Injection Of Blood Research Articles

IL-10 protects against OPC ferroptosis by regulating lipid reactive oxygen species levels post stroke

Accumulation of reactive oxygen species (ROS), especially on lipids, induces massive cell death in neurons and oligodendrocyte progenitor cells (OPCs) and causes severe neurologic deficits post stroke. While small compounds, such as deferoxamine, lipostatin-1, and ferrostatin-1, have been shown to be effective in reducing lipid ROS, the mechanisms by which endogenously protective molecules act against lipid ROS accumulation and subsequent cell death are still unclear, especially in OPCs, which are critical for maintaining white matter integrity and improving long-term outcomes after stroke. Here, using mouse primary OPC cultures, we demonstrate that interleukin-10 (IL-10), a cytokine playing roles in reducing neuroinflammation and promoting hematoma clearance, significantly reduced hemorrhage-induced lipid ROS accumulation and subsequent ferroptosis in OPCs. Mechanistically, IL-10 activated the IL-10R/STAT3 signaling pathway and upregulated the DLK1/AMPK/ACC axis. Subsequently, IL-10 reprogrammed lipid metabolism and reduced lipid ROS accumulation. In addition, in an autologous blood injection intracerebral hemorrhagic stroke (ICH) mouse model, deficiency of the endogenous Il-10, specific knocking out Il10r or Dlk1 in OPCs, or administration of ACC inhibitor was associated with increased OPC cell death, demyelination, axonal sprouting, and the cognitive deficits during the chronic phase of ICH and vice versa. These data suggest that IL-10 protects against OPC loss and white matter injury by reducing lipid ROS, supporting further development of potential clinical applications to benefit patients with stroke and related disorders.

Kv1.3 Blockade Alleviates White Matter Injury through Reshaping M1/M2 Phenotypes via the NF-κB Signaling Pathway after Intracerebral Hemorrhage.

White matter injury (WMI) in basal ganglia usually induces long-term disability post intracerebral hemorrhage (ICH). Kv1.3 is an ion channel expressed in microglia and induces neuroinflammation after ICH. Here, we investigated the functions and roles of Kv1.3 activation-induced inflammatory response in WMI and the Kv1.3 blockade effect on microglia polarization after ICH. Mice ICH model was constructed by autologous blood injection. The expression of Kv1.3 was measured using immunoblot, real-time quantitative polymerase chain reaction (RT-qPCR), and immunostaining assays. Then, the effect of administration of 5-(4-Phenoxybutoxy) psoralen (PAP-1), a selectively pharmacological Kv1.3 blocker, was investigated using open field test (OFT) and basso mouse score (BMS). RT-qPCR, immunoblot, and enzyme-linked immunosorbent assay (ELISA) were taken to elucidate the expression of pro-inflammatory or anti-inflammatory factors around hematoma. PAP-1's function in regulating microglia polarization was investigated using immunoblot, RT-qPCR, and immunostaining assays. The downstream PAP-1 signaling pathway was determined by RT-qPCR and immunoblot. Kv1.3 expression was increased in microglia around the hematoma significantly after ICH. PAP-1 markedly improved neurological outcomes and the WMI by reducing pro-inflammatory cytokine accumulation and upregulating anti-inflammatory factors. Mechanistically, PAP-1 reduces NF-κB p65 and p50 activation, thus facilitating microglia polarization into M2-like microglia, which exerts this beneficial effect. PAP-1 reduced pro-inflammatory cytokines accumulation and increased anti-inflammatory factors by facilitating M2-like microglia polarization via the NF-κB signaling pathway. Thus, the current study shows that the Kv1.3 blockade is capable of ameliorating WMI by facilitating M2-like phenotype microglia polarization after ICH.

