Inflammation and angiogenesis are critical processes contributing to the progression of chronic subdural hematoma (CSDH). Tissue plasminogen activator (tPA), which is highly abundant in CSDH effusion, has been implicated not only in hematoma liquefaction but also in progressive hematoma enlargement. Notably, tPA expression has also been reported in intracranial neoplasms, where it contributes to the development of peritumoral edema, suggesting roles beyond fibrinolysis. We therefore hypothesized that tPA exerts non-fibrinolytic effects in the pathophysiology of CSDH. Twenty CSDH fluid specimens and eight outer membrane samples were analyzed. The concentrations of tPA and matrix metalloproteinase-9 (MMP-9) were markedly higher in CSDH fluid than in cerebrospinal fluid. Immunoblotting confirmed the presence of low-density lipoprotein receptor-related protein-1 (LRP-1), phosphorylated Mek (p-Mek), Mek, phosphorylated Erk (p-Erk), Erk, MMP-9, caspase-3, and cleaved caspase-3 in the outer membrane. Immunohistochemical analyses revealed that LRP-1, p-Erk, Erk, and MMP-9 were predominantly localized to vascular endothelial cells, whereas LRP-1, caspase-3, and cleaved caspase-3 were mainly expressed in fibroblasts within the outer membrane. Moreover, exposure of fibroblasts to CSDH effusion significantly attenuated staurosporine-induced cleaved caspase-3 expression in vitro. Collectively, these findings suggest that elevated tPA in CSDH effusion is associated with activation of LRP-1-dependent Mek-Erk signaling and increased MMP-9 expression, and may also be linked to anti-apoptotic responses in fibroblasts. These pathology-associated signaling features extend beyond the classical fibrinolytic role of tPA and may have therapeutic implications for refractory CSDH, warranting further functional and interventional studies.

Stem cell therapy employing stem cells from human exfoliated deciduous teeth (SHED) has demonstrated efficacy in treating peripheral nerve injury; however, the precise underlying mechanisms remain largely undefined. In this study, we investigated the effects of SHED on signal transducer and activator of transcription 3 (STAT3), a key mediator of inflammation following sciatic nerve injury (SNI). The left sciatic nerve was transected (cut group), sutured and wrapped with cellulose (suture group), or sutured and enveloped with SHED-soaked cellulose (SHED group). The L4-5 segments of the spinal cord were harvested up to 7 days post-SNI, and tissues were separated into ipsilateral and contralateral regions for molecular and immunohistochemical analyses. In the SHED group, the sciatic functional index showed significant improvement compared with the suture group beginning at 4 weeks postinjury, and tibialis anterior muscle mass was markedly restored at 12 weeks. STAT3 phosphorylation at Tyr705 (p-STAT3) was prominently elevated between 12 and 48 h post-SNI on the ipsilateral side, but not contralaterally. This phosphorylation was localized to motor neurons in the anterior horn and was substantially attenuated by SHED administration between 24 and 48 h postinjury. Moreover, interleukin (IL)-6 expression was significantly reduced at 12 h, while p-STAT3 and importin β1 levels were notably decreased between 12 and 24 h. Erk signaling was significantly activated in S100β-positive Schwann cells (SCs) on day 4 at the site of SNI in the SHED group. These results suggest that SHED mitigate neuroinflammation by suppressing IL-6 expression and modulating STAT3 activation, while concurrently enhancing remyelination through Erk signaling activation in SCs at the injury site. Collectively, these findings underscore the therapeutic promise of SHED as a potent and innovative intervention for peripheral nerve avulsion injuries.

