Seeing is believing: in situ/operando optical microscopy for probing electrochemical energy systems

This review discusses a range of in situ/operando techniques based on optical microscopy reported in literatures for studying electrochemical energy systems. Compared to other techniques (scanning probe microscopy, electron microscopy, X-ray microscopy), optical microscopy offers many advantages including the simplicity of the instrument and operation, cost effectiveness, and nondestructive nature. In the past few decades, significant advances in the field of optical microscopy have been made, enabling new opportunities of more elaborate studies on electrochemical energy systems. Herein, different methodologies are compared, with the emphasis on experimental setup designs and findings, to illustrate their aptness

Additional file 1 of X chromosome rearrangement associated with premature ovarian insufficiency as diagnosed by molecular cytogenetic methods: a case report and review of the literature

Supplementary Material

Numbers of viable α-motor neurons in the anterior horn of spinal cord.

<p>The numbers of viable α-motor neurons were greater in C_0.01-C_0.5 groups than in the NS group. The best dosage was 0.1 mg/kg. There was no significant difference among the C_0.005, C₁, and NS groups. NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg. * <i>P</i><0.05 vs. the NS group.</p

Neurological and histopathological outcome at 48 hours after repercussion.

<p>Incidence is expressed as absolute numbers. Number of viable α-motor neurons is expressed as median (25th and 75th percentiles).</p><p>NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg. * <i>P</i><0.05 vs. the NS group.</p

Incidence of paraplegia and neurological dysfunction.

<p>Data are expressed as absolute numbers.</p><p>I/R = ischemia-reperfusion; 6 h = 6 hours after reperfusion; 24 h = 24 hours after reperfusion; 48 h = 48 hours after reperfusion. * <i>P</i><0.05 vs. the sham group.</p

Tarlov scores at different time points after reperfusion.

<p>Tarlov scores were significantly higher in C_0.01-C_0.5 groups than in the NS group at 24 and 48 hours after reperfusion. The best dosage was 0.1 mg/kg. There was no significant difference among the C_0.005, C₁, and NS groups. Tarlov score: 0 = paraplegia with no lower-extremity movement; 1 = poor lower-extremity movement but unresistant to gravity; 2 = good lower-extremity motor function with resistance to gravity, but unable to draw legs or hop; 3 = ability to draw leg and hop but not normally; 4 = normal lower-extremity motor function. NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg; 6 h = 6 hours; 24 h = 24 hours; 48 h = 48 hours. * <i>P</i><0.05 vs. the NS group.</p

Serum electrolytes concentration (mmol/L).

<p>Data are expressed as mean ± SD.</p><p>NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg; T0 = baseline; T1 = 30 minutes after ischemia; T2 = 30 minutes after reperfusion; T3 = 1 hour after reperfusion. * <i>P</i><0.05 vs. the NS group. # <i>P</i><0.05 vs. before aortic occlusion.</p

Changes of hemodynamics among different dosage groups.

<p>Clenbuterol (1 mg/kg) reduced DBP from T4 to T9, especially at T7, accompanied with the decrease of MAP. There were no significant differences in HR and SBP. NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg; HR = heart rate; SBP = systolic blood pressure; DBP = diastolic blood pressure; MAP = mean arterial pressure; T0 = baseline; T1 = the onset of ischemia; T2 = 5 minutes after ischemia; T3 = 10 minutes after ischemia; T4 = 15 minutes after ischemia; T5 = 20 minutes after ischemia; T6 = the onset of reperfusion; T7 = 5 minutes after reperfusion; T8 = 10 minutes after reperfusion; T9 = 15 minutes after reperfusion; T10 = 20 minutes after reperfusion; T11 = 30 minutes after reperfusion.</p

Hematoxylin and eosin staining in the anterior horn of spinal cord.

<p>(A) The sham group showed no specific histopathological change. (B) The I/R group showed marked vacuolization and significant loss of α-motor neurons. (C) The NS group showed a similar histopathological appearance to the I/R group. (E–H) Histopathological damage was attenuated in C_0.01, C_0.05, C_0.1, and C_0.5 groups. The α-motor neurons were preserved most in the C_0.1 group. (D and I) The C_0.005 and C₁ groups showed no significant neuroprotection (original magnification, 40× object lens). I/R = ischemia-reperfusion; NS = normal saline; C_0.005-C₁ = clenbuterol 0.005–1 mg/kg.</p

Table_1_Investigating the shared genetic architecture between hypothyroidism and rheumatoid arthritis.docx

BackgroundThere is still controversy regarding the relationship between hypothyroidism and rheumatoid arthritis (RA), and there has been a dearth of studies on this association. The purpose of our study was to explore the shared genetic architecture between hypothyroidism and RA.MethodsUsing public genome-wide association studies summary statistics of hypothyroidism and RA, we explored shared genetics between hypothyroidism and RA using linkage disequilibrium score regression, ρ-HESS, Pleiotropic analysis under a composite null hypothesis (PLACO), colocalization analysis, Multi-Trait Analysis of GWAS (MTAG), and transcriptome-wide association study (TWAS), and investigated causal associations using Mendelian randomization (MR).ResultsWe found a positive genetic association between hypothyroidism and RA, particularly in local genomic regions. Mendelian randomization analysis suggested a potential causal association of hypothyroidism with RA. Incorporating gene expression data, we observed that the genetic associations between hypothyroidism and RA were enriched in various tissues, including the spleen, lung, small intestine, adipose visceral, and blood. A comprehensive approach integrating PLACO, Bayesian colocalization analysis, MTAG, and TWAS, we successfully identified TYK2, IL2RA, and IRF5 as shared risk genes for both hypothyroidism and RA.ConclusionsOur investigation unveiled a shared genetic architecture between these two diseases, providing novel insights into the underlying biological mechanisms and establishing a foundation for more effective interventions.</p