Validity of D-penicillamine in experimental cerebral vasospasm therapy

BackgroundCerebral vasospasm is a reversible vessel constriction following subarachnoid hemorrhage. Immunoreactive and inflammatory mechanisms induce long-term vasoconstriction and vessel dilatation inhibition. We hypothesized that D-penicillamine depresses this process given that it reduces the concentration of free oxygen (O2) radicals. We evaluated the effects of D-penicillamine on cerebral vasospasm in rabbits induced with subarachnoid hemorrhage, achieved by autologous blood injection in the basal cistern. Materials and methodsFour experimental groups were studied: Group 1: basilar angiography, Group 2: basilar angiography + D-penicillamine, Group 3: subarachnoid hemorrhage (SAH), and Group 4: SAH + D-penicillamine. Vessel diameter and cerebral vasospasm were evaluated angiographically in each group. Vascular degeneration was studied by electron microscopy of the basilar artery. Free O2 radicals were investigated based on measurements of the levels of vascular superoxide dismutase and malondialdehyde. Myasthenia gravis–like side effects of D-penicillamine application were analyzed by electromyography and electron microscopy of the orbicularis oculi muscle. ResultsWe detected a 9.03% decrease in basilar artery constriction in Group 4 compared with Group 3. In addition, levels of free O2 radicals were reduced in Groups 2 and 4. Application of D-penicillamine resulted in the prevention of basilar artery wall degeneration, without myasthenia gravis–like side effects. ConclusionOur study indicated that D-penicillamine application induced vasodilatation and had anti-inflammatory effects.

Establishment of a rat model of severe spontaneous intracerebral hemorrhage

BackgroundSevere intracerebral hemorrhage (ICH) is the most devastating subtype of stroke resulting in high mortality and disability. At present, the development of targeted treatments to minimize the high morbidity and mortality is limited partly due to the lack of a severe ICH animal model. In this study, we aimed to establish an accurate severe ICH model in rats and examine the pathological and physiological changes associated with ICH. MethodsA rat model of severe ICH model was established by intrastriatal injection of autologous blood using different blood volumes (ICH 100 µL group, ICH 130 µL group, ICH 160 µL group, ICH 170 µL group, and ICH 180 µL group). The mortality was assessed during the 28-day post-ICH period. Short- and long-term neurological deficits were evaluated using the Longa method, foot fault, falling latency, and Morris water maze tests. Brain water content, hematoma volume, hemoglobin content, and magnetic resonance imaging were assessed to determine the extent of brain injury. Immunofluorescence staining was conducted to examine microglial activation and neuronal apoptosis. Hematoxylin and eosin (H&E) staining, lung water content, and western blotting were used to assess lung injury following ICH. ResultsThe mortality of ICH rats increased significantly with an increase in autologous blood injection. The 28-day mortality in the 100 µL, 130 µL, 160 µL, 170 µL, and 180 µL ICH groups were 5%, 20%, 40%, 75%, and 100%, respectively. A significantly higher 28-day mortality was observed in the ICH 160 µL group compared to the ICH 100 µL group. The ICH 160 µL group exhibited significantly increased neurological deficits, brain edema, hematoma volume, and hemoglobin content compared to the sham group. Compared with the sham operation group, the activation of microglia and neuronal death in ICH 160 µL rats increased. The use of H&E staining and western blotting demonstrated that disruption of the intra-alveolar structure, alveolar edema, and infiltration of inflammatory cells and cytokines into the lung tissue were more severe in the ICH 160 µL group than the sham group. ConclusionsA severe ICH model in rats was successfully established using an injection of autologous blood at a volume of 160 µL. This model may provide a valuable tool to examine the pathological mechanisms and potential therapeutic interventions of severe ICH.

The phosphokinase activity of IRE1ɑ prevents the oxidative stress injury through miR-25/Nox4 pathway after ICH.

