Fiber orientation and crimp level might control the auxetic effect of biological tissues.

We propose an analytical micromechanical model for studying the lamellar-composite-like structure of fibrous soft tissue. The tissue under consideration is made up of several lamellae, and is designed to resemble the annulus fibrosus (AF) tissue or media layer of arterial tissue, for example. The collagen fibers are arranged in parallel in each lamella and the fiber orientation differs from one lamella to its neighbors. The parallel fibers in each lamella of AF tissue, for example, have been observed to have a crimped microstructure. The proposed model incorporates this quality, considering fiber waviness as a sinusoidal shape and taking into account the fiber dispersion in different layers, where both fiber and matrix are considered as solid phases. We find that collagen-fiber waviness and layer orientation have a significant influence on Poisson's ratio. The effective Poisson's ratio predicted by the proposed model demonstrates that the crimped collagen fiber microstructure might weaken the auxetic effect of fibrous soft tissue, which might explain why, as the literature suggests, the auxetic behavior is more difficult to observe than large Poisson's ratios. As opposed to the many studies that use the well-known hyperelastic fiber-based constitutive model, in which out-of-plane expansion is often observed, the present work explains the auxetic response found in modeling and in experimental data from the perspective of collagen fiber microstructure.

Phyllosticta rizhaoensis sp. nov. causing leaf blight of Ophiopogon japonicus in China.

Ophiopogon japonicus (Asparagaceae) is a perennial grass species which can be cultivated as an ornamental and medicinal plant. From April 2021 to September 2022, a serious leaf blight disease of O. japonicus was discovered in Rizhao City, Shandong Province, China. The initial disease symptoms were small yellow spots, finally developing as tip blight, often associated with many small, black, semi-immersed pycnidial conidiomata formed in lesions. To obtain isolates of the causal agent for this disease, samples were randomly collected from O. japonicus diseased leaves in Rizhao City. In total 97 Phyllosticta isolates were obtained from samples, and studied using morphological features and multi-locus phylogenetic analyses of a combined dataset using the internal transcribed spacers (ITS), the 28S large subunit of ribosomal RNA (LSU), and partial translation elongation factor 1-alpha (tef), actin (act) and glyceraldehyde-3-phosphate dehydrogenase (gapdh) loci. Phylogenetically, these Phyllosticta isolates formed a clade in the P. concentrica species complex, and clustered with P. pilospora and P. spinarum. Morphologically, isolates in this clade differed from P. pilospora and P. spinarum by the size of conidiogenous cells and conidia, and the absence of an apical conidial appendage. As a result, these isolates were described as a novel species Phyllosticta rizhaoensis. Pathogenicity was confirmed using Koch's postulates, which showed that P. rizhaoensis could induce leaf blight symptoms on O. japonicus in China. Citation: Wang C-B, Wang T-T, Ma C-Y, Xue H, Li Y, Piao C-G, Jiang N (2023). Phyllosticta rizhaoensis sp. nov. causing leaf blight of Ophiopogon japonicus in China. Fungal Systematics and Evolution 11: 43-50. doi: 10.3114/fuse.2023.11.03.

ICAM-1 suppresses tumor metastasis by inhibiting macrophage M2 polarization through blockade of efferocytosis.

Efficient clearance of apoptotic cells (efferocytosis) can profoundly influence tumor-specific immunity. Tumor-associated macrophages are M2-polarized macrophages that promote key processes in tumor progression. Efferocytosis stimulates M2 macrophage polarization and contributes to cancer metastasis, but the signaling mechanism underlying this process is unclear. Intercellular cell adhesion molecule-1 (ICAM-1) is a transmembrane glycoprotein member of the immunoglobulin superfamily, which has been implicated in mediating cell-cell interaction and outside-in cell signaling during the immune response. We report that ICAM-1 expression is inversely associated with macrophage infiltration and the metastasis index in human colon tumors by combining Oncomine database analysis and immunohistochemistry for ICAM-1. Using a colon cancer liver metastasis model in ICAM-1-deficient (ICAM-1(-/-)) mice and their wild-type littermates, we found that loss of ICAM-1 accelerated liver metastasis of colon carcinoma cells. Moreover, ICAM-1 deficiency increased M2 macrophage polarization during tumor progression. We further demonstrated that ICAM-1 deficiency in macrophages led to promotion of efferocytosis of apoptotic tumor cells through activation of the phosphatidylinositol 3 kinase/Akt signaling pathway. More importantly, coculture of ICAM-1(-/-) macrophages with apoptotic cancer cells resulted in an increase of M2-like macrophages, which was blocked by an efferocytosis inhibitor. Our findings demonstrate a novel role for ICAM-1 in suppressing M2 macrophage polarization via downregulation of efferocytosis in the tumor microenvironment, thereby inhibiting metastatic tumor progression.

