NIP45 controls the magnitude of the type 2 T helper cell response.

Nuclear factor of activated T cell (NFAT) transcription factors are key regulators of gene transcription within immune cells. The NFAT-interacting protein, (NIP45), augments NFAT-driven IL-4 expression by a mechanism that relies on arginine methylation. To establish the function of NIP45 in vivo, we generated mice with a targeted deletion of the gene encoding this cofactor. NIP45-deficient T helper cells displayed profound defects in the expression of NFAT-regulated cytokine genes, including IL-4. Whereas NIP45 deficiency does not interfere with T helper cell NFAT activation or lineage-specific transcription-factor expression, NIP45 acts as an enhancer for the assembly of protein arginine methyltransferase 1 and the protein arginine methyltransferase 1-linked histone 4 arginine 3 methylation with the IL-4 promoter. Our study reveals an essential role for NIP45 in promoting robust cytokine expression in vivo, which is required for the efficient handling of parasites. We propose that NIP45 acts as a molecular rheostat serving to amplify the type-2 immune response.

Identification of the target self-antigens in reperfusion injury.

Reperfusion injury (RI), a potential life-threatening disorder, represents an acute inflammatory response after periods of ischemia resulting from myocardial infarction, stroke, surgery, or trauma. The recent identification of a monoclonal natural IgM that initiates RI led to the identification of nonmuscle myosin heavy chain type II A and C as the self-targets in two different tissues. These results identify a novel pathway in which the innate response to a highly conserved self-antigen expressed as a result of hypoxic stress results in tissue destruction.

Endothelial keratoplasty: the relationship between donor tissue storage time and donor endothelial survival.

PURPOSE: To evaluate the relationship between storage time in Optisol GS (Bausch & Lomb, St. Louis, MO) and postoperative cell loss after Descemet's stripping automated endothelial keratoplasty (DSAEK) surgery. DESIGN: Retrospective analysis of a noncomparative, interventional case series. PARTICIPANTS: Three hundred sixty-two eyes of 265 patients undergoing DSAEK surgery for Fuchs' endothelial dystrophy. METHODS: Storage times (death to surgery) of donor tissue were recorded for 362 eyes undergoing DSAEK surgery. Donor cell loss at 6, 12, and 24 months was recorded. Analysis of storage times with endothelial cell loss was performed using a Pearson correlation coefficient and an independent samples Student t test. MAIN OUTCOME MEASURES: Percentage of donor endothelial cell loss as measured by specular microscopy of central endothelial cell density (ECD). RESULTS: The mean storage time was 98.95 ± 33 hours (range, 20.65-186.02 hours). The mean percent endothelial cell loss from before to after surgery was 29 ± 16% at 6 months (n = 362), 31 ± 16% at 12 months (n = 263), and 32 ± 20% at 24 months (n = 98). Storage time did not correlate significantly with endothelial cell loss at any postoperative time point (6 months: r = -0.047, P = 0.373; 12 months: r = -0.023, P = 0.709; 24 months: r = -0.14, P = 0.169). The mean cell loss for corneas stored 0 to 4 days (n = 55) was 32 ± 17% at 2 years and the mean cell loss for corneas stored for more than 4 days (n = 43) was 30 ± 18% at 2 years (P = 0.57). At the extremes of storage time, 10 corneas stored for the shortest time (1.5 days) had a 1-year cell loss of 33% and 10 corneas stored for the longest time (7 days) had a 1-year cell loss of 30% (P = 0.45). CONCLUSIONS: No correlation was found between the characteristic of storage time and the decline of ECD. Surgeons should not make special requests to the eye bank for short storage times with the hope of improving donor endothelial survival. The upper limit of donor storage time as it relates to acceptable postoperative endothelial cell loss is not known.

Surgical hospitalist: can this be a program for your group?

