Astaxanthin: Past, Present, and Future.

Astaxanthin (AX), a lipid-soluble pigment belonging to the xanthophyll carotenoids family, has recently garnered significant attention due to its unique physical properties, biochemical attributes, and physiological effects. Originally recognized primarily for its role in imparting the characteristic red-pink color to various organisms, AX is currently experiencing a surge in interest and research. The growing body of literature in this field predominantly focuses on AXs distinctive bioactivities and properties. However, the potential of algae-derived AX as a solution to various global environmental and societal challenges that threaten life on our planet has not received extensive attention. Furthermore, the historical context and the role of AX in nature, as well as its significance in diverse cultures and traditional health practices, have not been comprehensively explored in previous works. This review article embarks on a comprehensive journey through the history leading up to the present, offering insights into the discovery of AX, its chemical and physical attributes, distribution in organisms, and biosynthesis. Additionally, it delves into the intricate realm of health benefits, biofunctional characteristics, and the current market status of AX. By encompassing these multifaceted aspects, this review aims to provide readers with a more profound understanding and a robust foundation for future scientific endeavors directed at addressing societal needs for sustainable nutritional and medicinal solutions. An updated summary of AXs health benefits, its present market status, and potential future applications are also included for a well-rounded perspective.

Accuracy of a portable accelerometer-based navigation system for cup placement and intraoperative leg length measurement in total hip arthroplasty: a cross-sectional study.

BACKGROUND: Complications after total hip arthroplasty (THA) are frequently the consequence of malpositioned components or leg length discrepancy after surgery. Recently, a new version of a portable, accelerometer-based hip navigation system (New HipAlign) was made available with a change in the method of measuring cup abduction and the addition of a leg length measurement function. The purposes of this study were to investigate cup positioning and to examine the accuracy of leg length measurement with New HipAlign. METHODS: Cups were implanted and intraoperative leg length change was measured using New HipAlign in 60 THAs through a posterior approach in the lateral decubitus position. The cup position and radiographic leg length change were determined postoperatively on pelvic radiograph and computed tomography scans. We previously compared cup positioning with a previous version of a portable, accelerometer-based hip navigation system (Previous HipAlign) and conventional surgical techniques. Cup positioning in this study was compared with the results of out previous study using Previous HipAlign. RESULTS: The mean cup abduction of 40.3° ± 4.9° (range, 26° to 53°) and the mean cup anteversion of 15.8° ± 5.6° (range, 6.7° to 29.5°) were found. The deviation of the postoperative measured angles from the target cup position was 3.7° ± 3.3° for cup abduction and 5.9° ± 3.6° for cup anteversion. 56/60 of the cups were inside the Lewinnek safe zone. Compared with our previous study using Previous HipAlign, there were no significant differences with regard to cup abduction, cup anteversion, the deviation from the target cup position for cup abduction, the value of deviation for cup anteversion, and the number of cups inside the Lewinnek safe zone (P = 0.218, 0.334, 0.651, 0.797, 0.592). The mean difference between the intraoperative and radiographic leg length changes was + 0.8 ± 3.4 mm. There was significant correlation between the intraoperative and radiographic leg length changes (r = 0.804, P = 0.000). CONCLUSIONS: Use of New HipAlign allowed for accurate cup placement and reliable leg length measurement during THA. TRIAL REGISTRATION: Clinical trial is defined as 'any research study that prospectively assigns human participants or groups of humans to one or more health-related interventions to evaluate the effects on health outcome' by the World Health Organization (WHO). Because this study is not a clinical trial, trial registration is not needed.

A simple angle-measuring instrument for measuring cemented stem anteversion during total hip arthroplasty.