Endoplasmic reticulum (ER) stress and oxidative stress are the major pathologies encountered after intracerebral hemorrhage (ICH). Inositol-requiring enzyme-1 alpha (IRE1α) is the most evolutionarily conserved ER stress sensor, which plays a role in monitoring and responding to the accumulation of unfolded/misfolded proteins in the ER lumen. Recent studies have shown that ER stress is profoundly related to oxidative stress in physiological or pathological conditions. The purpose of this study was to investigate the role of IRE1α in oxidative stress and the potential mechanism. A mouse model of ICH was established by autologous blood injection. The IRE1α phosphokinase inhibitor KIRA6 was administrated intranasally at 1 h after ICH, antagomiR-25 and agomiR-25 were injected intraventricularly at 24 h before ICH. Western blot analysis, RT-qPCR, immunofluorescence staining, hematoma volume, neurobehavioral tests, dihydroethidium (DHE) staining, H2O2 content, brain water content, body weight, Hematoxylin and Eosin (HE) staining, Nissl staining, Morris Water Maze (MWM) and Elevated Plus Maze (EPM) were performed. Endogenous phosphorylated IRE1α (p-IRE1α), miR-25-3p, and Nox4 were increased in the ICH model. Administration of KIRA6 downregulated miR-25-3p expression, upregulated Nox4 expression, promoted the level of oxidative stress, increased hematoma volume, exacerbated brain edema and neurological deficits, reduced body weight, aggravated spatial learning and memory deficits, and increased anxiety levels. Then antagomiR-25 further upregulated the expression of Nox4, promoted the level of oxidative stress, increased hematoma volume, exacerbated brain edema and neurological deficits, whereas agomiR-25 reversed the effects promoted by KIRA6. The IRE1α phosphokinase activity is involved in the oxidative stress response through miR-25/Nox4 pathway in the mouse ICH brain.

Use of Ultrasound-Guided Tendon Fenestration and Injection Procedures for Treatment of Tendinosis

Introduction. Overuse injuries such as tendinosis are a common complaint at sports medicine clinics. When conservative management for tendinosis has failed, ultrasound-guided tendon fenestration and injection procedures such as dry needling, needling tenotomy, autologous whole blood injections, and prolotherapy can be utilized for treatment. This study examined the effectiveness of these procedures for pain improvement and ability to return to activity for patients with tendinosis. Methods. This study included patients 15 years or older who underwent at least one treatment for tendinosis at a sports medicine clinic between January 1, 2014 through April 17, 2019. A CPT code query was used to screen patient charts for study inclusion. Results. In total, 680 patients’ data were reviewed, and 343 patients met inclusion criteria. Patients underwent a total of 598 unique procedures. Dry needling represented most procedures (62.8%, n=375). Most patients reported diminished pain at follow up (73.0%, n=268). Prolotherapy had the highest percentage of patients reporting diminished pain (81.0%, n=17). Most patients were able to return to activity (47.4%, n=172) at follow-up. A greater proportion of patients with autologous whole blood injection were able to return to activity (60.7%, n=85). Conclusions. Most patients with tendinosis who underwent tendon fenestration or injection procedures reported diminished pain at follow-up. Autologous whole blood injection may be more likely to diminish patient pain and allow return to activity than other procedure types. More research is needed across all anatomical sites to compare the generalized effectiveness of these procedures.

Azithromycin reduces hemoglobin-induced innate neuroimmune activation

Neonatal intraventricular hemorrhage (IVH) releases blood products into the lateral ventricles and brain parenchyma. There are currently no medical treatments for IVH and surgery is used to treat a delayed effect of IVH, post-hemorrhagic hydrocephalus. However, surgery is not a cure for intrinsic brain injury from IVH, and is performed in a subacute time frame. Like many neurological diseases and injuries, innate immune activation is implicated in the pathogenesis of IVH. Innate immune activation is a pharmaceutically targetable mechanism to reduce brain injury and post-hemorrhagic hydrocephalus after IVH. Here, we tested the macrolide antibiotic azithromycin, which has immunomodulatory properties, to reduce innate immune activation in an in vitro model of microglial activation using the blood product hemoglobin (Hgb). We then utilized azithromycin in our in vivo model of IVH, using intraventricular blood injection into the lateral ventricle of post-natal day 5 rat pups. In both models, azithromycin modulated innate immune activation by several outcome measures including mitochondrial bioenergetic analysis, cytokine expression and flow cytometric analysis. This suggests that azithromycin, which is safe for neonates, could hold promise for modulating innate immune activation after IVH.

