How I do it: angiography-assisted full endoscopic treatment of spinal dural arteriovenous fistula.

BACKGROUND: Spinal dural arteriovenous fistula (sDAVF) is a rare vascular malformation that leads to serious neurological symptoms. We treat a 52-year-old man with sDAVF in the thoracic segment exhibiting uncoordinated gait. METHOD: Thoracic MRI of the lesion indicated myelomalacia and dilated blood vessels, while DSA revealed the right T6 radicular artery as the feeding arteriole. A full endoscopic obliteration of the lesion was performed under angiography guidance in a hybrid operation room. CONCLUSION: The case underscores the importance of a multidisciplinary and individualized approach to successfully manage sDAVF using a fully endoscopic approach.

Comprehensive Thione-Derived Perylene Diimides and Their Bio-Conjugation for Simultaneous Imaging, Tracking, and Targeted Photodynamic Therapy.

In this study, the chromophore 3,4,9,10-perylenetetracarboxylic diimide (PDI) is anchored with phenyl substituents at the imide N site, followed by thionation, yielding a series of thione products 1S-PDI-D, 2S-cis-PDI-D, 2S-trans-PDI-D, 3S-PDI-D, and 4S-PDI-D, respectively, with n = 1, 2, 3, and 4 thione. The photophysical properties are dependent on the number of anchored thiones, where the observed prominent lower-lying absorption is assigned to the S0 → S2(ππ*) transition and is red-shifted upon increasing the number of thiones; the lowest-lying excited state is ascribed to a transition-forbidden S1(nπ*) configuration. All nS-PDIs are non-emissive in solution but reveal an excellent two-photon absorption cross-section of >800 GM. Supported by the femtosecond transient absorption study, the S1(nπ*) → T1(ππ*) intersystem crossing (ISC) rate is > 1012 s-1, resulting in ∼100% triplet population. The lowest-lying T1(ππ*) energy is calculated to be in the order of 1S-PDI-D > 2S-cis-PDI-D ∼ 2S-trans-PDI-D > 3S-PDI-D > 4S-PDI-D, where the T1 energy of 1S-PDI-D (1.10 eV) is higher than that (0.97 eV) of the 1O2 1Δg state. 1S-PDI-D is further modified by either conjugation with peptide FC131 on the two terminal sides, forming 1S-FC131, or linkage with peptide FC131 and cyanine5 dye on each terminal, yielding Cy5-1S-FC131. In vitro experiments show power of 1S-FC131 and Cy5-1S-FC131 in recognizing A549 cells out of other three lung normal cells and effective photodynamic therapy. In vivo, both molecular composites demonstrate outstanding antitumor ability in A549 xenografted tumor mice, where Cy5-1S-FC131 shows superiority of simultaneous fluorescence tracking and targeted photodynamic therapy.

Recognizing the Importance of Fast Nonisothermal Crystallization for High-Performance Two-Dimensional Dion-Jacobson Perovskite Solar Cells with High Fill Factors: A Comprehensive Mechanistic Study.

Two-dimensional (2D) Dion-Jacobson (DJ) perovskite solar cells (PSCs), despite their advantage in versatility of n-layer variation, are subject to poor photovoltaic efficiency, particularly in the fill factor (FF), compared to their three-dimensional counterparts. To enhance the performance of DJ PSCs, the process of growing crystals and hence the corresponding morphology of DJ perovskites are of prime importance. Herein, we report the fast nonisothermal (NIT) crystallization protocol that is previously unrecognized for 2D perovskites to significantly improve the morphology, orientation, and charge transport of the DJ perovskite films. Comprehensive mechanistic studies reveal that the NIT effect leads to the secondary crystallization stage, forming network-like channels that play a vital role in the FF's leap-forward improvement and hence the DJ PSC's performance. As a whole, the NIT crystallized PSCs demonstrate a high power conversion efficiency and an FF of up to 19.87 and 86.16%, respectively. This research thus provides new perspectives to achieve highly efficient DJ PSCs.

The neuroprotective effects of AMN082 on neuronal apoptosis in rats after traumatic brain injury.