Background:Osteoarthritis (OA) is a degenerative joint disease involving cartilage loss and inflammation. Traditional histological evaluation is limited. Micro-computed tomography (micro-CT) offers non-invasive three-dimensional (3D) joint visualization but lacks detailed cartilage assessment. This study developed and evaluated a novel micro-CT-based scoring system for joint structure in a rat model of mono-iodoacetate (MIA)-induced OA. Methods:OA was induced in the right knees of 24 Wistar male rats using varying MIA concentrations (0.2, 0.5, 1, 3 mg). After 28 days, knee joints were scanned using micro-CT and segmented into 10 compartments. Degenerative changes in each compartment were scored (0-4), and a total joint score was calculated. Histological evaluation using a modified Mankin score was performed on sagittal sections of the patellar groove. Interobserver reliability and correlations between micro-CT joint scores and Mankin scores were analyzed statistically. Results:The micro-CT 3D imaging scoring system demonstrated excellent interobserver reliability [interclass correlation coefficient (ICC) >0.75 for most compartments]. Micro-CT joint scores revealed statistically significant differences in joint degeneration between the highest MIA dose group (3 mg) and the lower dose groups (0.2 and 0.5 mg). Notably, micro-CT could differentiate between the 0.2 mg and 1mg groups, which was not fully reflected in histological scores. A strong correlation was found between the total micro-CT joint score and the modified Mankin score (ρ=0.8, P<0.001). Conclusions:The novel micro-CT-based 3D imaging scoring system provides a reliable method for quantifying gross degenerative changes in rat knee joints in the MIA-induced OA model. While it does not directly assess cartilage, its correlation with histological findings suggests its utility as a complementary tool for evaluating overall joint degeneration.

INTRODUCTION: Spinal cord injury (SCI) precipitates profound enduring deficits. Recently, cell transplantation therapy has emerged as a noteworthy intervention for SCI. Although stem cells derived from human exfoliated deciduous teeth (SHED) present an enticing therapeutic prospect, their precise mode of action remains elusive. METHODS: Employing a rat clip compression SCI model, we partitioned the animals randomly into three cohorts: SCI, SCI + PBS, and SCI + SHED. Subsequent to SCI induction, we assessed the impact of SHED on motor function via the Basso, Beattie, and Bresnahan score, along with the inclined plane method. We scrutinized the signal transduction pathway, particularly the JAK and STAT3 pathway, the apoptotic pathway, and the expression of neurocan, a member of the chondroitin sulfate proteoglycans. RESULTS: SHED treatment notably ameliorated functional recovery beginning on day 14 compared to the controls. Western blot analysis revealed that SHED significantly attenuated the expression of GFAP and phosphorylated (p-) STAT3 at Tyr705 on day 10, albeit not on day 5. Immunohistochemistry unveiled that p-STAT3 at Tyr705 was chiefly expressed in GFAP-positive astrocytes on day 10 post-SCI, with its expression curtailed by SHED administration. Furthermore, SHED treatment substantially triggered the expression of cleaved caspase 3 in GFAP-positive astrocytes on day 10 post-SCI, without such effects observed on day 5. Neurocan expression was also markedly diminished following SHED injection on day 10 post-SCI. CONCLUSIONS: Our findings elucidate the pivotal role of SHED in mitigating astrogliosis and glial scar formation between days 5 and 10 post-SCI, plausibly through astrocyte apoptosis, ultimately culminating in neurological functional enhancements thereafter. Thus, our data unveil one of the neuroprotective mechanisms of SHED during the subacute phase following SCI, contributing to enhanced functional recovery post-SCI.

Angiogenesis is one of the growth mechanisms of chronic subdural hematoma (CSDH). Pericytes have been implicated in the capillary sprouting during angiogenesis and are involved in brain ischemia and diabetic retinopathy. This study examined the pericyte expressions in CSDH outer membranes obtained during trepanation surgery. Eight samples of CSDH outer membranes and 35 samples of CSDH fluid were included. NG2, N-cadherin, VE-cadherin, Tie-2, endothelial nitric oxide synthase (eNOS), platelet-derived growth factor (PDGF) receptor-β (PDGFR-β), a well-known marker of pericytes, phosphorylated PDGFR-β at Tyr751, and β-actin expressions, were examined using western blot analysis. PDGFR-β, N-cadherin, and Tie-2 expression levels were also examined using immunohistochemistry. The concentrations of PDGF-BB in CSDH fluid samples were measured using enzyme-linked immunosorbent assay kits. NG2, N-cadherin, VE-cadherin, Tie-2, eNOS, PDGFR-β, and eNOS expressions in CSDH outer membranes were confirmed in all cases. Furthermore, phosphorylated PDGFR-β at Tyr751 was also detected. In addition, PDGFR-β, N-cadherin, and Tie-2 expressions were localized to the endothelial cells of the vessels within CSDH outer membranes by immunohistochemistry. The concentration of PDGF-BB in CSDH fluids was significantly higher than that in cerebrospinal fluid. These findings indicate that PDGF activates pericytes in the microvessels of CSDH outer membranes and suggest that pericytes are crucial in CSDH angiogenesis through the PDGF/PDGFR-β signaling pathway.

