Injection Of Autologous Blood Research Articles

Baihui (DU20)-penetrating-Qubin (GB7) acupuncture regulates microglia polarization through miR-34a-5p/Klf4 signaling in intracerebral hemorrhage rats.

Intracerebral hemorrhage (ICH) is the most devastating subtype of stroke with high morbidity and mortality. The previous study has confirmed the therapeutic effect of Baihui (DU20)-penetrating-Qubin (GB7) acupuncture on ICH, while the related mechanism is left to be revealed. The aim of this study was to investigate the relevant mechanisms. ICH rat models were established utilizing the autologous blood injection method and the beneficial effect was found after DU20-penetrating-GB7 acupuncture along with decreased miR-34a-5p levels in the perihemorrhagic penumbra. Inversely, upregulating miR-34a-5p expression inhibited microglia M2 polarization while accelerated M1 polarization through targeting Krüppel-like factor 4 (Klf4), and thereby diminished the protective effect of DU20-penetrating-GB7 acupuncture on ICH. The results suggested the therapeutic effect of DU20-penetrating-GB7 acupuncture on ICH might be attributed to its modulation on microglia polarization through miR-34a-5p/Klf4 signaling.

Effectiveness of Autologous Blood and Steroid Injection in Tennis Elbow Based on Visual Analog Score Pain Score and Nirschl Stage

Introduction: Lateral epicondylitis or Tennis elbow is one of the most common causes of lateral elbow pain. Local steroid injection is a time tested treatment for providing symptomatic relief. Local injection of autologous blood in a case of lateral epicondylitis provides pain relief due to its cellular and humoral factor and triggers a healing cascade.
 Aims: This study aims to compare the outcomes of the autologous blood injection and local corticosteroid injection in the treatment of tennis elbow.
 Methods: This is a Hospital based study on conducted in the Department of Orthopedics at Nepalgunj Medical College from July 2018 to June 2019. 42 patients with unilateral tennis elbow were divided into two groups-Group A-21 patients (Autologous Blood Injection) and Group B-21 patients (Steroid Injection). Group A received 2 ml of autologous venous blood and mixed with 1 ml of 2% lignocaine solution; Group B patients received 80 mg (in 2 ml) of methyl Prednisolone acetate and 1ml of 2% lignocaine solution. Visual Analogue Scale pain score and Nirschl stage of patients were evaluated before injection and at 2, 6, and 12 weeks of injection were noted and analyzed.
 Results: Preinjection mean VAS pain score was - 7.48±0.75, 7.52±0.68 in Group A, and Group B respectively while the Nirschl stage was 5.62±0.59 and 5.6±0.5 in group A and B, these scores among two group was not statistically significant. At 2 weeks follow up both groups showed improvement without any significant difference between two groups (p=0.84 and 0.549), while group A had better improvement in VAS pain score at 6 weeks (p=0.001). At 12 weeks follow-up within each group, there was significant VAS pain and Nirschl stage improvement (p=0.001) but there was no significant difference between the two groups.
 Conclusion: Injection of autologous blood and corticosteroid injection is equally effective in the treatment of Tennis elbow at 12 weeks final follow-up.

LncRNA Blnc1 mediates the permeability and inflammatory response of cerebral hemorrhage by regulating the PPAR-γ/SIRT6/FoxO3 pathway