BACKGROUND: The aim of this study was to investigate whether AMN082 exerts its neuroprotective effect by attenuating glutamate receptor-associated neuronal apoptosis and improving functional outcomes after traumatic brain injury (TBI). METHODS: Anesthetized male Sprague-Dawley rats were divided into the sham-operated, TBI + vehicle, and TBI + AMN082 groups. AMN082 (10 mg/kg) was intraperitoneally injected 0, 24, or 48 h after TBI. In the 120 min after TBI, heart rate, mean arterial pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) were continuously measured. Motor function, the infarct volume, neuronal nitrosative stress-associated apoptosis, and N-methyl-D-aspartate receptor 2A (NR2A) and NR2B expression in the pericontusional cortex were measured on the 3rd day after TBI. RESULTS: The results showed that the AMN082-treated group had a lower ICP and higher CPP after TBI. TBI-induced motor deficits, the increase in infarct volume, neuronal apoptosis, and 3-nitrotyrosine and inducible nitric oxide synthase expression in the pericontusional cortex were significantly improved by AMN082 therapy. Simultaneously, AMN082 increased NR2A and NR2B expression in neuronal cells. CONCLUSIONS: We concluded that intraperitoneal injection of AMN082 for 3 days may ameliorate TBI by attenuating glutamate receptor-associated nitrosative stress and neuronal apoptosis in the pericontusional cortex. We suggest that AMN082 administration in the acute stage may be a promising strategy for TBI.

Iatrogenic pseudoaneurysm of the superficial temporal artery following craniectomy from a scalp hook retractor penetrating injury: Case report and literature review.

BACKGROUND: Iatrogenic pseudoaneurysms in scalp vessels are an uncommon complication after cranial surgery. This paper reports a case of scalp pseudoaneurysm in the superficial temporal artery (STA) after forceful hook retraction in craniectomy and reviews the relevant literature. CASE DESCRIPTION: A 36-year-old man with history of hypertension and depression presented to the emergency department with head injury after using sedation medication. Brain computed tomography (CT) revealed a 2-cm-thick right parietal extradural hematoma (EDH) with parietal skull fracture, a bilateral lower frontotemporal contusional intracerebral hematoma, diffuse subarachnoid hemorrhage, and a right frontotemporoparietal subdural hematoma. To prevent EDH progression, frontotemporal emergency craniectomy to remove the EDH was performed. The next day, a firm, painful mass measuring 3 × 3.5 cm2 was discovered over the right frontal scalp. The mass was close to the site where the scalp hook retractor had been placed during surgery. Sonography revealed pulsatile blood flow with an arterial feeder inside the mass. CT angiography revealed a 1 × 1.2 × 0.7 cm3 pseudoaneurysm in the right frontal scalp from the frontal branch of the STA. We scheduled a resection of the pseudoaneurysm and combined cranioplasty on the 29th postoperative day. The pseudoaneurysm was resected en bloc. The patient was discharged with clear consciousness and intact muscle power. CONCLUSION: The complications of STA pseudoaneurysms caused by scalp hook retractors are rare and not yet well reported. Surgeons must avoid injuring the STA when using a scalp hook retractor.

Tuning Electron-Withdrawing Strength on Phenothiazine Derivatives: Achieving 100 % Photoluminescence Quantum Yield by NO2 Substitution.

The weak fluorescence (quantum yield <1 % in cyclohexane) of phenothiazine (PTZ) impedes its further application. In addition, the nitro group (NO2 ) is a well-known fluorescence quencher. Interestingly, we obtained a highly fluorescent chromophore by combining these two moieties, forming 3-nitrophenothiazine (PTZ-NO2 ). For comparison, a series of PTZ derivatives bearing electron-withdrawing groups (EWGs; CN and CHO) or electron-donating groups (EDGs; OMe) at the 3-position have been designed and synthesized. The phenothiazines bearing EWGs exhibited enhanced emission compared with the parent PTZ or EDG derivatives. Computational approaches unveiled that for PTZ and PTZ-OMe, the transitions are from HOMOs dominated by π orbitals to LUMOs of mixed sulfur nonbonding-π* orbitals, and hence are partially forbidden. In contrast, the EWGs lower the energy level of the lone-pair electrons on the sulfur atom, thereby suppressing the mixing of the nonbonding orbital with the π* orbital in the LUMO, such that the allowed ππ* transition becomes dominant. This work thus demonstrates a judicious chemical design to fine-tune the transition character in PTZ analogues, with PTZ-NO2 attaining 100 % emission quantum yields in nonpolar solvent.

