PTEN expression can be used as a switch between senescence and apoptosis in breast cancer cells according to a logical model of the G2/M checkpoint.

Worldwide, the second-highest mortality rate is caused by breast cancer (BC). The most studied BC cell line is MCF-7 because it exhibits strong consistency with clinical cases and is a good system for analyzing tumors with functional estrogen receptors (ER-positive cancers). In this paper, we introduce the first theoretical method for describing PTEN-loss-induced cellular senescence (PICS), which is an increase in cellular senescence caused by PTEN knockout, utilizing a logical model of the G2/M checkpoint. We predict that PTEN expression acts as a switch between cell phenotypes associated with senescence and apoptosis. We show that PICS is induced by the activity of the positive feedback between AKT and mTORC2, and that overexpression of PTEN will disrupt the feedback, abrogating senescence and only leading to arrest or apoptosis. Furthermore, we demonstrate that miR-21 can be used as a target against proliferation control because its knockout is equivalent to PTEN overexpression. We think the findings can be used to motivate new strategies for MCF-7 strain proliferation control.

A dynamic Boolean network reveals that the BMI1 and MALAT1 axis is associated with drug resistance by limiting miR-145-5p in non-small cell lung cancer.

Patients with non-small cell lung cancer (NSCLC) are often treated with chemotherapy. Poor clinical response and the onset of chemoresistance limit the anti-tumor benefits of drugs such as cisplatin. According to recent research, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA related to cisplatin resistance in NSCLC. Furthermore, MALAT1 targets microRNA-145-5p (miR-145), which activates Krüppel-like factor 4 (KLF4) in associated cell lines. B lymphoma Mo-MLV insertion region 1 homolog (BMI1), on the other hand, inhibits miR-145 expression, which stimulates Specificity protein 1 (Sp1) to trigger the epithelial-mesenchymal transition (EMT) process in pemetrexed-resistant NSCLC cells. The interplay between these molecules in drug resistance is still unclear. Therefore, we propose a dynamic Boolean network that can encapsulate the complexity of these drug-resistant molecules. Using published clinical data for gain or loss-of-function perturbations, our network demonstrates reasonable agreement with experimental observations. We identify four new positive circuits: miR-145/Sp1/MALAT1, BMI1/miR-145/Myc, KLF4/p53/miR-145, and miR-145/Wip1/p38MAPK/p53. Notably, miR-145 emerges as a central player in these regulatory circuits, underscoring its pivotal role in NSCLC drug resistance. Our circuit perturbation analysis further emphasizes the critical involvement of these new circuits in drug resistance for NSCLC. In conclusion, targeting MALAT1 and BMI1 holds promise for overcoming drug resistance, while activating miR-145 represents a potential strategy to significantly reduce drug resistance in NSCLC.

The lncRNA DLX6-AS1/miR-16-5p axis regulates autophagy and apoptosis in non-small cell lung cancer: A Boolean model of cell death.

Long non-coding RNA (lncRNA) distal-less homeobox 6 antisense RNA 1 (DLX6-AS1) is elevated in a variety of cancers, including non-small cell lung cancer (NSCLC) and cervical cancer. Although it was found that the microRNA-16-5p (miR-16), which is known to regulate autophagy and apoptosis, had been downregulated in similar cancers. Recent research has shown that in tumors with similar characteristics, DLX6-AS1 acts as a sponge for miR-16 expression. However, the cell death-related molecular mechanism of the DLX6-AS1/miR-16 axis has yet to be investigated. Therefore, we propose a dynamic Boolean model to investigate gene regulation in cell death processes via the DLX6-AS1/miR-16 axis. We found the finest concordance when we compared our model to many experimental investigations including gain-of-function genes in NSCLC and cervical cancer. A unique positive circuit involving BMI1/ATM/miR-16 is also something we predict. Our results suggest that this circuit is essential for regulating autophagy and apoptosis under stress signals. Thus, our Boolean network enables an evident cell-death process coupled with NSCLC and cervical cancer. Therefore, our results suggest that DLX6-AS1 targeting may boost miR-16 activity and thereby restrict tumor growth in these cancers by triggering autophagy and apoptosis.