A shortage of general surgeons is creating issues for the coverage of many emergency departments. This article outlines a new way of thinking about how to diagnosis and treat this problem. Learn the basics behind the possible creation of a surgical hospitalist program from assessing the need; reviewing physician issues; computing the financial analysis; understanding the political and bureaucratic issues; and, finally, recruiting to fill the positions.

Prevention of lipopolysaccharide-induced microangiopathy by gp49B1: evidence for an important role for gp49B1 expression on neutrophils.

gp49B1 is expressed on mast cells and inhibits immunoglobulin E-dependent activation and inflammation in vivo. We now show that gp49B1 is expressed on neutrophils and prevents neutrophil-dependent vascular injury in response to lipopolysaccharide (LPS). The intradermal (i.d.) injection of LPS into gp49B1-null (gp49B-/-) but not gp49B1-sufficient (gp49B+/+) mice elicited macroscopic hemorrhages by 24 h, which were preceded on microscopic analyses by significantly more intravascular thrombi (consisting of neutrophils, platelets, and fibrin) that occluded venules and by more tissue neutrophils than in gp49B+/+ mice. However, there were no differences in the number of intact (nondegranulating) mast cells or the tissue levels of mediators that promote neutrophil recruitment. Hemorrhage was prevented by depleting neutrophils, blocking beta2 integrin-intercellular adhesion molecule 1 interactions, or inhibiting coagulation. These characteristics indicate that gp49B-/- mice are exquisitely sensitive to a local Shwartzman reaction (LSR) after a single i.d. injection of LPS, whereas in the classic LSR, a second exposure is required for increased beta2 integrin function, intravascular neutrophil aggregation, formation of occlusive thrombi, and hemorrhage. Moreover, LPS increased gp49B1 expression on neutrophils in vivo. The results suggest that gp49B1 suppresses the LPS-induced increase in intravascular neutrophil adhesion, thereby providing critical innate protection against a pathologic response to a bacterial component.

Mast cells are an essential hematopoietic component for polyp development.

It is generally agreed that most colon cancers develop from adenomatous polyps, and it is this fact on which screening strategies are based. Although there is overwhelming evidence to link intrinsic genetic lesions with the formation of these preneoplastic lesions, recent data suggest that the tumor stromal environment also plays an essential role in this disease. In particular, it has been suggested that CD34(+) immature myeloid precursor cells are required for tumor development and invasion. Here we have used mice conditional for the stabilization of beta-catenin or defective for the adenomatous polyposis coli (APC) gene to reinvestigated the identity and importance of tumor-infiltrating hematopoietic cells in polyposis. We show that, from the onset, polyps are infiltrated with proinflammatory mast cells (MC) and their precursors. Depletion of MC either pharmacologically or through the generation of chimeric mice with genetic lesions in MC development leads to a profound remission of existing polyps. Our data suggest that MC are an essential hematopoietic component for preneoplastic polyp development and are a novel target for therapeutic intervention.

Body Weight as an Indicator of Vulnerability to Domestic Cat Predation for Juveniles of Three Species of Cottontail Rabbits (Sylvilagus spp.) in Colorado, USA: Implications for Release Criteria.

Cottontail rabbits (Sylvilagus spp.) are frequently admitted to wildlife rehabilitation facilities due to predation by domestic cats (Felis catus). Our retrospective study (2015-19) of three species (Sylvilagus audubonii, Sylvilagus floridanus, and Sylvilagus nuttallii) indicated that once juveniles reached a weight over 220 g, they were unlikely to present due to domestic cat interactions. This information should be incorporated into release criteria for these species.

Precut tissue for Descemet's stripping automated endothelial keratoplasty: vision, astigmatism, and endothelial survival.