AimsIntracerebral hemorrhage (ICH) induces serious neuroinflammation and damage of blood-brain barrier. We aim to investigate the role of brown fat enriched lncRNA 1 (Blnc1) in the development of ICH in mice. MethodsAn ICH model was established with autologous blood injection in C57BL/6 mice, and Blnc1 siRNA was injected intracranially. Blnc1 levels were detected and brain injury was evaluated at day 3. Primary brain microvascular endothelial cells (BMVECs) were isolated from new born mice and gain- and loss-of-function experiments were performed to investigate the role of Blnc1. Then, ICH cell model was established by treating BMVECs with oxygen and glucose deprivation (OGD) plus hemin, and Blnc1 siRNA was transfected into the cells. BMVEC functions, including viability, invasion, apoptosis, permeability and secretion of inflammatory cytokines were analyzed. Key findingsBlnc1 was upregulated in perihematomal edema, hematoma and microvessel in the brain of ICH mice. Blnc1 negatively regulated viability and migration, and facilitated apoptosis, permeability and inflammatory cytokine secretion in BMVECs. Silencing Blnc1 restrained OGD plus hemin-caused reduction of BMVEC viability and migration and the induction of apoptosis, permeability and inflammation response, and suppressed PPAR-γ/SIRT6-mediated FoxO3 activation, which could be reversed by T0070907 (PPAR-γ inhibitor). Downregulation of Blnc1 ameliorated ICH-induced nerve injury, brain edema, blood brain barrier destruction, inflammation response and hematoma. Moreover, Blnc1 levels were positively correlated with PPAR-γ levels, and Blnc1 interference suppressed PPAR-γ/SIRT6-mediated activation of FoxO3 signaling in ICH mice. SignificanceSilencing Blnc1 alleviated nerve injury and inflammatory response caused by ICH through activating PPAR-γ/SIRT6/FoxO3 pathway.

Corticosteroids vs autologous blood injection for lateral epicondylitis

Background:There is limited evidence to assess the evaluation of the safety and effectiveness of autologous blood injections in the treatment of lateral epicondylitis patients. For this study, the aim was to compare the efficiency of corticosteroid and autologous blood injections for the treatment of lateral epicondylitis in a retrospective cohort trial in our single center.Methods:After being approved by the institutional review committee of Chongqing General Hospital (IRB# 2018.417.C, November 9, 2018), we performed a single-center, retrospective study between November 2018 and January 2020. All participants provided written informed consent. The criteria for inclusion in our experiment are as follows: over 18 years old; with the history of at least 6 months of lateral epicondylitis; and the palpation of lateral epicondyle tenderness; visual analog scale (≥4). In the group A, the patient were injected the autologous blood. In group B, the patients were immersed with 0.5% of bupivacaine (1 ml) and local corticosteroids (2 ml) at lateral epicondyle. The outcomes were composed of a visual analog scores of subjective pain severity over the past 24 hours as the primary result; and limb function in various tasks of daily activity measured with disabilities of the arm, shoulder, and hand quick questionnaire scores, the maximum grip strength and the modified scores of Nirschl, as secondary results. All the results were assessed before the injection and at 4 weeks and 8 weeks after the injection. For all examination, when the P value was less than .05, it would be defined to be a statistically significant difference.Results:The results of this study would provide new information about the influence of autologous blood injections in treating the lateral epicondylitis.Trial registration:This study protocol was registered in Research Registry (researchregistry6263).

Autologous blood injection for the treatment of chronic recurrent temporomandibular joint dislocation in neurological disorder - A case report

Autologous blood injection (ABI) into the articular cavity, It is one of the treatments for recurrent temporomandibular joint dislocation, was recently reintroduced, here we present a case report of the management of recurrent temporomandibular joint dislocation by Autologous blood injection (ABI) in a 45 -year-old neurologically disabled female. After the treatment, the left condylar process had settled just beneath the articular tubercle, the dislocation had improved, the patient was able to close her mouth & patient was followed on 3rd day, 15th day, 1 month, 3rd month, 6th month, 1 year for 1 year. Keywords: Autologous blood injection, ABI, Temporomandibular joint dislocation, TMJ.

Acyl-CoA synthetase long chain family member 4 plays detrimental role in early brain injury after subarachnoid hemorrhage in rats by inducing ferroptosis.

AimsAcyl‐CoA synthetase long chain family member 4 (ACSL4) is closely related to tumor genesis and development in certain tissues. However, the function of ACSL4 in early brain injury (EBI) caused by subarachnoid hemorrhage (SAH) is unclear. In this study, we investigated the expression patterns and role of ACSL4 in SAH and post‐SAH EBI using a rat model of SAH.MethodsThe rat model of SAH was induced by autologous blood injection into the prechiasmatic cistern of rats. We also used two specific inhibitors of ferroptosis (Ferrostatin‐1 and Liproxstatin‐1) to investigate the role of ferroptosis in EBI.ResultsWe found that ACSL4 levels in brain tissue increased significantly in post‐SAH EBI. Inhibiting the expression of ACSL4 using small interfering RNAs alleviated inflammation, blood‐brain barrier (BBB) impairment, oxidative stress, brain edema, and behavioral and cognitive deficits, and increased the number of surviving neurons, after SAH. Similar effects were obtained by suppressing ferroptosis.ConclusionsACSL4 exacerbated SAH‐induced EBI by mediating ferroptosis. These findings may provide a theoretical basis for potential therapy aimed at alleviating post‐SAH EBI.