BACKGROUND: During total hip arthroplasty (THA), the accurate placement of the femoral components is an important determinant of the success of the procedure. This study assessed the accuracy of cemented stem placement using a new angle-measuring instrument. The primary objective was to investigate the accuracy of the intraoperative measurements of cemented stem anteversion obtained using the angle-measuring instrument. Our secondary objective was to evaluate the accuracy of stem positioning performed using the angle-measuring instrument. METHODS: We compared the intraoperative stem anteversion measurements obtained using the angle-measuring instrument with postoperative stem anteversion measurements obtained using computed tomography in 149 hips (measurement accuracy). We also compared the target angle and postoperative stem anteversion in 105 hips (implantation accuracy). RESULTS: The mean amount of intraoperative stem anteversion was 37.9° ± 10.1°, and the mean amount of postoperative stem anteversion was 37.0° ± 10.4°. The mean measurement accuracy was 0.9° ± 6.1°, and the absolute measurement accuracy was 4.9° ± 3.7°. The correlation coefficient for the relationship between the intraoperative and postoperative stem anteversion measurements was 0.824 (p = 0.000). The mean amount of target angle was 37.4° ± 7.6°, and the mean amount of postoperative stem anteversion was 35.9° ± 9.1°. The mean implantation accuracy was 1.4° ± 5.6°, and the mean absolute implantation accuracy was 4.3° ± 3.6°. The correlation coefficient for the relationship between the target angle and postoperative stem anteversion was 0.795 (p = 0.000). CONCLUSIONS: The angle-measuring instrument measured intraoperative stem anteversion accurately, and cemented stem was implanted accurately during THA with the angle-measuring instrument.

Portable Accelerometer-Based Navigation System for Cup Placement of Total Hip Arthroplasty: A Prospective, Randomized, Controlled Study.

BACKGROUND: Malposition of the acetabular component during total hip arthroplasty (THA) is associated with increased risk of dislocation, reduced range of motion, and accelerated wear. The purpose of this study is to compare cup positioning with a portable, accelerometer-based hip navigation system and conventional surgical technique. METHODS: In a prospective, randomized, clinical study, cups were implanted with a portable, accelerometer-based hip navigation system (navigation group; n = 55) or conventional technique (conventional group; n = 55). THA was conducted in the lateral position and through posterior approach. The cup position was determined postoperatively on pelvic radiograph and computed tomography scans. RESULTS: An average cup abduction of 39.2° ± 4.6° (range, 27° to 50°) and an average cup anteversion of 14.6° ± 6.1° (range, 1° to 27.5°) were found in the navigation group, and an average cup abduction of 42.9° ± 8.0° (range, 23° to 73°) and an average cup anteversion of 11.6° ± 7.7° (range, -12.1° to 25°) in the conventional group. A smaller variation in the navigation group was indicated for cup abduction (P = .001). The deviations from the target cup position were significantly lower in the navigation group (P = .001, .016). While only 37 of 55 cups in the conventional group were inside the Lewinnek safe zone, 51 of 55 cups in the navigation group were placed inside this safe zone (P = .006). The navigation procedure took a mean of 10 minutes longer than the conventional technique. CONCLUSION: Use of the portable, accelerometer-based hip navigation system can improve cup positioning in THA.

Erythropoietin, a putative neurotransmitter during hypoxia, is produced in RVLM neurons and activates them in neonatal Wistar rats.

Recent studies indicate that erythropoietin (EPO) is present in many areas of the brain and is active in the restoration of impaired neurons. In this study, we examined the presence of EPO and its role in bulbospinal neurons in the rostral ventrolateral medulla (RVLM). Hypoxia is often accompanied by a high blood pressure (BP). We hypothesized that EPO is produced in response to hypoxia in RVLM neurons and then activates them. To investigate whether RVLM neurons are sensitive to EPO, we examined the changes in the membrane potentials (MPs) of bulbospinal RVLM neurons using the whole cell patch-clamp technique during superfusion with EPO. A brainstem-spinal cord preparation was used for the experiments. EPO depolarized the RVLM neurons, and soluble erythropoietin receptor (SEPOR), an antagonist of EPO, hyperpolarized them. Furthermore, hypoxia-depolarized RVLM neurons were significantly hyperpolarized by SEPOR. In histological examinations, the EPO-depolarized RVLM neurons showed the presence of EPO receptor (EPOR). The RVLM neurons that possessed EPORs showed the presence of EPO and hypoxia-inducible factor (HIF)-2α. We also examined the levels of HIF-2α and EPO messenger RNA (mRNA) in the ventral sites of the medullas (containing RVLM areas) in response to hypoxia. The levels of HIF-2α and EPO mRNA in the hypoxia group were significantly greater than those in the control group. These results suggest that EPO is produced in response to hypoxia in RVLM neurons and causes a high BP via the stimulation of those neurons. EPO may be one of the neurotransmitters produced by RVLM neurons during hypoxia.