The critical role of catalase in prooxidant and antioxidant function of p53.

The tumor suppressor p53 is an important regulator of intracellular reactive oxygen species (ROS) levels, although downstream mediators of p53 remain to be elucidated. Here, we show that p53 and its downstream targets, p53-inducible ribonucleotide reductase (p53R2) and p53-inducible gene 3 (PIG3), physically and functionally interact with catalase for efficient regulation of intracellular ROS, depending on stress intensity. Under physiological conditions, the antioxidant functions of p53 are mediated by p53R2, which maintains increased catalase activity and thereby protects against endogenous ROS. After genotoxic stress, high levels of p53 and PIG3 cooperate to inhibit catalase activity, leading to a shift in the oxidant/antioxidant balance toward an oxidative status, which could augment apoptotic cell death. These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively.

First Report of Root-Knot Nematode Meloidogyne arenaria on Atractylodis macrocephalae in China.

Atractylodis macrocephalae is an important Chinese herbal medicine plant and its rhizome is of high medicinal value. In recent years, a severe decline in yield has been observed in Bozhou City (China's largest A. macrocephalae producing area), Anhui Province, China. A survey for plant-parasitic nematodes was conducted in this area from June to September 2011. Stunted plants displayed chlorotic or necrotic lower leaves near the ground part by the growth reduction; examination of the roots of stunted plants revealed the presence of galls typical of infestation by root knot nematode. Root nodules were found on the tap and lateral roots caused the fleshy tap root deformity. The incidence of diseased plants was estimated to be 45%, and yield loss was quantified as 43.5%. Nematodes were extracted from the root samples as previously described (4) and identified by morphology, enzyme analysis, and molecular characterization. Morphology of the female perineal patterns and measurements of the second-stage juveniles (J2s) matched those of the original description of Meloidogyne arenaria. Enzyme analysis of the esterase (Est) phenotype was also typical of the AII phenotype in M. arenaria (2). DNA was extracted according to a modified protocol (1), and the rDNA-internal transcribed spacer (ITS1_5.8S_ITS2) region was amplified with universal primers V5367 (5'-TTGATTACGTCCCTGCCCTTT-3') and 26S (5'-TTTCACTCGCCGTTACTAAGG-3'). PCR yielded a fragment of 764 bp and the purified product was sequenced by Sanger's dideoxy chain termination method (ABI3730). Sequences were identical to that of M. arenaria in GenBank (Accession No. AF387092) (3). Amplification of the D2/D3 fragments of the 28S RNA with universal primers D2A (5'-ACAAGTACCGTGAGGGAAAGTTG-3') and D3B (5'-TCGGAAGGAACCAGCTACTA-3') yielded a PCR fragment of 758 bp. These sequences were also identical to that of M. arenaria in GenBank (Accession No. AF435803). For further confirmation, amplification of the IGS region with universal primers 5S (5'-TTAACTTGCCAGATCGGACG-3') and 18S (5'-TCTAATGAGGGAACCAGCTACTA-3') yielded a PCR fragment of 713 bp. These sequences were 99.64% homologous to that of M. arenaria (GenBank Accession No. MAU42342). To our knowledge, this is the first report of M. arenaria species on A. macrocephalae in China. The fleshy tap root of A. macrocephalae is the main edible part of the plant, and the damage caused by root knot nematode will potentially reduce the yield and quality of this herb. References: (1) J. L. Cenis et al. Phytopathology 83:76, 1993. (2) P. R. Esbenshade and A. C. Triantaphyllou. J. Nematol. 17:6, 1985. (3) T. C. Vrain et al. Appl Nematol. 15:563, 1992. (4) L. F. Wang et al. Forest Res. 14:484, 2001.

A 3-year prospective radiographic evaluation of marginal bone level around different implant systems.