Subarachnoid Hemorrhage Increases Level of Heme Oxygenase-1 and Biliverdin Reductase in the Choroid Plexus.

Subarachnoid hemorrhage is a specific, life-threatening form of hemorrhagic stroke linked to high morbidity and mortality. It has been found that the choroid plexus of the brain ventricles forming the blood-cerebrospinal fluid barrier plays an important role in subarachnoid hemorrhage pathophysiology. Heme oxygenase-1 and biliverdin reductase are two of the key enzymes of the hemoglobin degradation cascade. Therefore, the aim of present study was to investigate changes in protein levels of heme oxygenase-1 and biliverdin reductase in the rat choroid plexus after experimental subarachnoid hemorrhage induced by injection of non-heparinized autologous blood to the cisterna magna. Artificial cerebrospinal fluid of the same volume as autologous blood was injected to mimic increased intracranial pressure in control rats. Immunohistochemical and Western blot analyses were used to monitor changes in the of heme oxygenase-1 and biliverdin reductase levels in the rat choroid plexus after induction of subarachnoid hemorrhage or artificial cerebrospinal fluid application for 1, 3, and 7 days. We found increased levels of heme oxygenase-1 and biliverdin reductase protein in the choroid plexus over the entire period following subarachnoid hemorrhage induction. The level of heme oxygenase-1 was the highest early (1 and 3 days) after subarachnoid hemorrhage indicating its importance in hemoglobin degradation. Increased levels of heme oxygenase-1 were also observed in the choroid plexus epithelial cells at all time points after application of artificial cerebrospinal fluid. Biliverdin reductase protein was detected mainly in the choroid plexus epithelial cells, with levels gradually increasing during subarachnoid hemorrhage. Our results suggest that heme oxygenase-1 and biliverdin reductase are involved not only in hemoglobin degradation but probably also in protecting choroid plexus epithelial cells and the blood-cerebrospinal fluid barrier from the negative effects of subarachnoid hemorrhage.

Activation of the Melanocortin-1 Receptor by NDP-MSH Attenuates Oxidative Stress and Neuronal Apoptosis through PI3K/Akt/Nrf2 Pathway after Intracerebral Hemorrhage in Mice.

Oxidative stress and neuronal apoptosis play crucial roles in secondary brain injury (SBI) after intracerebral hemorrhage (ICH). Recently, Nle4-D-Phe7-α-melanocyte-stimulating hormone (NDP-MSH), a synthetic agonist of the melanocortin-1 receptor (Mc1r), has been proved to inhibit neuroinflammatory in several diseases. This study is aimed at exploring if NDP-MSH could reduce oxidative stress and neuronal apoptosis following ICH, as well as the potential mechanism. A mouse ICH model was induced by autologous blood injection. NDP-MSH was intraperitoneally injected at 1 h after ICH. Mc1r siRNA and PI3K inhibitor LY294002 were administrated to inhibit the expression of Mc1r and phosphorylation of PI3K, respectively. Neurological test, brain water content, enzyme-linked immunosorbent assay (ELISA), terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), immunofluorescence, and Western blot analysis were utilized in this study. The results exhibited that Mc1r was mainly expressed in neurons, and its level in the ipsilateral hemisphere was significantly elevated after ICH. NDP-MSH treatment significantly attenuated the neurological deficits and brain water content 24 hours after ICH, which was accompanied by the inhibition of oxidative stress and neuronal apoptosis. The administration of NDP-MSH after ICH significantly promoted the expression of Mc1r, p-PI3K, p-Akt, and p-Nrf2, followed by an increase of Bcl-2 and reduction of cleaved caspase-3. Conversely, downregulating the expression of Mc1r and phosphorylation of PI3K aggravated the neurological deficits and brain edema at 24 hours after ICH, meanwhile, the effect of NDP-MSH on the expression of Mc1r, p-PI3K, p-Akt, p-Nrf2, Bcl-2, and cleaved caspase 3 was also abolished. In conclusion, our data suggest that the activation of Mc1r by NDP-MSH ameliorates oxidative stress and neuronal apoptosis through the PI3K/Akt/Nrf2 signaling pathway after ICH in mice.

