[Determination of chlorate and perchlorate in infant formula by ultra-high performance liquid chromatography-tandem mass spectrometry].

OBJECTIVE: To establish a method for determination of perchlorate and chlorate in infant formula by ultra-high performance liquid chromatography-tandem mass spectrometry(UPLC-MS/MS). METHODS: Chlorate-~(18)O_3 and perchlorate-~(18)O_4 were added to the samples, and the filtrate was collected and analyzed by UPLC-MS/MS by vortex mixing, extraction, centrifugation and filtration. The mobile phase was 20 mmol/L ammonium formate and acetonitrile. The Waters Torus~(TM) DEA(2.1 mm×100 mm, 1.7 µm)column was used to separate chlorate and perchlorate. The negative spray ionization(ESI-) was used. The multi-response monitoring(MRM) mode was used for monitoring. The internal standard method was used for quantification. RESULTS: The linear relationships of chlorate and perchlorate were good in the range of 0.2-200 µg/L and 0.1-100 µg/L(R~2& gt; 0.999), respectively. The detection limits(LOD, S/N=3) of chlorate and perchlorate were 0.35 µg/kg and 0.12 µg/kg, respectively, and the quantitative limits(LOQ, S/N=10) of chlorate and perchlorate were 1.16 µg/kg and 0.40 µg/kg, respectively. At the addition levels of 15.0, 75.0 and 150 µg/kg, the chlorate recovery was 91.9%-102.8% and the relative standard deviation(RSD, n=6) was 2.5%-4.4%. At the addition levels of 7.5, 37.5 and 75.0 µg/kg, the recovery rate of perchlorate was 91.3%-106.3% and the RSD(n=6) was 2.6%-3.9%. CONCLUSTION The method is simple, rapid, sensitive and accurate, and is suitable for simultaneous analysis of perchlorate and chlorate in various complex substrates.

Potential exposure to metals and health risks of metal intake from Tieguanyin tea production in Anxi, China.

The metal content of Tieguanyin tea from Anxi, Southeast China, was studied. Leaching experiments were designed based on the local tea-drinking habits, and tea infusions were prepared using three types of water and two methods of soaking tea. Twelve metals (Cd, As, Cr, Pb, Se, Sb, Ag, Tl, Cu, Zn, Be, and Ba) were measured by inductively coupled plasma mass spectrometry (ICP-MS), and a human health risk assessment was performed. The results showed that the quality of water used for steeping tea has a direct effect on the leaching concentrations of metals in the tea infusion and this effect can be reduced by using pure water or commercially available drinking water. Further, the two tea-soaking methods used by local residents can reduce the metal intake. The health risk assessment determined that the carcinogenic risk values of Cr, As, and Pb (Cr > Pb > As) were within an acceptable range (10-7-10-4); therefore, the concentrations of these metals in tea infusions do not pose substantial carcinogenic risk to tea drinkers. The results also indicate that the high concentrations of Tl in the tea infusions pose a substantial noncarcinogenic risk and may result from the dissolution characteristics of Tl and the water quality.

Retraction note to: Association between triglyceride-glucose index and colorectal polyps: A retrospective cross-sectional study.

[This retracts the article on p. 55 in vol. 16, PMID: 38464818.].

Association between triglyceride-glucose index and colorectal polyps: A retrospective cross-sectional study.

BACKGROUND: Colorectal polyps (CPs) are frequently occurring abnormal growths in the colorectum, and are a primary precursor of colorectal cancer (CRC). The triglyceride-glucose (TyG) index is a novel marker that assesses metabolic health and insulin resistance, and has been linked to gastrointestinal cancers. AIM: To investigate the potential association between the TyG index and CPs, as the relation between them has not been documented. METHODS: A total of 2537 persons undergoing a routine health physical examination and colonoscopy at The First People's Hospital of Kunshan, Jiangsu Province, China, between January 2020 and December 2022 were included in this retrospective cross-sectional study. After excluding individuals who did not meet the eligibility criteria, descriptive statistics were used to compare characteristics between patients with and without CPs. Logistic regression analyses were conducted to determine the associations between the TyG index and the prevalence of CPs. The TyG index was calculated using the following formula: Ln [triglyceride (mg/dL) × glucose (mg/dL)/2]. The presence and types of CPs was determined based on data from colonoscopy reports and pathology reports. RESULTS: A nonlinear relation between the TyG index and the prevalence of CPs was identified, and exhibited a curvilinear pattern with a cut-off point of 2.31. A significant association was observed before the turning point, with an odds ratio (95% confidence interval) of 1.70 (1.40, 2.06), P < 0.0001. However, the association between the TyG index and CPs was not significant after the cut-off point, with an odds ratio (95% confidence interval) of 0.57 (0.27, 1.23), P = 0.1521. CONCLUSION: Our study revealed a curvilinear association between the TyG index and CPs in Chinese individuals, suggesting its potential utility in developing colonoscopy screening strategies for preventing CRC.

Peripheral nerve lesion induces an up-regulation of Spy1 in rat spinal cord.