A logical model of Ewing sarcoma cell epithelial-to-mesenchymal transition supports the existence of hybrid cellular phenotypes.

Ewing sarcoma (ES) is a highly aggressive pediatric tumor driven by the RNA-binding protein EWS (EWS)/friend leukemia integration 1 transcription factor (FLI1) chimeric transcription factor, which is involved in epithelial-mesenchymal transition (EMT). EMT stabilizes a hybrid cell state, boosting metastatic potential and drug resistance. Nevertheless, the mechanisms underlying the maintenance of this hybrid phenotype in ES remain elusive. Our study proposes a logical EMT model for ES, highlighting zinc finger E-box-binding homeobox 2 (ZEB2), miR-145, and miR-200 circuits that maintain hybrid states. The model aligns with experimental findings and reveals a previously unknown circuit supporting the mesenchymal phenotype. These insights emphasize the role of ZEB2 in the maintenance of the hybrid state in ES.

A Boolean model of the oncogene role of FAM111B in lung adenocarcinoma.

The ultimate goal of this study is to analyze the gene regulation between FAM111B and p53 in lung adenocarcinoma using Boolean networks. Recent studies have shown that downregulation of FAM111B enhances the G2/M cell cycle checkpoint in the respective cell lines. Upregulation of p53 directly downregulates FAM111B, which is directed to affect cell cycle controllers Cdc25C and Cdk1/CyclinB, thereby controlling G2/M cell cycle arrest. As for apoptosis, down-regulation of FAM111B by p53 directly regulates the BAG3/Bcl-2 axis, which triggers apoptotic cell death. However, the molecular mechanisms involving p53 and FAM111B in G2/M checkpoint regulation are still unknown. Thus, we present a Boolean model of the G2/M checkpoint considering the effect of p53 and FAM111B. Our model indicates that the cell fate between the two cellular phenotypes, arrest, and apoptosis, at the G2/M checkpoint is non-deterministic and is controlled by p53. The model was compared with the experimental data involving gain- or loss-of-function genes and achieved a fair agreement. The model predicts a positive circuit involving p53/FAM111B/BAG3. Our circuit perturbation analysis suggests that this circuit may be essential for controlling cell-fate decisions at the G2/M checkpoint. Our model supports that FAM111B is an engaging target for drug development in lung adenocarcinoma.

Quadra-Stable Dynamics of p53 and PTEN in the DNA Damage Response.

Cell fate determination is a complex process that is frequently described as cells traveling on rugged pathways, beginning with DNA damage response (DDR). Tumor protein p53 (p53) and phosphatase and tensin homolog (PTEN) are two critical players in this process. Although both of these proteins are known to be key cell fate regulators, the exact mechanism by which they collaborate in the DDR remains unknown. Thus, we propose a dynamic Boolean network. Our model incorporates experimental data obtained from NSCLC cells and is the first of its kind. Our network's wild-type system shows that DDR activates the G2/M checkpoint, and this triggers a cascade of events, involving p53 and PTEN, that ultimately lead to the four potential phenotypes: cell cycle arrest, senescence, autophagy, and apoptosis (quadra-stable dynamics). The network predictions correspond with the gain-and-loss of function investigations in the additional two cell lines (HeLa and MCF-7). Our findings imply that p53 and PTEN act as molecular switches that activate or deactivate specific pathways to govern cell fate decisions. Thus, our network facilitates the direct investigation of quadruplicate cell fate decisions in DDR. Therefore, we concluded that concurrently controlling PTEN and p53 dynamics may be a viable strategy for enhancing clinical outcomes.

A comparison of sutureless flanged fixation and 4-point Gore-Tex fixation for scleral-fixated intraocular lenses: a pilot study.