Spinal cord injury (SCI) induces devastating permanent deficits. Recently, cell transplantation therapy has become a notable treatment for SCI. Although stem cells from human exfoliated deciduous teeth (SHED) are an attractive therapy, their precise mechanism of action remains to be elucidated. In this study, we explored one of the neuroprotective mechanisms of SHED treatment at the subacute stage after SCI. We used a rat clip compression SCI model. The animals were randomly divided into three groups: SCI, SCI + phosphate-buffered saline (PBS), and SCI + SHED. The SHED or PBS intramedullary injection was administered immediately after SCI. After SCI, we explored the effects of SHED on motor function, as assessed by the Basso-Beattie-Bresnahan score and the inclined plane method, the signal transduction pathway, especially the Janus kinase (JAK) and the signal transducer and activator of transcription 3 (STAT3) pathway, the apoptotic pathway, and the expression of neurocan, one of the chondroitin sulfate proteoglycans. SHED treatment significantly improved functional recovery from Day 14 relative to the controls. Western blot analysis showed that SHED significantly reduced the expression of glial fibrillary acidic protein (GFAP) and phosphorylated STAT3 (p-STAT3) at Tyr705 on Day 10 but not on Day 5. However, SHED had no effect on the expression levels of Iba-1 on Days 5 or 10. Immunohistochemistry revealed that p-STAT3 at Tyr705 was mainly expressed in GFAP-positive astrocytes on Day 10 after SCI, and its expression was reduced by administration of SHED. Moreover, SHED treatment significantly induced expression of cleaved caspase 3 in GFAP-positive astrocytes only in the epicenter lesions on Day 10 after SCI but not on Day 5. The expression of neurocan was also significantly reduced by SHED injection on Day 10 after SCI. Our results show that SHED plays an important role in reducing astrogliosis and glial scar formation between Days 5 and 10 after SCI, possibly via apoptosis of astrocytes, ultimately resulting in improvement in neurological functions thereafter. Our data revealed one of the neuroprotective mechanisms of SHED at the subacute stage after SCI, which improved functional recovery after SCI, a serious condition.

OBJECTIVE:To explore whether methotrexate (MTX) prevents joint destruction and improves pain-related behaviors in the acute phase of knee osteoarthritis (OA) induced by monosodium iodoacetate (MIA) in a rat model.METHODS:Twenty of 25 male Wistar rats (10-14 weeks old) received 3 mg MIA via intra-articular injection into their right knee and were then administered a vehicle control (n=10) or 3 mg/kg MTX orally weekly (n=10). We assessed differences in pain-related behavior, spontaneous lifting behavior, micro-computed tomography (CT), histopathology, and expression of pain- and inflammatory-related genes using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) between the two groups for 4 weeks. Five rats were used as untreated controls to assess pain- and inflammatory-related mRNA expression in the dorsal root ganglia (DRG) and knee joints using RT-qPCR.RESULTS:Joint destruction and mechanical hyperalgesia were observed in the vehicle group. Decreases in mechanical pain thresholds for the knee joint and calf muscles were improved after MTX administration; however, joint damage assessed by micro-CT and histopathology was not significantly inhibited by MTX administration, while upregulation levels of transient receptor potential cation channel, subfamily V, member 1 (TRPV-1) (P<0.01) and brain-derived neurotrophic factor (BDNF) (P=0.02) mRNA in the DRG and nerve growth factor NGF mRNA (P=0.03) in the affected knee joints were significantly suppressed in the MTX group compared with the vehicle group at week 4.CONCLUSION:Our results imply that MTX administration improves pain-related behaviors and suppresses expression of pain-related mRNAs in the DRG and knee joint; however, MTX is not expected to prevent cartilage degeneration in MIA-induced OA in rat knee.