Spy1, as a member of the Speedy/RINGO family and a novel activator of cyclin-dependent kinases, was shown to promote cell cycle progression and cell survival in response to DNA damage. While its expression and roles in nervous system lesion and repair were still unknown. Here, we performed an acute sciatic nerve injury model in adult rats and studied the dynamic changes of Spy1 expression in lumbar spinal cord. Temporally, Spy1 expression was increased shortly after sciatic nerve crush and peaked at day 2. Spatially, Spy1 was widely expressed in the lumbar spinal cord including neurons and glial cells. While after injury, Spy1 expression was increased predominantly in astrocytes and microglia, which were largely proliferated. Moreover, there was a concomitant up-regulation of CDK2 activity and down-regulation of p27. Collectively, we hypothesized peripheral nerve injury induced an up-regulation of Spy1 in lumbar spinal cord, which was associated with glial proliferation.

Peripheral nerve injury induces down-regulation of Foxo3a and p27kip1 in rat dorsal root ganglia.

FOXO3a, as a forkhead transcription factor, can control cell cycle through transcriptionally down-regulating p27(kip1) level, which is a key regulator of the mammalian cell cycle and a good candidate to regulate multiple aspects of neurogenesis. To elucidate their expression and function in nervous system lesion and repair, we performed an acute sciatic nerve crush model and studied differential expressions of Foxo3a and p27(kip1) in lumbar dorsal root ganglia. Temporally, Foxo3a protein level was reduced 1 day after injury, and following Foxo3a down-regulation, p27(kip1) mRNA and protein levels were also decreased after injury. Spatially, decreased levels of Foxo3a and p27(kip1) were predominant in neurons and glial cells, which were regenerating axons and largely proliferated after injury, respectively. Together with previous reports, we hypothesized decreased levels of Foxo3a and p27(kip1) in lumbar dorsal root ganglia were implicated in axonal regeneration and the proliferation of glial cells after sciatic nerve injury.

Temporal-spatial expressions of p27kip1 and its phosphorylation on Serine-10 after acute spinal cord injury in adult rat: Implications for post-traumatic glial proliferation.

P27kip1, as a member of Cip/Kip family of cyclin-dependent kinase inhibitors, plays important roles in cell cycle regulation and neurogenesis in the developing central nervous system. Serine-10 is the major phosphorylation site of p27kip1, and post-translational regulation of p27kip1 by different phosphorylation events is critical for its function. To elucidate the expressions and possible functions of p27kip1 and its phosphorylation in central nervous system lesion and repair, we performed an acute spinal cord contusion injury model in adult rats. Our work studied the temporal-spatial expression patterns of p27kip1 and Serine-10 phosphorylated p27kip1 (p-p27s10). Western blot analysis showed p27kip1 level significantly decreased at day 3 after damage, while p-p27s10 was detected at a high-level at the same time reaching the uninjured level. Moreover, immunofluorescence double labeling suggested these changes were striking in microglia and astrocytes, which were largely proliferated. Immunohistochemical analysis revealed subcellular localization changes of p27kip1 and p-p27s10 staining between nucleus and cytoplasm after injury in about 20% of total positive cells including neurons and glial cells. We also investigated the increased interactions of p27kip1 and p-p27s10 with CRM1 3 days after injury by co-immunoprecipitation studies. Taken together, we hypothesized spinal cord injury stimulated mitogenic signals to induce a serine-threonine kinase KIS (kinase interacting stathmin) to phosphorylate p27kip1 on Serine-10, so that p27kip1 could bind to CRM1 and be exported from nuclei for degradation. Such an event facilitated cell cycle progression of glial cells, especially microglia and astrocytes which had a prevalent proliferation.

A relationship between p27(kip1) and Skp2 after adult brain injury: implications for glial proliferation.

S-phase-associated kinase protein-2 (Skp2) is involved in ubiquitination and proteasome-mediated degradation of p27(kip1), which plays an important role in mammalian cell-cycle regulation and neurogenesis in the developing central nervous system. To investigate their expression and function in central nervous system injury and repair, we used a brain-penetrating injury model in adult rats. Western blot analysis showed a significant downregulation of p27(kip1) and a concomitant upregulation of Skp2 following brain injury, and their expression profiles were temporally correlative (r = -0.910, p = 0.037). Immunofluorescence double-labeling revealed that p27(kip1) was highly expressed in neurons (51%), astrocytes (72%), and microglia (76%) in the sham group, while its expression was decreased prominently in microglia (26%) and astrocytes (32%) at 3 days after injury. Meanwhile, Skp2 expression was very low in all cell types in the sham group; however, 3 days after injury, its expression was increased significantly in microglia (51%) and astrocytes (31%) (p < 0.001), and less significantly in neurons (8%) (p = 0.038), and the astrocytes and microglia had proliferated. We also examined the expression profiles of CDK2, threonine-187 phosphorylated p27(kip1), proliferating cell nuclear antigen (PCNA), and Ki67, and their changes correlated with the expression profiles of p27(kip1) and Skp2. Moreover, co-immunoprecipitation data suggested that the protein-protein interactions between p27(kip1) and Skp2 were enhanced after injury. Taken with results of previous reports, we hypothesize the Skp2 is related to the downregulation of p27(kip1) expression after brain injury, and such an event may be associated with glial proliferation, including that of astrocytes and microglia.