ObjectiveTo investigate the protective effect of α-ketoglutarate （α-KG） on hepatic lipid deposition in offspring caused by arsenic exposure during pregnancy. Methods8-week-old institute of cancer research （ICR） mice were mated in a ratio of 2∶1 between females and males， and the detection of vaginal plugs confirmed pregnant. A total of 32 pregnant mice were randomly divided into four groups： control group， arsenic group， α-KG group， arsenic+α-KG group. On gestational day 0-16 （GD0-GD16）， the arsenic and arsenic+α-KG groups were exposed to sodium arsenite （NaAsO₂ ，15 mg/L） in drinking water everyday， and the α-KG and arsenic+α-KG groups were gavaged with α-KG （2 g/kg） everyday. On GD16， pregnant mice were euthanized to collect fetal liver， and fetal body weight and crown-rump length were measured. Gene expression differences between the control group and the arsenic group were analyzed by transcriptome. The total triglycerides （TGs） and subtypes in fetal liver were detected by liquid chromatography tandem mass spectrometry （LC-MS/MS）. Oil red O staining was used to observe the histopathological changes in the liver. Quantitative polymerase chain reaction （qPCR） was used to detect the expression level of genes related to lipid synthesis， transport， and degradation， and phosphatidylinositol 3' -kinase/ protein kinase B （PI3K/AKT） in the liver of fetus. ResultsTranscriptomics analysis showed that 2 144 genes were downregulated and 1 675 genes were upregulated in the arsenic exposed fetal liver； body weight and crown-rump length were reduced （P_TuKey<0.05）； the level of hepatic TGs was elevated in arsenic group （P_TuKey<0.05）； oil-red O staining showed a significant increase in lipid droplets in arsenic group （P_TuKey<0.01）； the expression of lipid synthesis-related genes were significantly upregulated （P_TuKey<0.05）； the expression of β-oxidation-related genes and lipid degradation-related genes were downregulated （P_TuKey<0.05）； the expression of PI3K， AKT decreased（P_TuKey<0.05）. Compared with the arsenic group， the body weight and crown-rump length of fetus increased in the arsenic+α-KG group （P_TuKey<0.05）； the level of hepatic TGs decreased in the arsenic+α-KG group （P_TuKey<0.05）； oil red O staining showed lipid droplets significantly decreased （P_TuKey<0.01）； the expression of lipid synthesis-related genes were downregulated （P_TuKey<0.05）， the expression of β-oxidation-related genes and lipid degradation-related genes were upregulated （P_TuKey<0.05）； the expression levels of PI3K and AKT increased （P_TuKey<0.05）. Conclusionα-KG alleviated hepatic lipid deposition in offspring exposed to arsenic during pregnancy through activating PI3K/AKT signaling pathway.

AIM: To investigate the association between dyslipidemia and macular hard exudates(HEs)in non-proliferative diabetic retinopathy(NPDR)secondary to type 2 diabetes mellitus(T2DM).METHODS: NPDR patients attending the outpatient ophthalmology clinic from January 2021 to December 2023 were selected and divided into three groups according to the severity of macular HEs. Group A: None or minimal HEs; Group B: Definite HEs; Group C: Prominent HEs. Total cholesterol(TC), triglycerides(TG), low-density lipoprotein cholesterol(LDL-C), high-density lipoprotein cholesterol(HDL-C), lipoprotein(a)[Lp(a)] levels and other lipid-related indicators were routinely measured. The correlation between these indicators and HEs was analyzed.RESULTS:Group A(24 eyes)consisted of 9 males and 15 females with the mean age of 54.71±6.15 y, group B(52 eyes)consisted of 20 males and 32 females with the mean age of 55.08±6.27 y, group C(14 eyes)consisted of 9 males and 5 females with the mean age of 53.93±6.08 y. The concentration of TC, TG, LDL-C and Lp(a)was highest in group C, followed by group B and lowest in group A with statistically significant differences(P<0.001). There were no statistically significant differences between the three groups for fasting plasma glucose(FPG), glycated hemoglobin A1c(HbA1c), creatinine(Cr), and HDL-C(P>0.05). The results of multivariate Logistic regression analysis showed that elevated levels of TC, TG, LDL-C, and Lp(a)were associated with the presence of macular HEs. Receiver operating characteristiccurve analysis showed that the area under the curve(AUC)for TC, TG, LDL-C, Lp(a), and their combination in predicting macular HEs in NPDR were 0.785, 0.718, 0.784, 0.742, and 0.911, respectively, with the combined model demonstrating the highest predictive performance.CONCLUSION: Dyslipidemia is closely associated with the development and progression of macular HEs in patients with NPDR and T2DM. The levels of TC, TG, LDL-C, and Lp(a)were correlated with the severity of macular HEs, suggesting that dyslipidemia may be involved in the pathological process of macular HEs formation.