The acupuncture point “Hegu” (LI4) has been used for treating peripheral circulatory failure, which is located in the area covered by the superficial branch of the radial nerve (SBRN). SBRN has branches reaching arteries, so-called vascular branches (VBs), which are thought to be involved in the arterial constriction. The distribution areas of the VBs from the SBRN have been reported, but the positional relationship between these distribution areas and the acupuncture points are not known. To examine the positional relationship between LI4 and VBs from the SBRN, forty hands were examined to assess the positional relationship between the acupuncture points “Erjian” (LI2), “Sanjian” (LI3), LI4, and “Yangxi” (LI5) in the Yangming Large Intestine Meridian of Hand, which are located in the area covered by SBRN, and the VBs from the SBRN. After the VBs were identified, the distances from the acupuncture points (LI2, LI3, LI4, and LI5) to the point where the VBs reached the radial artery or the first dorsal metacarpal artery were measured. VBs reaching the radial arteries were observed in all specimens. The mean distances from LI2, LI3, LI4, and LI5 to the point where the VBs reached the radial artery were 64.2 ± 8.2 mm, 42.0 ± 7.5 mm, 4.3 ± 4.3 mm, and 33.0 ± 4.8 mm, respectively. LI4 was significantly closer than the other acupuncture points (P<0.01). The nerve fibers of the VBs adjacent to the radial artery were confirmed using hematoxylin and eosin staining. Our findings provide anatomical evidence that stimulation at LI4 is used for treating peripheral circulatory failure such as Raynaud’s disease. LI4 is significant because it is located at a source point, making it clinically important.

Chronic subdural hematoma (CSDH) is considered an angiogenic and inflammatory disease. Chemokines attract leukocytes, and invading neutrophils and monocytes/macrophages play important roles in wound healing. However, no studies have been reported regarding changes in expression of chemokines in CSDH fluid after trepanation surgery. We randomly divided patients who underwent trepanation surgery into two groups. One was the irrigation group, in which irrigation of CSDH fluids was performed and a drainage tube was placed (n = 10). The other was the non-irrigation group, in which a drainage tube was inserted without irrigation (n = 10). CSDH fluids were collected during the trepanation surgery, immediately after surgery and on day 1 through the drainage tube. The concentrations of interleukin-8 (IL-8), growth-regulated oncogene-α (GRO-α), epithelial neutrophil-activating peptide 78 (ENA-78), monocyte chemoattractant protein-1 (MCP-1), interferon-γ-induced protein-10 (IP-10), tissue plasminogen activator (tPA), von Willebrand factor (vWF), eotaxin-3, and myeloperoxidase (MPO) in each CSDH fluid sample were measured using enzyme-linked immunosorbent assay kits. After irrigation, concentrations of all chemokines decreased. However, concentrations of IL-8, GRO-α, ENA-78, MCP-1, and MPO were significantly increased on day 1 compared with concentrations during surgery with or without irrigation. In contrast, there were no changes in concentrations of IP-10, eotaxin-3, tPA, or vWF after trepanation surgery. Moreover, there were significant relationships among concentrations of IL-8, GRO-α, ENA-78, and MCP-1 during the surgery and on day 1. In CSDH fluids, chemokines that attract neutrophils, such as IL-8, GRO-α, ENA-78, and macrophage-attracting MCP-1, appear first after trepanation surgery, whereas lymphocyte-attracting IP-10 and eosinophil-attracting eotaxin-3 levels do not change within 1 day of surgery. These findings suggest that neutrophils and macrophages may play important roles in the healing process of CSDH at an early stage.

To elucidate the relationship between chronic pain conditions with cast immobilization and autonomic function, we investigated the functional changes of the autonomic nervous system in conscious rats with chronic post-cast pain (CPCP) induced by a two-week cast immobilization of one hind limb. We telemetrically examined the time courses of systolic arterial blood pressure (SBP), heart rate (HR), and the middle-frequency (MF) component obtained from the power spectral analysis of SBP variability as a vasomotor sympathetic index. We also investigated the baroreflex sensitivity to phentolamine, an α-adrenoceptor antagonist, and the SBP and HR responses to a low ambient temperature (LT; 9.0 ± 0.2°C) exposure, a sympathetic stimulant. Rats exposed to cast immobilization exhibited mechanical allodynia lasting for at least 10 weeks after cast removal in the calf area (skin and muscle) of the bilateral hind limbs. Under resting conditions, the SBP, HR, and MF components were significantly increased during cast immobilization (all p < 0.001). Following cast removal, these parameters gradually decreased and within 1 week reached lower than baseline levels, lasting for over 10 weeks. Phentolamine administration (10 mg/kg, intraperitoneally) significantly decreased the SBP before and during cast immobilization (before, p < 0.001; during, p = 0.001) but did not lower the SBP after cast removal. The baroreflex gain after phentolamine administration, calculated as the HR increase divided by the SBP reduction, was significantly increased after cast removal (p = 0.002). The SBP increase on LT exposure was significantly greater after cast removal than that before cast immobilization, suggesting hypersensitivity to sympathetic neurotransmitters. These results revealed that, in the CPCP model, sympathetic activation was augmented during cast immobilization, which then decreased after cast removal and remained below normal levels with persisting pain behaviors. Additionally, the responsiveness of the autonomic nervous system was impaired in the CPCP model.