RETRACTED: Long noncoding RNA MEG3 contributes to dysfunction of brain microvascular endothelial cells after intracerebral hemorrhage by regulating the miR-1930-5p/Mllt1 axis

Intracerebral hemorrhage (ICH) is a subtype of stroke and causes disability and death worldwide. The roles of long noncoding RNAs (lncRNAs) in brain function and neurological diseases have been revealed. LncRNA maternally expressed gene 3 (MEG3) is involved in neurological impairment, but its role in ICH remains unknown. The aim of this research is to explore the role of MEG3 in ICH. Here, we established an ICH mouse model via intracerebral injection of autologous blood. Primary brain microvascular endothelial cells (BMECs) were treated with oxygen-and-glucose-deprivation (OGD) plus hemin to establish the model in vitro. We observed that MEG3 expression was significantly upregulated in both ICH mouse model and OGD/hemin (OGD/H) induced BMECs. The downregulation of MEG3 suppressed cell apoptosis and the activation of NOD-like receptor family protein 3 (NLRP3) inflammasome in OGD/H-induced BMECs. In ICH mice, MEG3 downregulation inhibited cell apoptosis and improved brain dysfunction. Mechanistically, MEG3 was confirmed to act as a molecular sponge for microRNA (miR)-1930-5p, and Mllt1 was a downstream target for miR-1930-5p. MEG3 competitively bound with miR-1930-5p to upregulate Mllt1. We further verified that Mllt1 overexpression reversed the inhibitory effect of miR-1930-5p in OGD/H-induced BMECs. In conclusion, lncRNA MEG3 promoted the dysfunction of BMECs by modulating the miR-1930-5p/Mllt1 axis, which provides a potential target in gene therapy for brain injury following ICH.

Effect of manual acupuncture of "Shuigou" (GV26)"Neiguan" (PC6) on neurological function and expression of apoptosis-related factors in brain tissues surrounding hematoma in intracerebral hemorrhage rats

To observe the effect of manual acupuncture stimulation of "Shuigou" (GV26) and "Neiguan" (PC6) on neurological function and expression of Caspase-3 and Caspase-9 in brain tissues around the intracerebral hematoma in rats with acute intracerebral hemorrhage (ICH), so as to explore its possible mechanisms underlying improvement of ICH. Ninety-six male SD rats were randomly divided into 4 groups: control, model, acupoint and non-acupoint (24 rats in each group). The ICH model was established by injection of the rat's autologous blood into the caudate nucleus. According to the time-points of 6, 24, 48 and 72 h after ICH, each of the 4 groups was further divided into 4 subgroups. For rats of the acupoint group, the PC6 on both sides was manually stimulated by manipulating the needle with lifting-thrusting-twisting reducing techniques, while the GV26 was stimulated with strong "sparrow-pecking" method for 10 times, then, left the needles in the acupoints for 30 min. For rats of the non-acupoint group, two non-acupoints: mid-spot below the bilateral axilla and the spot 3 mm above the left side of the coccyx tip were stimulated with the same methods to PC6 and GV26, respectively. For rats of the 6 h and 24 h subgroups, the intervention was given once after waking up from modeling, and for those of the 48 and 72 h subgroups, the intervention was conducted once a day for 2 or 3 times, respectively. The neurological severity score (NSS) was used to evaluate the degree of neurological function. The immunoactivity (expression) of Caspase-3 and Caspase-9 proteins of the hematoma focus of the brain was detected by immunohistochemistry. Following modeling, the NSS and the expression levels of Caspase-3 and Caspase-9 proteins in the brain tissues surrounding the hematoma at each time-points (6, 24, 48 and 72h) after modeling were significantly increased in the model group relevant to the control group (P<0.01, P<0.05). Compared with the model group, the NSS at 72h and the expression levels of Caspase-3 and Caspase-9 proteins at 6, 24, 48 and 72h were significantly down-regulated in the acupoint group (P<0.05) rather than in the non-acupoint group (P>0.05). Acupuncture of GV26 and PC6 can improve the neurological function in rats with ICH, which may be related to its function in reducing the expression of Caspase-3 and Caspase-9 proteins (apoptosis-related proteins) in the brain.

