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Background In the Republic of Korea, which medical specialties should take the responsibility for primary care and what the role of primary care should be are still unclear. In this study, we focused on the comprehensiveness of primary care to identify related factors. Methods The National Health Insurance Service (NHIS)-National Sample Cohort is a population-based cohort, sampled in the 2002 NHIS database and followed up until 2015. We used data collected from January 2014 to December 2015, including 20,423,832 outpatient visits in 19,557 office-based clinics. The Korean government has designated 52 simple or minor disease groups (SMDGs) to enhance the experience of patients who attend primary care for managing those diseases. We assessed comprehensiveness for each clinic as the number of SMDGs treated in each clinic for 2 years. We also identified the factors related to higher comprehensiveness, using logistic regression for analysis. Results The clinics included in the study had provided treatment for an average of 14 SMDGs during a 2-year period. Compared to general practitioners, internal medicine physicians presented higher comprehensiveness with an odds ratio (OR) of 2.29 (95% confidence interval [CI], 2.03-2.59), and family medicine physicians illustrated higher comprehensiveness (OR, 4.96; 95% CI, 3.59-6.83). Other specialties showed lower comprehensiveness than general practitioners. Clinics located in the capital city and metropolitan area tended to have lower comprehensiveness. Clinics hiring more doctors and having hospitalization facility showed higher comprehensiveness. Conclusion General physician, internal medicine, and family medicine are the fields providing comprehensive medical care in Korea. Clinics located in metropolitan area and capital city show lower comprehensiveness. The number of physicians is related to higher comprehensiveness of clinics.

Acadesine (ACA), a pharmacological activator of AMP-activated protein kinase (AMPK), showed a promising beneficial effect in a mouse model of colitis, indicating this drug as an alternative tool to manage IBDs. However, ACA displays some pharmacodynamic limitations precluding its therapeutical applications. Our study was aimed at evaluating the in vitro and in vivo effects of FA-5 (a novel direct AMPK activator synthesized in our laboratories) in an experimental model of colitis in rats. A set of experiments evaluated the ability of FA5 to activate AMPK and to compare the efficacy of FA5 with ACA in an experimental model of colitis. The effects of FA-5, ACA, or dexamethasone were tested in rats with 2,4-dinitrobenzenesulfonic acid (DNBS)-induced colitis to assess systemic and tissue inflammatory parameters. In in vitro experiments, FA5 induced phosphorylation, and thus the activation, of AMPK, contextually to the activation of SIRT-1. In vivo, FA5 counteracted the increase in spleen weight, improved the colon length, ameliorated macroscopic damage score, and reduced TNF and MDA tissue levels in DNBS-treated rats. Of note, FA-5 displayed an increased anti-inflammatory efficacy as compared with ACA. The novel AMPK activator FA-5 displays an improved anti-inflammatory efficacy representing a promising pharmacological tool against bowel inflammation.

Background: The progression of coronavirus disease-2019 (COVID-19) is less well-studied in asymptomatic patients. The study aimed to understand the clinical characteristics of asymptomatic COVID-19 patients at the time of admission and follow-up their occurrence of symptoms during hospitalization.Methods: Patients were divided into two groups—those with no symptoms until discharge (group A) and those who had symptoms that developed during hospitalization (group B). Baseline and clinical characteristics were retrospectively measured, and logistic regression analysis was performed to identify risk factors for deterioration during hospital stay.Results: Overall, 223 patients were enrolled in the study, including 42 and 181 patients in groups A and B, respectively. Patients were older in group B than in group A. They developed cough as the most common symptom. Abnormal initial chest X-ray (CXR) and higher levels of C-reactive protein were frequently observed in group B than in group A. Moreover, 5 patients required mechanical support, including hi-flow nasal cannular and mechanical ventilation in group B. Five patients were transferred to tertiary hospitals owing to deterioration, and 4 patients succumbed to COVID-19. The risk factors for deterioration were age over 75 years, diabetes mellitus, and C-reactive protein > 1.Conclusions: Even when the patients have no symptoms at admission, we recommend close monitoring of symptoms during hospital stay in patients who present with risk factors at the time of admission.