The aim of this study was to evaluate the change of marginal bone level radiographically around three different implant systems after 3 years in function. Fifty-four patients were included and randomly assigned to three treatment groups of rough-surface implants (TiUnite, n = 37), hybrid of smooth and rough-surface implants (Restore, n = 38) and rough surface with microthread implants (Hexplant, n = 45). Clinical and radiographic examinations were conducted at the time of implant loading (baseline), 1 and 3 years after loading. A three-level mixed-effect analysis of covariance (ancova) was used to test the significance of the mean marginal bone change of the three implant groups. A total 120 of 135 implants completed the study. None of the implants failed to integrate. Significant differences were noted in the marginal bone loss recorded for the three groups (P < 0.0001). At 3 years, the rough surface with microthread implants had a mean crestal bone loss of 0.59 +/- 0.30 mm; the rough-surface implants, 0.95 +/- 0.27 mm; and the hybrid surface implants, 1.05 +/- 0.34 mm. Within the limitations of this study, rough-surface implants with microthread at the coronal part might have a long-term positive effect in maintaining the marginal bone level against functional loading in comparison with implants without these two features.

Marginal bone loss around three different implant systems: radiographic evaluation after 1 year.

This study was designed to radiographically evaluate the effect of surface macro-and microstructures within the coronal portion of the external hex implant at the marginal bone change after loading. The fifty-four patients included in the study were randomly assigned to treatment groups with rough-surface implants (TiUnite, n = 45), a hybrid of smooth and rough surface implants (Restore, n = 45) or rough-surface with microthreads implants (Hexplant, n = 45). Clinical and radiographic examinations were conducted at the time of implant loading (baseline) and at 1-year post-loading. A three-level mixed-effect ancova was used to test the significance of the mean marginal bone change of the three implant groups from baseline to 1-year follow-up. At 1-year, significant differences were noted in marginal bone loss recorded for the three groups (P < 0.0001). The rough surface with microthread implants had a mean crestal bone loss of 0.42 +/- 0.27 mm; the rough surface implants, 0.81 +/- 0.27 mm; and the hybrid surface implants, 0.89 +/- 0.41 mm. Within the limitations of this study, a rough surface with microthreads at the coronal part of implant maintained the marginal bone level against functional loading better than implants without these two features.

Ribonucleotide reductase small subunit p53R2 suppresses MEK-ERK activity by binding to ERK kinase 2.

The p53-dependent RR small subunit (p53R2) protein, a newly identified member of the ribonucleotide reductase family, plays a key role in the p53-dependent cellular response to DNA. Several recent studies have suggested that p53R2 also plays an important role in suppressing the invasive potential of human cancer cells. However, the cellular mechanism that regulates invasiveness remains largely unknown. In this study, we show that p53R2 interacts with MEK2 (extracellular signal-regulated kinase (ERK) kinase 2-mitogen-activated protein kinase (MAPK) kinase 2), the molecule immediately upstream of ERK in the Ras-Raf-MAPK signaling cascade. In co-immunoprecipitation and immunofluorescence analyses, we found that p53R2 and MEK2 interact physically in cultured mammalian cells, and that the p53R2 segment comprising amino acids 161-206 is critical for this interaction. Moreover, serum-induced phosphorylation of MEK1/2 and ERK1/2 was greatly augmented in human cancer cells expressing small-interfering RNA against p53R2. On the other hand, phosphorylation of MEK1/2 and ERK1/2 in human cancer cells was markedly attenuated by overexpression of p53R2. Furthermore, MEK2 was required for p53R2 knockdown-induced enhancement of the invasive ability and anchorage-independent growth of human lung cancer H1299 cells. Taken together, these findings show that p53R2 negatively modulates serum-induced MEK-ERK activity and inhibits the MEK-ERK-mediated malignancy potential of human cancer cells.

Cell cycle and immune-related processes are significantly altered in chronic GVHD.