Although the methods for medical education continue to evolve due to the development of medicines, the cadaver dissection course still plays a fundamental role. The cadaver dissection course allows students to learn to handle instruments correctly while actively exploring three-dimensional anatomy. However, dissection comes with the risk of accidental injury. In recent years, the number of classes offered for the cadaver dissection course has decreased while the amount of knowledge required in clinical medicine has increased. Simulation-based education (SBE) has been proven to be an effective educational method that enhances the development of practical skills by integrating learners' knowledge and skills. This study aimed to investigate the effect of SBE as a preparatory education course when taken prior to a medical student's enrollment in the cadaver dissection course. In the present study, an SBE assuming practical cadaver dissection course was performed in the Clinical Simulation Center. The frequency of injury rates per 1000 h of cadaver dissection course was significantly less in 2017 and 2018 compared to that in 2016. Two years after the implementation of the SBE, average student self-efficacy scores and written examination scores significantly increased, whereas self-contentment scores were relatively unchanged. The results showed that the implementation of SBE decreased the incidence of injuries and improved students' overall self-efficacy scores and increased acquisition of knowledge evident on written examination score. Therefore, SBE as a preparatory education course may effectively promote the combined development of dissection skills and anatomical knowledge in the subsequent fundamental cadaver dissection course.

BACKGROUND:The recurrent peroneal nerve (RPN) branches from the common peroneal nerve or the deep peroneal nerve and it innervates to the lower patellar region. It has recently been reported that damage to the RPN causes pain in the lower patellar region; therefore, this study examined the recurrent position and the innervation pattern of the RPN.METHODS:Cases of knee deformity or atrophy were excluded, and 50 legs (25 males and 25 females) of 34 cadavers (15 males and 19 females) were examined to assess the recurrent position and the innervation pattern of the RPN.RESULTS:The recurrent position of the RPN was 27.9 ± 3.6 mm from the tip of the fibula. The RPN innervated to the patellar tendon in five of the 50 legs (10%), to the infrapatellar fat pad in 13 legs (26%), and to both the patellar tendon and the infrapatellar fat pad in 20 legs (40%), and to neither the patellar tendon nor the infrapatellar fat pad in 12 legs (24%). No significant sex differences were observed in the recurrent position and the innervation pattern of the RPN.CONCLUSIONS:In all cases, the recurrent position of the RPN was almost fixed from the tip of the fibula. The RPN frequently innervated to the patellar tendon or the infrapatellar fat pad (76%) in both males and females. These findings would be useful in knee surgery to preserve the RPN or for the diagnosis of pain in the lower patellar region.

The sagittal band of the finger is an aponeurosis-like structure surrounding the metacarpophalangeal joint. Sagittal band rupture causes extensor tendon dislocation from the dorsal side of the metacarpophalangeal joint. The thumb has two extensor tendons: extensor pollicis longus and extensor pollicis brevis tendons. Multiple studies have reported variations of extensor pollicis brevis tendon insertion. However, it remains unclear how the thumb sagittal band envelopes the extensor pollicis longus and extensor pollicis brevis tendons. This study investigated the anatomical relationship between the sagittal band and the two extensor tendons of the thumb. One hundred hands (47 right, 53 left) from 54 cadavers were examined to assess the detailed structure of the thumb sagittal band and extensor pollicis longus and extensor pollicis brevis tendons. We found that the thumb sagittal band enveloped both the tendons either separately (type I) or collectively (type II). Thirty-four cases (34.0%) were type I and 66 cases (66.0%) were type II. The extensor pollicis longus and extensor pollicis brevis tendons enveloped in the type I thumb sagittal band were inserted on different sites, respectively, whereas those tendons enveloped in the type II thumb sagittal band were inserted on the same sites. This study demonstrated that differences in the type of thumb sagittal band are closely associated with variations in extensor pollicis brevis tendon insertion. We predicted that these differences contribute to the sliding distance between the extensor pollicis brevis and extensor pollicis longus tendons and affect the pathophysiology of extensor tendon dislocation.