ObjectiveTo explore the ameliorative effect of the endoplasmic reticulum stress inhibitor 4-phenylbutyric acid （4-PBA） on bile acid metabolism disorders induced by bacterial lipopolysaccharide （LPS） in late-pregnant mice， and to clarify the regulatory mechanism of endoplasmic reticulum stress （ERS） in intrahepatic cholestasis of pregnancy （ICP）. MethodsTwenty-four pregnant mice were divided into control group， LPS group， 4-PBA group， and LPS+4-PBA group. On the 16th day of pregnancy， the LPS group received intraperitoneal injection of LPS （200 μg/kg） and the 4-PBA group received injection of 4-PBA （150 mg/kg）. In the LPS+4-PBA group， 4-PBA was intraperitoneally injected first， followed by LPS administration 1 h later. Serum total bile acid （TBA）， liver injury markers， bile acid profiles， and the expression of key genes and proteins were detected 6 h after LPS treatment. ResultsLPS exposure increased serum TBA levels in pregnant mice（P<0.05）， activated ERS markers and inflammatory factors， and downregulated bile acid transporters and the expression of the rate limiting enzyme CYP7A1（all P<0.05）. 4-PBA intervention effectively inhibited ERS， reduced TBA levels（P<0.05）， and upregulated Ntcp， Bsep， Mdr3， and Mrp3 gene expression（all P<0.05）. ConclusionERS plays an important role in LPS interference with the homeostasis of bile acid metabolism during pregnancy. Inhibiting ERS can improve bile stasis by regulating bile acid transporters， providing a theoretical basis for targeted therapy of ICP.

ObjectiveTo construct a risk prediction model for chronic atrophic gastritis （CAG） that combines disease and syndrome by integrating spleen deficiency and blood stasis syndrome scores， gastric stem cell marker analysis， and network pharmacology and to elucidate the mechanism link between spleen deficiency， blood stasis， and gastric stem cell dysregulation. MethodsA total of 60 patients were stratified into high-risk CAG， low-risk CAG， and non-atrophic groups based on the operative link for gastritis assessment （OLGA）/operative link for gastric intestinal metaplasia assessment （OLGIM） stages. General data and syndrome scores of the patients were collected. Immunohistochemistry was employed to measure the protein levels of leucine-rich repeat-containing G protein-coupled receptor 5 （LGR5）， trefoil factor 2 （TFF2）， and β-catenin in gastric mucosa across groups. Transcriptomic data （GSE130823） from the Gene Expression Omnibus （GEO） database were analyzed to validate the expression of these molecular markers at the gene level. A Firth penalized maximum likelihood logistic regression model was employed to integrate clinical， molecular， and TCM syndrome data to develop a CAG risk prediction model. Finally， network pharmacology analysis was conducted on spleen-invigorating herbs （Astragali Radix， Atractylodis Macrocephalae Rhizoma， and Dioscorea Rhizoma） and blood-activating herbs （Hedyotis diffusa， Salviae Miltiorrhizae Radix et Rhizoma， and Curcumae Rhizoma） to identify overlapping targets between these herbs and differentially expressed genes between low-grade intraepithelial neoplasia （LGIN） and gastritis， thereby clarifying the role of spleen deficiency and blood stasis in CAG progression from a pharmacological perspective. ResultsHigh-risk CAG patients exhibited higher blood stasis scores （4.60±1.50，2.62±1.32， P<0.01）， progressive nuclear accumulation of β-catenin （A 0.28-0.53， P<0.01）， and an increased LGR5⁺/TFF2⁺ ratio （A 1.02-1.92， P<0.01）. Blood stasis scores were correlated with LGR5/TFF2 imbalance （P=0.03） and activation of the Wnt/β-catenin signaling pathway （CTNNB1 increase， log₂=0.78）. The integrated prediction model （blood stasis score≥5 + β-catenin>0.38 + LGR5/TFF2>1.5） outperformed a pure biomarker approach ［Area Under the Curve （AUC） 0.92，0.89， ΔAUC=0.03， P=0.02］. Moreover， network pharmacology revealed 66 overlapping targets between spleen-invigorating/blood-activating herbs and LGIN， which were functionally enriched in mucosal repair and anti-oxidative stress， and negatively correlated with the Wnt/β-catenin signaling pathway （P<0.01）. ConclusionThis study developed an integrated risk prediction model for CAG by combining TCM spleen deficiency and blood stasis syndromes with gastric stem cell molecular markers. Furthermore， it proposed for the first time the "blood stasis-Wnt/β-catenin-stem cell axis" hypothesis， preliminarily elucidating that spleen deficiency and blood stasis may exacerbate gastric stem cell dysregulation and promote malignant transformation of CAG through hypoxia-induced Wnt activation. This provides a theoretical foundation and a translational tool for risk stratification and multi-target TCM intervention in CAG.