Post trabeculectomy hypotonous maculopathy: Miraculous result with autologous blood injection in a young lad

A 28-year-old male patient was referred to us for the management of hypotonous maculopathy developed post trabeculectomy for angle recession glaucoma. After examination, the patient was advised cycloplegics, oral and topical steroids, but maculopathy had not settled even after treatment for 3 weeks and so scleral patch grafting was done. Post grafting also macular folds persisted and a part of the graft was exposed and so amniotic membrane grafting was done, still hypotony persisted with the development of neurosensory detachments. The over-filtration hypotonus maculopathy finally resolved with peri bleb injection of autologous whole blood.

Клинические случаи острого кератоконуса

During the ten-year follow-up period, hydrops corneae was diagnosed in 5 (6 eyes) out of 266 patients (1.8%) with keratoconus. The age of the patients ranged from 14 to 57 years. In 2 patients, acute keratoconus was the first manifestation of corneal ectasia. Decompensation of chronic keratoconus was observed in the period from 1 to 19 years from the onset of the disease. In all patients, autologous blood injection into the anterior chamber in the acute period of the disease made it possible to stop corneal edema and corneal syndrome in a short time. Hemoplombing of the anterior chamber in acute keratoconus makes it possible to stabilize the process in the cornea for a sufficiently long time and delay (avoid) reconstructive intervention as much as possible. Keywords: acute keratoconus, hydrops corneae.

The Neuroprotective Effects and Probable Mechanisms of Everolimus in a Rat Model of Intracerebral Hemorrhage.

Mammalian target of rapamycin (mTOR) is a central regulator of cellular growth and homeostasis. Changes in mTOR activity are often observed in many neurological diseases, such as stroke. Intracerebral hemorrhage (ICH) is associated with high mortality and morbidity. However, there are currently no treatments that have been shown to enhance outcomes following ICH, so new treatments are urgently required. In this study, a selective mTOR inhibitor, everolimus, was applied to investigate the outcome after ICH and the possible underlying mechanism. The ICH model was established by autologous blood injection. Everolimus (50 and 100µg/kg) was administered intraperitoneally for 14 consecutive days' post-operation. The neurological functions were examined at 3, 7, and 14days' post-ICH. Samples of brain tissue were collected to perform histopathological and immunohistochemical (NF-k-positive cell) examinations. Besides, the striatum was used to evaluate parameters related to oxidative stress (superoxide dismutase (SOD) activity, malondialdehyde (MDA), and total thiol levels) and inflammation markers (TNF-α and NO). Everolimus ameliorated ICH-induced neurological deficits. In addition, treatment with everolimus reduced infarct volume and NF-k-β positive cells as compared to the ICH group. Furthermore, everolimus significantly increased total thiol content and SOD activity while significantly reducing MDA, NO, and TNF- levels as compared to the ICH group. Collectively, our investigation showed that everolimus improves ICH outcome and modulates oxidative stress and inflammation after ICH. Treatment with rapamycin reduced neurological deficient, oxidative stress, and inflammation in a rat model of intracerebral hemorrhage.

Autologous Whole-Blood Versus Corticosteroid Local Injection in Treatment of Plantar Fasciitis: A Randomized Single Blind Placebo-Controlled Study.