Hip stability after total hip arthroplasty predicted by intraoperative stability test and range of motion: a cross-sectional study.

BACKGROUND: Dislocation continues to be a common complication following total hip arthroplasty (THA). A larger intraoperative range of motion (ROM) is believed to minimize dislocation risk, and intraoperative stability tests have been used to assess the ROM. However, it is not clear whether or not intraoperative stability tests can predict hip stability after THA. It is also unclear which angles are required in intraoperative stability tests. We investigated the usefulness of intraoperative stability tests, and other risk factors to predict hip stability after THA. METHODS: Patients operated by single surgeon at one hospital from June 2009 to December 2013 were evaluated. This study included 185 hips with 32 mm metal femoral head. The range of internal rotation with 90° hip flexion (IR angle) was measured as an intraoperative stability test. The variables studied as risk factors included age, height, weight, gender, cerebral dysfunction, preoperative diagnosis, history of previous hip surgery, and IR angle. RESULTS: Mean IR angle was statistically different between patients with dislocation and patients without dislocation (59.5° vs 69.6°: p = 0.006). Cerebral dysfunction and a history of previous hip surgery were statistically related with prevalence of dislocation (p = 0.021, and p = 0.011). The receiver-operating characteristic curve analysis suggested that the cutoff points for IR angle were 51° and 67°. Dislocation rate in larger IR angle group was significantly lower than the rate in smaller IR angle group when patients were divided by 51° (p = 0.002). Logistic regression analyses showed that significant risk factors were cerebral dysfunction (OR: 5.3 (95%CI 1.1-25.9); p = 0.037), history of previous hip surgery (OR: 8.6 (95%CI 1.2-63.0); p = 0.035), and IR angle (OR: 10.4 (95%CI 1.9-57.1); p = 0.007). CONCLUSIONS: The results showed that intraoperative stability test, especially the IR angle, was a useful method to predict hip stability after THA, and a larger intraoperative ROM reduced the likelihood of dislocation. 51° and 67° were indicated as cutoff points for IR angle. Cerebral dysfunction and a history of previous hip surgery are also risk factors for the incidence of dislocation after THA. TRIAL REGISTRATION: This is a retrospective study, not a clinical trial defined by the World Health Organization (WHO).

Fibrinogen γ-Chain Peptide-Coated Adenosine 5' Diphosphate-Encapsulated Liposomes Rescue Mice From Lethal Blast Lung Injury via Adenosine Signaling.

