Posterior scleral reinforcement surgery effectively slows the rate of high myopic progression in children.

PURPOSE: To investigate the rate of axial length elongation and high myopia progression in operated eyes before and after posterior scleral reinforcement (PSR) surgery. METHODS: This was a retrospective study. Children with pathological myopia treated with PSR at Beijing Tongren Hospital between May 2013 and May 2020 were recruited into the PSR surgery group. Children matched for age and myopia were recruited into the control group. All children underwent comprehensive ophthalmologic examinations. The presurgical and postsurgical rates of axial length elongation and myopic (spherical equivalent) progression were calculated. RESULTS: A total of 35 PSR patients were included in the study. The mean age was 6.5±3.0 years (range 2 to 14 years). Mean follow-up was 544 days (range 216 to 1657 days). The rate of axial length elongation was significantly less after posterior scleral reinforcement surgery (0.505±0.048mm per year prior to surgery; 0.382±0.045mm per year after surgery, P<0.001). The rate of myopic progression decreased after posterior scleral reinforcement surgery (1.162±0.118 D per year prior to surgery; 0.153±0.437 D per year after surgery, P=0.0239). There was no statistically significant difference in axial length elongation or myopic progression between pre-inclusion and post-inclusion in the control group. Moreover, the children's best-corrected visual acuity was significantly improved after posterior scleral reinforcement surgery (P<0.001). CONCLUSION: Posterior scleral reinforcement surgery effectively decreased the rate of high myopic progression and axial length elongation in children.

Interconversion of Molybdenum or Tungsten d2 Styrene Complexes with d0 1-Phenethylidene Analogues.

Upon addition of 5-15% PhNMe2H+X- (X = B(3,5-(CF3)2C6H3)4 or B(C6F5)4) to Mo(NAr)(styrene)(OSiPh3)2 (Ar = N-2,6-i-Pr2C6H3) in C6D6 an equilibrium mixture of Mo(NAr)(styrene)(OSiPh3)2 and Mo(NAr)(CMePh)(OSiPh3)2 is formed over 36 h at 45 °C (Keq = 0.36). A plausible intermediate in the interconversion of the styrene and 1-phenethylidene complexes is the 1-phenethyl cation, [Mo(NAr)(CHMePh)(OSiPh3)2]+, which can be generated using [(Et2O)2H][B(C6F5)4] as the acid. The interconversion can be modeled as two equilibria involving protonation of Mo(NAr)(styrene)(OSiPh3)2 or Mo(NAr)(CMePh)(OSiPh3)2 and deprotonation of the α or ß phenethyl carbon atom in [Mo(NAr)(CHMePh)(OSiPh3)2]+. The ratio of the rate of deprotonation of [Mo(NAr)(CHMePh)(OSiPh3)2]+ by PhNMe2 in the α position versus the ß position is ∼10, or ∼30 per Hß. The slow step is protonation of Mo(NAr)(styrene)(OSiPh3)2 (k1 = 0.158(4) L/(mol·min)). Proton sources such as (CF3)3COH or Ph3SiOH do not catalyze the interconversion of Mo(NAr)(styrene)(OSiPh3)2 and Mo(NAr)(CMePh)(OSiPh3)2, while the reaction of Mo(NAr)(styrene)(OSiPh3)2 with pyridinium salts generates only a trace (∼2%) of Mo(NAr)(CMePh)(OSiPh3)2 and forms a monopyridine adduct, [Mo(NAr)(CHMePh)(OSiPh3)2(py)]+ (two diastereomers). The structure of [Mo(NAr)(CHMePh)(OSiPh3)2]+ has been confirmed in an X-ray study; there is no structural indication that a ß proton is activated through a CHß interaction with the metal. W(NAr)(CMePh)(OSiPh3)2 is also converted into a mixture of W(NAr)(CMePh)(OSiPh3)2 and W(NAr)(styrene)(OSiPh3)2 (Keq = 0.47 at 45 °C in favor of the styrene complex) with 10% [PhNMe2H][B(C6F5)4] as the catalyst; the time required to reach equilibrium is approximately the same as in the Mo system.

Platinum(II) Di-ω-alkenyl Complexes as "Slow-Release" Precatalysts for Heat-Triggered Olefin Hydrosilylation.