Autologous whole-blood intralesional injection has attracted interest as a possible means of treatment for chronic plantar fasciitis. We contrasted its effectiveness with that of corticosteroids, which have a longer history of success in treating tendinopathies such as plantar fasciitis. In order to monitor the disease's progress naturally, we also compared them with a placebo. Sixty clinically diagnosed patients were taken up for intralesional injection of autologous whole blood (AWB), corticosteroid, and normal saline as placebo mixed with 2 mL of lignocaine after dividing them into three groups. Two doses were given and followed up in the third, sixth, and 12th weeks. The evaluation was done according to the visual analog scale (VAS) and the number of tablets of paracetamol (PCM) 500 mg consumed for the following period. When compared to the placebo group in the third, sixth, and 12th weeks, the corticosteroid group exhibited a significant improvement with a p<0.001 in the VAS score, whereas the autologous whole blood group showed no meaningful difference. When compared to the placebo group at the sixth and 12th weeks, the AWB group's VAS score showed a statistically significant difference with a p>0.001. At each follow-up, the placebo group consumed more analgesics than the corticosteroid group, with a p<0.001. Only in the third week of follow-up did AWB demonstrate a statistically significant difference in PCM consumption as compared to the corticosteroid group. Statistically significant improvement was seen in both the AWB group and corticosteroid group as compared to the placebo group. The corticosteroid group achieved earlier and superior relief of pain while AWB had a longer lasting effect. Therefore, study results indicate almost similar results in short-term studies.

Intra-cochlear Flushing Reduces Tissue Response to Cochlear Implantation.

Intraoperative trauma leading to bleeding during cochlear implantation negatively impacts residual hearing of cochlear implant recipients. There are no clinical protocols for the removal of blood during implantation, to reduce the consequential effects such as inflammation and fibrosis which adversely affect cochlear health and residual hearing. This preclinical study investigated the implementation of an intra-cochlear flushing protocol for the removal of blood. Three groups of guinea pigs were studied for 28 days after cochlear implantation; cochlear implant-only (control group); cochlear implant with blood injected into the cochlea (blood group); and cochlear implant, blood injection, and flushing of the blood from the cochlea intraoperatively (flush group). Auditory brainstem responses (ABRs) in addition to tissue response volumes were analyzed and compared between groups. After implantation, the blood group exhibited the highest ABR thresholds when compared to the control and flush group, particularly in the high frequencies. On the final day, the control and blood group had similar ABR thresholds across all frequencies tested, whereas the flush group had the lowest thresholds, significantly lower at 24 kHz than the blood and control group. Analysis of the tissue response showed the flush group had significantly lower tissue responses in the basal half of the array when compared with the blood and control group. Flushing intra-cochlear blood during surgery resulted in better auditory function and reduced subsequent fibrosis in the basal region of the cochlea. This finding prompts the implementation of a flushing protocol in clinical cochlear implantation. N/A Laryngoscope, 134:1410-1416, 2024.

Galectin-3 promotes brain injury by modulating the phenotype of microglia via binding TLR-4 after intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) is a stroke subtype with high mortality and disability rate, and neuroinflammation is involved in secondary brain injury. Galectin-3 (Gal-3) is one of the scaffold proteins of Galectins. Studies have indicated that Gal-3 plays an important role in the physiological and pathological state of the nervous system. Here we focus on the role of Gal-3 in ICH, especially in neuroinflammation. Injection of autologous blood into the right basal ganglia was used to simulate ICH injury, and the level of Gal-3 in brain was regulated by related means. The changes of Gal-3 were detected by western blot and immunofluorescence, the level of neuroinflammation by immunofluorescence staining and ELISA. Apoptosis and neuron loss were detected by TUNEL staining FJB staining and Nissl staining, and neurological deficits were judged by neurobehavioral tests. The protein level of Gal-3 increased at 24 h after ICH. Downregulation of Gal-3 level can reduce the infiltration of M1-type microglia and peripheral inflammatory cells, thus alleviating post-ICH neuroinflammation, and reducing cell apoptosis and neuron loss in brain tissue. ICH-induced neurological damage was rescued. Meanwhile, the promotion in the expression level of Gal-3 increased neuroinflammatory activation and nerve cell death, aggravating ICH-induced brain injury. This study proves that Gal-3 is involved in neuroinflammation and nerve damage after ICH. Gal-3 expression should not be encouraged early on to prevent neuroinflammation. which provides a new possibility for clinical treatment for ICH patients.