Currently, the pathogenesis of chronic GVHD is unclear. To elucidate the molecular characteristics underlying chronic GVHD, we analyzed the gene expression profiles of 21 mononuclear cell samples from allogeneic hematopoietic stem cell transplantation (HSCT) recipients. Self organizing map (SOM) clustering showed that the entire expression profiles of chronic GVHD samples were clearly different from those of the non-GVHD samples, and significance analysis of microarray (SAM) demonstrated that 120 genes, including PTDSS1, VAV1 and CD3D, were up-regulated, and 5 genes, including calnexin, were down-regulated in GVHD patients. Gene ontology annotation revealed that these genes are related to the phosphorous metabolism and lipid biosynthesis. Quantitative real time polymerase chain reaction (qRT-PCR) experiments validated the up-regulation of PTDSS1, VAV1 and CD3D in separate samples. Pathway-wise global test revealed that differential gene expression in cell cycle and T cell immune-associated pathways were significant between GVHD patients and non-GVHD patients. Seventeen classifier genes selected using a PAM (prediction analysis of microarray) algorithm showed favorable performance (prediction accuracy=0.85) for identifying patients with chronic GVHD. In conclusion, we identified differentially expressed genes and pathways in chronic GVHD patients using microarray analysis, and we also selected diagnostic genes predicting chronic GVHD status.

Tumor suppressor function of Betaig-h3 gene in radiation carcinogenesis.

Interaction between cell and extracellular matrix (ECM) plays a crucial role in tumor invasiveness and metastasis. Using an immortalized human bronchial epithelial (BEP2D) cell model, we showed previously that expression of a list of genes including Betaig-h3 (induced by transforming growth factor-beta), DCC (deleted in colorectal cancer), p21(cipl), c-fos, Heat shock protein (HSP27) and cytokeratin 14 were differentially expressed in several independently generated, radiation-induced tumor cell lines (TL1-TL5) relative to parental BEP2D cells. Our previous data further demonstrated that loss of tumor suppressor gene(s) as a likely mechanism of radiation carcinogenesis. In the present study, we chose Betaig-h3 and DCC that were downregulated in tumorigenic cells for further study. Restored expression of Betaig-h3 gene, not DCC gene, by transfecting cDNA into tumor cells resulted in a significant reduction in tumor growth. While integrin receptor alpha 5 beta 1 was overexpressed in tumor cells, its expression was corrected to the level found in control BEP2D cells after Betaig-h3 transfection. These data suggest that Betaig-h3 gene is involved in tumor progression by regulating integrin alpha 5 beta 1 receptor. Furthermore, exogenous TGF- beta 1 induced expression of Betaig-h3 gene and inhibited the growth of both control and tumorigenic BEP2D cells. Therefore, downregulation of Betaig-h3 gene may results from the decreased expression of upstream mediators such as TGF-beta. The findings provide strong evidence that the Betaig-h3 gene has tumor suppressor function in radiation-induced tumorigenic human bronchial epithelial cells and suggest a potential target for interventional therapy.

Overexpression of Betaig-h3 gene downregulates integrin alpha5beta1 and suppresses tumorigenicity in radiation-induced tumorigenic human bronchial epithelial cells.

Interaction between cell and extracellular matrix plays a crucial role in tumour invasion and metastasis. Using an immortalised human bronchial epithelial (BEP2D) cell model, the study here shows that expression of Betaig-h3 gene, which encodes a secreted adhesion molecule induced by transforming growth factor-beta, is markedly decreased in several independently generated, radiation-induced tumour cell lines (TL1-TL5) relative to parental BEP2D cells. Transfection of Betaig-h3 gene into tumour cells resulted in a significant reduction in tumour growth. While integrin receptor alpha5beta1 was overexpressed in tumour cells, its expression was corrected to the level found in control BEP2D cells after Betaig-h3 transfection. These data suggest that Betaig-h3 gene is involved in tumour progression by regulating integrin receptor alpha5beta1. The findings provide strong evidence that the Betaig-h3 gene has tumour suppressor function in human BEP2D cell model and suggest a potential target for interventional therapy.

Laparoscopic features of primary biliary cirrhosis in AMA-positive and AMA-negative patients.