We describe the synthesis, characterization, and catalytic hydrosilylation activity of platinum(II) di-ω-alkenyl compounds of stoichiometry PtR2, where R = CH2SiMe2(vinyl) (1) or CH2SiMe2(allyl) (2), and their adducts with 1,5-cyclooctadiene (COD), dibenzo[a,e]cyclooctatetraene (DBCOT), and norbornadiene (NBD), which can be considered as slow-release sources of the reactive compounds 1 and 2. At loadings of 0.5 × 10-6-5 × 10-6 mol %, 1-COD is an active hydrosilylation catalyst that exhibits heat-triggered latency: no hydrosilylation activity occurs toward many olefin substrates even after several hours at 20 °C, but turnover numbers as high as 200000 are seen after 4 h at 50 °C, with excellent selectivity for formation of the anti-Markovnikov product. Activation of the PtII precatalyst occurs via three steps: slow dissociation of COD from 1-COD to form 1, rapid reaction of 1 with silane, and elimination of both ω-alkenyl ligands to form Pt0 species. The latent catalytic behavior, the high turnover number, and the high anti-Markovnikov selectivity are a result of the slow release of 1 from 1-COD at room temperature, so that the concentration of Pt0 during the initial stages of the catalysis is negligible. As a result, formation of colloidal Pt, which is known to cause side reactions, is minimized, and the amounts of side products are very small and comparable to those seen for platinum(0) carbene catalysts. The latent reaction kinetics and high turnover numbers seen for 1-COD after thermal triggering make this compound a potentially useful precatalyst for injection molding or solvent-free hydrosilylation applications.

Nature of the Short Rh-Li Contact between Lithium and the Rhodium ω-Alkenyl Complex [Rh(CH2CMe2CH2CH═CH2)2].

We describe the preparation of the cis-bis(η1,η2-2,2-dimethylpent-4-en-1-yl)rhodate(I) anion, cis-[Rh(CH2CMe2CH2CH═CH2)2]-, and the interaction of this species with Li+ both in solution and in the solid state. For the lithium(diethyl ether) salt [Li(Et2O)][Rh(CH2CMe2CH2CH═CH2)2], VT-NMR and 1H{7Li} NOE NMR studies in toluene-d8 show that the Li+ cation is in close proximity to the dz2 orbital of rhodium. In the solid-state structure of the lithium(12-crown-4) salt [Li(12-crown-4)2][Li{Rh(CH2CMe2CH2CH═CH2)2}2], one lithium atom is surrounded by two [Rh(CH2CMe2CH2CH═CH2)2]- anions, and in this assembly there are two unusually short Rh-Li distances of 2.48 Å. DFT calculations, natural energy decomposition, and ETS-NOCV analysis suggest that there is a weak dative interaction between the 4dz2 orbitals on the Rh centers and the 2pz orbital of the Li+ cation. The charge-transfer term between Rh and Li+ contributes only about the 1/5 of the total interaction energy, however, and the principal driving force for the proximity of Rh and Li in compounds 1 and 2 is that Li+ is electrostatically attracted to negative charges on the dialkylrhodiate anions.

Microscale vacuum distillation apparatus for high-boiling, air- and heat-sensitive liquids.

We describe a simple apparatus that enables the vacuum distillation of ~0.2 mL of air- and water-sensitive, high-boiling liquids. The apparatus should be useful in teaching laboratories, and also to practicing chemists.

The effect of increased intra-abdominal pressure on orbital subarachnoid space width and intraocular pressure.

In accordance with the trans-lamina cribrosa pressure difference theory, decreasing the trans-lamina cribrosa pressure difference can relieve glaucomatous optic neuropathy. Increased intracranial pressure can also reduce optic nerve damage in glaucoma patients, and a safe, effective and noninvasive way to achieve this is by increasing the intra-abdominal pressure. The purpose of this study was to observe the changes in orbital subarachnoid space width and intraocular pressure at elevated intra-abdominal pressure. An inflatable abdominal belt was tied to each of 15 healthy volunteers, aged 22-30 years (12 females and 3 males), at the navel level, without applying pressure to the abdomen, before they laid in the magnetic resonance imaging machine. The baseline orbital subarachnoid space width around the optic nerve was measured by magnetic resonance imaging at 1, 3, 9, and 15 mm behind the globe. The abdominal belt was inflated to increase the pressure to 40 mmHg (1 mmHg = 0.133 kPa), then the orbital subarachnoid space width was measured every 10 minutes for 2 hours. After removal of the pressure, the measurement was repeated 10 and 20 minutes later. In a separate trial, the intraocular pressure was measured for all the subjects at the same time points, before, during and after elevated intra-abdominal pressure. Results showed that the baseline mean orbital subarachnoid space width was 0.88 ± 0.1 mm (range: 0.77-1.05 mm), 0.77 ± 0.11 mm (range: 0.60-0.94 mm), 0.70 ± 0.08 mm (range: 0.62-0.80 mm), and 0.68 ± 0.08 mm (range: 0.57-0.77 mm) at 1, 3, 9, and 15 mm behind the globe, respectively. During the elevated intra-abdominal pressure, the orbital subarachnoid space width increased from the baseline and dilation of the optic nerve sheath was significant at 1, 3 and 9 mm behind the globe. After decompression of the abdominal pressure, the orbital subarachnoid space width normalized and returned to the baseline value. There was no significant difference in the intraocular pressure before, during and after the intra-abdominal pressure elevation. These results verified that the increased intra-abdominal pressure widens the orbital subarachnoid space in this acute trial, but does not alter the intraocular pressure, indicating that intraocular pressure is not affected by rapid increased intra-abdominal pressure. This study was registered in the Chinese Clinical Trial Registry (registration number: ChiCTR-ONRC-14004947).