Treatment with Marstacimab for People with Severe Hemophilia a or B: a Plain Language Summary of the results from a short-term study and a longer-term study

What is this summary about? This is a summary of the results from two clinical studies of treatment for men with severe hemophilia A or B. The studies were published in the British Journal of Haematology. People with hemophilia either have low amounts of clotting factors or are missing certain clotting factors in their blood. The severity of hemophilia is found out by a blood test. There are medicines that people with hemophilia can take to replace the missing clotting factor. However, sometimes the body thinks the clotting factor used to treat hemophilia is a foreign substance and produces antibodies to destroy it (called inhibitors) which may slow down or stop blood clotting. What were the results? The studies showed that men with hemophilia had fewer bleed events while taking marstacimab than before this treatment. The results were similar for all doses of marstacimab tested. Overall, the side effects with marstacimab were generally acceptable. Two men had to stop taking marstacimab because of side effects in the short-term study. The most common side effects were high blood pressure and injection site reactions. Most of these reactions were mild or moderate. What do the results mean? These studies showed that marstacimab could help prevent bleeding in men with hemophilia A or B, with or without inhibitors. The results of this study may differ from those of other studies. Physicians should make treatment decisions based on all available evidence and not just on the results of a single study. Larger studies of marstacimab involving more people with hemophilia A or B have started.

Inflammatory regulation by restraining M2 microglial polarization: Neurodestructive effects of Kallikrein-related peptidase 8 activation in intracerebral hemorrhage

Intracerebral hemorrhage (ICH) is a cerebrovascular disease. Kallikrein-related peptidase 8 (KLK8) is a serine peptidase, while its role in ICH remains unclarified. Western blot (WB) showed that KLK8 was upregulated in rat perihematomal tissues 24 h following autologous blood injection. KLK8 overexpression aggravated behavioral deficits and increased water content and Fluoro-Jade B (FJB)-positive neuron numbers in brain tissue of rats. Immunofluorescence (IF) assay showed that overexpressed-KLK8 promoted Iba-1 and iNOS expression in perihematomal tissue of rats. Overexpressed-KLK8 increased COX-2, iNOS, and Arg-1 expression and the content of IL-6, IL-1β, and TNF-α in perihematomal tissue of rats, confirmed by WB and ELISA. IF staining confirmed the expression of CCR5 was co-expressed with Iba-1, and the WB results shown increased CCR5 expression and decreased p-PKA and p-CREB expression in perihematomal tissue. Maraviroc (MVC, CCR5 inhibitor) administration rescued KLK8-induced behavioral deficits and brain injury (decreased water content and FJB-positive neuron numbers) in rats. Additionally, MVC suppressed p-PKA and p-CREB expression and the content of IL-6, IL-1β, and TNF-α in perihematomal tissue, induced by overexpressed-KLK8. Co-IP confirmed the binding of CCR5 and CCL14 in HMC3 cells. Transwell assay shown that KLK8 plus CCL4 promoted the chemotactic activity of cells, which was rescued by MVC. The biological function of KLK8/CCL14/CCR5 axis in ICH injury was also proved by MVC administration in HMC3 cells. Overall, our work revealed that KLK8 overexpression aggravated ICH process and involved in microglial activation. KLK8 might activate CCL14 thereby turning on downstream CCR5/PKA/CREB pathway, providing a theoretical basis for future therapy.

Minocycline attenuates hydrocephalus and inhibits iron accumulation, ependymal damage and epiplexus cell activation after intraventricular hemorrhage in aged rats

