Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet:

Article Snippet: MyD88 (-/-) mice were obtained from the Jackson Lab (strain # 009088) and were originally developed by Hou et al ( ).

Techniques: Produced

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) NanoString-based analysis of Toll-like receptor ( Tlr ) and MyD88 expression in the brainstem of 45-day old control and Ndufs4 (-/-) mice (see Methods ). Black – Ndufs4 (Ctl), Red – Ndufs4 (-/-) (see Methods ). p-values reflect multiple testing corrected (Holm-Šídák method) pairwise t-tests. *p<0.05, ns and those not shown – not significant. B ) Taqman probe-based qPCR analysis of Tlr7, Tlr9 , and MyD88 expression in 50-day old control and Ndufs4 (-/-) mouse brainstem samples. Normalized to actin, included in each reaction. Black – Ndufs4 (Ctl), Red – Ndufs4 (-/-) (see Methods ). Relative expression calculated using relative standard curve approach. *p<0.05, ns – not significant, by Holm-Šídák method multiple-testing corrected pairwise t-tests with Welch’s correction (no assumption regarding standard deviation).

Article Snippet: MyD88 (-/-) mice were obtained from the Jackson Lab (strain # 009088) and were originally developed by Hou et al ( ).

Techniques: Expressing, Control, Standard Deviation

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on overall weight trajectory in Nduf4 (-/-) mice (see Results, , ). Replicates (n’s) as indicated. B) Maximum weights of individual animals in A). Replicates (n’s) as indicated in A). ANOVA and pairwise comparisons were not statistically significant. C) Impact of enrofloxacin and MyD88 disruption on the onset of cachexia (weight loss) in Nduf4 (-/-) mice. No curves significantly different by pairwise log-rank comparison. Replicates (n’s) as indicated.

Article Snippet: MyD88 (-/-) mice were obtained from the Jackson Lab (strain # 009088) and were originally developed by Hou et al ( ).

Techniques: Disruption, Comparison

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on ataxia onset in Nduf4 (-/-) mice. n’s as indicated. The dot (MyD88(-/-) cohort) represents an animal which died prior to presenting with ataxia. P-value shown indicates pairwise log-rank test comparisons between curves indicated - **p<0.005. B) Impact of enrofloxacin and MyD88 disruption on the onset of clasping in Nduf4 (-/-) mice. n’s as indicated. The dot (MyD88(-/-) cohort) represents an animal which died prior to presenting with clasping. P-value shown indicates pairwise log-rank test comparisons between curves indicated - **p<0.005.

Article Snippet: MyD88 (-/-) mice were obtained from the Jackson Lab (strain # 009088) and were originally developed by Hou et al ( ).

Techniques: Disruption

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on survival in Nduf4 (-/-) mice (see Methods , introduction). P-values shown indicate pairwise log-rank test comparisons between curves indicated - **p=0.0087, *p<0.013. n’s as indicated. B) Cause of death in mice from A). FDIC – found dead in cage, cause of death unknown. C) Summary of findings. Enrofloxacin treatment modestly accelerates disease progression in the Ndufs4 (-/-) model, while loss of MyD88 modestly slows disease progression and extends survival.

Article Snippet: MyD88 (-/-) mice were obtained from the Jackson Lab (strain # 009088) and were originally developed by Hou et al ( ).

Techniques: Disruption, Biomarker Discovery

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet:

Article Snippet: Genotyping of Ndufs4 and MyD88 was performed according to the Jackson Laboratory methods (for strains #009088 and #027058).

Techniques: Produced

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) NanoString-based analysis of Toll-like receptor ( Tlr ) and MyD88 expression in the brainstem of 45-day old control and Ndufs4 (-/-) mice (see Methods ). Black – Ndufs4 (Ctl), Red – Ndufs4 (-/-) (see Methods ). p-values reflect multiple testing corrected (Holm-Šídák method) pairwise t-tests. *p<0.05, ns and those not shown – not significant. B ) Taqman probe-based qPCR analysis of Tlr7, Tlr9 , and MyD88 expression in 50-day old control and Ndufs4 (-/-) mouse brainstem samples. Normalized to actin, included in each reaction. Black – Ndufs4 (Ctl), Red – Ndufs4 (-/-) (see Methods ). Relative expression calculated using relative standard curve approach. *p<0.05, ns – not significant, by Holm-Šídák method multiple-testing corrected pairwise t-tests with Welch’s correction (no assumption regarding standard deviation).

Article Snippet: Genotyping of Ndufs4 and MyD88 was performed according to the Jackson Laboratory methods (for strains #009088 and #027058).

Techniques: Expressing, Control, Standard Deviation

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on overall weight trajectory in Nduf4 (-/-) mice (see Results, , ). Replicates (n’s) as indicated. B) Maximum weights of individual animals in A). Replicates (n’s) as indicated in A). ANOVA and pairwise comparisons were not statistically significant. C) Impact of enrofloxacin and MyD88 disruption on the onset of cachexia (weight loss) in Nduf4 (-/-) mice. No curves significantly different by pairwise log-rank comparison. Replicates (n’s) as indicated.