Chronic subdural hematoma (CSDH) is an angiogenic disease that is involved with many inflammatory mediators. Tie2 is predominantly expressed in the embryonic endothelium and plays an important role in the maturation and stabilization of the vasculature. Angiopoietin (Ang)1 and Ang2 are well-known ligands of the Tie2 receptor. We examined the expression of Ang1 and Ang2 in CSDH fluid and the expression of Tie-2 receptor and components of the angiogenic signaling pathways in the outer membrane of CSDH. Twenty-five samples of CSDH fluid and eight samples of outer membrane of CSDH were included. The concentrations of Ang1 and Ang2 in the CSDH fluid were measured using enzyme-linked immunosorbent assay (ELISA) kits. The expression of Tie2, phosphoinositide 3-kinase (PI3K), protein kinase B (Akt) mechanistic target of rapamycin (mTOR), G beta L, 70 kDa ribosomal protein S6 kinase (p70S6K), eukaryotic initiation factor 4E (eIF-4E), and beta-actin was examined by a Western blot analysis. The expression of Tie2, Akt, and mTOR was also examined by immunohistochemistry. The concentration of Ang2 in CSDH fluid was significantly higher than that in the serum or cerebrospinal fluid (CSF), and also higher than that of Ang1 in CSDH fluid. Tie2, PI3K, Akt, mTOR, G beta L, p70S6K, and eIF-4E were detected in all cases. In addition, Tie2, Akt, and mTOR were localized in the endothelial cells of vessels in the CSDH outer membrane. Our data suggest that Ang2, although not Ang1, in CSDH fluid promotes angiogenesis in endothelial cells through the Tie2 receptor. The Ang2/Tie2 signaling pathway might therefore be a useful therapeutic target for treating the growth of intractable CSDH.

The mechanism of severe pain occurring because of physical disuse, such as complex regional pain syndrome Type I, has not been elucidated so far. Therefore, to investigate this mechanism, we have developed a model called a chronic post-cast pain (CPCP) model. Oxidative stress-related factors generated in a fixed limb may be triggers for nociceptive signals due to physical disuse. On the basis of the results of our previous studies, we speculated that oxidative stress-related factors in immobilized hind limbs may also be triggers of nociceptive signals due to physical disuse. In this study, we aimed to clarify whether an oxidative stress-related factor is involved in the induction of nociceptive signals. The time course of oxidative damage in the soleus (slow-twitch fiber) and gastrocnemius (fast-twitch fiber) muscles was evaluated by immunostaining of 8-hydroxy-2′-deoxyguanosine (a marker of oxidative damage in DNA). We also investigated the effects of tempol, a scavenger of superoxide, on oxidative damage in DNA, spontaneous pain-related behaviors (licking and/or biting and flinching), and the activation of spinal dorsal horn neurons (c-Fos). Systemic administration of tempol before cast removal attenuated oxidative damage to DNA in immobilized skeletal muscles, suppressed spontaneous pain-related behavior, and suppressed the activation of spinal dorsal horn neurons. We suggest that superoxide generated in immobilized skeletal muscles after cast removal is one of the peripheral factors that trigger nociceptive signals.