Intracerebral hemorrhage is primarily a disease of the elderly and it is frequently accompanied by intraventricular hemorrhage (IVH) which can lead to posthemorrhagic hydrocephalus and poor prognosis. Red blood cell iron has been implicated in brain injury after cerebral hemorrhage. The current study examined using T2* magnetic resonance imaging (MRI) to detect periventricular iron deposition after IVH and investigated the effects of minocycline on hydrocephalus in an aged rat IVH model. It had three parts. In part 1, male aged rats received a 200 μl injection of saline or autologous blood into the lateral ventricle and were euthanized at day 14. In parts 2 and 3, aged IVH rats were treated with vehicle or minocycline and euthanized at day 7 or 14. Rats underwent MRI to quantify hydrocephalus and iron deposition followed by brain histology and immunohistochemistry. Periventricular iron overload was found after IVH using T2* MRI and confirmed by histology. IVH also caused ventricular wall damage and increased the number of CD68(+) choroid plexus epiplexus cells. Minocycline administration reduced iron deposition and ventricular volume at days 7 and 14 after IVH, as well as ventricle wall damage and epiplexus cell activation. In summary, IVH-induced hydrocephalus is associated with periventricular iron deposition, ependymal damage and choroid plexus epiplexus cell activation in aged rats. Minocycline attenuated those effects and might be a potential treatment for posthemorrhagic hydrocephalus in the elderly.

Autologous Blood Injections in Temporomandibular Hypermobility: A Systematic Review.

The injection of autologous blood (AB) is one of the methods of treatment of recurrent dislocations in the temporomandibular joints (TMJs). Due to the low invasiveness of this technique, it is reasonable to evaluate it in accordance with the standards of evidence-based medicine. The purpose of this systematic review is to identify primary studies on AB injection for the treatment of TMJ hypermobility and assess the therapy for effectiveness. This systematic review was conducted in accordance with the current "Preferred Reporting Items for Systematic Reviews and Meta-Analyses" guidelines. Controlled randomized trials comparing dislocation episode rates, range of motion in the TMJ, or articular pain intensity were adopted as the eligibility criteria. Final searches were conducted on 11 June 2023 using Bielefeld Academic Search Engine, Elsevier Scopus, and the National Library of Medicine: PubMed. Trials were assessed using the "Oxford Center for Evidence-Based Medicine 2011 Levels of Evidence" scale and "A revised Cochrane risk-of-bias tool for randomized trials". The results of the individual studies were tabulated, syntheses were illustrated in graphs. Twenty two studies involving 982 patients were included in the qualitative analysis, of which seven studies involving 390 patients were subject to quantitative analysis. None of the included randomized controlled trials presented a high risk of bias, 75% of them raised some concerns. In a three-month observation, administration of AB was more efficient in limiting temporomandibular dislocations than hypertonic dextrose (1 study, 32 patients, relative risk = 0.33, odds ratio = 0.29) and no difference in outcomes was observed between intracavitary and pericapsular administration compared to pericapsular injection alone (2 studies, 70 patients, relative risk = 1.00, odds ratio = 1.00). Injections of AB into the temporomandibular joints are effective in preventing further TMJ dislocation episodes in 75-94% of patients. This study received no funding.

Modulation of autophagy in the rats with acute intracerebral hemorrhage by acupuncture based on JNK pathway

To investigate the effects of acupuncture on JNK pathway and autophagy level in rats with intracerebral hemorrhage （ICH） and explore the partial mechanism of acupuncture against ICH. SD rats were randomly divided into blank group, model group and acupuncture group. Each group was divided into Day 1, Day 3 and Day 7 subgroups respectively, with 5 rats in each group. The autologous blood injection was adopted to duplicate rat model of ICH. In the acupuncture group, the needle was inserted from "Baihui" （GV20） towards "Qubin" （GB7） on the affected side, stimulating for 30 min each time, once daily； the same acupuncture technique was opera-ted in each subgroup for 1, 3 and 7 days, separately. Using Bederson scale, the neurological deficit was evaluated in each group. Western blot was adopted to detect the protein expression levels of Beclin1, LC3Ⅰ/Ⅱ, phosphorylated c-Jun amino-terminal kinase （p-JNK） and the phosphorylated （p）-c-Jun around hematoma lesion of the brain tissue of rats in each group. After treatment, the neurological deficit score of rats in the model group was higher than that of the blank group at each time point （P<0.05）, and the score of the acupuncture group started declining since the 3rd day of treatment when compared with the model group （P<0.05）. At each time point, compared with the blank group, the protein expression levels of LC3Ⅰ/Ⅱ, Beclin1, p-c-Jun and p-JNK was increased （P<0.01）. Compared with the model group, the protein expression level of LC3Ⅰ/Ⅱ was reduced （P<0.05）； the protein expression levels of Beclin1, p-c-Jun and p-JNK was increased （P<0.05, P<0.01） on day 3 and 7 in the acupuncture group. Acupuncture can activate the JNK pathway in the brain tissue of rats with ICH and increase the level of autophagy, thereby improving the neurological function of the rats with ICH.