Article Snippet: Genotyping of Ndufs4 and MyD88 was performed according to the Jackson Laboratory methods (for strains #009088 and #027058).

Techniques: Disruption, Comparison

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on ataxia onset in Nduf4 (-/-) mice. n’s as indicated. The dot (MyD88(-/-) cohort) represents an animal which died prior to presenting with ataxia. P-value shown indicates pairwise log-rank test comparisons between curves indicated - **p<0.005. B) Impact of enrofloxacin and MyD88 disruption on the onset of clasping in Nduf4 (-/-) mice. n’s as indicated. The dot (MyD88(-/-) cohort) represents an animal which died prior to presenting with clasping. P-value shown indicates pairwise log-rank test comparisons between curves indicated - **p<0.005.

Article Snippet: Genotyping of Ndufs4 and MyD88 was performed according to the Jackson Laboratory methods (for strains #009088 and #027058).

Techniques: Disruption

Journal: bioRxiv

Article Title: MyD88 deficiency modestly attenuates disease in a Leigh syndrome mouse model while enrofloxacin accelerates disease

doi: 10.64898/2026.05.13.724988

Figure Lengend Snippet: A) Impact of enrofloxacin and MyD88 disruption on survival in Nduf4 (-/-) mice (see Methods , introduction). P-values shown indicate pairwise log-rank test comparisons between curves indicated - **p=0.0087, *p<0.013. n’s as indicated. B) Cause of death in mice from A). FDIC – found dead in cage, cause of death unknown. C) Summary of findings. Enrofloxacin treatment modestly accelerates disease progression in the Ndufs4 (-/-) model, while loss of MyD88 modestly slows disease progression and extends survival.

Article Snippet: Genotyping of Ndufs4 and MyD88 was performed according to the Jackson Laboratory methods (for strains #009088 and #027058).

Techniques: Disruption, Biomarker Discovery

Journal: Physiological Reports

Article Title: Water intake regulates mucosal immunity in rat jejunal villi via IL ‐1β, IL ‐6, and IL ‐10

doi: 10.14814/phy2.70891

Figure Lengend Snippet: (a) Effects of water intake on changes in lymph volume collected over set intervals of 60 min in rat jejunum‐derived lymph vessels in the absence (white column) and presence of a MyD88 inhibitor (oblique line column). (b) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐1β in the lymph. (c) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐6 in the lymph. (d) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐10 in the lymph. The error bars represent the SDs.

Article Snippet: Clodronate‐containing liposomes (catalog no 16001004, Sigma‐Aldrich, USA) and an inhibitor of MyD88 (catalog no 2‐29328 Novus Bio, USA) are purchased.

Techniques: Derivative Assay, Concentration Assay

Journal: iScience

Article Title: Protective effect of Zymosan-A against radiation-induced premature ovarian insufficiency in a murine model

doi: 10.1016/j.isci.2026.115027

Figure Lengend Snippet: The TLR2-NF-κB signaling pathway plays a critical role in the radioprotective effect of Zymosan-A (A) Heatmap of differential gene expression between wild-type mice and Zymosan-A mice. (B) Scatterplot of differently expressed genes in ovary tissue after Zymosan-A treatment. Each dot stands for a gene. Red and green color dots indicate an increase or decrease, respectively. (C) Pathway enrichment analysis of KEGG pathways within the core network. (D) RNA level to verify the expression of DEGs, including TLR2, CCL3, CCL5, AKT1, MYD88, and IκBκB. (E) The expression of TLR2-NF-κB pathway-related proteins. (F) The serum E2 level, AMH level, FSH level, and LH level were measured at TLR2 KO + IR + NS group and TLR2 KO + IR + Zymosan-A group. (G) The cell viability in siTLR2 + NS + IR group and siTLR2 + Zymosan-A + IR group (error bars represent the mean ± SD of independent experiments; N.S., no statistical difference, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; n = 3).

Article Snippet: The following antibodies were used: TLR2 (Cat no: 17236-1-AP, 1:1000, Proteintech), BCL-2 (Cat no: 60178-1-Ig, 1:1000, Proteintech), BAX (Cat no: 60267-1-Ig, 1:1000, Proteintech), PCNA (Cat no: 13110, 1:1000, CST), Cleaved Caspase-3 (Cat no: 9661, 1:1000, CST) and GAPDH (Cat no:5174, 1:1000, CST), p -IKKα/β (Cat no: 2697, 1:1000, CST), p-P65 (Cat no: 3033, 1:1000, CST), TLR2 (Cat no: 66645-1-Ig, 1:1000, Proteintech), Myd88 (Cat no: 50010, 1:1000, CST).

Techniques: Gene Expression, Expressing