PURPOSE: To report 6 and 12 month results using precut tissue for Descemet's stripping automated endothelial keratoplasty (DSAEK) and correlate donor characteristics with clinical outcomes. DESIGN: Prospective, noncomparative, interventional case series. PARTICIPANTS: We reviewed 100 donor corneas precut for 100 eyes of 90 DSAEK patients. METHODS: Our first 100 consecutive cases of DSAEK with precut tissue were entered into a prospective protocol. Donor characteristics and the visual, refractive, topographic, and specular microscopy results at 6 and 12 months were analyzed. Correlation analysis comparing donor characteristics with clinical outcomes was performed. MAIN OUTCOME MEASURES: Six- and 12-month postoperative best spectacle-corrected visual acuity (BSCVA), refractive astigmatism, topographic keratometry (K), and specular endothelial cell densities (ECD) were measured prospectively and then compared with preoperative values. Donor characteristics analyzed included death to preservation time, death to surgery time, precutting resection to surgery time, and graft thickness. RESULTS: Six months after DSAEK surgery, BSCVA improved from 20/83 to 20/38. (P<0.01). In eyes with no known comorbidity (n = 60), 92% had a vision of >/=20/40 at 6 months and 20% obtained > or =20/20. Astigmatism changed an average of 0.09 diopters (D) and K changed by +0.09 D, both of which were not significant and were stable to 12 months. The postoperative mean ECD (n = 65) was 1918 cells/mm(2) at 6 months, and represented a 31% cell loss from preoperatively (P<0.001). The mean ECD (n = 61) was 1990 cells/mm(2) at 12 months, and represented a 29% cell loss from preoperatively (P<0.001) with no significant change from 6 to 12 months (P = 0.172). Improvement of visual acuity from preoperative to postoperative in eyes without comorbidity was not correlated with any donor characteristic. Greater endothelial cell loss correlated with higher preoperative ECD levels (P<0.001) and with a trend toward longer precut resection to surgery times at both 6 months (P = 0.049) and 12 months (P = 0.051). CONCLUSIONS: Precut tissue by Eye Banks for use in DSAEK surgery provides an improvement in vision with no significant change in astigmatism. Donor endothelial cell loss from 6 to 12 months is stable and is comparable with reports involving tissue that is cut intraoperatively. FINANCIAL DISCLOSURE(S): Proprietary or commercial disclosures may be found after the references.

Endothelial keratoplasty for Fuchs' dystrophy with cataract: complications and clinical results with the new triple procedure.

PURPOSE: To report the immediate postoperative complications and the 6- and 12-month clinical results in a large series of cases undergoing the new triple-procedure Descemet's stripping automated endothelial keratoplasty (DSAEK) and concurrent cataract surgery. DESIGN: Prospective, noncomparative, interventional case series. PARTICIPANTS: Three hundred fifteen eyes of 233 patients with Fuchs' corneal dystrophy were evaluated for the complications of dislocation and iatrogenic primary graft failure (IPGF). Two hundred three eyes of 149 patients had 6-month postoperative data available for other outcome analysis. METHODS: A standardized technique of DSAEK with extensive use of cohesive viscoelastic was performed in all 315 eyes with Fuchs' dystrophy, and 225 of those eyes had cataract surgery concurrently. Of the 203 eyes with 6-month data, concurrent phacoemulsification with intraocular lens placement (triple procedure) was performed in 149 of those eyes. MAIN OUTCOME MEASURES: The complications of graft dislocation and IPGF were recorded for all eyes. Six- and 12-month postoperative best spectacle-corrected visual acuity (BSCVA), refractive spherical equivalent (SE), and central donor endothelial cell density (ECD) were measured prospectively and then compared with preoperative values for the triple-procedure eyes. RESULTS: There were 4 dislocations (4%) among the 90 straight DSAEK cases and 4 dislocations (1.8%) among the 225 triple-procedure cases (P = 0.327). There was not a single case of IPGF in any of the 315 DSAEK cases. After the triple procedure, the BSCVA in eyes without comorbidity (n = 122) improved with 93% at 20/40 or better at 6 months and 97% at 20/40 or better at 12 months. Refractive SE at 6 months averaged 0.11+/-1.08 diopters (D), with 73% of eyes within 1 D of emmetropia and 95% within 2 D of emmetropia. The postoperative mean ECD was 1955 cells/mm(2) at 6 months (n = 125) and 1979 cells/mm(2) at 12 months (n = 89) and represented a 32% cell loss from that before surgery (P<0.001) for both postoperative time points. CONCLUSIONS: The new triple-procedure DSAEK combined with cataract surgery provides rapid visual recovery and allows selection of an appropriate intraocular lens. Dislocations are rare (1.8%) and primary graft failure did not occur.