Accumulating evidence indicates many brain functions are mediated by epigenetic regulation of neural genes, and their dysregulations result in neuronal disorders. Experiences such as learning and recall, as well as physical exercise, induce neuronal activation through epigenetic modifications and by changing the noncoding RNA profiles. Animal models, brain samples from patients, and the development of diverse analytical methods have broadened our understanding of epigenetic regulation in the brain. Diverse and specific epigenetic changes are suggested to correlate with neuronal development, learning and memory, aging and age-related neuronal diseases. Although the results show some discrepancies, a careful comparison of the data (including methods, regions and conditions examined) would clarify the problems confronted in understanding epigenetic regulation in the brain. [BMB Reports 2016; 49(12): 671-680].

The striped catfish (Pangasianodon hypophthalmus) is a facultative air-breathing fish that is cultured in freshwater culture systems in Mekong Delta, Viet Nam. We report the effects of increased CO2 concentrations (7, 14, and 21 mmHg) and CO2 at different temperatures (27, 30, and 33 °C) on: (i) acid-base status and stress indicators (plasma glucose and cortisol); and (ii) growth parameters including weight, daily weight gain (DWG), specific growth rate (SGR), food conversion ratio (FCR), and digestive enzyme activity in P. hypophthalmus juveniles. The results show that there were stress responses via increases of glucose and cortisol concentrations, sharp decreases in pHe (extracellular pH) and increases in PaCO2 (partial pressure of CO2). Acid-base regulation appeared at the latter stage of CO2 exposure (from 24 h) at elevated temperatures with a related increase of plasma HCO3−. Digestive enzyme activities tended to reduce, typically pepsin at the high CO2 exposures of 14 and 21 mmHg after 60 days. Although survival rate fluctuated from 95 to 100% for all treatments, the lowest weight (56 g/fish) was found in the treatment of 21 mmHg CO2 whereas the control was 75 g/fish after 3 months of culture. In addition, DWG and SGR were relatively similar between the treatments of 7 mmHg CO2 and 14 mmHg CO2 at all three temperatures, whereas higher CO2 concentration led to significantly higher FCR at all CO2 exposures. In conclusion, there were no significant negative impacts of elevated temperatures (27–33 °C) and CO2 exposures (7–21 mmHg) in isolation and in combination on physiological responses, although there was decreased growth performance at the highest concentration of CO2 (21 mmHg).

Twelve new 2-quinolizinylbenzimidazole and 2-naphthalylbenzimidazole derivatives with various 5- and 6-positioned substituents (aza, H, CH3, Cl, NO2, NH2, OCH3), have been synthesized in moderate to excellent yields via the condensation of 4-oxo-4H-quinolizinecarbaldehyde or naphthalenecarbaldehyde with substituted o-phenylenediamines, o-nitroaniline, and 2,3-pyridinediamine using sodium metabisulfite or sodium hydrosulfite under microwave irradiation. The new benzimidazole derivatives were screened for their cytotoxic activity against the human breast cancer cell line (MCF-7). The results showed on one hand that 2-(substituted quinolizinyl)-1H-benzimidazoles (12b–f) were less active (3–6 fold) than the positive control Tamoxifen (CC50 = 6.52 μM), and on the other hand, among the 2-(substituted naphthalyl)-1H-benzimidazoles series (13a–f), compounds 6,7,8-trimethoxy-3-(5-chloro-1H-benzo[d]imidazol-2-yl)naphthalen-1-ol (13c) (CC50 = 7.48 μM) and 6,7,8-trimethoxy-3-(5-methoxy-1H-benzo[d]imidazol-2-yl)naphthalen-1-ol (13f) (CC50 = 6.43 μM) were found to be as active as Tamoxifen.