ObjectiveTo construct a risk prediction model for chronic atrophic gastritis （CAG） that combines disease and syndrome by integrating spleen deficiency and blood stasis syndrome scores， gastric stem cell marker analysis， and network pharmacology and to elucidate the mechanism link between spleen deficiency， blood stasis， and gastric stem cell dysregulation. MethodsA total of 60 patients were stratified into high-risk CAG， low-risk CAG， and non-atrophic groups based on the operative link for gastritis assessment （OLGA）/operative link for gastric intestinal metaplasia assessment （OLGIM） stages. General data and syndrome scores of the patients were collected. Immunohistochemistry was employed to measure the protein levels of leucine-rich repeat-containing G protein-coupled receptor 5 （LGR5）， trefoil factor 2 （TFF2）， and β-catenin in gastric mucosa across groups. Transcriptomic data （GSE130823） from the Gene Expression Omnibus （GEO） database were analyzed to validate the expression of these molecular markers at the gene level. A Firth penalized maximum likelihood logistic regression model was employed to integrate clinical， molecular， and TCM syndrome data to develop a CAG risk prediction model. Finally， network pharmacology analysis was conducted on spleen-invigorating herbs （Astragali Radix， Atractylodis Macrocephalae Rhizoma， and Dioscorea Rhizoma） and blood-activating herbs （Hedyotis diffusa， Salviae Miltiorrhizae Radix et Rhizoma， and Curcumae Rhizoma） to identify overlapping targets between these herbs and differentially expressed genes between low-grade intraepithelial neoplasia （LGIN） and gastritis， thereby clarifying the role of spleen deficiency and blood stasis in CAG progression from a pharmacological perspective. ResultsHigh-risk CAG patients exhibited higher blood stasis scores （4.60±1.50，2.62±1.32， P<0.01）， progressive nuclear accumulation of β-catenin （A 0.28-0.53， P<0.01）， and an increased LGR5⁺/TFF2⁺ ratio （A 1.02-1.92， P<0.01）. Blood stasis scores were correlated with LGR5/TFF2 imbalance （P=0.03） and activation of the Wnt/β-catenin signaling pathway （CTNNB1 increase， log₂=0.78）. The integrated prediction model （blood stasis score≥5 + β-catenin>0.38 + LGR5/TFF2>1.5） outperformed a pure biomarker approach ［Area Under the Curve （AUC） 0.92，0.89， ΔAUC=0.03， P=0.02］. Moreover， network pharmacology revealed 66 overlapping targets between spleen-invigorating/blood-activating herbs and LGIN， which were functionally enriched in mucosal repair and anti-oxidative stress， and negatively correlated with the Wnt/β-catenin signaling pathway （P<0.01）. ConclusionThis study developed an integrated risk prediction model for CAG by combining TCM spleen deficiency and blood stasis syndromes with gastric stem cell molecular markers. Furthermore， it proposed for the first time the "blood stasis-Wnt/β-catenin-stem cell axis" hypothesis， preliminarily elucidating that spleen deficiency and blood stasis may exacerbate gastric stem cell dysregulation and promote malignant transformation of CAG through hypoxia-induced Wnt activation. This provides a theoretical foundation and a translational tool for risk stratification and multi-target TCM intervention in CAG.

