Objective:To investigate the influencing factors of secondary osteoporosis in stroke patients with hemiplegia, and to construct a nomogram prediction model and evaluate it.Methods:The study subjects were 110 patients with hemiplegia after stroke who were treated in our hospital from Jun. 2019 to Jun. 2023, and were divided into osteoporosis group and non-osteoporosis group by bone mineral density detection. Clinical data and laboratory indicators were collected. Single factor analysis and binary Logistic multiple factor regression analysis were used to screen the influencing factors. R software (R3.3.2) and software package rms were used to construct the nomogram prediction model.Results:There were 52 patients with osteoporosis and 58 patients without osteoporosis. In the osteoporosis group, the proportion of female, unilateral anterior circulation multiple infarction and less sunlight was significantly higher than that in the non-osteoporosis group, with statistical significance ( χ2=8.27, 14.77 and 6.96, respectively, P<0.05). Systolic blood pressure (159.32±21.72 vs. 151.67±19.52), total cholesterol (4.29±0.50 vs. 3.57±0.42), LDL-C (2.87±0.33 vs. 2.04±0.31), Hcy (3.81±2.51 vs. The level of 112.33±2.47 was significantly higher than that of the non-osteoporosis group, and the difference was statistically significant ( t was 5.23, 8.38, 7.98 and 5.63, respectively, P<0.001). The level of albumin (38.15±5.21 vs. 33.26±5.73) was significantly lower than that of the non-osteoporosis group. The difference was statistically significant ( t=4.90, P<0.05). Binary Logistic regression analysis showed that female, higher total cholesterol, LDL-C, Hcy levels and less sun exposure were independent risk factors for secondary osteoporosis in stroke patients with hemiplegia ( P<0.05). ROC curve analysis results showed that the area under the curve of the established model to predict secondary osteoporosis in stroke hemiplegia patients was 0.891 (0.833-0.949), and the sensitivity and specificity were 80.8% and 79.3%, respectively. Conclusion:The categorization and consistency of the nomogram model based on the influencing factors of secondary osteoporosis in patients with stroke hemiplegia are good, which can provide a certain reference for the identification and early intervention of high-risk groups with stroke hemiplegia.

BACKGROUND: Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome is a severe congenital disorder characterized by vaginal hypoplasia caused by dysplasia of the Müllerian duct. Patients with MRKH syndrome often require nonsurgical or surgical treatment to achieve satisfactory vaginal length and sexual outcomes. The extracellular matrix has been successfully used for vaginal reconstruction. METHODS: In this study, we developed a new biological material derived from porcine vagina (acellular vaginal matrix, AVM) to reconstruct the vagina in Bama miniature pigs. The histological characteristics and efficacy of acellularization of AVM were evaluated, and AVM was subsequently transplanted into Bama miniature pigs to reconstruct the vaginas. RESULTS: Macroscopic analysis showed that the neovaginas functioned well in all Bama miniature pigs with AVM implants. Histological analysis and electrophysiological evidence indicated that morphological and functional recovery was restored in normal vaginal tissues. Scanning electron microscopy showed that the neovaginas had mucosal folds characteristics of normal vagina. No significant differences were observed in the expression of CK14, HSP47, and a-actin between the neovaginas and normal vaginal tissues. However, the expression of estrogen receptor (ER) was significantly lower in the neovaginas than in normal vaginal tissues. In addition, AVM promoted the expression of b-catenin, c-Myc, and cyclin D1. These results suggest that AVM might promotes vaginal regeneration by activating the b-catenin/cMyc/cyclin D1 pathway. CONCLUSION This study reveals that porcine-derived AVM has potential application for vaginal regeneration.