Short term results of a single autologous whole blood injection for treatment of resistant tennis elbow

&lt;p&gt;&lt;strong&gt;Background:&lt;/strong&gt; Lateral epicondylitis commonly called tennis elbow is a common cause of elbow pain and involves degeneration of common extensor origin with no unanimously supported algorithm for the treatment. Recently, autologous blood injection has been reported for the treatment of resistant cases. We present the short term results of a single shot of autologous whole blood for the treatment of resistant tennis elbow.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;The study was conducted on 56 patients who fulfilled the other inclusion criteria’s. 2 ml of autologous whole blood was introduced just proximal to the lateral epicondyle and the contents were injected on the under surface of the extensor carpi radialis group of muscles. Pain severity using VAS and Nirschl Staging was assessed before injection and re-evaluation was done at 4 weeks, 12 weeks and 6 months.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results:&lt;/strong&gt; Before the procedure average pain score was 7.5(range 5-9). The average Nirschl stage was 5.5 (range 4-7). After autologous blood injections the average pain score decreased to 4 at 4 weeks, 2.8 at 12 weeks and 2.5 at 6 months. The average Nirschl stage decreased to 3.53 at 4 weeks, 2.45 at 12 weeks and 2.3 at 6months. The reduction was statistically significant (p&amp;lt;0.001). 28 out of 56 patients (50%) were completely relieved of pain with a pain score of 0 at 6 months. There was no major complication.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions:&lt;/strong&gt; A single injection of autologous whole blood for resistant tennis elbow is an economical and effective treatment and has an excellent safety profile.&lt;/p&gt;

Hemorrhagic Descemet's Membrane Detachment in Nonpenetrating Glaucoma Surgery.

To describe 5 representative cases of hemorrhagic Descemet's membrane (DM) detachment in glaucoma surgery that had different origins, mechanisms and treatments. Clinical records of patients that had undergone a nonpenetrating glaucoma surgery, with a diagnosis of hemorrhagic DM detachment were reviewed for demographic data, clinical findings and treatment applied. Five patients with hemorrhagic DM detachment were included in this case series. They all had different causes, namely a massive hemorrhage at the end of a canaloplasty procedure, a needling maneuver, autologous blood injection, Swan syndrome, and frequent eye rubbing. Hematoma evacuation was performed in 4 eyes, 1 of them from under the scleral flap of the deep sclerectomy and 3 of them through a surgical or laser perforation in DM. Air tamponade was done in most of these cases. One of these cases required transcorneal suture fixation. One case was observed expectantly. All cases successfully recovered but peripheral corneal stain was persistent in 2 cases. Hemorrhagic DM detachment is a rare but potential vision-threatening complication in glaucoma surgery. Different mechanisms may cause the bleeding and there are several techniques available to approach this complication. Pre-Descemet hematoma should be drained to avoid permanent corneal stain and air/gas tamponade may help to prevent recurrences.

Inhibition of lysophosphatidic acid receptor 1 attenuates neuroinflammation via PGE2/EP2/NOX2 signalling and improves the outcome of intracerebral haemorrhage in mice

Lysophosphatidic acid receptor 1 (LPA1) plays a critical role in proinflammatory processes in the central nervous system by modulating microglia activation. The aim of this study was to explore the anti-inflammatory effects and neurological function improvement of LPA1 inhibition after intracerebral haemorrhage (ICH) in mice and to determine whether prostaglandin E2 (PGE2), E-type prostaglandin receptor 2 (EP2), and NADPH oxidase 2 (NOX2) signalling are involved in LPA1-mediated neuroinflammation. ICH was induced in CD1 mice by autologous whole blood injection. AM966, a selective LPA1 antagonist, was administered by oral gavage 1 h and 12 h after ICH. The LPA1 endogenous ligand, LPA was administered to verify the effect of LPA1 activation. To elucidate potential inflammatory mechanisms of LPA1, the selective EP2 activator butaprost was administered by intracerebroventricular injection with either AM966 or LPA1 CRISPR knockout (KO). Water content of the brain, neurobehavior, immunofluorescence staining, and western blot were performed. After ICH, EP2 was expressed in microglia whereas LPA1 was expressed in microglia, neurons, and astrocytes, which peaked after 24 h. AM966 inhibition of LPA1 improved neurologic function, reduced brain oedema, and suppressed perihematomal inflammatory cells after ICH. LPA administration aggravated neurological deficits after ICH. AM966 treatment and LPA1 CRISPR KO both decreased the expressions of PGE2, EP2, NOX2, NF-κB, TNF-α, IL-6, and IL-1β expressions after ICH, which was reversed by butaprost. This study demonstrated that inhibition of LPA1 attenuated neuroinflammation caused by ICH via PGE2/EP2/NOX2 signalling pathway in mice, which consequently improved neurobehavioral functions and alleviated brain oedema. LPA1 may be a promising therapeutic target to attenuate ICH-induced secondary brain injury.