BACKGROUND AND STUDY AIMS: Antimitochondrial antibody (AMA)-negative primary biliary cirrhosis (PBC) has been difficult to diagnose. Laparoscopic features of AMA-negative PBC were evaluated in comparison with those of AMA-positive PBC and autoimmune hepatitis. PATIENTS AND METHODS: 71 patients who fulfilled the diagnostic criteria for PBC were enrolled in the study; 48 were AMA-positive and 23 were AMA-negative. As a disease control, 46 autoimmune hepatitis patients were included. Both the frequency and specificity of each laparoscopic finding were evaluated. A laparoscopic scoring system was introduced, which used, common and uncommon laparoscopic findings, and was evaluated for the diagnosis of AMA-negative PBC. RESULTS: The characteristic laparoscopic findings for AMA-positive PBC were yellowish-white marking (92 %), dark-brown discoloration (73 %), gentle undulation (67 %), reddish patch (38 %), and yellowish-white nodules (32 %). On the other hand, laparoscopic findings such as trench-like depression, reddish markings, and wide and small depressions were uncommon in PBC compared with autoimmune hepatitis. The frequencies of characteristic and uncommon laparoscopic findings did not differ statistically between AMA-positive and AMA-negative PBC, but were different between AMA-positive or AMA-negative PBC and autoimmune hepatitis. Scores based on common and uncommon laparoscopic findings were 5.5 +/- 1.5 (mean +/- SD) in AMA-positive PBC, 5.6 +/- 2.0 in AMA-negative PBC, and - 0.30 +/- 0.5 in autoimmune hepatitis. CONCLUSION: The laparoscopic findings in AMA-negative PBC did not differ from those of AMA-positive PBC. A laparoscopic scoring system may be helpful in the diagnosis of AMA-negative PBC.

Analysis of p16 and p21(Cip1) expression in tumorigenic human bronchial epithelial cells induced by asbestos.

Although asbestos is carcinogenic to humans, the mechanism(s) by which it induces cancer is unknown. Using tumor cell lines generated previously by asbestos treatment of immortalized human bronchial epithelial (BEP2D) cells, we examined alterations in p16 and p21(Cip1) genes together with their protein levels. Results were compared with untreated BEP2D cells, normal human bronchial epithelial cells (NHBE), as well as non-tumorigenic fusion cell lines generated by fusing tumor cells with BEP2D cells. No deletion in the p16 gene was found in any of the tumor cell lines examined. Although p16 protein was expressed at a similar level in tumor and BEP2D cells, there was a fourfold decrease in its expression among NHBE cells. In contrast, both the protein and mRNA expression levels of p21(Cip1) were decreased by about threefold in tumor cell lines when compared with either BEP2D or NHBE cells, which had a similar expression level. Expression of p21(Cip1) mRNA was restored to the control level in all the fusion cell lines examined. The results suggested that down regulation of p21(Cip1) expression is linked to the tumorigenic conversion of BEP2D cells by asbestos.

Molecular alterations in tumorigenic human bronchial and breast epithelial cells induced by high LET radiation.

Carcinogenesis is a multi-stage process with sequence of genetic events governing the phenotypic expression of a series of transformation steps leading to the development of metastatic cancer. In the present study, immortalized human bronchial (BEP2D) and breast (MCF-10F) cells were irradiated with graded doses of either 150 keV/micrometer alpha particles or 1 GeV/nucleon 56Fe ions. Transformed cells developed through a series of successive steps before becoming tumorigenic in nude mice. Cell fusion studies indicated that radiation-induced tumorigenic phenotype in BEP2D cells could be completely suppressed by fusion with non-tumorigenic BEP2D cells. The differential expressions of known genes between tumorigenic bronchial and breast cells induced by alpha particles and their respective control cultures were compared using cDNA expression array. Among the 11 genes identified to be differentially expressed in BEP2D cells, three (DCC, DNA-PK and p21(CIP1)) were shown to be consistently down-regulated by 2 to 4 fold in all the 5 tumor cell lines examined. In contrast, their expressions in the fusion cell lines were comparable to control BEP2D cells. Similarly, expression levels of a series of genes were found to be altered in a step-wise manner among tumorigenic MCF-10F cells. The results are highly suggestive that functional alterations of these genes may be causally related to the carcinogenic process.

Delayed induction of alpha B-crystallin in activated glia cells of hippocampus in kainic acid-treated mouse brain.