Oyster sperm bindin is a combinatorial fucose lectin with remarkable intra-species diversity.

Sperm of the oyster, Crassostrea gigas, have ring-shaped acrosomes that, after exocytosis, bind the sperm to the egg vitelline layer. Isolated acrosomal rings contain proteins of various sizes: 35-, 48-, 63-, 75- and 88-kDa. These proteins, called bindins, have identical 24-residue signal peptides and conserved 97-residue N-terminal sequences, and they differ in mass because of the presence of between 1 and 5 tandemly repeated 134-residue fucose-binding lectin (F-lectin) domains. Southern blots suggest that oyster bindin is a single copy gene, but F-lectin repeat number and sequence are variable within and between individuals. Eight residues in the F-lectin fucose-binding groove are subject to positive diversifying selection, indicating a history of adaptive evolution at the lectin's active site. There is one intron in the middle of each F-lectin repeat, and recombination in this intron creates many combinations of repeat halves. Alternative splicing creates many additional size and sequence variants of the repeat array. Males contain full-length bindin cDNAs of all 5 possible sizes, but only one or two protein mass forms exist in each individual. Sequence analysis indicates that recombination and alternate splicing create hundreds, possibly thousands, of different bindin sequences in C. gigas. The extreme within-species sequence variation in the F-lectin sequence of oyster bindin is a novel finding; most male gamete-recognition proteins are much less variable. In experimental conditions oyster eggs have poor polyspermy blocks, and bindin diversity could be an evolutionary response by sperm to match egg receptors that have diversified to avoid being fertilized by multiple sperm.

Clostridial Enterotoxemia and Coccidiosis in Weanling Cottontail Rabbits ( Sylvilagus audubonii, Sylvilagus floridanus, Sylvilagus nuttallii) from Colorado, USA.

Wild cottontail rabbits ( Sylvilagus spp.), especially young individuals, are one of the most frequent wildlife species presented for rehabilitation at wildlife rehabilitation centers. These species are challenging to rehabilitate, with gastrointestinal (GI) disease being a major cause of morbidity and mortality during the weaning stage. Two organisms, Clostridium spiroforme and Eimeria spp., are frequently associated with GI disease in young domestic rabbits ( Oryctolagus cuniculus) and can result in high rates of morbidity and mortality in this species. Here we present evidence that these two pathogens also play an important role in GI disease in young cottontail rabbits ( Sylvilagus audubonii, Sylvilagus floridanus, Sylvilagus nuttallii) undergoing rehabilitation.

Endothelial keratoplasty a simplified technique to minimize graft dislocation, iatrogenic graft failure, and pupillary block.

PURPOSE: Endothelial keratoplasty is an exciting alternative to full-thickness penetrating keratoplasty for replacing the diseased endothelium, yet 3 of the major complications seen are dislocation of the donor tissue, primary graft failure (PGF), and pupillary block from the residual, supportive air bubble. Surgical strategies were developed to reduce the likelihood of occurrence of these complications in our first 200 consecutive Descemet's stripping automated endothelial keratoplasty (DSAEK) cases. DESIGN: Prospective, noncomparative, interventional case series. PARTICIPANTS: Two hundred eyes of 172 patients with corneal edema. METHODS: An institutional review board-approved, prospective protocol of endothelial keratoplasty was initiated. Four different surgeons performed DSAEK for the initial 200 consecutive cases using a technique of peripheral recipient bed scraping for donor edge adherence and leaving a residual supportive air bubble, which was freely mobile, and

Precut tissue in Descemet's stripping automated endothelial keratoplasty donor characteristics and early postoperative complications.