Standardized Tendon Fenestration with Injection of Autologous Blood for Treatment of Lateral Epicondylitis

Lateral epicondylitis (LE) of the elbow is often treated with conservative methods. Several techniques including injections with different substances are widely performed. No standardization exists. This prospective study describes the results of the short-term follow-up of 56 patients with mean age 48 years (range: 30–68 years) treated with the Instant Tennis Elbow Cure Medical device, which fenestrates the injured tendon in a standardized way through a holder of 12 small needles. Depth and position of the needles are determined beforehand by ultrasonography. Unprepared autologous blood was injected through the holder in the tendon. Visual analog pain scale (VAS) decreased significantly in rest by 61% and during activity by 47% after 6 weeks. VAS decreased significantly in rest by 79% and during activity by 66% after 3 months. VAS did not remain significantly different after 6 months. Satisfaction rates were 71% after 6 weeks and 82% after 6 months. This suggests that the therapeutical effect sustains and in some cases increases over time. Patient Related Tennis Elbow Evaluation score ameliorated after 3 months by 71%. Comparative studies are needed to confirm this effect versus other techniques as physiotherapy, shockwave therapy, and injections with other substances.

Effectiveness of autologous blood injection in reducing the rate of pneumothorax after percutaneous lung core needle biopsy

To assess the effectiveness and safety of autologous intraparenchymal blood patch (IBP) application in reducing the frequency of pneumothorax (PTX) after percutaneous transthoracic pulmonary core needle biopsy. The records of patients who underwent the transthoracic pulmonary core needle biopsy procedure under CT guidance between January 2015 and October 2018 were screened retrospectively. Patients whose traversed pulmonary parenchymal length was ≥20 mm during biopsy were included in the study irrespective of lesion size. The IBP procedure was made a department policy in November 2017; patients who underwent biopsy after this date comprised the IBP group, while those who underwent the procedure before this date comprised the control group. IBP recipients received 2-5 mL of autologous blood injection to the needle tract. Demographic data, procedural reports, tomography images, and the follow-up records of patients were assessed. A total of 262 patients were included in the study. Of the 91 patients that received an IBP, PTX developed in 13 (14.1%), with 7 (7.7%) requiring a thoracic tube. Of the 171 patients who did not receive an IBP, PTX developed in 45 (26.3%), with 19 (11.1%) requiring a thoracic tube. Patients who received an autologous IBP showed a significantly lower rate of PTX development versus those who did not (P = 0.01). Similarly, a significantly lower number of patients who received the blood patch required chest tube placement (P = 0.015). Autologous IBP is a safe, inexpensive and easy to use method that reduces the rate of PTX development and thoracic tube application after percutaneous core needle biopsies of the lung.

Elevated miR-29a Contributes to Axonal Outgrowth and Neurological Recovery After Intracerebral Hemorrhage via Targeting PTEN/PI3K/Akt Pathway.