Purpose: Scleral-fixation of intraocular lenses (IOLs) provides an option for eyes that lack sufficient capsular support for in-the-bag IOL placement. The latest techniques for lens fixation include use of a novel suture material, Gore-Tex, and a sutureless method, with flanged intrascleral fixation. The purpose of this pilot study was to compare these methods in terms of anatomic and clinical outcomes. Methods: A total of 35 eyes of patients 18-60 years of age who presented with aphakia, subluxated lens, or ectopia lentis were randomized into two groups. Group A (15 eyes) underwent flanged intrascleral IOL fixation using the Yamane technique; group B (20 eyes) underwent 4-point transscleral fixation of IOL using Gore-Tex suture. The following parameters were compared between groups on day 1, week 3, and month 6 postoperatively: logMAR uncorrected and best-corrected visual acuity, retinoscopy, IOL centration on slit-lamp biomicroscopy, and IOL tilt on ultrasound biomicroscopy. Results: Postoperative visual acuity was better in group B: uncorrected, logMAR 0.89 ± 0.22 versus 0.72 ± 0.24 (P = 0.046); best-corrected, logMAR 0.51 ± 0.18 versus 0.37 ± 0.26 (P = 0.016). No significant difference was found in postoperative retinoscopy and astigmatism between groups. IOL tilt (>100 µm) occurred in 8 cases in group A and in 9 cases in group B; 87% in group A and 100% in group B were well centered. Complications in both groups were minimal. Conclusions: In our small study cohort, both sutureless flanged IOL fixation and Gore-Tex sutured scleral IOL fixation resulted in excellent visual rehabilitation of patients with aphakia and subluxated lenses. Patients who underwent Gore-Tex suture fixation experienced better postoperative visual acuity, IOL centration, and stability.

Network analysis reveals that the tumor suppressor lncRNA GAS5 acts as a double-edged sword in response to DNA damage in gastric cancer.

The lncRNA GAS5 acts as a tumor suppressor and is downregulated in gastric cancer (GC). In contrast, E2F1, an important transcription factor and tumor promoter, directly inhibits miR-34c expression in GC cell lines. Furthermore, in the corresponding GC cell lines, lncRNA GAS5 directly targets E2F1. However, lncRNA GAS5 and miR-34c remain to be studied in conjunction with GC. Here, we present a dynamic Boolean network to classify gene regulation between these two non-coding RNAs (ncRNAs) in GC. This is the first study to show that lncRNA GAS5 can positively regulate miR-34c in GC through a previously unknown molecular pathway coupling lncRNA/miRNA. We compared our network to several in-vivo/in-vitro experiments and obtained an excellent agreement. We revealed that lncRNA GAS5 regulates miR-34c by targeting E2F1. Additionally, we found that lncRNA GAS5, independently of p53, inhibits GC proliferation through the ATM/p38 MAPK signaling pathway. Accordingly, our results support that E2F1 is an engaging target of drug development in tumor growth and aggressive proliferation of GC, and favorable results can be achieved through tumor suppressor lncRNA GAS5/miR-34c axis in GC. Thus, our findings unlock a new avenue for GC treatment in response to DNA damage by these ncRNAs.

The Wnt pathway can stabilize hybrid phenotypes in the epithelial-mesenchymal transition: A logical modeling approach.

The Wnt pathway is important to regulate a variety of biochemical functions and can contribute to cancer development through its influence on the epithelial-mesenchymal transition (EMT). Multiple circuits have been reported to participate in the regulation of the Wnt signaling, however, the way these circuits coordinately regulate this signaling is still unclear. Moreover, the mechanisms responsible for the appearance of hybrid phenotypes (cells presenting both E and M features) are not well determined. The hybrid phenotype can present much higher metastatic potential than the mesenchymal phenotype. In this study, we propose a Boolean model of the Wnt pathway signaling contemplating recent published biochemical information on hepatocarcinoma. The model presents good coherence with experimental data for perturbed and wild-type cases. With the model, we propose two new molecular circuits involving several molecules that can stabilize hybrid states during the EMT. Moreover, we found that the two well studied circuits, AKT1/ß-catenin and SNAIL1/miR-34, can cooperate with the predicted ones to favor the stabilization of the hybrid states. These findings highlight some possible unrecognized mechanisms during Wnt signaling and may provide alternative therapeutic strategies to control cancer metastatization.