OBJECTIVES: Fibrinogen γ-chain (dodecapeptide HHLGGAKQAGDV)-coated adenosine 5'-diphosphate-encapsulated liposomes can accumulate via dodecapeptide HHLGGAKQAGDV interactions at bleeding sites where they release adenosine 5'-diphosphate that is rapidly metabolized to adenosine, which has tissue-protective effects. We investigated the efficacy of fibrinogen γ-chain (dodecapeptide HHLGGAKQAGDV)-coated adenosine 5'-diphosphate-encapsulated liposomes to treat blast lung injury, with a focus on adenosine signaling. DESIGN: Controlled animal study. SETTING: University research laboratory. SUBJECTS: Adult male C57BL/6 mice. INTERVENTIONS: Mice were pretreated with fibrinogen γ-chain (dodecapeptide HHLGGAKQAGDV)-coated adenosine 5'-diphosphate-encapsulated liposomes, dodecapeptide HHLGGAKQAGDV-(phosphate-buffered saline)-liposomes, adenosine 5' diphosphateliposomes, or phosphate-buffered saline-liposomes. Five minutes after treatment the mice received a single laser-induced shock wave (1.8 J/cm) that caused lethal blast lung injury, and their survival times and lung injuries were then assessed. We also evaluated the therapeutic effect of posttreatment with fibrinogen γ-chain (dodecapeptide HHLGGAKQAGDV)-coated adenosine 5'-diphosphate-encapsulated liposomes or H12-(phosphate-buffered saline)-liposomes 1 minute after laser-induced shock wave exposure. To examine the effect of adenosine signaling, adenosine A2A receptor (ZM241385) or adenosine A2B receptor (PSB 1115) antagonists were administered to the mice 1 hour before the pretreatment with fibrinogen γ-chain (dodecapeptide HHLGGAKQAGDV)-coated adenosine 5'-diphosphate-encapsulated liposomes that was followed by laser-induced shock wave exposure. MEASUREMENTS AND MAIN RESULTS: Pre- and posttreatment with fibrinogen γ-chain (dodecapeptide HHLGGAKQAGDV)-coated adenosine 5'-diphosphate-encapsulated liposomes significantly increased mouse survival [fibrinogen γ-chain (dodecapeptide HHLGGAKQAGDV)-coated adenosine 5'-diphosphate-encapsulated liposomes: 58% survival vs H12-(phosphate-buffered saline)-liposomes: 8%; p < 0.05 (posttreatment)] and mitigated pulmonary tissue damage/hemorrhage and neutrophil accumulation after laser-induced shock wave exposure. fibrinogen γ-chain (dodecapeptide HHLGGAKQAGDV)-coated adenosine 5'-diphosphate-encapsulated liposomes accumulated at pulmonary vessel injury sites after laser-induced shock wave exposure with both pre- and posttreatment. Furthermore, pretreatment with fibrinogen γ-chain (dodecapeptide HHLGGAKQAGDV)-coated adenosine 5'-diphosphate-encapsulated liposomes reduced albumin and macrophage inflammatory protein-2 levels in bronchoalveolar lavage fluid. Although fibrinogen γ-chain (dodecapeptide HHLGGAKQAGDV)-coated adenosine 5'-diphosphate-encapsulated liposomes pretreatment did not affect blood coagulation activity in the injured mice, its beneficial effect on blast lung injury was significantly abrogated by A2A or A2B adenosine receptor antagonists (A2A antagonist: 17% survival; A2B antagonist: 33% vs dimethyl sulfoxide control: 80%; p < 0.05, respectively). CONCLUSIONS: Fibrinogen γ-chain (dodecapeptide HHLGGAKQA GDV)-coated adenosine 5'-diphosphate-encapsulated liposomes may be effective against blast lung injury by promoting tissue-protective adenosine signaling and could represent a novel controlled-release drug delivery system.

Optical Coherence Tomography Angiography in a Patient with Optic Atrophy After Non-arteritic Anterior Ischaemic Optic Neuropathy.

A 75-year-old female noticed a lower visual field (VF) defect in the right eye. A diagnosis of non-arteritic anterior ischaemic optic neuropathy (NAION) was made. The lower VF defect in the right eye did not change after onset. Optical coherence tomography (OCT) angiograms on the disc and the macula showed decreased retinal perfusion in the upper retina of the right eye. Retinal nerve fibre layer loss and ganglion cell complex loss in the upper retina were also seen in the right eye. OCT angiography could non-invasively detect the decrease of the retinal perfusion due to NAION.

Treatment with fibrinogen γ-chain peptide-coated, adenosine 5'-diphosphate-encapsulated liposomes as an infusible hemostatic agent against active liver bleeding in rabbits with acute thrombocytopenia.