PURPOSE: To describe donor characteristics of eye bank-prepared precut tissue used in Descemet's stripping automated endothelial keratoplasty (DSAEK) and report any increase in immediate postoperative complications associated with its use. DESIGN: Prospective, noncomparative, interventional case series. PARTICIPANTS: One hundred donor corneas deemed appropriate for transplant and 100 eyes undergoing DSAEK for endothelial dysfunction. METHODS: Precut donor tissue was evaluated in a prospective study of 100 consecutive cases of DSAEK surgery. Donor characteristics and the immediate postoperative complications of donor tissue dislocation and graft failure with the use of precut tissue were recorded and analyzed. MAIN OUTCOME MEASURES: Preoperative donor characteristics (age, time from death to preservation, time from death to implantation, time from cut to implantation, residual stromal bed thickness, pre- and postcut endothelial density), rate of dislocation, and rate of primary graft failure. RESULTS: Average donor age was 57.6+/-10.8 years, average time from death to preservation was 9.8+/-3.2 hours, average time from death to implantation was 94.5+/-33.5 hours, and average time from cut to implantation was 26.0+/-17.4 hours. The average residual stromal bed thickness was 169+/-36 microns. The average endothelial cell density (ECD) after cutting was 2709+/-292 cells/mm(2) (n = 100). In the subgroup of donors in whom pre-resection and postresection endothelial cell densities were available (n = 80), the average ECD before cutting was 2743+/-253 cells/mm(2) and the average ECD after cutting was 2644+/-257 cells/mm(2). This average cell loss of 3.7% was statistically significant (P<0.001). There was only 1 dislocation in this entire series of 100 eyes. There were no primary graft failures. CONCLUSION: The use of precut tissue in DSAEK had a low rate of early postoperative complications such as graft dislocation (1%) and primary graft failure (0%). A wide range of donor characteristics such as donor age, death to transplantation time, precutting to transplantation time, and donor lenticule thickness resulted in excellent adhesion of the tissue and clear grafts.

Endothelial cell loss after Descemet's stripping endothelial keratoplasty in a large prospective series.

PURPOSE: To report the donor endothelial cell loss in the first year after Descemet's stripping endothelial keratoplasty (DSEK) for the treatment of endothelial dysfunction. DESIGN: Prospective noncomparative interventional case series. PARTICIPANTS: Eighty eyes of 78 patients with corneal edema. METHODS: Eighty eyes with endothelial failure were entered into a prospective study of endothelial keratoplasty (EK). The donor central endothelial cell density (ECD) was recorded postoperatively at 6 months (n = 80) and 12 months (n = 80) and then compared with the preoperative eye bank measurements. The subsets of eyes with the donor prepared manually (DSEK; n = 19) and the donor prepared with a microkeratome (Descemet's stripping automated EK [DSAEK]; n = 61) were also evaluated and compared. MAIN OUTCOME MEASURES: Preoperative and postoperative central ECDs were prospectively evaluated and the cell loss calculated for each postoperative time point. RESULTS: The average and standard deviation ECD at 6 months was 1908+/-354 cells/mm(2), representing a mean cell loss from preoperative donor cell measurements of 34+/-12%. At 12 months, ECD was 1856+/-371 cells/mm(2) (35+/-13% cell loss). The 1% additional cell loss from 6 to 12 months was not significant (P = 0.233). In the subset of DSEK eyes (n = 19), the cell loss from preoperatively to 6 months was 34%, and at 12 months it was 39%. In the subset of DSAEK eyes (n = 61), the cell loss from preoperatively to 6 months was 34%, and at 12 months it was 34%. There was no statistical difference between the cell loss from DSEK and that from DSAEK at 6 months (P = 0.884) or at 12 months (P = 0.224). CONCLUSIONS: Descemet's stripping EK using our surgical technique has a mean donor endothelial cell loss of 34% at the 6-month postoperative examination, and this average cell loss remains relatively stable up to at least 1 year. We found no difference in cell loss between the DSEK and DSAEK techniques over this 1-year postoperative period.