Upon viral infection, the 2', 5'-oligoadenylate synthetase (OAS)-ribonuclease L (RNaseL) system works to cleave viral RNA, thereby blocking viral replication. However, it is unclear whether OAS proteins have a role in regulating gene expression. Here, we show that OAS1 and OAS3 act as negative regulators of the expression of chemokines and interferonresponsive genes in human macrophages. Clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-associated protein-9 nuclease (Cas9) technology was used to engineer human myeloid cell lines in which the OAS1 or OAS3 gene was deleted. Neither OAS1 nor OAS3 was exclusively responsible for the degradation of rRNA in macrophages stimulated with poly(I:C), a synthetic surrogate for viral double-stranded (ds)RNA. An mRNA sequencing analysis revealed that genes related to type I interferon signaling and chemokine activity were increased in OAS1-/- and OAS3-/- macrophages treated with intracellular poly(I:C). Indeed, retinoic-acid-inducible gene (RIG)-I- and interferon-induced helicase C domain-containing protein (IFIH1 or MDA5)-mediated induction of chemokines and interferon-stimulated genes was regulated by OAS3, but Toll-like receptor 3 (TLR3)- and TLR4-mediated induction of those genes was modulated by OAS1 in macrophages. However, stimulation of these cells with type I interferons had no effect on OAS1- or OAS3-mediated chemokine secretion. These data suggest that OAS1 and OAS3 negatively regulate the expression of chemokines and interferon-responsive genes in human macrophages. [BMB Reports 2019; 52(2): 133-138].

Genetic and epigenetic alterations play prominent roles in hepatocarcinogenesis and their appearance varies depending on etiological factors, race and tumor progression. Intriguingly, distinct patterns of these genetic and epigenetic mutations are coupled not only to affect each other, but to trigger different types of tumorigenesis. The patterns and frequencies of somatic variations vary depending on the nature of the surrounding chromatin. On the other hand, epigenetic alterations often induce genomic instability prone to mutation. Therefore, genetic mutations and epigenetic alterations in hepatocellular carcinoma appear to be inseparable factors that accelerate tumorigenesis synergistically. We have summarized recent findings on genetic and epigenetic modifications, their influences on each other’s alterations and putative roles in liver tumorigenesis.

Twelve new 2-quinolizinylbenzimidazole and 2-naphthalylbenzimidazole derivatives with various 5- and 6-positioned substituents (aza, H, CH3, Cl, NO2, NH2, OCH3), have been synthesized in moderate to excellent yields via the condensation of 4-oxo-4H-quinolizinecarbaldehyde or naphthalenecarbaldehyde with substituted o-phenylenediamines, o-nitroaniline, and 2,3-pyridinediamine using sodium metabisulfite or sodium hydrosulfite under microwave irradiation. The new benzimidazole derivatives were screened for their cytotoxic activity against the human breast cancer cell line (MCF-7). The results showed on one hand that 2-(substituted quinolizinyl)-1H-benzimidazoles (12b–f) were less active (3–6 fold) than the positive control Tamoxifen (CC50 = 6.52 μM), and on the other hand, among the 2-(substituted naphthalyl)-1H-benzimidazoles series (13a–f), compounds 6,7,8-trimethoxy-3-(5-chloro-1H-benzo[d]imidazol-2-yl)naphthalen-1-ol (13c) (CC50 = 7.48 μM) and 6,7,8-trimethoxy-3-(5-methoxy-1H-benzo[d]imidazol-2-yl)naphthalen-1-ol (13f) (CC50 = 6.43 μM) were found to be as active as Tamoxifen.