BACKGROUND: We evaluated the hemostatic efficacy of H12-(adenosine 5'-diphosphate [ADP])-liposomes in the setting of active liver bleeding in rabbits with dilutional thrombocytopenia after massive transfusion. STUDY DESIGN AND METHODS: Acute thrombocytopenia (platelet [PLT] count < 50 × 10(9) /L) was induced in rabbits by repeated blood withdrawal and isovolemic transfusion of autologous washed red blood cells. Liver hemorrhage was initiated by a penetrating liver injury. Subsequently, the animals received tamponade treatment for the liver hemorrhage for 5 minutes and were intravenously administered H12-(ADP)-liposomes with PLT-poor plasma (PPP), PLT-rich plasma (PRP), PPP alone, H12-(phosphate-buffered saline [PBS])-liposome/PPP, or H12-(ADP)-liposomes/PPP plus fibrinogen concentrate during the tamponade. RESULTS: Administration of H12-(ADP)-liposomes/PPP rescued 60% of the rabbits from the liver hemorrhage; PRP administration rescued 50%. In contrast, rabbits receiving PPP or H12-(PBS)-liposome/PPP achieved only 10 or 17% survival, respectively, for the first 24 hours. H12-(ADP)-liposomes/PPP as well as PRP consistently reduced bleeding volumes and shortened clotting times (CTs) in comparison to PPP administration. Specifically, bleeding volumes in the initial 5 minutes averaged 11 mL (H12-(ADP)-liposomes/PPP) and 17 mL (PRP) versus 30 mL (PPP; p < 0.05); CTs averaged 270 and 306 seconds versus 401 seconds (p < 0.05). H12-(ADP)-liposomes were observed at the bleeding site with thrombus formation, suggesting an induction of thrombi. Neither macro- nor microthrombi were detected in the lung, kidney, spleen, or liver in rabbits treated with H12-(ADP)-liposomes. Supplementation of fibrinogen to H12-(ADP)-liposomes/PPP did not significantly improve rabbit survival. CONCLUSIONS: H12-(ADP)-liposomes might be a safe and effective therapeutic tool during damage control surgery for trauma patients with acute thrombocytopenia and massive bleeding.

Long-Term Outcomes of Three Cases That Underwent a Muscle Transposition Procedure Without Tenotomy Caused by Abducens Palsy.

Few reports have discussed long-term outcomes of muscle transposition procedures. In this study, cases with abducens palsy treated with a muscle transposition procedure were followed for 12, 25, or 26 years. The preoperative alignments were esotropia of 65 degrees, 47 prism dioptres (PD), and 24 PD, respectively. Orthophoria was postoperatively achieved in all cases. The postoperative alignment in one case deteriorated at 8 years postoperatively, although orthophoria were maintained in the other two cases. These findings indicate that it is possible that esotropia can recur even though orthophoria was maintained for several years postoperatively in some cases that underwent a muscle transposition procedure.

Successful Repair of a Traumatic Medial Rectus Laceration with the Aid of Computed Tomography.

A 79-year-old woman suffered ocular trauma from an umbrella. Exotropia of the left eye was observed, and the left eye could not adduct to the midline. Both edges of the lacerated medial rectus were sutured together with the aid of preoperative computed tomography (CT), which showed posterior muscle belly widening due to posterior slippage toward the equator. The alignment and ocular movement were improved postoperatively. Repairing a lacerated medial rectus is difficult because its edge slips into the muscle cone posteriorly. Preoperative CT was useful in identifying the posterior portion of the lacerated muscle, enabling successful repair.

Early weight-bearing after periacetabular osteotomy leads to a high incidence of postoperative pelvic fractures.