Objective:To analyze the relationship between allergen reactivity, atopic disease history and clinical features in patients with chronic inducible urticaria (CIndU) .Methods:A retrospective analysis was conducted on clinical data and follow-up results from 168 patients with CIndU in the Department of Dermatology, Southwest Hospital of Army Medical University from June 2014 to June 2015. Associations were analyzed between allergen reactivity, atopic disease history and clinical characteristics (including patient global assessment [PGA] scores, pruritus intensity, dermatology life quality index [DLQI], proportions of cases with complicated angioedema, natural course, etc.) in patients with different CIndU subtypes. Chi-square test, Mann-Whitney U test and Kaplan-Meier survival analysis were used for statistical analysis. Results:Among the 168 patients with CIndU, 117 were diagnosed with symptomatic dermographism (SD) , 32 with cold contact urticaria (CCU) , 5 with heat contact urticaria (HCU) , and 14 with cholinergic urticaria (CholU) ; there were 46 (39.3%) , 14 (43.8%) , 3, and 9 patients with positive skin prick test (SPT) among the patients with SD, CCU, HCU and CholU respectively, and no significant difference was observed in the positive rate of SPT among patients with different CIndU subtypes ( χ2 = 3.86, P = 0.283) . The SPT-positive CIndU patients showed significantly increased PGA scores, pruritus scores, DLQI scores and proportions of cases with complicated angioedema compared with the SPT-negative patients (all P<0.05) ; the CIndU patients with a personal or family history of atopic diseases also showed significantly increased PGA and DLQI scores compared with those without (both P < 0.05) . For different CIndU subtypes, the pruritus scores, PGA scores, DLQI scores, and proportions of cases with complicated angioedema were significantly higher in the SPT-positive SD patients than in the SPT-negative SD patients (all P < 0.05) ; the DLQI scores were significantly higher in the SPT-positive CholU patients than in the SPT-negative CholU patients ( Z = -2.28, P = 0.019) ; the pruritus scores were significantly higher in the CCU patients with a personal or family history of atopic diseases than in those without ( Z =-2.41, P = 0.022) . Conclusion:The allergen reactivity and atopic disease history of CIndU patients were associated with disease severity, pruritus intensity, quality of life, and the proportion of cases with complicated angioedema, but their relationship with the natural course of CIndU needs to be confirmed by further studies.

Pure drug-assembled nanomedicines (PDANs) are currently under intensive investigation as promising nanoplatforms for cancer therapy. However, poor colloidal stability and less tumor-homing ability remain critical unresolved problems that impede their clinical translation. Herein, we report a core-matched nanoassembly of pyropheophorbide a (PPa) for photodynamic therapy (PDT). Pure PPa molecules are found to self-assemble into nanoparticles (NPs), and an amphiphilic PEG polymer (PPa-PEG

Objective: To investigate the in vitro and in vivo effects of apatinib in esophageal squamous cell carcinoma and the underlying mechanisms. Methods: The esophageal cancer cells, KYSE-150 and ECA-109, were divided into control group and apatinib treatment group at the concentrations of 2.5, 5, 10, 20 and 40 μmol/L respectively. All of experiments were performed in triplicate. MTT and colony formation assays were used to measure cell proliferation. Transwell assay was used to determine the migration capacity. The effect of apatinib on cell cycle and apoptosis was analyzed by flow cytometry. The expression of VEGF and VEGFR-2 was measured by real-time quantitative PCR (qRT-PCR). The concentration of VEGF in the cell supernatant was assessed by enzyme-linked immunosorbent assay (ELISA). The expression levels of MEK, ERK, p-MEK, p-ERK, JAK2, STAT3 and p-STAT3 after VEGF stimulation were detected by Western blot. Furthermore, the nude mice xenograft model was established. The tumor-bearing mice were randomly divided into control group, apatinib low dose treatment group (250 mg) and apatinib high dose treatment group (500 mg), respectively. Tumor inhibition rates of different groups were calculated. And then the expressions of VEGF and VEGFR2 were detected in xenograft tissues by immunohistochemical staining. Results: In the presence of 20 μmol/L and 40 μmol/L of apatinib for 24 hours, the migration cell numbers of KYSE-150 and ECA-109 were 428.67±4.16 and 286.67±1.53 as well as 1 123.67±70.00 and 477.33±26.84, respectively, that were significantly lower than control group (P<0.05 for all). In addition, after treatment with 10 μmol/L, 20 μmol/L and 40 μmol/L of apatinib for 7 days on KYSE-150 and ECA-109, the