BACKGROUND:The authors found that when the bilateral percutaneous vertebral augmentation is used to treat osteoporotic vertebral compression fractures with a total bone cement injection of 4 mL or more,different distribution patterns were usually presented on the X-rays;however,there were few reports addressing the effects of these patterns of bone cement distribution on the biomechanical properties of fractural vertebrae. OBJECTIVE:To further explore the biomechanical effects of different bone cement filling doses and distribution patterns on biomechanics of the fractural vertebrae using the finite element method. METHODS:The L1-L3 finite element models of osteoporosis were established,and the vertebral compression fractures were simulated in L2.Four distribution patterns bilateral partial fusion(FH type),full fusion(FO type),symmetrical separation(SA type),and asymmetric segregation(SN type)were simulated in 4 and 6 mL injections in the osteoporotic vertebral compression fracture models,respectively,and a total of nine sets of models were obtained.These models were solved under the same boundary conditions and compared with the stress and displacement of the L2 fractural vertebra. RESULTS AND CONCLUSION:(1)The maximum stresses of the nine groups of models were concentrated in the L2 fractural area,and the maximum stress and maximum displacement of each filling model were lower than in the osteoporotic vertebral compression fracture model,indicating the effectiveness of bone cement filling in the treatment of osteoporotic vertebral compression fracture.(2)Compared with 4 mL bone cement filling,6 mL bone cement filling could significantly reduce the stress of fractured vertebrae and enhance the strength of fractured vertebrae while improving the stability of fractured vertebrae.(3)In the same state of movement,the FH type stress was the least,followed by the SA type,both of which were close.FO type stress was the largest,especially in the lateral bend,which might be associated with its cluster shape resulting in the concentration of lateral stress.In the aspect of displacement,FH type was the least and FO type was the largest.(4)The results show that increased dose of bone cement injection reduces fractural vertebral stress and improves stability,but increases the risk of leakage.Bilateral symmetrical dispersed bone cement(FH type,SA type)is superior in restoring vertebral strength and stability than full fusion(FO type),asymmetric separated(SN type)bone cement.Therefore,when clinically performing bilateral percutaneous vertebral augmentation treatment of osteoporotic vertebral compression fractures,the bilateral symmetric dispersions of the distribution are first guaranteed;priority is recommended for FH type distribution,for appropriate stress stimulation and best stability.

ObjectiveTo investigate the mechanism of Tangbikang dry paste in the prevention and treatment of type 2 diabetic peripheral neuropathy （DPN） based on the glyoxalase-1 （GLO-1）/advanced glycation end products （AGE）/receptor for advanced glycation end products （RAGE） pathway. MethodsA total of 56 Sprague-Dawley rats were randomly divided， with eight assigned to the normal group. The remaining 48 rats were fed a high-fat diet combined with intraperitoneal injection of streptozotocin （STZ） to induce a type 2 diabetes mellitus （T2DM） model. Based on blood glucose levels， the rats were randomly assigned to the model group， Tanglin group （13.5 mg·kg^-1）， metformin group （135 mg·kg^-1）， and Tangbikang dry paste low-， medium-， and high-dose groups （3， 6， 12 g·kg^-1）. Successful modeling of DPN was confirmed by a decrease in mechanical pain threshold in the model group at week 4. Fasting blood glucose， body weight， and mechanical pain threshold were measured every 4 weeks. After 16 weeks of intervention， the pathological morphology of the sciatic nerve was observed using hematoxylin-eosin （HE） staining. The expression of RAGE， AGE， protein kinase C （PKC）， and collagen （COL） in the sciatic nerve was assessed by immunohistochemistry. The mRNA expression of RAGE， PKC， Toll-like receptor （TLR）， COL， and GLO-1 was detected using real-time quantitative PCR （Real-time PCR）. Serum levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， creatinine （CREA）， urea （UREA）， interleukin-6 （IL-6）， and tumor necrosis factor （TNF）-α were measured by enzyme-linked immunosorbent assay （ELISA）. ResultsCompared with the normal group， the model group showed significantly increased fasting blood glucose （P<0.01）， decreased body weight and mechanical pain threshold （P<0.01）， and elevated serum AST， ALT， CREA， UREA， IL-6， and TNF-α levels （P<0.01）. The expression of RAGE， AGE， and PKC in the sciatic nerve was significantly increased （P<0.01）， while COL expression was decreased （P<0.01）. The mRNA expression of TLR， RAGE， and PKC was upregulated （P<0.01）， whereas COL and GLO-1 mRNA levels were downregulated （P<0.01）. Histological examination showed irregular nerve morphology， axonal alterations， and myelin degeneration. Compared with the model group， fasting blood glucose levels in the Tangbikang dry paste high-dose group at all time points and in the medium-dose group at weeks 4 and 16 were significantly reduced （P<0.05， P<0.01）. No significant changes in body weight were observed across all Tangbikang dose groups. The mechanical pain threshold was elevated at different time points after administration in all Tangbikang groups （P<0.05， P<0.01）. Serum IL-6 and TNF-α levels were decreased in all dose groups （P<0.05， P<0.01）. The expression of RAGE， AGE， and PKC in the sciatic nerve was reduced （P<0.01）， while COL expression was increased （P<0.01）. The mRNA expression of TLR， RAGE， and PKC was downregulated （P<0.01）， whereas GLO-1 mRNA expression was upregulated （P<0.05， P<0.01）. Additionally， COL mRNA expression was significantly increased in the low- and high-dose groups （P<0.01）. Pathological changes in the sciatic nerve were milder in all Tangbikang groups compared to the model group. ConclusionTangbikang dry paste significantly improves DPN， and its mechanism may be associated with the regulation of the GLO-1/AGE/RAGE signaling pathway.