Purpose: To examine the positional relationship between the medial canthal tendon (MCT) and the common canalicular orifice (CCO) in cadavers. Methods: This experimental anatomical study was conducted using 75 orbits from 48 embalmed Japanese cadavers fixed in 10% buffered formalin (24 orbits from 17 males and 51 orbits from 31 females; 38 right and 37 left; mean age at time of death, 84.1 +/- 9.2 years). The vertical width of the MCT on the level of the medial orbital rim and the angle between the MCT and axial plane were measured. In addition, the vertical distance from the CCO to the lower edge of the MCT was measured. Positive values of the distance were indicated when the CCO was located below the lower edge of the MCT. Results: The vertical distance from the CCO to the lower edge of the MCT was -1.43 +/- 1.31 mm. Only 13 orbits (17.3%) showed the CCO located on the same level (2 orbits, 2.7%) or below the lower edge of the MCT (11 orbits, 14.7%), while the CCO was located above the lower edge of the MCT in 62 orbits (82.7%). In multiple regression analyses, both the MCT width and angle between the MCT and axial plane were not correlated with the distance (P> 0.050). Conclusions: As the CCO was mostly found to be located above the inferior margin of the MCT, the creation of the bony window up to the MCT's inferior margin is not sufficient in external dacryocystorhinostomy to completely expose the CCO. (C) 2019 Elsevier GmbH. All rights reserved.

Objectives This study aimed to clarify the positional relationship between the left brachiocephalic vein and its surrounding vessels and to analyse the association between this positional relationship and ageing. Method Chest contrast-enhanced computed tomography was performed for 100 adults. The contact number between left brachiocephalic vein and surrounding vessels (aorta, brachiocephalic artery, left common carotid artery and left subclavian artery) was determined. The correlations of ageing with the cross-sectional areas of left brachiocephalic vein crossing brachiocephalic artery and left common carotid artery and peripheral end of left brachiocephalic vein were analysed. Results LBV was in contact with aorta in 19, brachiocephalic artery in 97, left common carotid artery in 90 and left subclavian artery in 21 patients. There were significant negative correlations of ageing with the cross-sectional areas of left brachiocephalic vein crossing brachiocephalic artery and left common carotid artery and peripheral end of left brachiocephalic vein. Conclusions Brachiocephalic artery and left common carotid artery have easy contact with left brachiocephalic vein. There was a negative relationship between the cross-sectional area of left brachiocephalic vein and age.

Physical disuse could lead to a state of chronic pain typified by complex regional pain syndrome type I due to fear of pain through movement (kinesiophobia) or inappropriate resting procedures. However, the mechanisms by which physical disuse is associated with acute/chronic pain and other pathological signs remain unresolved. We have previously reported that inflammatory signs, contractures, disuse muscle atrophy, spontaneous pain-like behaviors, and chronic widespread mechanical hyperalgesia based on central plasticity occurred after 2 weeks of cast immobilization in chronic post-cast pain (CPCP) rat model. In this study, we also demonstrated dystrophy-like changes, both peripheral nociceptive signals and activation of the central pain pathway in CPCP rats. This was done by the following methods: (1) vascular permeability (Evans blue dye) and inflammatory- and oxidative stress-related messenger RNA changes (real-time quantitative polymerase chain reaction); (2) immunofluorescence of pERK and/or c-Fos expression in the spino-parabrachio-amygdaloid pathway; and (3) blockade of nociceptive-related signals using sciatic nerve block. Furthermore, we demonstrated tactile allodynia using an optogenetic method in a transgenic rat line (W-TChR2V4), cold allodynia using the acetone test, and activation of dorsal horn neurons in the chronic phase associated with chronic mechanical hyperalgesia using c-Fos immunofluorescence. In addition, we showed that nociceptive signals in the acute phase are involved in chronic pathological pain-like behaviors by studying the effects of sciatic nerve block. Thus, we conclude that physical disuse contributes to dystrophy-like changes, spontaneous pain-like behavior, and chronic widespread pathological pain-like behaviors in CPCP rats after 2 weeks of cast immobilization.

Abstract In this experimental anatomic study, the authors examined the number and distribution of muscle spindles in the levator palpebrae superioris (LPS) muscle of human adults. This study included 11 orbits from 11 cadavers (mean age at death, 81.9 years). The LPS muscles were harvested and equally divided into 5 sections using transverse incisions. Muscle spindles were counted in each section. Consequently, muscle spindles were identified in 4 (36.4%) of the 11 orbits studied. One to 4 muscle spindles were identified in each of these 4 orbits. All muscle spindles were found in the most proximal section (the muscle origin), and no muscle spindles were identified in the other sections. The results indicate that the LPS muscle is associated with a smaller number of muscle spindles as compared with the rest of the extraocular muscles. Since higher muscle spindle numbers are associated with finer motor movements, eyelid opening does not seem to require much precision, compared to ocular movement.