Spontaneous Spinal Epidural Hematoma After Normal Spontaneous Delivery with Epidural Analgesia: Case Report and Literature Review.

BACKGROUND: Pregnancy is a known risk factor for spontaneous spinal epidural hematoma. During cesarean section or vaginal delivery, the unstable hemodynamic status that may occur owing to fluctuation of intra-abdominal pressure increases the possibility of spontaneous spinal epidural hematoma. During labor and the postpartum period, neurologic symptoms may be masked by labor pain or anesthesia block, which makes early diagnosis difficult, especially in the obstetric clinic without a neurologist or neurosurgeon. CASE DESCRIPTION: A 28-year-old woman who had a normal spontaneous delivery under epidural anesthesia developed bilateral lower limb flaccid paralysis and loss of sensation 12.5 hours after delivery. Magnetic resonance imaging showed a 5.2 × 0.9 × 2 cm spinal epidural hematoma with severe spinal cord stenosis at the T2-T5 level with no evidence of a vascular anomaly. After emergent evacuation of the spinal epidural hematoma, lower limb muscle power improved from 0/5 to 1/5, and sensation gradually returned to bilateral lower limbs 22 days postoperatively. Deep vein thrombosis developed at 35 days postoperatively, and an inferior vena cava filter was implanted with urokinase infusion for thrombolytic therapy. She was discharged on day 52 after admission, and lower limb muscle power returned to normal after 3 months. CONCLUSIONS: Clinicians should observe postpartum women for signs of myelopathy or back tenderness and closely monitor neurologic function until anesthesia has run its course. A prompt diagnosis can enable prompt intervention.

The Short-Term Effects of Isolated Traumatic Brain Injury on the Heart in Experimental Healthy Rats.

BACKGROUND: To date, cardiac dysfunction after traumatic brain injury (TBI) has not been consistent. In this study, we hypothesized that TBI may play a role in the development of new-onset cardiac dysfunction in healthy experimental rats. MATERIALS AND METHODS: Anesthetized healthy male Sprague-Dawley rats were divided into two groups: a sham-operated control group and a TBI group. The brain was injured with 2.4 atm percussion via a fluid percussion injury model. During the 120 min after TBI, we continuously measured brain parameters, including intracranial pressure (ICP) and cerebral perfusion pressure (CPP), and cardiac parameters, such as heart rate (HR), inter-ventricular septum dimension (IVSD), left ventricular internal dimension diastole (LVIDd), end-diastolic volume (EDV), ejection fraction (EF), fractional shortening (FS), and LV mass diastole (LVd mass) by cardiac echo. On days 1, 3, 7, and 14 after TBI, the brain damage volume was evaluated with triphenyltetrazolium chloride; the physiological parameters of the heart, including HR, IVSd, LVIDd, EDV, EF, FS, and LVd mass, were evaluated with cardiac echo; the morphology of cardiomyocytes was examined by hematoxylin and eosin (HE) and Masson trichrome staining; and the biomarkers of cardiac injury troponin I and B-type natriuretic peptide (BNP) were also examined. RESULTS: Compared to sham-operated controls, the TBI groups had higher ICP, lower CPP, and higher brain neuronal apoptosis and infarction contusion volume. The impact of TBI on heart function showed hyperdynamic response trends in IVSd, LVIDd, EDV, EF, FS, and LVd mass within 30 min after TBI; however, EF and FS exhibited eventual decreasing trends. Simultaneously, the values of the biomarkers troponin I and BNP were within normal limits, and HE and Mass trichrome staining revealed no significant differences between the sham-operated control group and the TBI group. CONCLUSIONS: Our results suggest that TBI due to 2.4 atm fluid percussion injury in healthy experimental rats may cause significant damage to the brain and affect the heart function as investigated by cardiac echo but not as investigated by HE and Masson trichrome stainings or troponin I and BNP evaluation.

Unveiling the structural features of nonnative trimers of human superoxide dismutase 1.

