Analysis of internal astigmatism and higher order aberrations in eyes implanted with a new diffractive multifocal toric intraocular lens

Background

To evaluate the intraocular lens (IOL) position by analyzing the postoperative axis of internal astigmatism as well as the higher-order aberration (HOA) profile after cataract surgery following the implantation of a diffractive multifocal toric IOL

Methods

Prospective study including 51 eyes with corneal astigmatism of 1.25D or higher of 29 patients with ages ranging between 20 and 61 years old. All cases underwent uneventful cataract surgery with implantation of the AT LISA 909 M toric IOL (Zeiss). Visual, refractive and corneal topograpy changes were evaluated during a 12-month follow-up. In addition, the axis of internal astigmatism as well as ocular, corneal, and internal HOA (5-mm pupil) were evaluated postoperatively by means of an integrated aberrometer (OPD Scan II, Nidek).

Results

A significant improvement in uncorrected distance and near visual acuities (p?<?0.01) was found, which was consistent with a significant correction of manifest astigmatism (p?<?0.01). No significant changes were observed in corneal astigmatism (p?=?0.32). With regard to IOL alignment, the difference between the axes of postoperative internal and preoperative corneal astigmatisms was close to perpendicularity (12 months, 87.16°?±?7.14), without significant changes during the first 6 months (p?≥?0.46). Small but significant changes were detected afterwards (p?=?0.01). Additionally, this angular difference correlated with the postoperative magnitude of manifest cylinder (r?=?0.31, p?=?0.03). Minimal contribution of intraocular optics to the global magnitude of HOA was observed.

Conclusions

The diffractive multifocal toric IOL evaluated is able to provide a predictable astigmatic correction with apparent excellent levels of optical quality during the first year after implantation.     

Quantification of astrocyte volume changes during ischemia in situ reveals two populations of astrocytes in the cortex of GFAP/EGFP mice

Energy depletion during ischemia leads to disturbed ionic homeostasis and accumulation of neuroactive substances in the extracellular space, subsequently leading to volume changes in astrocytes. Confocal microscopy combined with 3D reconstruction was used to quantify ischemia-induced astrocyte volume changes in cortical slices of GFAP/EGFP transgenic mice. Twenty-minutes of oxygen-glucose deprivation (OGD) or oxygen-glucose deprivation combined with acidification (OGD(pH 6.8)) revealed the presence of two distinct astrocytic populations, the first showing a large volume increase (HR astrocytes) and the second displaying a small volume increase (LR astrocytes). In addition, changes in resting membrane potential (V(m)), measured by the patch-clamp technique, supported the existence of two astrocytic populations responding differently to ischemia. Although one group markedly depolarized during OGD or OGD(pH 6.8), only small changes in V(m) toward more negative values were observed in the second group. Conversely, acidification (ACF(pH 6.8)) led to a uniform volume decrease in all astrocytes, accompanied by only a small depolarization. Interestingly, two differently responding populations were not detected during acidification. Differences in the expression of inwardly rectifying potassium channels (Kir4.1), glial fibrillary acidic protein (GFAP), and taurine levels in cortical astrocytes were detected using immunohistochemical methods. We conclude that two distinct populations of astrocytes are present in the cortex of GFAP/EGFP mice, based on volume and V(m) changes during exposure to OGD or OGD(pH 6.8). Immunohistochemical analysis suggests that the diverse expression of Kir4.1 channels and GFAP as well as differences in the accumulation of taurine might contribute to the distinct ability of astrocytes to regulate their volume.     

Gastric pentadecapeptide BPC 157 as an effective therapy for muscle crush injury in the rat

PURPOSE: Stable gastric pentadecapeptide BPC 157 accelerates the healing of a transected Achilles tendon and a transected quadriceps muscle. It may also be of clinical relevance as a systemic and local peptide treatment for crush injury of a major muscle, such as gastrocnemius muscle complex. BPC 157 is effective without a carrier, and it is presently undergoing trials for inflammatory bowel disease, and no toxicity has so far been reported. METHODS: In crushed rats (force delivered 0.727 Ns/cm(2)), BPC 157 was applied either intraperitoneally or locally, as a thin cream layer, immediately after injury (sacrifice at 2 h), and once a day for 14 days. RESULTS: BPC 157 improved muscle healing, macroscopically (less hematoma and edema, no post-injury leg contracture), microscopically, functionally, and also based on enzyme activity (creatine kinase, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase). CONCLUSION: BPC 157, at all investigated intervals, given locally or intraperitoneally, accelerated post-injury muscle healing and also helped to restore the full function.     

Hyperbaric oxygenation alters temporal expression pattern of superoxide dismutase 2 after cortical stab injury in rats

Aim

To evaluate the effect of hyperbaric oxygen therapy (HBOT) on superoxide dismutase 2 (SOD2) expression pattern after the cortical stab injury (CSI).

