Comparison of visual outcomes after epiretinal membrane surgery

AbstractPurposeTo elucidate the anatomical and visual outcomes of patients with idiopathic epiretinal membranes (ERM) who underwent vitrectomy, membrane removal only, or with internal limiting membrane (ILM) peeling under the assistance of different dyes.MethodsA retrospective chart review of patients with idiopathic ERM who received surgical treatment between January 2004 and December 2009. The patients were grouped according to the usage of staining materials assisting ILM peeling. Group 1 consisted of 61 eyes that underwent conventional vitrectomy and ERM peeling without staining-assisted ILM peeling. Group 2 consisted of 20 eyes with triamcinolone acetonide-assisted ILM peeling following conventional vitrectomy. Group 3 consisted of 23 eyes with indocyanine green-assisted ILM peeling following conventional vitrectomy.ResultsThis study included 104 eyes from 104 patients. There was no significant difference in age, sex, preoperative visual acuity, retinal thickness or follow-up duration among the three groups. Overall, the mean best-corrected visual acuity improved significantly from baseline 0.15 to postoperative 0.41 (p<0.0001). Among the three groups, the mean logarithm minimum angle of resolution acuity markedly improved. There was no significant difference in postoperative visual acuity among groups. As measured by ocular coherent tomography, the mean central foveal thickness decreased from 465.21±86.18 to 299.16±70.14μm. Although there was no difference between groups, postoperative retinal thickness was thicker than that observed in the normal population. The incidence of recurrent ERM was 13.1% in Group 1 and 0% in Groups 2 and 3; this incidence was significantly higher than in the conventional surgery group. Visual outcome was statistically more deteriorated in recurrent cases than in non-recurrent cases (p=0.011).ConclusionsERM surgeries with or without dye-assisted ILM peeling showed similar results. Moreover, the incidence of recurrence is lower in the ILM peeling groups and plays a primary role in determining the final postoperative vision outcome

Antinociceptive effects of morphine and naloxone in mu-opioid receptor knockout mice transfected with the MORS196A gene

<p>Abstract</p> <p>Background</p> <p>Opioid analgesics such as morphine and meperidine have been used to control moderate to severe pain for many years. However, these opioids have many side effects, including the development of tolerance and dependence after long-term use, which has limited their clinical use. We previously reported that mutations in the mu-opioid receptors (MOR) S196L and S196A rendered them responsive to the opioid antagonist naloxone without altering the agonist phenotype. In MORS196A knock-in mice, naloxone and naltrexone were antinociceptive but did not cause tolerance or physical dependence. In this study we delivery this mutated MOR gene into pain related pathway to confirm the possibility of <it>in vivo </it>transfecting MORS196A gene and using naloxone as a new analgesic agent.</p> <p>Methods</p> <p>The MOR-knockout (MOR-KO) mice were used to investigate whether morphine and naloxone could show antinociceptive effects when MORS196A gene was transfected into the spinal cords of MOR-KO mice. Double-stranded adeno-associated virus type 2 (dsAAV2) was used to deliver the MORS196A-enhanced green fluorescence protein (EGFP) gene by microinjected the virus into the spinal cord (S2/S3) dorsal horn region. Tail-flick test was used to measure the antinociceptive effect of drugs.</p> <p>Results</p> <p>Morphine (10 mg/kg, s.c.) and naloxone (10 mg/kg, s.c.) had no antinociceptive effects in MOR-KO mice before gene transfection. However, two or three weeks after the MOR-S196A gene had been injected locally into the spinal cord of MOR-KO mice, significant antinociceptive effects could be induced by naloxone or morphine. On the other hand, only morphine but not naloxone induced significant tolerance after sub-chronic treatment.</p> <p>Conclusion</p> <p>Transfecting the MORS196A gene into the spinal cord and systemically administering naloxone in MOR-KO mice activated the exogenously delivered mutant MOR and provided antinociceptive effect without causing tolerance. Since naloxone will not activate natural MOR in normal animals or humans, it is expected to produce fewer side effects and less tolerance and dependence than traditional opioid agonists do.</p