ObjectiveTo investigate the role of 4-week high-intensity interval training (HIIT) in modulating the metabolic homeostasis of the pyruvate-lactate axis in the hippocampus of rats with chronic unpredictable mild stress (CUMS) to improve their depressive-like behavior. MethodsForty-eight SPF-grade 8-week-old male SD rats were randomly divided into 4 groups: the normal quiet group (C), the CUMS quiet group (M), the normal exercise group (HC), and the CUMS exercise group (HM). The M and HM groups received 8 weeks of CUMS modeling, while the HC and HM groups were exposed to 4 weeks of HIIT starting from the 5th week (3 min (85%-90%) S_max+1 min (50%-55%) S_max, 3-5 cycles, S_max is the maximum movement speed). A lactate analyzer was used to detect the blood lactate concentration in the quiet state of rats in the HC and HM groups at week 4 and in the 0, 2, 4, 8, 12, and 24 h after exercise, as well as in the quiet state of rats in each group at week 8. Behavioral indexes such as sucrose preference rate, number of times of uprightness and number of traversing frames in the absenteeism experiment, and other behavioral indexes were used to assess the depressive-like behavior of the rats at week 4 and week 8. The rats were anesthetized on the next day after the behavioral test in week 8, and hippocampal tissues were taken for assay. LC-MS non-targeted metabolomics, target quantification, ELISA and Western blot were used to detect the changes in metabolite content, lactate and pyruvate concentration, the content of key metabolic enzymes in the pyruvate-lactate axis, and the protein expression levels of monocarboxylate transporters (MCTs). Results4-week HIIT intervention significantly increased the sucrose preference rate, the number of uprights and the number of traversed frames in the absent field experiment in CUMS rats; non-targeted metabolomics assay found that 21 metabolites were significantly changed in group M compared to group C, and 14 and 11 differential metabolites were significantly dialed back in the HC and HM groups, respectively, after the 4-week HIIT intervention; the quantitative results of the targeting showed that, compared to group C, lactate concentration in the hippocampal tissues of M group, compared with group C, lactate concentration in hippocampal tissue was significantly reduced and pyruvate concentration was significantly increased, and 4-week HIIT intervention significantly increased the concentration of lactate and pyruvate in hippocampal tissue of HM group; the trend of changes in blood lactate concentration was consistent with the change in lactate concentration in hippocampal tissue; compared with group C, the LDHB content of group M was significantly increased, the content of PKM2 and PDH, as well as the protein expression level of MCT2 and MCT4 were significantly reduced. The 4-week HIIT intervention upregulated the PKM2 and PDH content as well as the protein expression levels of MCT2 and MCT4 in the HM group. ConclusionThe 4-week HIIT intervention upregulated blood lactate concentration and PKM2 and PDH metabolizing enzymes in hippocampal tissues of CUMS rats, and upregulated the expression of MCT2 and MCT4 transport carrier proteins to promote central lactate uptake and utilization, which regulated metabolic homeostasis of the pyruvate-lactate axis and improved depressive-like behaviors.