Methods

CSI was performed on 88 male Wistar rats, divided into control, sham, lesioned, and HBO groups. HBOT protocol was the following: pressure applied was 2.5 absolute atmospheres, for 60 minutes, once a day for consecutive 3 or 10 days.‎ The pattern of SOD2 expression and cellular localization was analyzed using real-time polymerase chain reaction, Western blot, and double-label fluorescence immunohistochemistry. Neurons undergoing degeneration were visualized with Fluoro-Jade^®B.

Results

CSI induced significant transient increase in SOD2 protein levels at day 3 post injury, which was followed by a reduction toward control levels at post-injury day 10. At the same time points, mRNA levels for SOD2 in the injured cortex were down-regulated. Exposure to HBO for 3 days considerably down-regulated SOD2 protein levels in the injured cortex, while after 10 days of HBOT an up-regulation of SOD2 was observed. HBOT significantly increased mRNA levels for SOD2 at both time points compared to the corresponding L group, but they were still lower than in controls. Double immunofluorescence staining revealed that 3 days after CSI, up-regulation of SOD2 was mostly due to an increased expression in reactive astrocytes surrounding the lesion site. HBOT attenuated SOD2 expression both in neuronal and astroglial cells. Fluoro-Jade^®B labeling showed that HBOT significantly decreased the number of degenerating neurons in the injured cortex.

Conclusion

HBOT alters SOD2 protein and mRNA levels after brain injury in a time-dependent manner.Traumatic brain injury (TBI) is among the most disabling injuries and represents the major health problem worldwide (1). TBI involves primary and secondary injury. Primary injury is the result of immediate mechanical damage of neural pathways that occurs at the time of injury and triggers a cascade of events known as secondary injury, which causes further damage to the brain. Secondary injury evolves over time and may persist for months to years after TBI causing primarily unaffected neurons to degenerate. Therefore, it should be considered as a chronic disease process and main target for potential therapies (2,3).As a part of secondary post-injury cascade, oxidative stress, among the other events, is a prominent one (1). It has been demonstrated that reactive oxygen species (ROS), if exceed the capacity of the anti-oxidative defense, lead to oxidative stress and cellular damage after brain trauma (4-6). Additionally, it has been shown that depletion of antioxidant systems following trauma could adversely affect synaptic function and plasticity (7).The first line of defense against ROS is in the place where it all begins – mitochondria. Manganese superoxide dismutase (SOD2), located in the mitochondrial inner membrane and matrix, is a critical antioxidant enzyme that catalyzes the dismutation of superoxide radical to oxygen and hydrogen peroxide. In different brain pathologies, the induction of SOD2 varies and depends on the type of injury (8), and most data point out the neuroprotective role of SOD2 in brain injury (9,10). In addition, experiments with SOD2 deficient mice who suffered from early degeneration have shown how essential this enzyme was for normal brain functioning (11,12). It has also been found that SOD2 expression was directly correlated with the grade of brain tumors in humans (13).Despite the amount of work that has been done in order to better understand TBI, an adequate therapy is still lacking. In the past decade, hyperbaric oxygen therapy (HBOT) became one of the more frequently used medical tools and it appears to be a good therapeutic solution for a variety of conditions (14). Beneficial effects of HBOT as adjuvant therapy with surgery were also observed in the treatment of complex war injuries. Irrespectively of the type of surgical strategy applied, HBOT significantly reduced the frequency of wound complications and the time to wound stabilization (15). HBOT is a therapeutic approach where the patient is exposed to 100% oxygen at pressures higher than ambient (1 atmosphere absolute [1 ATA]). This leads to an increased blood oxygen level, which than can penetrate to ischemic areas more deeply than under normobaric conditions (16-18). In our recently published article (19), we have shown that HBOT can recover locomotor performances in rats after the brain injury. Although there is a large body evidence that HBOT is useful as a therapy for brain injury (18-23), there is also data indicating that the use of hyperbaric oxygen can have serious side effects (14,24-26). The main concern in HBOT is oxidative stress and/or oxygen toxicity that can affect multiple organs. ‎However, these unwelcome side-effects have often been dependent on treatment parameters – pressure and duration of the ‎treatment (25,27,28). The data on the exact mechanisms by which HBOT exerts its positive effects are deficient. Thus, in the present study we investigated the effect of HBOT on temporal expression pattern and cellular distribution of SOD2 after cortical stub injury (CSI).     

Impact of the BDNF Val66Met Polymorphism on Cognition: Implications for Behavioral Genetics

Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin growth factor family and is implicated as a modulator of neuronal survival and differentiation, synaptic plasticity, and higher order cognitive functions such as learning and memory. A common single-nucleotide polymorphism (SNP) has been identified in the human BDNF gene (BDNF Val66Met) that leads to decreased BDNF secretion and impairments in specific forms of learning in humans. To better understand the impact of this SNP on biological function, the authors generated a mouse model containing the BDNF Met allele, which they found to replicate the key phenotypes observed in humans and provided further insight into the functional impact of this SNP in vivo. They used a "bottom-up" approach to study the BDNF SNP, which provided external validation in biologically less complex, genetically uniform systems, which minimized the variability inherent in human studies. In this review, the authors discuss the impact of the BDNF SNP on learning and memory while providing arguments for the relevance of a vertically integrated approach to studying human genetic variants.