BACKGROUND: It has not been shown whether accelerated rehabilitation following periacetabular osteotomy (PAO) is effective for early recovery. The purpose of this retrospective study was to compare complication rates in patients with standard and accelerated rehabilitation protocols who underwent PAO. METHODS: Between January 2002 and August 2011, patients with a lateral center-edge (CE) angle of < 20°, showing good joint congruency with the hip in abduction, pre- or early stage of osteoarthritis, and age younger than 60 years were included in this study. We evaluated 156 hips in 138 patients, with a mean age at the time of surgery of 30 years. Full weight-bearing with two crutches started 2 months postoperatively in 73 patients (80 hips) with the standard rehabilitation protocol. In 65 patients (76 hips) with the accelerated rehabilitation protocol, postoperative strengthening of the hip, thigh and core musculature was begun on the day of surgery as tolerated. The exercise program included active hip range of motion, and gentle isometric hamstring and quadriceps muscle sets; these exercises were performed for 30 minutes in the morning and 30 minutes in the afternoon with a physical therapist every weekday for 6 weeks. Full weight-bearing with two axillary crutches started on the day of surgery as tolerated. Complications were evaluated for 2 years. RESULTS: The clinical results at the time of follow-up were similar in the two groups. The average periods between the osteotomy and full-weight-bearing walking without support were 4.2 months and 6.9 months in patients with the accelerated and standard rehabilitation protocols (P < 0.001), indicating that the accelerated rehabilitation protocol could achieve earlier recovery of patients. However, postoperative fractures of the ischial ramus and posterior column of the pelvis were more frequently found in patients with the accelerated rehabilitation protocol (8/76) than in those with the standard rehabilitation protocol (1/80) (P = 0.013). CONCLUSION: The accelerated rehabilitation protocol seems to have advantages for early muscle recovery in patients undergoing PAO; however, postoperative pelvic fracture rates were unacceptably high in patients with this protocol.

High blood pressure enhances brain stem neuronal nitric oxide synthase activity in Dahl salt-sensitive rats.

The aims of the present study were to determine the mechanism underlying enhanced neuronal nitric oxide synthase (nNOS) activity in the brain of hypertensive Dahl salt-sensitive (DSS) rats and the consequences of enhanced nNOS activity. Male DSS rats were fed either a regular (0.4% NaCl) or high-salt (8% NaCl) diet, with or without 0.25% nifedipine, for 4 weeks. The effects of nifedipine, which lowers blood pressure peripherally, on central nNOS were determined by measuring nNOS activity, as well as the number of nNOS-positive neurons in the brain stem and diencephalon. The effects of chronic (12 days) infusion of 7 µg (0.5 µL/h, i.c.v.) S-methyl-L-thiocitrulline (SMTC; a stereoselective competitive nNOS inhibitor) on mean arterial pressure were assessed in conscious DSS rats using a radiotelemetry system. In addition, the number of central nNOS-positive neurons was compared between DSS and salt-insensitive Sprague-Dawley rats. Normalization of blood pressure by nifedipine attenuated the increase in nNOS activity in the brain stem of DSS rats. Chronic i.c.v. infusion of SMTC further enhanced hypertension in DSS rats. Feeding of a high-salt diet increased nNOS-positive neurons in the lateral parabrachial nucleus, rostral ventrolateral medulla and nucleus tractus solitarius of DSS compared with Sprague-Dawley rats, whereas nNOS-positive neurons in the paraventricular nucleus remained downregulated in DSS rats. The results of the present study suggest that hypertension, rather than a high-salt diet, increases central nNOS activity in hypertensive DSS rats to buffer high blood pressure. However, this compensatory response may be insufficient to relieve salt-induced hypertension.

Mismatch between peripheral and central demands in salt-sensitive hypertensive Dahl rats.

Sympathetic nerve activity in essential hypertension, which accounts for 90% of all hypertension cases, is in general thought to be elevated regardless of whether there is salt sensitivity or insensitivity. The cause is thought to be an abnormality in the sympathetic center. On the other hand, neuronal nitric oxide synthase-expressing neurons that function to inhibit the sympathetic center are clearly activated in the salt-sensitive hypertensive Dahl rat model. How is this related to sympathetic hyperactivity and hypertension? Also, how is hypertension associated with peripheral vessel contractility and renal function? Human life is supported by the body's various essential functions. The circulatory system links all these functions into one system that cannot be separated. Blood pressure is the driving force of this circulatory system, and both the central and peripheral demands determine the output. We examined the 'mismatch' between these two sides and its association with hypertension.