The Drosophila mid-oogenesis stages are notable as the time when most maternal mRNAs become localized at discrete regions of the oocyte. Microtubule rearrangement occurs during this period and is critical for the localization of axis-determining maternal mRNAs. We have identified shot as a key player in establishing the cytoskeletal arrangement required for the spatial localization of axis-determining maternal mRNAs. We also found that the spatial distribution of the Shot protein is regulated by its mRNA localization. Our results suggest that the RNA localization mechanism is used not only for restricted accumulation of patterning molecules but also for the microtubule organization that leads to the initial development of oocyte polarity.

In Drosophila, mushroom bodies are centers for higher order behavior. Mushroom body neurons consist of three distinct types of neuronal cells, alpha, alpha'/beta', and alpha/beta, which are all generated by the same neuroblasts. The mechanism by which a single neuroblast generates three different types of mushroom body neurons is a compelling area of research. Here, we report that bunched (bun) is expressed only in alpha/beta-type mushroom body neurons and that mutation of the bun gene only affects the development of alpha/beta neurons. Reduced bun expression causes decreased and premature arrest of neuroblast cell division, which results in reduced numbers of alpha/beta neurons and thin axon bundled formation. We propose that bun acts as a specific factor in regulating neuroblast mitotic activity during the development of alpha/beta neurons.

In response to persistent mycobacteria infection, the host induces a granuloma, which often fails to eradicate bacteria and results in tissue damage. Diverse host receptors are required to control the formation and resolution of granuloma, but little is known concerning their regulatory interactions. Here we show that Mincle, the inducible receptor for mycobacterial cord factor, is the key switch for the transition of macrophages from cytokine expression to high nitric oxide production. In addition to its stimulatory role on TLR-mediated transcription, Mincle enhanced the translation of key genes required for nitric oxide synthesis through p38 and eIF5A hypusination, leading to granuloma resolution. Thus, Mincle has dual functions in the promotion and subsequent resolution of inflammation during anti-mycobacterial defence using both transcriptional and translational controls., Resolution of granulomas in mycobacterial infection requires macrophages to switch from cytokine to nitric oxide (NO) production. Here the authors show that Mincle stimulates translation of the key NO synthesis genes by a mechanism dependent on p38-mediated hypusination of eiF5A.

It has been generally accepted that Hwangryunjihwang-tang (H-tang) is a useful prescription for treating polydipsia and to prevent obesity induced by a high-fat diet. The aim of this study was to clarify whether H-tang improved reproductive dysfunction caused by obesity in mice. Mice were fed a high density protein and lipid diet for 4 weeks, followed by administration of H-tang at 480 mg/kg body weight per day for 4 days. Thereafter, changes of body weight, ovulation rate, in vitro and in vivo fertilization, embryonic development and implantation rate were measured. H-tang markedly reduced the body weight of obese mice fed a high-fat diet, but not mice fed a normal diet. H-tang significantly improved ovulation rates, in vitro and in vivo fertilization rates and embryonic development. These results indicate pharmacological reversal of reproductive dysfunction caused by obesity, perhaps by adjusting internal secretions and metabolic functions.

Transcription mediators are evolutionarily conserved from yeast to human. We previously reported the specific in vivo roles of mediators during development. Transcriptional mediators including med-6, med-7, and med-10 were shown to be involved in the regulated transcription of specific genes, but not in the transcription of ubiquitous genes. In this report we have identified and characterized the Caenorhabditis elegans med-7 gene. A genetic mutation in the med-7 gene was identified by comparing genetic and physical maps and determining the molecular lesion. let-49 was found to have a nonsense mutation in the coding region of the med-7 gene. The identification of let-49 as the med-7 gene was confirmed by rescue experiments. The phenotype of the let-49 mutation indicated that the med-7 gene is required for normal postembryonic development. RNAi experiments showed that med-7 is also involved in embryogenesis and the gonad and germ cell development.

