The ammonium-oxidizing microbial community was investigated in a granular sludge anaerobic ammonium-oxidizing (anammox) reactor that was operated for about 1 year with high anaerobic ammonium ...oxidation activity (up to 0.8 kg NH₄⁺-N m⁻³ day⁻¹). A Planctomycetales-specific 16S rRNA gene library was constructed to analyse the diversity of the anaerobic ammonium-oxidizing bacteria (AnAOB). Most of the specifically amplified sequences (15/16) were similar to each other (> 99%) but were distantly related to all of the previously recognized sequences (< 94%), with the exception of an unclassified anammox-related clone, KSU-1 (98%). An ammonia monooxygenase (amoA) gene library was also analysed to investigate the diversity of 'aerobic' ammonium-oxidizing bacteria (AAOB) from the β-Proteobacteria. Most of the amoA gene fragments (53/55) clustered in the Nitrosomonas europaea-Nitrosococcus mobilis group which has been reported to prevail under oxygen-limiting conditions. The quantitative results from real-time polymerase chain reaction (PCR) amplification showed that the dominant AnAOB comprised approximately 50% of the total bacterial 16S rRNA genes in the reactor, whereas the AAOB of β-Proteobacteria represented only about 3%. A large fragment (4008 bp) of the rRNA gene cluster of the dominant AnAOB (AS-1) in this reactor sludge was sequenced and compared with sequences of other Planctomycetales including four anammox-related candidate genera. The partial sequence of hydrazine-oxidizing enzyme (hzo) of dominant AnAOB was also identified using new designed primers. Based on this analysis, we propose to tentatively name this new AnAOB Candidatus'Jettenia asiatica'.
The magnetic resonance image study identified a 6 × 3.3-cm cystic lesion in the left CPA, causing mass effect on the pons and cerebellum, consistent with an AC (Figure 1). Spontaneous resolution of ...ACs in various locations has been reported in the literature. 3,4 Most reported cases occur in children and involved the supratentorial region. CONFLICT OF INTEREST STATEMENT The authors declare no conflicts of interest.
Magnetic resonance imaging (MRI) serves as a crucial diagnostic tool, aiding in the identification of NVC and exclusion of other alternative etiologies. Following the surgery, the patient experienced ...complete remission of symptoms, and no recurrence was observed during the 2-year follow-up period. CONFLICT OF INTEREST STATEMENT All authors declare no conflict of interest.
The
genus (Lauraceae) had been extensively utilized in folk medicine due to its broad range of bioactivities. In the present study, a series of chromatographic separations of the methanol extract of ...stems of
led to the identification of thirty eight compounds totally. Among these, biscinnamophilin (1), machilupins A-C (2-4), machilutone A (5), and machilusoxide A (6) were new compounds reported for the first time. In addition, 5 was characterized with a unprecedented carbon skeleton. Other known compounds, including the major compounds cinnamophilin (7) and
-dihydroguaiaretic acid (8), are identified by comparison of their physical and spectroscopic data with reported values. One of the reported compounds, cinnamophilin A (10), should be revised as dehydroguaiaretic acid (9) after careful comparison of all the
H and
C NMR data. Moreover, the neuroprotective activity of cinnamophilin (7) was examined in a primary cortical neuron culture and the results indicated that 7 was effective against glutamate induced excitotoxicity.
In posterior spine surgery, retractors exert pressure on paraspinal muscles, elevating intramuscular pressure and compromising blood flow, potentially causing muscle injury during ...ischemia–reperfusion. Ginkgo biloba extract (EGb 761), known for its antioxidant and free radical scavenging properties and its role in treating cerebrovascular diseases, is investigated for its protective effects against muscle ischemia–reperfusion injury in vitro and in vivo. Animals were randomly divided into the control group, receiving normal saline, and experimental groups, receiving varying doses of EGb761 (25/50/100/200 mg/kg). A 2‐h hind limb tourniquet‐induced ischemia was followed by reperfusion. Blood samples collected pre‐ischemia and 24 h post‐reperfusion, along with muscle tissue samples after 24 h, demonstrated that EGb761 at 1000 μg/mL effectively inhibited IL‐6 and TNF‐α secretion in RAW 264.7 cells without cytotoxicity. EGb761 significantly reduced nitric oxide (NO) and malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity, and increased glutathione (GSH) levels compared to the control after 24 h. Muscle tissue sections revealed more severe damage in the control group, indicating EGb761's potential in mitigating inflammatory responses and oxidative stress during ischemia–reperfusion injury, effectively protecting against muscle damage.