A Boolean Model of the Proliferative Role of the lncRNA XIST in Non-Small Cell Lung Cancer Cells.

The long non-coding RNA X inactivate-specific transcript (lncRNA XIST) has been verified as an oncogenic gene in non-small cell lung cancer (NSCLC) whose regulatory role is largely unknown. The important tumor suppressors, microRNAs: miR-449a and miR-16 are regulated by lncRNA XIST in NSCLC, these miRNAs share numerous common targets and experimental evidence suggests that they synergistically regulate the cell-fate regulation of NSCLC. LncRNA XIST is known to sponge miR-449a and miR-34a, however, the regulatory network connecting all these non-coding RNAs is still unknown. Here we propose a Boolean regulatory network for the G1/S cell cycle checkpoint in NSCLC contemplating the involvement of these non-coding RNAs. Model verification was conducted by comparison with experimental knowledge from NSCLC showing good agreement. The results suggest that miR-449a regulates miR-16 and p21 activity by targeting HDAC1, c-Myc, and the lncRNA XIST. Furthermore, our circuit perturbation simulations show that five circuits are involved in cell fate determination between senescence and apoptosis. The model thus allows pinpointing the direct cell fate mechanisms of NSCLC. Therefore, our results support that lncRNA XIST is an attractive target of drug development in tumor growth and aggressive proliferation of NSCLC, and promising results can be achieved through tumor suppressor miRNAs.

Dynamical modeling of miR-34a, miR-449a, and miR-16 reveals numerous DDR signaling pathways regulating senescence, autophagy, and apoptosis in HeLa cells.

Transfection of tumor suppressor miRNAs such as miR-34a, miR-449a, and miR-16 with DNA damage can regulate apoptosis and senescence in cancer cells. miR-16 has been shown to influence autophagy in cervical cancer. However, the function of miR-34a and miR-449a in autophagy remains unknown. The functional and persistent G1/S checkpoint signaling pathways in HeLa cells via these three miRNAs, either synergistically or separately, remain a mystery. As a result, we present a synthetic Boolean network of the functional G1/S checkpoint regulation, illustrating the regulatory effects of these three miRNAs. To our knowledge, this is the first synthetic Boolean network that demonstrates the advanced role of these miRNAs in cervical cancer signaling pathways reliant on or independent of p53, such as MAPK or AMPK. We compared our estimated probability to the experimental data and found reasonable agreement. Our findings indicate that miR-34a or miR-16 may control senescence, autophagy, apoptosis, and the functional G1/S checkpoint. Additionally, miR-449a can regulate just senescence and apoptosis on an individual basis. MiR-449a can coordinate autophagy in HeLa cells in a synergistic manner with miR-16 and/or miR-34a.

Dynamical Analysis of a Boolean Network Model of the Oncogene Role of lncRNA ANRIL and lncRNA UFC1 in Non-Small Cell Lung Cancer.

Long non-coding RNA (lncRNA) such as ANRIL and UFC1 have been verified as oncogenic genes in non-small cell lung cancer (NSCLC). It is well known that the tumor suppressor microRNA-34a (miR-34a) is downregulated in NSCLC. Furthermore, miR-34a induces senescence and apoptosis in breast, glioma, cervical cancer including NSCLC by targeting Myc. Recent evidence suggests that these two lncRNAs act as a miR-34a sponge in corresponding cancers. However, the biological functions between these two non-coding RNAs (ncRNAs) have not yet been studied in NSCLC. Therefore, we present a Boolean model to analyze the gene regulation between these two ncRNAs in NSCLC. We compared our model to several experimental studies involving gain- or loss-of-function genes in NSCLC cells and achieved an excellent agreement. Additionally, we predict three positive circuits involving miR-34a/E2F1/ANRIL, miR-34a/E2F1/UFC1, and miR-34a/Myc/ANRIL. Our circuit- perturbation analysis shows that these circuits are important for regulating cell-fate decisions such as senescence and apoptosis. Thus, our Boolean network permits an explicit cell-fate mechanism associated with NSCLC. Therefore, our results support that ANRIL and/or UFC1 is an attractive target for drug development in tumor growth and aggressive proliferation of NSCLC, and that a valuable outcome can be achieved through the miRNA-34a/Myc pathway.