In Vitro Evaluation of Skin-Related Physicochemical Properties and Biological Activities of Astaxanthin Isomers.

Dietary astaxanthin exists predominantly as the all-E-isomer; however, certain amounts of the Z-isomers are universally present in the skin, whose roles remain largely unknown. The aim of this study was to investigate the effects of the astaxanthin E/Z-isomer ratio on skin-related physicochemical properties and biological activities using human dermal fibroblasts and B16 mouse melanoma cells. We revealed that astaxanthin enriched in Z-isomers (total Z-isomer ratio = 86.6%) exhibited greater UV-light-shielding ability and skin antiaging and skin-whitening activities, such as anti-elastase and anti-melanin formation activities, than the all-E-isomer-rich astaxanthin (total Z-isomer ratio = 3.3%). On the other hand, the all-E-isomer was superior to the Z-isomers in singlet oxygen scavenging/quenching activity, and the Z-isomers inhibited type I collagen release into the culture medium in a dose-dependent manner. Our findings help clarify the roles of astaxanthin Z-isomers in the skin and would help in the development of novel skin health-promoting food ingredients.

Trigeminal interpolaris/caudalis transition neurons mediate reflex lacrimation evoked by bright light in the rat.

Abnormal sensitivity to bright light can cause discomfort or pain and evoke protective reflexes such as lacrimation. Although the trigeminal nerve is probably involved, the mechanism linking luminance to somatic sensory nerve activity remains uncertain. This study determined the effect of bright light on second-order ocular neurons at the ventral trigeminal interpolaris/caudalis transition (Vi/Vc) region, a major termination zone for trigeminal sensory fibers that innervate the eye. Most Vi/Vc neurons (80.9%) identified by responses to mechanical stimulation of the ocular surface also encoded bright light intensity. Light-evoked neural activity displayed a long latency to activation (> 10 s) and required transmission through the trigeminal root ganglion. Light-evoked neural activity was inhibited by intravitreal injection of phenylephrine or l-N(G) -nitro-arginine methyl ester (L-NAME), suggesting a mechanism coupled to vascular events within the eye. Laser Doppler flowmetry revealed rapid light-evoked increases in ocular blood flow that occurred prior to the increase in Vi/Vc neural activity. Synaptic blockade of the Vi/Vc region by cobalt chloride prevented light-evoked increases in tear volume, whereas blockade at the more caudal spinomedullary junction (Vc/C1) had no effect. In summary, Vi/Vc neurons encoded bright light intensity and were inhibited by drugs that alter blood flow to the eye. These results support the hypothesis that light-responsive neurons at the Vi/Vc transition region are critical for ocular-specific functions such as reflex lacrimation, whereas neurons at the caudal Vc/C1 junction region probably serve other aspects of ocular nociception.

Depletion of CD206+ M2-like macrophages induces fibro-adipogenic progenitors activation and muscle regeneration.

Muscle regeneration requires the coordination of muscle stem cells, mesenchymal fibro-adipogenic progenitors (FAPs), and macrophages. How macrophages regulate the paracrine secretion of FAPs during the recovery process remains elusive. Herein, we systemically investigated the communication between CD206+ M2-like macrophages and FAPs during the recovery process using a transgenic mouse model. Depletion of CD206+ M2-like macrophages or deletion of CD206+ M2-like macrophages-specific TGF-ß1 gene induces myogenesis and muscle regeneration. We show that depletion of CD206+ M2-like macrophages activates FAPs and activated FAPs secrete follistatin, a promyogenic factor, thereby boosting the recovery process. Conversely, deletion of the FAP-specific follistatin gene results in impaired muscle stem cell function, enhanced fibrosis, and delayed muscle regeneration. Mechanistically, CD206+ M2-like macrophages inhibit the secretion of FAP-derived follistatin via TGF-ß signaling. Here we show that CD206+ M2-like macrophages constitute a microenvironment for FAPs and may regulate the myogenic potential of muscle stem/satellite cells.

