needed to modify the disease. We found that moderate-dose PD-1 in combination with influenza vaccine effectively attenuated cognitive deficit and prevented amyloid-β pathology build-up in APP/PS1 mice in a mechanism dependent on recruitment of peripheral monocyte-derived macrophages into the brain. Eliminating peripheral macrophages abrogated the beneficial effect. Moreover, by comparing CD11b+ compartments in the mouse parenchyma, we observed an elevated subset of Ly6C+ microglia-like cells, which are reportedly derived from peripheral monocytes.