Tubercular Osteomyelitis of the Orbit Presenting as Periorbital Cellulitis.

PURPOSE: Osteomyelitis of the orbital bones presenting as an orbital cellulitis is a rare form of extrapulmonary tuberculosis (TB). We report a rare case of tubercular osteomyelitis of the orbital bones presenting as a periorbital cellulitis. CASE REPORT: A seven-year-old female child presented to our tertiary eye care center with swelling involving the right eyelids and the right cheek for two months. She had been provisionally diagnosed elsewhere as pre-septal cellulitis and had been given oral antibiotics. We clinically diagnosed her as orbital cellulitis, but her non-responsiveness to intravenous antibiotics prompted us to get a contrast enhanced computed tomography (CECT) of the orbit and paranasal sinuses, which was suggestive of tubercular etiology. However, the patient had no foci for TB elsewhere. We used a relatively new, but rapid test, called Cartridge-based Nucleic Acid Amplification Test (CBNAAT) on the pus aspirate which was positive for TB. Thereafter, the patient was started on anti-tubercular treatment to which she responded wonderfully. CONCLUSION: A high index of suspicion should be kept for TB infection in cases of orbital cellulitis with unusual clinical behavior in an endemic region such as India.

Derivation and validation of gray-box models to estimate noninvasive in-vivo percentage glycated hemoglobin using digital volume pulse waveform.

Glycated hemoglobin and blood oxygenation are the two most important factors for monitoring a patient's average blood glucose and blood oxygen levels. Digital volume pulse acquisition is a convenient method, even for a person with no previous training or experience, can be utilized to estimate the two abovementioned physiological parameters. The physiological basis assumptions are utilized to develop two-finger models for estimating the percent glycated hemoglobin and blood oxygenation levels. The first model consists of a blood-vessel-only hypothesis, whereas the second model is based on a whole-finger model system. The two gray-box systems were validated on diabetic and nondiabetic patients. The mean absolute errors for the percent glycated hemoglobin (%HbA1c) and percent oxygen saturation (%SpO2) were 0.375 and 1.676 for the blood-vessel model and 0.271 and 1.395 for the whole-finger model, respectively. The repeatability analysis indicated that these models resulted in a mean percent coefficient of variation (%CV) of 2.08% and 1.74% for %HbA1c and 0.54% and 0.49% for %SpO2 in the respective models. Herein, both models exhibited similar performances (HbA1c estimation Pearson's R values were 0.92 and 0.96, respectively), despite the model assumptions differing greatly. The bias values in the Bland-Altman analysis for both models were - 0.03 ± 0.458 and - 0.063 ± 0.326 for HbA1c estimation, and 0.178 ± 2.002 and - 0.246 ± 1.69 for SpO2 estimation, respectively. Both models have a very high potential for use in real-world scenarios. The whole-finger model with a lower standard deviation in bias and higher Pearson's R value performs better in terms of higher precision and accuracy than the blood-vessel model.

Systems biology approach suggests new miRNAs as phenotypic stability factors in the epithelial-mesenchymal transition.

The epithelial-mesenchymal transition (EMT) is a cellular programme on which epithelial cells undergo a phenotypic transition to mesenchymal ones acquiring metastatic properties such as mobility and invasion. TGF-ß signalling can promote the EMT process. However, the dynamics of the concentration response of TGF-ß-induced EMT is not well explained. In this work, we propose a logical model of TGF-ß dose dependence of EMT in MCF10A breast cells. The model outcomes agree with experimentally observed phenotypes for the wild-type and perturbed/mutated cases. As important findings of the model, it predicts the coexistence of more than one hybrid state and that the circuit between TWIST1 and miR-129 is involved in their stabilization. Thus, miR-129 should be considered as a phenotypic stability factor. The circuit TWIST1/miR-129 associates with ZEB1-mediated circuits involving miRNAs 200, 1199, 340, and the protein GRHL2 to stabilize the hybrid state. Additionally, we found a possible new autocrine mechanism composed of the circuit involving TGF-ß, miR-200, and SNAIL1 that contributes to the stabilization of the mesenchymal state. Therefore, our work can extend our comprehension of TGF-ß-induced EMT in MCF10A cells to potentially improve the strategies for breast cancer treatment.