Modulation of autophagy in the rats with acute intracerebral hemorrhage by acupuncture based on JNK pathway

To investigate the effects of acupuncture on JNK pathway and autophagy level in rats with intracerebral hemorrhage （ICH） and explore the partial mechanism of acupuncture against ICH. SD rats were randomly divided into blank group, model group and acupuncture group. Each group was divided into Day 1, Day 3 and Day 7 subgroups respectively, with 5 rats in each group. The autologous blood injection was adopted to duplicate rat model of ICH. In the acupuncture group, the needle was inserted from "Baihui" （GV20） towards "Qubin" （GB7） on the affected side, stimulating for 30 min each time, once daily； the same acupuncture technique was opera-ted in each subgroup for 1, 3 and 7 days, separately. Using Bederson scale, the neurological deficit was evaluated in each group. Western blot was adopted to detect the protein expression levels of Beclin1, LC3Ⅰ/Ⅱ, phosphorylated c-Jun amino-terminal kinase （p-JNK） and the phosphorylated （p）-c-Jun around hematoma lesion of the brain tissue of rats in each group. After treatment, the neurological deficit score of rats in the model group was higher than that of the blank group at each time point （P<0.05）, and the score of the acupuncture group started declining since the 3rd day of treatment when compared with the model group （P<0.05）. At each time point, compared with the blank group, the protein expression levels of LC3Ⅰ/Ⅱ, Beclin1, p-c-Jun and p-JNK was increased （P<0.01）. Compared with the model group, the protein expression level of LC3Ⅰ/Ⅱ was reduced （P<0.05）； the protein expression levels of Beclin1, p-c-Jun and p-JNK was increased （P<0.05, P<0.01） on day 3 and 7 in the acupuncture group. Acupuncture can activate the JNK pathway in the brain tissue of rats with ICH and increase the level of autophagy, thereby improving the neurological function of the rats with ICH.

Autologous serum therapy in chronic urticaria patients

Background: Chronic urticaria is very common distressing dermatoses. CU is caused by autoimmune mechanisms in approximately 30-50% of patients. Repeated injection of autologous whole blood or autologous serum, a form of therapy also known as autohaemotherapy, can be very effective in CAU patients. Aim was to assess the effectiveness of autologous serum therapy in chronic urticaria patients. Methods: All patients with CU attending the dermatology OPD of age &gt;18 years, and urticaria of duration &gt;6 weeks. After autologous serum skin test, autologous serum therapy was administered using autologous serum in a dose of 0.05 ml per kg body weight, injected IM in gluteus muscle weekly for nine weeks in all patients. Parameters of disease activity and severity were recorded at baseline and every week during treatment. End point of study was improvement in chronic modified urticaria total severity score after ninth dose of AST which was recorded at baseline and at 10th week. Results: Mean of MUTSS for ASST positive group and ASST negative group was 13.27±2.050 and 12.04±3.212 respectively which is statistically significant (p=0.043). Mean MUTSS post treatment in ASST positive group was 3.87±4.57 whereas in negative group it was 6.46±4.418 which was statistically significant (p=0.019). Conclusions: 42.3% patients of chronic urticaria were of autoimmune type and approximately half of them responded well to autologous serum therapy. This study found that serum therapy is effective in ASST positive patients with CU.