Teeth clenching and positive acceleration-induced cerebral arterial hypotension in rats.

INTRODUCTION: High positive acceleration (+Gz) stress is known to cause cerebral hypoperfusion, resulting in brain insults. Muscular contraction is reported to induce a pressor response. The effects of teeth clenching on cerebral hypoperfusion were examined. METHODS: The masseter muscle of anesthetized Sprague-Dawley rats was electrically stimulated to cause maximum clenching of the teeth. Arterial pressure at the level of the brain (APBr), heart rate, and central venous pressure were measured when rats were exposed to +1.5 Gz by using a centrifuge without an anti-C system. RESULTS: Acceleration of +1.5 Gz decreased APBr by 18.3 +/- 2.0 mmHg, which was reduced to 1.9 +/- 2.0 mmHg by masseter muscle contraction, but was not reduced by femoral muscle contraction. Stimulation of the masseter muscle but not the femoral muscle induced a pressor response of 11.8 +/- 2.1 mmHg, which was eliminated by dantrolene, a postsynaptic skeletal muscle relaxant. When masseter contraction was blocked by dantrolene, masseter stimulation did not reduce cerebral hypotension in the presence of +1.5-Gz acceleration (delta 18.9 +/- 2.6 mmHg). CONCLUSION: Our results suggest that teeth clenching induced a pressor response that prevented +Gz-induced cerebral hypotension, which suggests the possible development of a new anti-G method.

Severe hypotension during the decreasing phase of Gz stress in anesthetized rats wearing an anti-G suit.

INTRODUCTION: Physiological responses to +Gz stress have been reported in several studies. However, no reports exist on differences in arterial pressure responses between increasing and decreasing G phases. We hypothesized that +Gz stress and/or an anti-G support might disturb the circulation system and cause potential brain hypoperfusion, even if the anti-G support protects against G-induced loss of consciousness. METHODS: Dependency of +Gz magnitude, hemodynamic changes, renal sympathetic nerve activity (RSNA), and aortic blood flow (AoBF) were estimated in anesthetized rats to analyze the effects of +Gz stress and/or an anti-G support on arterial pressure at a level of the brain (APLB). The rats were exposed to +Gz using a centrifuge for small animals while wearing an anti-G suit. RESULTS: APLB remained at the control level while the anti-G suit was inflated. However, a decrease in APLB was observed twice during increasing and decreasing G phases using the anti-G suit. Hypotension in the decreasing C phase at +5 Gz was significantly deeper than that in the increasing G phase (47.5 +/- 7.7 vs. 29.6 +/- 3.0 mmHg). RSNA responses to Gz loads were greater in the decreasing G than in the increasing G phase (129.7 +/- 8.6 vs. 147.3 +/- 10.4%). Both AoBF and calculated vascular resistance were suppressed more significantly in the decreasing G than in the increasing G phase (38.3 +/- 4.4 vs. 34.4 +/- 3.4 ml x min(-1), 1.44 +/- 0.22 vs. 1.09 +/- 0.14 mmHg x min(-1) x ml(-1)). DISCUSSION: We conclude that transient excessive decreasing G hypotension may occur during the decreasing G phase, which may be due to anti-G suit functioning.

Astaxanthin as a Novel Mitochondrial Regulator: A New Aspect of Carotenoids, beyond Antioxidants.

Astaxanthin is a member of the carotenoid family that is found abundantly in marine organisms, and has been gaining attention in recent years due to its varied biological/physiological activities. It has been reported that astaxanthin functions both as a pigment, and as an antioxidant with superior free radical quenching capacity. We recently reported that astaxanthin modulated mitochondrial functions by a novel mechanism independent of its antioxidant function. In this paper, we review astaxanthin's well-known antioxidant activity, and expand on astaxanthin's lesser-known molecular targets, and its role in mitochondrial energy metabolism.