Towards DNA-damage induced autophagy: A Boolean model of p53-induced cell fate mechanisms.

How a cell determines a given phenotype upon damaged DNA is an open problem. Cell fate decisions happen at cell cycle checkpoints and it is becoming clearer that the p53 pathway is a major regulator of cell fate decisions involving apoptosis or senescence upon DNA damage, especially at G1/S. However, recent results suggest that this pathway is also involved in autophagy induction upon DNA damage. To our knowledge, in this work we propose the first model of the DNA damage-induced G1/S checkpoint contemplating the decision between three phenotypes: apoptosis, senescence, and autophagy. The Boolean model is proposed based on experiments with U87 glioblastoma cells using the transfection of miR-16 that can induce a DNA damage response. The wild-type case of the model shows that DNA damage induces the checkpoint and the coexistence of the three phenotypes (tristable dynamics), each with a different probability. We also predict that the positive feedback involving ATM, miR-16, and Wip1 has an influence on the tristable state. The model predictions were compared to experiments of gain and loss of function in other three different cell lines (MCF-7, A549, and U2OS) presenting agreement. For p53-deficient cell lines such as HeLa, H1299, and PC-3, our model contemplates the experimental observation that the alternative AMPK pathway can compensate this deficiency. We conclude that at the G1/S checkpoint the p53 pathway (or, in its absence, the AMPK pathway) can regulate the induction of different phenotypes in a stochastic manner in the U87 cell line and others.

Integrative data modeling from lung and lymphatic cancer predicts functional roles for miR-34a and miR-16 in cell fate regulation.

MiR-34a and miR-16 coordinately control cell cycle checkpoint in non-small cell lung cancer (NSCLC) cells. In cutaneous T-cell lymphoma (CTCL) cells miR-16 regulates a switch between apoptosis and senescence, however the role of miR-34a in this process is unclear. Both miRNAs share many common targets and experimental evidences suggest that they synergistically control the cell-fate regulation of NSCLC. In this work we investigate whether the coordinate action between miR-34a and miR-16 can explain experimental results in multiple cell lines of NSCLC and CTCL. For that we propose a Boolean model of the G1/S checkpoint regulation contemplating the regulatory influences of both miRNAs. Model validation was performed by comparisons with experimental information from the following cell lines: A549, H460, H1299, MyLa and MJ presenting excellent agreement. The model integrates in a single logical framework the mechanisms responsible for cell fate decision in NSCLC and CTCL cells. From the model analysis we suggest that miR-34a is the main controller of miR-16 activity in these cells. The model also allows to investigate perturbations of single or more molecules with the purpose to intervene in cell fate mechanisms of NSCLC and CTCL cells.

ATM/miR-34a-5p axis regulates a p21-dependent senescence-apoptosis switch in non-small cell lung cancer: a Boolean model of G1/S checkpoint regulation.

MicroRNA-34a-5p regulates the G1/S checkpoint in non-small cell lung cancer (NSCLC) cells. Forced expression of miR-34a-5p enhances p21 expression and promotes cellular senescence, whereas knockout of miR-34a-5p decreases senescence and increases apoptosis. This suggests that p21 is the main effector of a senescence-apoptosis switch in NSCLC cells; however, the molecular mechanisms controlling this switch are unclear. In this work, we propose a Boolean model of G1/S checkpoint regulation, contemplating the regulatory influences of p21 by miR-34a-5p. The predicted probabilities of our model are in excellent agreement with experimental data. Our model supports that p21 is the main effector of a senescence/apoptosis switch and that the disruption of the positive feedback involving ATM, miR-34a-5p, and the histone deacetylase HDAC1 abrogates senescence.