ObjectiveTo investigate the mechanism of Tangbikang dry paste in the prevention and treatment of type 2 diabetic peripheral neuropathy （DPN） based on the glyoxalase-1 （GLO-1）/advanced glycation end products （AGE）/receptor for advanced glycation end products （RAGE） pathway. MethodsA total of 56 Sprague-Dawley rats were randomly divided， with eight assigned to the normal group. The remaining 48 rats were fed a high-fat diet combined with intraperitoneal injection of streptozotocin （STZ） to induce a type 2 diabetes mellitus （T2DM） model. Based on blood glucose levels， the rats were randomly assigned to the model group， Tanglin group （13.5 mg·kg^-1）， metformin group （135 mg·kg^-1）， and Tangbikang dry paste low-， medium-， and high-dose groups （3， 6， 12 g·kg^-1）. Successful modeling of DPN was confirmed by a decrease in mechanical pain threshold in the model group at week 4. Fasting blood glucose， body weight， and mechanical pain threshold were measured every 4 weeks. After 16 weeks of intervention， the pathological morphology of the sciatic nerve was observed using hematoxylin-eosin （HE） staining. The expression of RAGE， AGE， protein kinase C （PKC）， and collagen （COL） in the sciatic nerve was assessed by immunohistochemistry. The mRNA expression of RAGE， PKC， Toll-like receptor （TLR）， COL， and GLO-1 was detected using real-time quantitative PCR （Real-time PCR）. Serum levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， creatinine （CREA）， urea （UREA）， interleukin-6 （IL-6）， and tumor necrosis factor （TNF）-α were measured by enzyme-linked immunosorbent assay （ELISA）. ResultsCompared with the normal group， the model group showed significantly increased fasting blood glucose （P<0.01）， decreased body weight and mechanical pain threshold （P<0.01）， and elevated serum AST， ALT， CREA， UREA， IL-6， and TNF-α levels （P<0.01）. The expression of RAGE， AGE， and PKC in the sciatic nerve was significantly increased （P<0.01）， while COL expression was decreased （P<0.01）. The mRNA expression of TLR， RAGE， and PKC was upregulated （P<0.01）， whereas COL and GLO-1 mRNA levels were downregulated （P<0.01）. Histological examination showed irregular nerve morphology， axonal alterations， and myelin degeneration. Compared with the model group， fasting blood glucose levels in the Tangbikang dry paste high-dose group at all time points and in the medium-dose group at weeks 4 and 16 were significantly reduced （P<0.05， P<0.01）. No significant changes in body weight were observed across all Tangbikang dose groups. The mechanical pain threshold was elevated at different time points after administration in all Tangbikang groups （P<0.05， P<0.01）. Serum IL-6 and TNF-α levels were decreased in all dose groups （P<0.05， P<0.01）. The expression of RAGE， AGE， and PKC in the sciatic nerve was reduced （P<0.01）， while COL expression was increased （P<0.01）. The mRNA expression of TLR， RAGE， and PKC was downregulated （P<0.01）， whereas GLO-1 mRNA expression was upregulated （P<0.05， P<0.01）. Additionally， COL mRNA expression was significantly increased in the low- and high-dose groups （P<0.01）. Pathological changes in the sciatic nerve were milder in all Tangbikang groups compared to the model group. ConclusionTangbikang dry paste significantly improves DPN， and its mechanism may be associated with the regulation of the GLO-1/AGE/RAGE signaling pathway.

The genome tagging project (GTP) plays a pivotal role in addressing a critical gap in the understanding of protein functions. Within this framework, we successfully generated a human influenza hemagglutinin-tagged sperm-specific protein 411 (HA-tagged Ssp411) mouse model. This model is instrumental in probing the expression and function of Ssp411. Our research revealed that Ssp411 is expressed in the round spermatids, elongating spermatids, elongated spermatids, and epididymal spermatozoa. The comprehensive examination of the distribution of Ssp411 in these germ cells offers new perspectives on its involvement in spermiogenesis. Nevertheless, rigorous further inquiry is imperative to elucidate the precise mechanistic underpinnings of these functions. Ssp411 is not detectable in metaphase II (MII) oocytes, zygotes, or 2-cell stage embryos, highlighting its intricate role in early embryonic development. These findings not only advance our understanding of the role of Ssp411 in reproductive physiology but also significantly contribute to the overarching goals of the GTP, fostering groundbreaking advancements in the fields of spermiogenesis and reproductive biology.
Animals ; Female ; Humans ; Male ; Mice ; Spermatids/metabolism* ; Spermatogenesis/physiology* ; Spermatozoa/metabolism* ; Thioredoxins/genetics*