The Drosophila RNA binding protein RBP9 and its Drosophila and human homologs, ELAV and the Hu family of proteins, respectively, are highly expressed in the nuclei of neuronal cells. However, biochemical studies suggest that the Hu proteins function in the regulation of mRNA stability, which occurs in the cytoplasm. In this paper, we show that RBP9 is expressed not only in the nuclei of neuronal cells but also in the cytoplasm of cystocytes during oogenesis. Despite the predominant expression of RBP9 in nerve cells, mutational analysis revealed a female sterility phenotype rather than neuronal defects for Rbp9 mutants. The female sterility phenotype of the Rbp9 mutants resulted from defects in oogenesis; the lack of Rbp9 activity caused the germarium region of the mutants to be filled with undifferentiated cystocytes. RBP9 appears to stimulate cystocyte differentiation by regulating the expression of bag-of-marbles (bam) mRNA, which encodes a developmental regulator of germ cells. RBP9 protein bound specifically to bam mRNA in vitro, which is required for cystocyte proliferation, and the number of cells that expressed BAM protein was increased 5- to 10-fold in the germarium regions of Rbp9 mutants. These results suggest that RBP9 protein binds to bam mRNA to down regulate BAM protein expression, which is essential for the initiation of cystocyte differentiation into functional egg chambers. In hypomorphic Rbp9 mutants, cystocytes differentiated into egg chambers; however, oocyte determination and positioning were perturbed. Therefore, the concentrated localization of RBP9 protein in the oocyte of the early egg chambers may be required for proper oocyte determination or positioning.

The purpose of this study was to assess the incidence and mortality of distal radius fracture among patients 50 years of age and older with diagnosis code (ICD10; S52.5, S52.6) and treatment code using a nationwide claims database from 2008 to 2012. All patients were followed using patient identification code to identify deaths. Standardized mortality ratios (SMRs) of distal radius fracture were calculated based on age and gender-specific rates in the entire Korean population. The number of distal radius fractures increased by 54.2% over the 5-year study (48,145 in 2008 and 74,240 in 2012). The incidence of distal radius fracture increased from 367.4/100,000 in 2008 to 474.1/100,000 in 2012. The cumulative mortality rate over the first 12 months after distal radius fracture was decreased from 2.0% (968/48,145) in 2008 to 1.4% (1,045/74,240) in 2012. The mean year mortality over 5 years in men (2.6%, 1,279/50,128) over the first 12 months was 1.7-times higher than in women (1.5%, 3,952/257,045). The mean of SMR of distal radius fracture at 1 year post-fracture was 1.45 in men and 1.17 in women. This study using a nationwide database demonstrates that the distal radius fractures are increasing with a decreasing mortality in Korea., Graphical Abstract

Objective To evaluate the clinical differences between patients with diabetes mellitus (DM) who have asymptomatic carpal tunnel syndrome (CTS) and those who have symptomatic CTS. Methods Sixty-three patients with DM were assessed using the Boston Carpal Tunnel Questionnaire (BCTQ), nerve conduction studies (NCS), and ultrasonographic evaluation of the cross-sectional area (CSA) of the median nerve. According to the BCTQ responses and NCS results, the patients were divided into the following three groups: group 1 (n=16), in which NCS results did not reveal CTS; group 2 (n=19), in which NCS results revealed CTS but the group scored 0 points on the BCTQ (asymptomatic); and group 3 (n=28), in which NCS results revealed CTS and the group scored >1 point on the BCTQ (symptomatic). The clinical findings, NCS results, and CSA of the median nerve were compared among the three groups. Results There were no significant differences in age, DM duration, glycated hemoglobin levels, and presence of diabetic polyneuropathy among the three groups. The peak latency of the median sensory nerve action potential was significantly shorter in group 1 than in groups 2 and 3 (p