BACKGROUND: Human SOD1 contains a single tryptophan residue (W32) which has been identified as a site of oxidative modification and a potentiator of aggregation involving in familial amyotrophic lateral sclerosis (fALS). In situ substitution of a tryptophan analog, 2,6-diazatryptophan ((2,6-aza)Trp) with its unique water-catalyzed proton transfer property, into proteins exhibits extraordinary sensitivity in the detection of subtle water-associated structural changes with only a few micro-molar concentration of samples. METHODS: A combination of size-exclusion chromatography and water-catalyzed fluorescent emission was utilized to probe the structural features of metastable SOD1 nonnative trimers, the potential neurotoxic species in the fALS. RESULTS: The monomer of apo-A4V SOD1 exhibits variable conformations and the fastest trimeric formation rate compared to that of wild type and I113T. The trimeric A4V SOD1 exhibits the least water molecules surrounding the W32, while I113T and the wild type appear to have more water molecules in the proximity of W32. A small molecule stabilizer, 5-fluorouridine, effects the structural conformation of SOD1 nonnative trimers. CONCLUSIONS: Our studies unveil new insights into water-associated structural changes of SOD1 nonnative trimers and demonstrate that in situ incorporation of (2,6-aza)Trp is a sensitive and powerful tool for probing subtle changes of water environments during protein aggregation. GENERAL SIGNIFICANCE: The water-sensitive probe, (2,6-aza)Trp, demonstrates superior sensitivity for detecting modulation of water microsolvation, structural conformation during oligomer formation and 5FUrd binding to both wild type and mutant SOD1.

The Neuroprotective Effects of Simvastatin on High Cholesterol Following Traumatic Brain Injury in Rats.

BACKGROUND: High cholesterol has been correlated with a greater risk of cerebrovascular diseases. Whether pre-existing high cholesterol exacerbates traumatic brain injury (TBI), and whether treatment with the cholesterol-lowering agent simvastatin has neuroprotective effects, especially anti-neuroinflammatory effects, after TBI are not well investigated. METHODS: Five-week-old male Sprague-Dawley rats were fed a high-fat diet for 8 weeks to induce hypercholesterolemia. Anesthetized male Sprague-Dawley rats were divided into 5 groups, including the sham-operated control, TBI control, and TBI with simvastatin treatment (4 mg/kg, 10 mg/kg, or 20 mg/kg) groups. Simvastatin was intraperitoneally injected at 0, 24, and 48 hours after TBI. Motor function was measured using an inclined plane. Neuronal apoptosis (maker Neu-N, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling), tumor necrosis factor-α expression in microglia (marker OX42) and astrocytes (marker glial fibrillary acidic protein), and Tumor necrosis factor-alpha receptor (TNFR) 1 and TNFR2 expression in neurons in the ischemic cortex were investigated using an immunofluorescence assay. All of the parameters were measured on the third day after TBI. RESULTS: TBI significantly increased the serum levels of cholesterol. The TBI-induced motor deficit was significantly attenuated by 4, 10, and 20 mg/kg simvastatin therapy on the third day after TBI. TBI-induced neuronal TNFR1 activation and apoptosis, as well as tumor necrosis factor-α expression in astrocytes in the ischemic cortex, were significantly attenuated by simvastatin, particularly when 20 mg/kg was administered. Simultaneously, the serum cholesterol remained high despite simvastatin treatment. CONCLUSIONS: The neuroprotection effects of simvastatin on the pre-existing hypercholesterolemia during TBI in rats may be related to its anti-neuroinflammatory effects but not to its cholesterol-lowing effects.

Postobliteration Arteriovenous Malformation Mimicking Malignant Change 30 Years After X-Knife Treatment-Case Report and Review of Literature.

BACKGROUND: Arteriovenous malformations (AVMs) are potentially dangerous vascular anomalies of the brain that can cause seizures or intracranial hemorrhage in patients if left untreated. Because full excision of these lesions is not always possible in deep or eloquent areas of the brain, radiosurgical advances have gone a long way in the control and treatment of AVMs. Postradiosurgery AVMs are followed closely via outpatient clinics with serial imaging every few months to assess AVM obliteration. Post X-knife treatment AVMs still carry with them some risk of rebleeding and even a chance of malignant transformation. CASE DESCRIPTION: In this article, we report a case of a post X-knife-treated arteriovenous malformation with the appearance of malignant change on magnetic resonance imaging and thallium-201 on follow-up 30 years after treatment. Imaging with magnetic resonance angiography showed obliteration of the lesion but progressive change in size with new soft tissue components, which suggests radiation-related secondary malignancy. CONCLUSIONS: Surgery was arranged, and pathology results indicate no malignant change.