The Effectiveness of a Peer-Staffed Crisis Respite Program as an Alternative to Hospitalization.

OBJECTIVE: This study assessed whether peer-staffed crisis respite centers implemented in New York City in 2013 as an alternative to hospitalization reduced emergency department (ED) visits, hospitalizations, and Medicaid expenditures for individuals enrolled in Medicaid. METHODS: This study used Medicaid claims and enrollment data for January 2009 through April 2016 to estimate impacts on ED visits, hospitalizations, and total Medicaid expenditures by using a difference-in-differences model with a matched comparison group. The study sample included 401 respite center clients and 1,796 members of the comparison group. RESULTS: In the month of crisis respite use and the 11 subsequent months, Medicaid expenditures were on average $2,138 lower per Medicaid-enrolled month and there were 2.9 fewer hospitalizations for crisis respite clients than would have been expected in the absence of the intervention (p<.01). CONCLUSIONS: Peer-staffed crisis respite services resulted in lowered rates of Medicaid-funded hospitalizations and health expenditures for participants compared with a comparison group. The findings suggest that peer-staffed crisis respites can achieve system-level impacts.

CCR3 is essential for skin eosinophilia and airway hyperresponsiveness in a murine model of allergic skin inflammation.

The CC chemokine receptor 3 (CCR3) is expressed by eosinophils, mast cells, and Th2 cells. We used CCR3(-/-) mice to assess the role of CCR3 in a murine model of allergic skin inflammation induced by repeated epicutaneous sensitization with ovalbumin (OVA), and characterized by eosinophil skin infiltration, local expression of Th2 cytokines, and airway hyperresponsiveness (AHR) to inhaled antigen. Eosinophils and the eosinophil product major basic protein were absent from the skin of sham and OVA-sensitized CCR3(-/-) mice. Mast cell numbers and expression of IL-4 mRNA were normal in skin of CCR3(-/-) mice, suggesting that CCR3 is not important for infiltration of the skin by mast cells and Th2 cells. CCR3(-/-) mice produced normal levels of OVA-specific IgE, and their splenocytes secreted normal amounts of IL-4 and IL-5 following in vitro stimulation with OVA, indicating effective generation of systemic Th2 helper responses. Recruitment of eosinophils to lung parenchyma and bronchoalveolar lavage (BAL) fluid was severely impaired in CCR3(-/-) mice, which failed to develop AHR to methacholine following antigen inhalation. These results suggest that CCR3 plays an essential role in eosinophil recruitment to the skin and the lung and in the development of AHR.

Descemet Membrane Endothelial Keratoplasty (DMEK) Tissue Preparation: A Donor Diabetes Mellitus Categorical Risk Stratification Scale for Assessing Tissue Suitability and Reducing Tissue Loss.

PURPOSE: This study assessed a novel diabetes mellitus (DM) rating scale in relation to its utility in reducing Descemet membrane endothelial keratoplasty (DMEK) tissue preparation failure. METHODS: A 5-point DM rating scale was defined, in which 1 demonstrated relatively good health associated with DM and 5 represented comorbidities associated with DM. A chart review from consecutive donors who had at least 1 tissue prepared for DMEK was performed. Using the donor profile, the first tissue processed from each donor was categorized according to the DM severity and if the tissue passed or failed the DMEK preparation. Failure rates per rating group were evaluated using logistic regression and odds of preparation failure. RESULTS: A total of 125 tissues prepared for DMEK were categorized based on the defined DM rating scale. Of these, 9 tissues were rated 1 (11.1% failure), 25 were rated 2 (0% failure), 31 were rated 3 (6.5% failure), 24 were rated 4 (16.7% failure), and 36 were rated 5 (30.6% failure). The odds ratios were significant for tissues rated as 5 and 3 (P < 0.05). No other rating categories were found to influence the odds of failure. A χ test comparing categories of low risk (1-3) and high risk (4-5) was also performed (P = 0.001). CONCLUSIONS: The DM rating scale does seem to stratify the risk of preparation failure associated with the severity of DM and associated comorbidities. Inclusion of some diabetic donors for the preparation of DMEK grafts may be warranted given proper screening of the donor history and application of the rating scale.