To evaluate the effect of gadoxetic acid enhancement on the detection and characterisation of focal hepatic lesions on T(2) weighted and diffusion weighted (DW) images.A total of 63 consecutive patients underwent T(2) weighted and DW imaging before and after gadoxetic acid enhancement. Two blinded readers independently identified all of the focal lesions using a five-point confidence scale and characterised each lesion using a three-point scale: 1, non-solid; 2, indeterminate; and 3, solid. For both T(2) weighted and DW imaging, the accuracies for detecting focal lesions were compared using the free-response receiver operating characteristic analysis; the accuracies for lesion characterisation were compared using the McNemar test between non-enhanced and gadoxetic acid-enhanced image sets. For hepatic lesions ≥ 1 cm, the lesion-to-liver contrast-to-noise ratio (CNR) and the apparent diffusion coefficient (ADC) were compared in the non-enhanced and enhanced image sets using the generalised estimating equations.For both T(2) weighted and DW images, the accuracies for detecting focal lesions (p ≥ 0.52) and those for lesion characterisation (p ≥ 0.63) did not differ significantly between the non-enhanced and enhanced image sets. The lesion-to-liver CNR was significantly higher on enhanced DW images than on non-enhanced DW images (p=0.02), although the difference was not significant for T(2) weighted imaging (p=0.65). The mean ADC values of lesions did not differ significantly on enhanced and non-enhanced DW imaging (p=0.75).The acquisition of T(2) weighted and DW images after administration of gadoxetic acid has no significant effect on the detection or characterisation of focal hepatic lesions, although it improves the lesion-to-liver CNR on DW images.

Pattern formation in the early development of many organisms relies on localized cytoplasmic proteins, which can be prelocalized as mRNAs. The Drosophila oskar gene, required both for posterior body patterning and germ cell determination, encodes one such mRNA. Localization of oskar mRNA is an elaborate process involving movement of the transcript first into the oocyte from adjacent interconnected nurse cells and then across the length of the oocyte to its posterior pole. We have mapped RNA regulatory elements that direct this localization. Using a hybrid lacZ/oskar mRNA, we identify several elements within the oskar 3 untranslated region that affect different steps in the process: the early movement into the oocyte, accumulation at the anterior margin of the oocyte and finally localization to the posterior pole. This use of multiple cis-acting elements suggests that localization may be orchestrated in a combinatorial fashion, thereby allowing localized mRNAs with ultimately different destinations to employ common mechanisms for shared intermediate steps.

To identify genes that function in the adult neural system, we screened pools of P element-mediated mutants and tested locomotor activity of homozygous flies. Of 1014 P element-mutagenized lines, 638 were homozygous viable. These lines were tested for climbing ability and lifespan. We isolated dGIPC, a Drosophila homolog of GIPC, that produced a 50% premature loss of locomotor activity and a 30% reduction in life span. We found that dGIPC is expressed in the central brain of adult flies, especially in glia and dopaminergic (DA) neurons. Inhibition of dGIPC expression in DA neurons significantly affected climbing ability and survival. In vertebrates, interactions between GIPC with dopamine receptors have been reported. Our findings, together with those obtained from vertebrate models, suggest that Drosophila dGIPC acts in the adult central nervous system and may be required to regulate the trafficking of dopamine receptors needed for proper functioning of dopaminergic neurons.

Rbp9 is a Drosophila RNA-binding protein that shares a high level of sequence similarity with Drosophila elav and human Hu proteins. Loss of function alleles of elav are embryonic lethal causing abnormal central nervous system (CNS) development, and Hu is implicated in the development of paraneoplastic neurological syndrome associated with small cell lung cancer. To elucidate the role of Rbp9, we generated Rbp9 mutant flies and examined them for symptoms related to paraneoplastic encephalomyelitis. Although Rbp9 proteins begin to appear from the middle of the pupal period in the cortex of the CNS, the Rbp9 mutants showed no apparent defects in development. However, as the mutant adult flies grew older, they showed reduced locomotor activities and lived only one-half of the life expectancy of wild-type flies. To understand the molecular mechanism underlying this symptom, gene expression profiles in Rbp9 mutants were analyzed and potential target genes were further characterized. Reduced expression of cell adhesion molecules was detected, and defects in the blood-brain barrier (BBB) of Rbp9 mutant brains could be seen. Putative Rbp9-binding sites were found in introns of genes that function in cell adhesion. Therefore, Rbp9 may regulate the splicing of cell adhesion molecules, critical for the formation of the BBB.