Small heat shock proteins have been implicated in playing a role in various cellular processes, including stress-induced cell death. In kainic acid (KA)-treated rat brain, the immunoreactivity of heat-shock protein 27 (HSP27) was markedly increased in glia cells of the limbic system. In the present study, we demonstrated that alpha B-crystallin, a member of the small heat-shock protein family, was strongly induced in reactive astrocytes in hippocampus after KA-induced seizure. The induction was localized mainly in the CA3 region of hippocampus, where massive neuronal loss occurred. We also demonstrated that the delayed induction of alpha B-crystallin and HSP27 immunoreactivities in the hippocampus of epileptic animals was repressed to the levels seen in control animals with preadministration of the selective nNOS inhibitor 7-nitroindazole (7-NI). This repression was reversed by coinjection of L-arginine, a substrate of NOS. Together, these data suggest a role for alpha B-crystallin and HSP27 in reactive gliosis and/or in delayed neuronal death proceeded after KA-induced seizure.

A contact lens electrode with built-in high intensity white light-emitting diodes. A contact lens electrode with built-in white LEDs.

We determined the clinical usefulness of a new contact lens electrode with built-in, white light-emitting diodes (LEDs) for full-field electroretinograms (ERGs). Three, high-brightness white LEDs were incorporated into a contact lens electrode and served as the source for the stimulus and the background. The stimulus intensity, stimulus duration and background illumination were regulated by a small LED control device. Maximum stimulus and background intensities were 3.9 and 3.6 log cd/m2, respectively. We successfully recorded intensity-response series for scotopic and photopic ERGs. We also recorded a duration-series for photopic ERGs, and ERGs that were comparable to the ISCEV standardized ERGs. The compactness and ease of using this system suggest that it will be clinically useful under different conditions.

Karyotype analysis of tumorigenic human bronchial epithelial cells transformed by chrysolite asbestos using chemically induced premature chromosome condensation technique.

We examined karyotypic changes of tumorigenic human bronchial epithelial cell lines transformed by asbestos fibers. Using Calyculin A mediated premature chromosome condensation (PCC) assay and Giemsa-trypsin banding, we showed that the common changes of all tumorigenic cell lines were the loss of one or two copies of chromosome 5, the monosomy of chromosome 19 and the increased trisomy of chromosome 8. The results indicate that the karyotypic change of chromosome 5, 8 and 19 could play an important role in asbestos-induced tumorigenic conversion of human bronchial epithelial cells from an immortalized to tumorigenic state.

Focal macular ERGs in eyes after removal of macular ILM during macular hole surgery.

PURPOSE: The removal of the internal limiting membrane (ILM) for traction maculopathy has recently been advocated. However, it is generally believed that the ILM plays an important role in retinal function, because it is the basal lamina of the Müller cells that are involved in the generation of the electroretinogram (ERG) b-wave. To date, there has been no objective assessment of retinal function on removing the ILM. In this study, the changes of each component of the focal macular electroretinograms (FMERGs) were investigated in eyes before and after the ILM was removed in the macular area during surgery for idiopathic macular holes (IMHs). METHODS: FMERGs were elicited by a 15 degrees stimulus centered on the fovea and monitored by an infrared fundus camera. FMERGs were recorded from 49 eyes of 48 patients with IMHs before and 6 weeks after anatomically successful macular hole surgery. Whether an eye had or did not have the ILM removed was randomly determined. The ILM was removed in 30 eyes (ILM-off group) and was not removed in 19 eyes (ILM-on group). Six months after surgery, the same examination was performed in 27 eyes of the ILM-off group and in 15 eyes of the ILM-on group. The amplitudes and implicit times of the a- and b-waves and the mean amplitudes and implicit times of the first three oscillatory potentials (OP1 to OP3) were compared before and after surgery within and between the groups. RESULTS: Visual acuity increased significantly after surgery in both groups. In the ILM-on group, the amplitude of the a- and b-waves and the OPs increased significantly 6 months after surgery (P: = 0.0093, P: = 0.0019, P: = 0.0024, respectively, paired t-test). In the ILM-off group, the a-wave amplitude and mean OP amplitudes were significantly larger 6 months after surgery (P: = 0.0077, P: = 0.0030, respectively, paired t-test). The b-wave amplitude, however, did not change significantly. The percentage increase in the b-wave amplitude 6 months after surgery was significantly higher in the ILM-on group (44.0%) than in the ILM-off group (15.0%; P: = 0.037, t-test). CONCLUSIONS: The removal of the ILM had no adverse effect on visual acuity. However, the selective delay of recovery of the FMERG b-wave 6 months after surgery suggests an alteration of retinal physiology in the macular region.