Spontaneous intracerebral hemorrhage (ICH) is a clinical challenge with high disability and lacks an effective treatment. miR-29a strongly expressed in the brain has been implicated in various neurological disorders. In this study, we investigated the biological roles of miR-29a in axonal outgrowth and neurological outcomes after ICH and relevant molecular mechanism. The rat model of ICH was established by injection of autologous whole blood into the right basal ganglia. First, a significant decrease in miR-29a level was found in perihematomal brain tissues and cerebrospinal fluid (CSF) after ICH in vivo and hemin-treated neurons in vitro. Further study documented that lentivirus-mediated miR-29a overexpression could remarkably attenuate hemorrhagic brain injury, promoted regenerative outgrowth of injured axons and improved neurobehavioral and cognitive impairments after ICH in rats. In addition, we also identified that overexpression of miR-29a obviously alleviated neuronal damage and mitochondrial dysfunctions, and facilitated neurite outgrowth in cultured neurons exposed to hemin in vitro. Furthermore, luciferase reporter assay showed that miR-29a directly targeted the 3'-UTR region of phosphatase and tensin homolog (PTEN) mRNA and negatively regulated its expression. More importantly, pharmacological inhibition of PTEN has similar neuroprotective effects as miR-29a overexpression involving activation of the PI3K/Akt pathway after hemorrhagic stroke. Collectively, these results suggested that elevated miR-29a could contribute to axonal outgrowth and neurological recovery through targeting PTEN/PI3K/Akt pathway after ICH, thereby providing a potential therapeutic target for patients with ICH.

Effects of ozone autohemotherapy on blood VEGF, TGF-β and PDGF levels after finger replantation.

The study aimed to confirm the important role of ozone autologous blood therapy (autohemotherapy) in promoting successful finger replantation and its possible influence mechanism. A total of 150 patients with severed finger replantation admitted to our hospital from March 2018 to March 2019 were selected. Patients were divided into observation group and control group according to different treatment methods. The observation group received additional ozone autologous blood treatment in the control group. We compared the number of white blood cells, visual analogue scale (VAS) scores, and the expression levels of vascular endothelial growth factor (VEGF), transforming growth factor-β (TGF-β), and platelet-derived growth factor (PDGF) in the two groups of patients before and after intervention. We also assessed the hospitalization time and survival time of the replanted finger in the two groups, as well as blood flow values (Vbcf). Compared with the observation group on the 1st day after the operation and the control group on the 7th day after the operation, the average white blood cell count of the observation group on the 7th day after the operation was significantly increased (P<0.05), and the VAS score was significantly decreased (P<0.05).48 hours after the operation, the average Vbcf value of the replanted finger was lower than that of the contralateral healthy finger (P<0.05). Compared with the control group, the Vbcf value of the replanted fingers in the observation group was higher, and the hospitalization time and finger survival time were shorter (P<0.05). At 7 days after operation, the serum VEGF, TGF-β and PDGF levels in the observation group were significantly higher than the 1 day after operation, before the operation and the control group (P<0.05). Intervention with ozone autohemotherapy after severed finger replantation can significantly increase the number of white blood cells, relieve postoperative pain, and improve the survival rate of the finger body. Ozone autohemotherapy also improves the microcirculation after anastomosis of the severed finger by up-regulating the expression of VEGF, TGF-β and PDGF in blood.

Recombinant CCL17 Enhances Hematoma Resolution and Activation of CCR4/ERK/Nrf2/CD163 Signaling Pathway After Intracerebral Hemorrhage in Mice.

Hematoma is a crucial factor leading to poor prognosis after intracerebral hemorrhage (ICH). Promoting microglial phagocytosis to enhance hematoma resolution may be an important therapeutic target for recovery after ICH. C-C chemokine receptor 4 (CCR4) is important for regulating immune balance in the central nervous system. However, whether CCR4 activation can attenuate hematoma after ICH remains unknown. We aimed to evaluate whether CCL17 (a specific ligand of CCR4) treatment can promote hematoma resolution through CCR4/ERK/Nrf2/CD163 pathway after ICH. A total of 261 adult male CD1 mice were used. Mice were subjected to intrastriatal injection of autologous blood to induce ICH and randomly assigned to receive recombinant CCL17 (rCCL17) or vehicle which was administered intranasally at 1h after ICH. To elucidate the underlying mechanism, C021, a selective inhibitor of CCR4 and ML385 and a selective inhibitor of Nrf2 were administered 1h prior to ICH induction. Clustered regularly interspaced short palindromic repeats (CRISPR) knockout for CD163 was administered by intracerebroventricular injection at 48h before ICH. Brain edema, short- and long-term neurobehavior evaluation, hematoma volume, hemoglobin content, western blot, and immunofluorescence staining were performed. Endogenous CCL17, CCR4, and CD163 expression increased and peaked at 72h after ICH. CCR4 was expressed by microglia. CCR4 activation with rCCL17 significantly improved neurobehavioral scores and reduced hematoma volume and brain edema compared with vehicle. Moreover, rCCL17 treatment significantly promoted phosphorylation of ERK1/2, increased the expression Nrf2, and upregulated CD163 expression after ICH. The protective effects of rCCL17 were abolished by administration of C021, ML385, and CD163 CRISPR knockout. This study demonstrated that CCR4 activation with rCCL17 promoted hematoma resolution by increasing CD163 expression and CCR4/ERK/Nrf2 pathway activation after ICH, thereby reducing brain edema and improving neurological function. Overall, our study suggests that CCR4 activation may be a potential therapeutic strategy to attenuate hematoma in early brain injury after ICH.