Mutants of the maternal posterior-group genes of Drosophila lack posterior body pattern elements and germ cells, both of which form through the action of determinants localized to the posterior pole of the oocyte. We report that transcripts of one of these genes, oskar, become localized to the posterior pole of oocytes shortly after the oocyte begins to differentiate visibly. Analysis of various posterior-group mutants reveals that localization of oskar mRNA is an early step in the posterior localization pathway. In addition, we find that nonsense oskar mutations disrupt osk mRNA localization, while missense oskar mutations do not.

Essential aspects of the innate immune response to microbial infection appear to be conserved between insects and mammals. Although signaling pathways that activate NF-κB during innate immune responses to various microorganisms have been studied in detail, regulatory mechanisms that control other immune responses to fungal infection require further investigation. To identify new Drosophila genes involved in antifungal immune responses, we selected genes known to be differentially regulated in SL2 cells by microbial cell wall components and tested their roles in antifungal defense using mutant flies. From 130 mutant lines, sixteen mutants exhibited increased sensitivity to fungal infection. Examination of their effects on defense against various types of bacteria and fungi revealed nine genes that are involved specifically in defense against fungal infection. All of these mutants displayed defects in phagocytosis or activation of antimicrobial peptide genes following infection. In some mutants, these immune deficiencies were attributed to defects in hemocyte development and differentiation, while other mutants showed specific defects in immune signaling required for humoral or cellular immune responses. Our results identify a new class of genes involved in antifungal immune responses in Drosophila., Author Summary The innate immune response is the first line of defense against microbial infections in insects and mammals. In Drosophila, multiple defense mechanisms that contribute to the innate immune response include antimicrobial peptides (AMP), reactive oxygen species, phagocytosis and melanization. A search for genes involved in these immune processes identified sixteen mutants that exhibited increased lethality after infection. The diverse functions annotated to these genes indicate the complexity of the regulatory mechanisms required for defense against fungal infection. Lineage specific transcription factors and chromatin modifiers appeared to be required for proper development of functional hemocytes, while cytoskeletal regulators were required for phagocytotic activities of hemocytes. In addition, we identified several genes involved in the immune signaling required for AMP synthesis or melanization. These results may lay the foundation for defining a new class of genes that are involved in humoral and cellular antifungal immune responses.

This study investigated the baseline predictors of best corrected visual acuity (BCVA) and central retinal thickness (CRT) at 6 months in patients with treatment-naïve branch retinal vein occlusion (BRVO) and central retinal vein occlusion (CRVO). This multicenter, interventional case series included 208 BRVO and 123 CRVO patients with follow-up period of 6 months or more. Outcome measures of BCVA (logMAR) included absolute change from baseline and a gain or loss of ≥ 0.3 from baseline. Outcome measures of CRT included absolute change from baseline and a measurement of ≤ 250 µm or ≥ 400 µm at 6 months. Univariate and multiple regression analyses were done to find baseline predictors. For BRVO, younger age, worse baseline BCVA, and shorter duration of symptom were associated with more gain in BCVA. For CRVO, worse baseline BCVA was associated with more gain in BCVA. For CRT outcomes, higher baseline CRT predicted greater decrease at 6 months in both BRVO and CRVO. Younger age and better baseline BCVA were associated with an increased likelihood of measurement of a ≤ 250 µm outcome for BRVO and CRVO, respectively. For CRVO, smoking was associated with greater decrease from baseline and decreased likelihood of measurement of a CRT ≥ 400 µm at 6 months. In conclusion, several baseline factors including age, symptom duration, and baseline BCVA and CRT are associated with BCVA and CRT outcomes at 6 months, which may help to predict disease course for RVO patients. Graphical Abstract