(1) Background: Inducing experimental stroke leads to biphasic immune responses, where the early activation of immune functions is followed by severe immunosuppression accompanied by spleen and ...thymus atrophy. Nicotinamide, a water-soluble B-group vitamin, is a known neuroprotectant against brain ischemia in animal models. We examined the effect of nicotinamide on the central and peripheral immune response in experimental stroke models. (2) Methods: Nicotinamide (500 mg/kg) or saline was intravenously administered to C57BL/6 mice during reperfusion after transiently occluding the middle cerebral artery or after LPS injection. On day 3, the animals were examined for behavioral performance and were then sacrificed to assess brain infarction, blood–brain barrier (BBB) integrity, and the composition of immune cells in the brain, thymus, spleen, and blood using flow cytometry. (3) Results: Nicotinamide reduced brain infarction and microglia/macrophage activation following MCAo (p < 0.05). Similarly, in LPS-injected mice, microglia/macrophage activation was decreased upon treatment with nicotinamide (p < 0.05), suggesting a direct inhibitory effect of nicotinamide on microglia/macrophage activation. Nicotinamide decreased the infiltration of neutrophils into the brain parenchyma and ameliorated Evans blue leakage (p < 0.05), suggesting that a decreased infiltration of neutrophils could, at least partially, be the result of a more integrated BBB structure following nicotinamide treatment. Our studies also revealed that administering nicotinamide led to retarded B-cell maturation in the spleen and subsequently decreased circulating B cells in the thymus and bloodstream (p < 0.05). (4) Conclusions: Cumulatively, nicotinamide decreased brain inflammation caused by ischemia–reperfusion injury, which was mediated by a direct anti-inflammatory effect of nicotinamide and an indirect protective effect on BBB integrity. Administering nicotinamide following brain ischemia resulted in a decrease in circulating B cells. This warrants attention with respect to future clinical applications.
Both Angelica sinensis (Oliv.) Diels (AS) and Ligusticum chuanxiong Hort. (LC) have been used to treat stroke in traditional Chinese medicine for centuries. Ferulic acid (FA), a component in both AS ...and LC, plays a role in neuroprotection. The purpose of this study was to investigate the effects of FA on cerebral infarct and the involvement of neuroprotective pathway. Rats underwent 2 hours and 24 hours of reperfusion after 90 min middle cerebral artery occlusion (MCAo). The cerebral infarct and neurological deficits were measured after 24 hours of reperfusion. Furthermore, the expression of superoxide radicals, intercellular adhesion molecule-1 (ICAM-1), myeloperoxidase (MPO), nuclear factor-kappaB (NF-kappaB) immunoreactive cells were assessed after 2 hours and 24 hours of reperfusion. Administration of 80 and 100 mg/kg of FA at the beginning of MCAo significantly reduced cerebral infarct and neurological deficit-score, similar results were obtained by 100 mg/kg of FA administered 30 min after MCAo. FA treatment (100 mg/kg i.v.) effectively suppressed superoxide radicals in the parenchyma lesion, and ICAM-1 immunoreactive vessels in the ischemic striatum after 2 hours of reperfusion. FA (100 mg/kg i.v.) reduced the expression of ICAM-1 and NF-kappaB in the ischemic cortex and striatum, also down-regulated MPO immunoreactive cells in the ischemic cortex after 24 hours of reperfusion. These results showed that the effect of FA on reducing cerebral infarct area and neurological deficit-score were at least partially attributed to the inhibition of superoxide radicals, ICAM-1 and NF-kappaB expression in transient MCAo rats.
Recent evidence shows that the NMDAR postsynaptic density‐95 (PSD‐95), growth‐associated protein‐43 (GAP‐43), and matrix metalloproteinase‐9 (MMP‐9) protein enhance neuroplasticity at the subacute ...stage of stroke. Here, we evaluated whether melatonin would modulate the PSD‐95, GAP‐43, and MMP‐9 proteins in cultured neurons exposed to glutamate excitotoxicity and in rats subjected to experimental stroke. Adult male Sprague–Dawley rats were treated with melatonin (5 mg/kg) or vehicle at reperfusion onset after transient occlusion of the right middle cerebral artery (tMCAO) for 90 min. Animals were euthanized for Western immunoblot analyses for the PSD‐95 and GAP‐43 proteins and gelatin zymography for the MMP‐9 activity at 7 days postinsult. Another set of animals was sacrificed for histologic and Golgi–Cox‐impregnated sections at 28 days postinsult. In cultured neurons exposed to glutamate excitotoxicity, melatonin significantly upregulated the GAP‐43 and PSD‐95 expressions and improved dendritic aborizations (P < 0.05, respectively). Relative to controls, melatonin‐treated stroke animals caused a significant improvement in GAP‐43 and PSD‐95 expressions as well as the MMP‐9 activity in the ischemic brain (P < 0.05). Consequently, melatonin also significantly promoted the dendritic spine density and reduced infarction in the ischemic brain, and improved neurobehaviors as well at 28 days postinsult (P < 0.05, respectively). Together, melatonin upregulates GAP‐43, PSD‐95, and MMP‐9 proteins, which likely accounts for its actions to improve neuroplasticity in cultured neurons exposed to glutamate excitotoxicity and to enhance long‐term neuroprotection, neuroplasticity, and brain remodeling in stroke rats.
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