Memory Impairment and Plasma BDNF Correlates of the BDNF Val66Met Polymorphism in Patients With Bipolar II Disorder

Studies suggest that a functional polymorphism of brain-derived neurotrophic factor (BDNF), polymorphism BDNF Val66Met affects cognitive functions, however, the effect is unclear in bipolar II (BD-II) disorder. We used the Wechsler Memory Scale-third edition (WMS-III), the presence of the BDNF Val66Met polymorphism, and plasma concentrations of BDNF to investigate the association between memory impairment and BDNF in BD-II disorder. We assessed the memory functions of 228 BD-II patients and 135 healthy controls (HCs). BD-II patients had significantly lower scores on five of the eight WMS-III subscales. In addition to education, the BDNF polymorphism were associated with the following subscales of WMS-III, auditory delayed memory, auditory delayed recognition memory and general memory scores in BD-II patients, but not in HC. Moreover, BD-II patients with the Val-homozygote scored significantly higher on the visual immediate memory subscale than did those with the Met/Met and Val/Met polymorphisms. The significantly positive effect of the Val-homozygote did not have a significantly positive effect on memory in the HC group, however. We found no significant association between BDNF polymorphisms and plasma concentrations of BDNF. The plasma BDNF was more likely to be associated with clinical characteristics than it was with memory indices in the BD-II group. The impaired memory function in BD-II patients might be dependent upon the association between the BDNF Val66Met polymorphism and peripheral BDNF levels

Associations Between Hepatitis B Virus Genotype and Mutants and the Risk of Hepatocellular Carcinoma

Background The risk of hepatocellular carcinoma (HCC) increases with increasing level of hepatitis B virus (HBV) in serum (viral load). However , it is unclear whether genetic characteristics of HBV, including HBV genotype and specific genetic mutations, contribute to the risk of HCC. We examined the HCC risk associated with HBV genotypes and common variants in the precore and basal core promoter (BCP) regions. Methods From January 5, 1991, to December 21, 1992 , baseline blood samples were collected from 2762 Taiwanese men and women who were seropositive for HBV surface antigen but had not been diagnosed with HCC; the samples were tested for HBV viral load by real-time polymerase chain reaction and genotyped by melting curve analysis. Participants who had a baseline serum HBV DNA level greater than 101 copies/ mL (n = 1526) were tested for the precore G 1896A and BCP A 1762T/G1764A mutants by direct sequencing. Incident cases of HCC were ascertained through follow-up examinations and computerized linkage to the National Cancer Registry and death certification profiles. A Cox proportional hazards model was used to estimate the risk of HCC associated with HBV genotype and precore and BCP mutants after adjustment for other risk factors. All statistical tests were two-sided . Results A total of 153 HCC cases occurred during 33847 person-years of follow-up. The HCC incidence rates per 100000 person-years for participants infected with HBV genotype B or C were 305.6 (95% confidence interval [CI] = 236.9 to 388.1) and 785.8 (95% CI = 626.8 to 972.9), respectively. Among participants with a baseline HBV DNA level of at least 10(4) copies/mL, HCC incidence per 100000 person-years was higher for those with the precore G1896 ( wild-type) variant than for those with the G1896A variant ( 955.5 [95% CI = 749.0 to 1201.4] vs 269.4 [95% CI = 172.6 to 400.9]) and for those with the BCP A1762T/G1764A double mutant than for those with BCP A1762/G1764 (wild-type) variant (1149.2 [95% CI = 872.6 to 1485.6] vs 358.7 [95% Cl = 255.1 to 490.4]). The multivariable-adjusted hazard ratio of developing HCC was 1.76 (95% CI = 1.19 to 2.61) for genotype C vs genotype B, 0.34 (95% CI = 0.21 to 0.57) for precore G1896A vs wild type, and 1.73 (95% CI = 1.13 to 2.67 ) for BCP A1762T/G1764A vs wild type. Risk was highest among participants infected with genotype C HBV and wild type for the precore 1896 variant and mutant for the BCP 1762/1764 variant ( adjusted hazard ratio = 2.99, 95% CI = 1.57 to 5.70 , P<.001). Conclusions HBV genotype C and specific alleles of BCP and precore were associated with risk of HCC. These associations were independent of serum HBV DNA level