Comparison of Plusoptix S12R photoscreener with cycloplegic retinoscopy and autorefraction in pediatric age group.

Purpose: To compare refractive measurements of noncycloplegic photoscreener Plusoptix S12R with cycloplegic retinoscopy, noncycloplegic autorefractor, and cycloplegic autorefractor in children. Methods: The study population (200 eyes of 100 children) was divided into two groups: Group 1 (age 3-7 years) and Group 2 (age 8-15 years). In Group 1, Plusoptix was compared with cycloplegic retinoscopy. In Group 2, Plusoptix was compared with cycloplegic retinoscopy and autorefraction. The second group was made because the younger group was found to be uncooperative for autorefraction. Paired t-test and Pearson's correlation were used for statistical analysis. Results: The mean difference in sphere (DS), spherical equivalent (DSE), and cylinder (DC) between cycloplegic retinoscopy and Plusoptix in Group 1 was 0.68 ± 0.55 (P < 0.001), 0.77 ± 0.61 (P < 0.001), and 0.18 ± 0.28 (P < 0.001), respectively. In Group 2, DS, DSE, and DC between cycloplegic retinoscopy and Plusoptix were 0.86 ± 0.49 (P < 0.001), 0.97 ± 0.51 (P < 0.001), and 0.23 ± 0.28 (P < 0.001); between cycloplegic autorefractor and Plusoptix were 0.69 ± 0.47 (P < 0.001), 0.74 ± 0.49 (P < 0.001), and 0.10 ± 0.31 (P = 0.002); and between noncycloplegic autorefractor and Plusoptix were - 0.25 ± 0.39 (P < 0.001), -0.19 ± 0.41 (P < 0.001), and 0.11 ± 0.31 (P < 0.001), respectively. Pearson's correlation coefficients of S, SE, and C between Plusoptix and cycloplegic retinoscopy were 0.948, 0.938, and 0.924 in Group 1 and 0.972, 0.972, and 0.946 in Group 2, and these values were statistically significant. Bland-Altman plots showed good agreement between cycloplegic retinoscopy and Plusoptix in both groups. Plusoptix gave axis values within 10° of cycloplegic retinoscopy in 81.56% of eyes in Group 1 and in 71.44% of eyes in Group 2. Conclusion: Plusoptix photoscreener can be used for prescription of axis of cylinder in children; however, other refractive measurements must be refined by cycloplegic retinoscopy.

Comparison of Manual Capsulorhexis and 25-Gauge Vitrectorhexis in Pediatric Cataract Surgery: A Pilot Study.

PURPOSE: To compare short-term visual outcomes (best corrected visual acuity [BCVA]), visual axis opacification, anterior (ACCC) and posterior (PCCC) continuous curvilinear capsulorhexis size, shape, and extension, and their decentration between manual capsulorhexis and 25-gauge vitrectorhexis in pediatric cataract surgery with intraocular lens (IOL) implantation. METHODS: Thirty eyes of children aged 3 to 8 years with developmental cataract were randomly selected for ACCC and PCCC by manual capsulorhexis forceps and 25-gauge vitrectomy cutter followed by IOL implantation and limited anterior vitrectomy. The size of the ACCC and PCCC was measured intraoperatively with calibrated capsulorhexis forceps. Patients were followed up for 3 months postoperatively and were evaluated for BCVA and visual axis opacification. Slit-lamp photographs of operated eyes were taken in retroillumination. The size in millimeters and decentration of the ACCC and PCCC from the center of the IOL were measured with the help of the Python imaging library. RESULTS: There was no statistically significant difference between BCVA (P > .05), visual axis opacification (P > .05), size of the ACCC (P > .05) and its decentration (P > .05), extension of the rhexis (P > .05), and size of the PCCC (P > .05) and its decentration (P > .05) between the two methods. CONCLUSIONS: In both groups, BCVA, visual axis opacification, and ACCC and PCCC size, shape, and decentration from the center of the IOL were comparable, making 25-gauge vitrectorhexis a good alternative to manual capsulorhexis. [J Pediatr Ophthalmol Strabismus. 2019;56(5):327-332.].