Pressure balance and imbalance in the optic nerve chamber: The Beijing Intracranial and Intraocular Pressure (iCOP) Study.

To determine the interdependence of intracranial pressure (ICP) and intraocular pressure (IOP) and how it affects optic nerve pressures, eight normal dogs were examined using pressure-sensing probes implanted into the left ventricle, lumbar cistern, optic nerve subarachnoid space in the left eye, and anterior chamber in the left eye. This allowed ICP, lumbar cistern pressure (LCP), optic nerve subarachnoid space pressure (ONSP) and IOP to be simultaneously recorded. After establishing baseline pressure levels, pressure changes that resulted from lowering ICP (via shunting cerebrospinal fluid (CSF) from the ventricle) were recorded. At baseline, all examined pressures were different (ICP0.001). As ICP was lowered during CSF shunting, IOP also dropped in a parallel time course so that the trans-lamina cribrosa gradient (TLPG) remained stable (ICP-IOP dependent zone). However, once ICP fell below a critical breakpoint, ICP and IOP became uncoupled and TLPG changed as ICP declined (ICP-IOP independent zone). The optic nerve pressure gradient (ONPG) and trans-optic nerve pressure gradient (TOPG) increased linearly as ICP decreased through both the ICP-IOP dependent and independent zones. We conclude that ICP and IOP are coupled in a specific pressure range, but when ICP drops below a critical point, IOP and ICP become uncoupled and TLPG increases. When ICP drops, a rise in the ONPG and TOPG creates more pressure and reduces CSF flow around the optic nerve. This change may play a role in the development and progression of various ophthalmic and neurological diseases, including glaucoma.

Intracranial pressure (ICP) and optic nerve subarachnoid space pressure (ONSP) correlation in the optic nerve chamber: the Beijing Intracranial and Intraocular Pressure (iCOP) study.

PURPOSE: Because a lowered intracranial pressure (ICP) is a possible mechanism of optic neuropathy, we wished to study the CSF dynamics in the optic nerve chamber by recording possible changes in the optic nerve subarachnoid space pressure (ONSP) and the impact on it when acutely lowering ICP. METHODS: In eight normal dogs pressure probes were implanted in the left brain ventricle, lumbar cistern, optic nerve subarachnoid space and in the anterior eye chamber. Following CSF shunting from the brain ventricle we monitored changes of ICP, lumbar cistern pressure (LCP), ONSP and intraocular pressure (IOP). RESULTS: At baseline, the pressures were different with ICP>LCP>ONSP but correlated with each other (P<0.001). The "trans-lamina cribrosa pressure gradient" (TLPG) was highest for IOP-ONSP, lower for IOP-LCP, and lowest for IOP-ICP (P<0.001). During CSF shunting the ICP gradually decreased in a linear fashion together with the ONSP ("ICP-depended zone"). But when the ICP fell below a critical breakpoint, ICP and ONSP became uncoupled and ONSP remained constant despite further ICP decline ("ICP-independent zone"). CONCLUSIONS: Because the parallel decline of ICP and ONSP breaks down when ICP decreases below a critical breakpoint, we interpret this as a sign of CSF communication arrest between the intracranial and optic nerve SAS. This may be caused by obstructions of either CSF inflow through the optic canal or outflow into the intra-orbital cavity. This CSF exchange arrest may be a contributing factor to optic nerve damage and the optic nerve chamber syndrome which may influence the loss of vision or its restoration.

Morphological and ultrastructural examination of senescence in Morchella elata.

In recent years, the artificial cultivation of Morchella mushrooms that belong to Elata Clade, including Morchella elata, has been developed rapidly in China. However, the prominent problem of spawn aging has been frustrating the morel farming. In this paper, aging in M. elata was achieved from 12 to 17 subcultures and lifespan of 1536-2256 h by successive subculturing. The lifespan can be roughly divided into juvenile phase and senescent phase with respect to the mycelia linear growth rate. After a certain period of rapid growth with almost constant rate at the juvenile phase, the isolate entered the senescent phase characterized by slow down of mycelia growth, producing pigments ahead of time and final death of the apical hyphae. The period of the senescent phase was definitely 240-288 h; while that of the juvenile phase was diverse relying on different isolates. Moreover, microscopic study showed that angles between the leading and primary hyphae increased constantly with aging. In senesced hyphal cells of M. elata, the typical characteristics of autophagy (enlargement of vacuoles and existence of organelles sequestrated lysosomes) and apoptosis (condensation of the cytoplasm and nuclear and plasmolysis) were observed. In addition, in the final stage of senescence, the apical hyphae collapsed with the plasma membrane and all the cellular organelles disrupted, indicated a necrotic mode of cell death. Taken together, these data revealed the involvement of autophagy, apoptosis and necrosis in senescence of M. elata. The characterization and molecular mechanism of autophagy, apoptosis and necrosis need further study and the systematic study of morel aging will be beneficial for the healthy development of morel farming.