Low peripheral levels of insulin growth factor-1 are associated with high incidence of delirium among elderly patients: A systematic review and meta-analysis

Introduction: Delirium, a serious condition observed in critically ill patients, clinically presents with impaired cognition and consciousness. The relationship between delirium and peripheral levels of insulin growth factor-1 (IGF-1) is unclear. Thus we conducted a meta-analysis to address this issue. Methods: Seven major electronic databases were searched from inception until October 2, 2017 to obtain relevant clinical variables to compare the difference in IGF-1 levels between delirious and non-delirious elderly in-patients. A random effects meta-analysis was conducted. Results: We studies 10 articles involving 294 delirious patients (mean age 73.0 years) and 604 non-delirious patients (mean age 76.9 years). We found that peripheral levels of IGF-1 in patients with delirium were significantly lower than in those without delirium (Hedges‘ g = −0.209, 95% confidence interval [CI] = −0.393 to −0.026, p = 0.025). Meta-regression analyses found that no variables such as percentage of cognitive impairment, mean age, and female proportion contribute to heterogeneity in terms of the entire population. Conclusions: Our data suggests that lower peripheral levels of IGF-1 could be associated with a higher incidence of delirium among elderly patients. Further prospective studies with larger sample sizes are needed to investigate the association between peripheral levels of IGF-1 and delirium

Mobile Cloud-Based Blood Pressure Healthcare for Education

Mercury, pneumatic, and electronic sphygmomanometers were widely used for traditional blood pressure (BP) measurement. Cloud BP database, and mobile information and communication technology (MICT) do not integrate to these BP measurement methods. Pen and papers were employed to record BP values for nurses and physicians, and recording errors are possible to occur. In the chapter, the cloud-based BP platform solution and advanced wireless hospital BP measurement technologies were studied. These cloud-based BT measurement technologies were used as teaching aids to train students of electrical and nursing fields for mobile BP healthcare and health promotion education, and hence interdisciplinary teaching and learning were conducted. The teachers include professors of electrical and nursing fields, physicians, hospital nurses, and the engineer and health management experts of Microlife. The interdisciplinary teaching and learning of mobile BP healthcare and health promotion for smart aging were conducted in the Department of Nursing Division, Chang Cung Memorial Hospital, Keelung Branch, Department of Nursing Ching Kuo Institute of Management and Health, School of Nursing Chung Shan Medical University, and Department of Electrical Engineering, National Taiwan Ocean University. The students of electrical and nursing fields participated for joint interdisciplinary learning. The concepts of interdisciplinary mobile BP healthcare learning and teaching involve nursing and technology, healthy aging, BP health care for smart aging, telenursing, BP care for smart aging, community/home telecare, and MICT. The objective of teaching and learning is training the design and making electrical engineers to understand BP healthcare and health promotion, and nurses to understand mobile BP healthcare and health promotion system for smart aging

Factors Affecting Painkillers, Sedatives/Hypnotics, Nicotine, and Unhealthy Alcohol Use Among Gay and Bisexual Men in Taiwan