The Possible Inhibition Effect of Lycium barbarum Polysaccharides on Rat Intracerebral Hemorrhage Secondary Neuronal Apoptosis through Intervening Endogenous/Exogenous Pathways of Apoptosis

AbstractObjective The aim of this study was to explore the inhibition effect and possible mechanism of Lycium barbarum polysaccharides (LBP) on rat intracerebral hemorrhage (ICH) secondary neuronal apoptosis.Materials and Methods High-, medium-, and low-dose LBP (50, 100, and 200 mg•kg) and nimodipine (10 mg•kg) groups were given once daily by 15-day gavage before operation, while the sham operation and ICH groups were given the equal volume of saline. An ICH model was established by autologous blood injection and the neurological function in each group was scored at 4, 8, 12, 24, and 48 hours after modeling. Furthermore, terminal deoxynucleotidyl transferase dUTP nick end labeling analysis was performed to detect neuronal apoptosis, while western blot, immunohistochemistry, and real-time-polymerase chain reaction were used to study the influence of LBP on ICH secondary neuronal apoptosis.Results The neurological function score was significantly decreased after ICH, and the intervention effect of a single drug was not evident. The apoptotic nerve cells increased significantly in the ICH group but decreased considerably in the LBP groups. Furthermore, tumor necrosis factor alpha (TNF-α) expression decreased significantly, while B-cell lymphoma 2 expression increased substantially in the high- and medium-dose LBP groups compared with ICH group, suggesting that LBP could reduce the effect of ICH. However, the impact of LBP did not correlate positively with the dose.Conclusion The application of LBP may not significantly improve neurological function after ICH, but it can inhibit rat ICH secondary neuronal apoptosis.

CT-guided blood tattoo for thoracoscopic excision of lung lesions in pediatric patients

BackgroundTo describe a single-institutional experience with an innovative technique using CT-guided injection of autologous blood for localization of nonpleural-based pulmonary nodules prior to thoracoscopic excisional biopsy in pediatric patients.MethodsA retrospective review of all patients under the age of 18 with lung lesions suspected to be malignant that were not pleural-based lesions and were not of adequate size to visualize at thoracoscopy, who underwent CT-guided blood tattoo (CGBT) localization between 2006–2019. CGBT was performed under general anesthesia by injecting 0.5–10 mL of autologous blood into the area of the lesions. The patients were then immediately transferred from interventional radiology to the operating room for thoracoscopic excision of the lesion. Demographics, location of lesions, indication for biopsy, and pathology were reviewed.ResultsIn eleven pediatric patients (ages ranging from 4–18 years), preoperative CGBT localization of pulmonary nodules resulted in successful thoracoscopic excisional biopsy. All resections were diagnostic and 82% (9/11 cases) represented a metastatic malignancy as confirmed by pathology. Malignant nodules ranged from 2 to 14 mm in size, while a 13 mm nodule in a patient with history of AML was determined to be an organizing pneumonia and a 12 mm nodule in a second patient revealed a caseating granuloma consistent with Crohn’s disease. One patient with a failed attempt at excisional biopsy without preoperative localization then underwent CGBT one week later with successful thoracoscopic excision of the nodule.ConclusionsCT-guided blood tattoo is a safe option for localization of nonpleural-based lung nodules prior to thoracoscopic excision in pediatric patients.