Optic neuropathy induced by experimentally reduced cerebrospinal fluid pressure in monkeys.

PURPOSE: To examine the influence of experimentally reduced cerebrospinal fluid pressure (CSFP) on retinal nerve fiber layer (RNFL) thickness and neuroretinal rim area of the optic nerve head. METHODS: This experimental study included nine monkeys that underwent implantation of a lumbar-peritoneal cerebrospinal fluid (CSF) shunt. In the study group (n = 4 monkeys), the shunt was opened to achieve a CSF of approximately 40 mm H2O, while the shunt remained closed in the control group (n = 5 monkeys). At baseline and in monthly intervals thereafter, optical coherence tomographic and photographic images of the optic nerve head and RNFL were taken of all monkeys. RESULTS: Two out of four monkeys in the study group showed bilaterally a progressive reduction in RNFL thickness between 12% and 30%, reduction in neuroretinal rim area and volume, and increase in cup-to-disc area ratios. A third monkey developed a splinter-like disc hemorrhage in one eye. The fourth monkey in the study group did not develop morphologic changes during follow-up, nor did any monkey in the control group. CONCLUSIONS: Experimental and chronic reduction in CSF in monkeys was associated with the development of an optic neuropathy in some monkeys.

Pharmacokinetic comparison of ketorolac after intracameral, intravitreal, and suprachoroidal administration in rabbits.

PURPOSE: To investigate the concentrations and pharmacokinetics of ketorolac in the rabbits by three different routes of administrations: a single intracameral, intravitreal, and suprachoroidal injection. METHODS: Fifty-four New Zealand white rabbits received ketorolac (250 µg/0.05 mL) in one eye by a single intracameral injection (group A, n = 18), single intravitreal injection (group B, n = 18), and single suprachoroidal injection (group C, n = 18). Drug concentrations in the vitreous, retina-choroid (RC), and plasma were determined by the methods of high-performance liquid chromatography at 0.5, 1, 2, 4, 8, and 24 hours after injection. The concentrations in the opposite eyes were also investigated. RESULTS: The mean maximum concentrations (Cmax) of ketorolac in the vitreous and RC were 0.378 ± 0.19 µg/mL and 3.15 ± 0.49 µg/g (at 0.5 hours), respectively, in group A; 156.2 ± 20.74 µg/mL (at 0.5 hours) and 208.0 ± 21.67 µg/g (at 1 hours), respectively, in group B; and 0.873 ± 0.34 µg/mL and 56.71 ± 22.64 µg/g (at 0.5 hours), respectively, in group C. In the RC, the area under the curve (AUC0-t) in group B (866.1 ± 52.67 µg/g·h) was higher (P < 0.01) than that in group C (77.10 ± 25.90 µg/g·h). The elimination half-life (t1/2) in group B (3.09 hours) was longer (P < 0.01) than that in group C (1.19 hours). In the control eyes, a drug level below 2 µg/g was detected in the RC in group C. Plasma concentrations were below 0.4 µg/mL in all 3 groups. Ketorolac was detectable in the RC till 24 hours after the intravitreal injection and 8 hours after the suprachoroidal injection. CONCLUSION: Intravitreal injection of ketorolac produced higher intraocular drug concentrations for a longer period compared with the other two routes. Suprachoroidal injection of ketorolac could reach an effective drug level in the RC with short half-lives and low drug levels in the vitreous. The plasma drug concentrations were low by all three routes.

Suprachoroidal injection of ketorolac tromethamine does not cause retinal damage.

Rabbit right eyes were injected with 3 or 6 mg ketorolac tromethamine into the suprachoroidal space. Electroretinography results demonstrated no abnormal changes in rod cell response, maximum rod cell or cone cell mixing reaction, oscillation potential, cone cell response, waveform, amplitude, and potential of 30 Hz scintillation response in right eyes before injection, and at 1, 2, and 4 weeks after injection. There was no difference between left (control) and right eyes. Under light microscopy, the histomorphology of cells in each retinal layer was normal at 4 weeks following 6 mg ketorolac tromethamine administration. These results indicate that a single suprachoroidal injection of 3 or 6 mg ketorolac tromethamine into rabbits was safe. Suprachoroidal space injection appears to be safe.