Substance use has become a major health problem globally for sexual minorities. However, few studies have explored multi-dimensional factors associated with smoking, drinking, and prescription drug use. We aimed to investigate the factors affecting painkiller, sedative/hypnotic, nicotine and unhealthy alcohol use among gay and bisexual men in Taiwan. We recruited 500 gay or bisexual men and assessed their experiences of using painkillers, sedatives/hypnotics, nicotine, alcohol and multi-dimensional factors with self-reported questionnaires. Multivariate logistic regression with a forward stepwise model was used to verify the factors associated with substance use. Overall, 9.4%, 5.4%, and 13.8% of the participants reported using painkillers, sedatives/hypnotics, and nicotine, respectively, and 5.6% reported unhealthy alcohol use. Victims of traditional homophobic bullying in childhood and adolescence were more likely to report nicotine use, sedative/hypnotic use, and unhealthy alcohol use in early adulthood than non-victims. Missing classes or truancy at senior high school was associated with painkiller and sedative/hypnotic use in early adulthood. Traditional homophobic bullying and missing classes or truancy in childhood and adolescence predicted substance use in early adulthood among the gay and bisexual men in this study. Timely preventions and interventions for substance use are crucial for gay and bisexual men, especially for those who experience homophobic bullying and missing classes or truancy

The Associations between Polysomnographic Parameters and Memory Impairment among Patients with Obstructive Sleep Apnea: A 10-Year Hospital-Based Longitudinal Study

Obstructive sleep apnea (OSA) has been associated with cognitive decline via several mechanisms, including intermittent hypoxemia, sleep fragmentation, and neuroinflammation. The neurological consequences of OSA have evolved into a major biopsychosocial concern in the elderly, especially memory impairment. We aimed to identify the polysomnographic (PSG) parameters capable of predicting memory impairment among OSA patients at or over age 50 with OSA. We reviewed the 10-year electronic medical records of OSA patients and compared the initial PSG parameters between those presenting and not presenting self-reported memory impairment. We conducted subgroup analyses based on OSA severity and performed multivariate analysis to correlate PSG parameters with memory impairment. The result showed that 25 out of the 156 (16%) investigated patients experienced self-reported memory impairment during follow-up. As compared to OSA patients without self-reported memory impairment, those reported with self-reported memory impairment had a higher oxygen desaturation index (ODI) (23.9 ± 17.8 versus 18.2 ± 12.0, p = 0.048). Regarding the associations between apnea-hypopnea index (AHI) as well as ODI and self-reported memory impairment among OSA subgroups classified by severity, the associations were only evident in the severe OSA subgroup in both univariate (p p = 0.005) and multivariate analyses (p = 0.014; p = 0.018). We concluded that AHI and ODI are the most relevant PSG parameters in predicting memory impairment in severe OSA patients

Neuron–Microglia Contacts Govern the PGE₂ Tolerance through TLR4-Mediated de Novo Protein Synthesis

Cellular and molecular mechanisms of the peripheral immune system (e.g., macrophage and monocyte) in programming endotoxin tolerance (ET) have been well studied. However, regulatory mechanism in development of brain immune tolerance remains unclear. The inducible COX-2/PGE2 axis in microglia, the primary innate immune cells of the brain, is a pivotal feature in causing inflammation and neuronal injury, both in acute excitotoxic insults and chronic neurodegenerative diseases. This present study investigated the regulatory mechanism of PGE2 tolerance in microglia. Multiple reconstituted primary brain cells cultures, including neuron–glial (NG), mixed glial (MG), neuron-enriched, and microglia-enriched cultures, were performed and consequently applied to a treatment regimen for ET induction. Our results revealed that the levels of COX-2 mRNA and supernatant PGE2 in NG cultures, but not in microglia-enriched and MG cultures, were drastically reduced in response to the ET challenge, suggesting that the presence of neurons, rather than astroglia, is required for PGE2 tolerance in microglia. Furthermore, our data showed that neural contact, instead of its soluble factors, is sufficient for developing microglial PGE2 tolerance. Simultaneously, this finding determined how neurons regulated microglial PGE2 tolerance. Moreover, by inhibiting TLR4 activation and de novo protein synthesis by LPS-binding protein (LBP) manipulation and cycloheximide, our data showed that the TLR4 signal and de novo protein synthesis are necessary for microglia to develop PGE2 tolerance in NG cells under the ET challenge. Altogether, our findings demonstrated that neuron–microglia contacts are indispensable in emerging PGE2 tolerance through the regulation of TLR4-mediated de novo protein synthesis