Murine hindlimb reperfusion injury can be initiated by a self-reactive monoclonal IgM.

BACKGROUND: Murine hindlimb reperfusion injury (I/R), is initiated by activation of the classical pathway of complement. Complement receptor-2 knockout mice (Cr2-/-) are protected from I/R injury due to defective B-1 cells with a resulting deficient natural immunoglobulin M (IgM) repertoire. Cr2-/- and wild type (WT) mice were studied to isolate the antibody or antibodies responsible for initiation of I/R. METHODS: IgM-secreting B-1 cell clones were produced with hybridoma technology from WT cells. Of 21 clones tested in murine I/R models, only 1 clone, CM22, was found to restore injury in protected mice. Cr2-/- mice reconstituted with IgM from individual clones, WT serum, or saline were subjected to 2 hours hindlimb ischemia and 3 hours reperfusion and compared with WT. RESULTS: Muscle injury in Cr2-/- mice reconstituted with CM22 was similar to injury in WT mice reconstituted with saline and Cr2-/- mice reconstituted with WT serum. This injury was 137% greater (P < .05) than in both Cr2-/- mice reconstituted with saline and those reconstituted with a different IgM clone, CM31. IgM and C3 deposition was found only on injured muscle of WT mice or Cr2-/- mice reconstituted with CM22 or WT serum. CONCLUSION: A single clone of self-reactive IgM, CM22, can initiate complement-dependent I/R injury.

Endothelial keratoplasty: endothelial cell loss after deep lamellar endothelial keratoplasty with retention of an open-loop anterior chamber intraocular lens.

PURPOSE: To prospectively assess the impact of a retained open-loop anterior chamber intraocular lens (ACIOLs) on endothelial cell loss after deep lamellar endothelial keratoplasty (DLEK). METHODS: Prospectively gathered central endothelial cell densities of eyes with open-loop ACIOLs after DLEK were examined at 6 months, 1 year, and 2 years. RESULTS: Nine eyes with an open-loop ACIOL were examined. Mean endothelial cell loss was 37% at 6 months (n = 9, P = 0.001), 36% at 1 year (n = 6, P = 0.001), and 41%, at 2 years (n = 5, P = 0.002) after surgery. CONCLUSION: Postoperative endothelial cell loss over the first 2 years in this small series of patients undergoing DLEK with retention of an open-loop ACIOL may be greater in the first 6-12 months but similar at 2 years when compared with that found in the literature for the DLEK procedure.

Endothelial cell damage in descemet stripping automated endothelial keratoplasty with the underfold technique: 6- and 12-month results.

PURPOSE: To evaluate the endothelial cell loss at 6 and 12 months after Descemet stripping automated endothelial keratoplasty (DSAEK) using a modified 40/60 underfolding technique and to compare this to the literature on other commonly used implantation techniques, such as the conventional 60/40-fold, gliding, and hitch suture techniques. METHODS: Endothelial cell density was measured prospectively, and cell loss was calculated at 6 and 12 months after endothelial keratoplasty using a recently described underfolding implantation technique. RESULTS: In this study, 305 eyes undergoing DSAEK were evaluated. Average endothelial cell loss was 26% at 6 months and 27% at 12 months, all statistically significant reductions from preoperative values (P < 0.01). The decrease in cell count from 6 months to 12 months was not statistically significant. CONCLUSIONS: This study demonstrates reduction in endothelial cell loss after DSAEK using the underfold technique when compared with previous reports on conventional folding techniques and similarity to previous reports on glide techniques at 6 and 12 months postoperatively (26% vs. 34% vs. 23% at 6 months). This offers an easy modification to a commonly used existing technique and improves endothelial cell survival after DSAEK.