colony formation rates were (65.12±25.48)%, (58.19±24.73)% and (29.10±22.40)% as well as (70.61±15.14)%, (61.12±17.21)% and (43.09±11.13)%, respectively. The colony formation rates of 20 μmol/L and 40 μmol/L of apatinib treatment groups were significantly lower than control group (100.00±0.00, P<0.05). The cell cycle ratio of G₂/M phase and apoptosis rate of control group and 20 μmol/L apatinib group in KYSE-150 cells were (12.14±2.13)% and (3.49±0.74)% as well as (26.27±3.30)% and (15.65±1.54)%, respectively. The corresponding ratios in ECA-109 cells were (3.44±0.57)% and (6.31±1.43)% as well as (22.64±2.36)% and (49.26±1.62)%, respectively. The results show that apatinib suppressed cell cycle progression at G₂/M phase and induced cell apoptosis in both KYSE-150 and ECA-109 cells (P<0.05 for all). In the presence of 20 μmol/L and 40 μmol/L of apatinib in KYSE-150 cells, the relative levels of VEGF mRNA were (42.57±10.43)% and (25.69±1.24)%, and those of VEGF-2 mRNA were (36.09±10.82)% and (13.99±6.54)%, which were all significantly decreased compared to control group (100.00±0.00, P<0.05 for all). For ECA-109 cells, the relative expression of VEGF and VEGFR2 showed similar tendency (P<0.05 for all). Moreover, after treatment with 20 μmol/L and 40 μmol/L of apatinib in KYSE-150 cells, the VEGF concentrations were (766.48±114.27) pg/ml and (497.40±102.18)pg/ml, which were significantly decreased compared to control group [(967.41±57.75) pg/ml, P<0.05)]. The results in ECA-109 were consistent (P<0.05). Furthermore, after treatment with 40 μmol/L of apatinib in KYSE-150 and ECA-109, the relative expression of p-MEK and p-ERK were 0.49±0.05 and 0.28±0.03 as well as 0.63±0.03 and 1.22±0.15, which were significantly lower than control group (1.23±0.19 and 0.66±0.07 as well as 1.03±0.20 and 1.76±0.20; P<0.05). The relative expression of STAT3, p-STAT3 in control group and experimental group were 0.96±0.15 and 0.85±0.16 as well as 0.62±0.09 and 0.36±0.13, respectively. The results showed that the protein levels of STAT3 and p-STAT3 were significantly lower than the control group (P<0.05 for all). The inhibition rates of apatinib in xenograft nude mice were 29.25% and 19.96% for 250 mg and 500 mg treatment groups. The concentration of VEGF were (25.11±4.12) pg/ml, (16.40±2.81) pg/ml and (15.04±4.88)pg/ml for control, 250 mg and 500 mg treatment groups, respectively. Conclusions Apatinib can inhibit cell proliferation, induce apoptosis and suppress migration of esophageal cancer cells in vitro and in vivo. This effect was mainly mediated via the alterations of Ras/Raf/MEK/ERK pathway and JAK2/STAT3 pathway.

Objective To investigate the in vitro and in vivo effects of apatinib in esophageal squamous cell carcinoma and the underlying mechanisms. Methods The esophageal cancer cells, KYSE?150 and ECA?109, were divided into control group and apatinib treatment group at the concentrations of 2.5, 5, 10, 20 and 40 μmol／L respectively. All of experiments were performed in triplicate. MTT and colony formation assays were used to measure cell proliferation. Transwell assay was used to determine the migration capacity. The effect of apatinib on cell cycle and apoptosis was analyzed by flow cytometry. The expression of VEGF and VEGFR?2 was measured by real?time quantitative PCR (qRT?PCR). The concentration of VEGF in the cell supernatant was assessed by enzyme?linked immunosorbent assay (ELISA). The expression levels of MEK, ERK, p?MEK, p?ERK, JAK2, STAT3 and p?STAT3 after VEGF stimulation were detected by Western blot. Furthermore, the nude mice xenograft model was established. The tumor?bearing mice were randomly divided into control group, apatinib low dose treatment group (250 mg) and apatinib high dose treatment group (500 mg), respectively.Tumor inhibition rates of different groups were calculated.And then the expressions of VEGF and VEGFR2 were detected in xenograft tissues by immunohistochemical staining. Results In the presence of 20 μmol／L and 40 μmol／L of apatinib for 24 hours, the migration cell numbers of KYSE?150 and ECA?109 were 428.67±4.16 and 286.67±1.53 as well as 1 123.67±70.00 and 477.33± 26.84, respectively, that were significantly lower than control group ( P＜0.05 for all). In addition, after treatment with 10 μmol／L, 20 μmol／L and 40 μmol／L of apatinib for 7 days on KYSE?150 and ECA?109, the colony formation rates were ( 65.12± 25.48)%, ( 58.19± 24.73)% and (29.10± 22.40)% as well as (70.61±15.14)%, (61.12±17.21)% and (43.09±11.13)%, respectively. The colony formation rates of 20 μmol／L and 40 μmol／L of apatinib treatment groups were significantly lower than control group (100.00±0.00, P＜0.05). The cell cycle ratio of G2／M phase and apoptosis rate of control group and 20 μmol／L apatinib group in KYSE?150 cells were (12.14±2.13)% and (3.49±0.74)% as well as (26.27±3.30)% and (15.65± 1.54)%, respectively. The corresponding ratios in ECA?109 cells were (3.44±0.57)% and (6.31±1.43)%as well as (22.64±2.36)% and (49.26± 1.62)%, respectively. The results show that apatinib suppressed cell cycle progression at G2／M phase and induced cell apoptosis in both KYSE?150 and ECA?109 cells (P＜0.05 for all). In the presence of 20 μmol／L and 40 μmol／L of apatinib in KYSE?150 cells, the relative levels of VEGF mRNA were (42.57± 10.43)% and ( 25.69± 1.24)%, and those of VEGF?2 mRNA were (36.09±10.82)% and (13.99±6.54)%, which were all significantly decreased compared to control group (100.00±0.00, P＜0.05 for all). For ECA?109 cells, the relative expression of VEGF and VEGFR2 showed similar tendency (P＜0.05 for all). Moreover, after treatment with 20 μmol／L and 40 μmol／L of apatinib in KYSE?150 cells, the VEGF concentrations were ( 766.48± 114.27) pg／ml and ( 497.40± 102.18) pg／ml, which were significantly decreased compared to control group [(967.41± 57.75) pg／ml, P＜0.05)]. The results in ECA?109 were consistent (P＜0.05). Furthermore, after treatment with 40 μmol／L of apatinib in KYSE?150 and ECA?109, the relative expression of p?MEK and p?ERK were 0.49±0.05 and 0.28±0.03 as well as 0.63±0.03 and 1.22±0.15, which were significantly lower than control group (1.23±0.19 and 0.66± 0.07 as well as 1.03±0.20 and 1.76±0.20; P＜0.05). The relative expression of STAT3, p?STAT3 in control group and experimental group were 0.96 ± 0.15 and 0.85 ± 0.16 as well as 0.62 ± 0.09 and 0.36 ± 0.13, respectively. The results showed that the protein levels of STAT3 and p?STAT3 were significantly lower than the control group (P＜0.05 for all). The inhibition rates of apatinib in xenograft nude mice were 29.25% and 19.96% for 250 mg and 500 mg treatment groups. The concentration of VEGF were (25.11±4.12) pg／ml, (16.40 ± 2.81) pg／ml and ( 15.04 ± 4.88) pg／ml for control, 250 mg and 500 mg treatment groups, respectively. Conclusions Apatinib can inhibit cell proliferation, induce apoptosis and suppress migration of esophageal cancer cells in vitro and in vivo. This effect was mainly mediated via the alterations of Ras／Raf／MEK／ERK pathway and JAK2／STAT3 pathway.

Objective To investigate the in vitro and in vivo effects of apatinib in esophageal squamous cell carcinoma and the underlying mechanisms. Methods The esophageal cancer cells, KYSE?150 and ECA?109, were divided into control group and apatinib treatment group at the concentrations of 2.5, 5, 10, 20 and 40 μmol／L respectively. All of experiments were performed in triplicate. MTT and colony formation assays were used to measure cell proliferation. Transwell assay was used to determine the migration capacity. The effect of apatinib on cell cycle and apoptosis was analyzed by flow cytometry. The expression of VEGF and VEGFR?2 was measured by real?time quantitative PCR (qRT?PCR). The concentration of VEGF in the cell supernatant was assessed by enzyme?linked immunosorbent assay (ELISA). The expression levels of MEK, ERK, p?MEK, p?ERK, JAK2, STAT3 and p?STAT3 after VEGF stimulation were detected by Western blot. Furthermore, the nude mice xenograft model was established. The tumor?bearing mice were randomly divided into control group, apatinib low dose treatment group (250 mg) and apatinib high dose treatment group (500 mg), respectively.Tumor inhibition rates of different groups were calculated.And then the expressions of VEGF and VEGFR2 were detected in xenograft tissues by immunohistochemical staining. Results In the presence of 20 μmol／L and 40 μmol／L of apatinib for 24 hours, the migration cell numbers of KYSE?150 and ECA?109 were 428.67±4.16 and 286.67±1.53 as well as 1 123.67±70.00 and 477.33± 26.84, respectively, that were significantly lower than control group ( P＜0.05 for all). In addition, after treatment with 10 μmol／L, 20 μmol／L and 40 μmol／L of apatinib for 7 days on KYSE?150 and ECA?109, the colony formation rates were ( 65.12± 25.48)%, ( 58.19± 24.73)% and (29.10± 22.40)% as well as (70.61±15.14)%, (61.12±17.21)% and (43.09±11.13)%, respectively. The colony formation rates of 20 μmol／L and 40 μmol／L of apatinib treatment groups were significantly lower than control group (100.00±0.00, P＜0.05). The cell cycle ratio of G2／M phase and apoptosis rate of control group and 20 μmol／L apatinib group in KYSE?150 cells were (12.14±2.13)% and (3.49±0.74)% as well as (26.27±3.30)% and (15.65± 1.54)%, respectively. The corresponding ratios in ECA?109 cells were (3.44±0.57)% and (6.31±1.43)%as well as (22.64±2.36)% and (49.26± 1.62)%, respectively. The results show that apatinib suppressed cell cycle progression at G2／M phase and induced cell apoptosis in both KYSE?150 and ECA?109 cells (P＜0.05 for all). In the presence of 20 μmol／L and 40 μmol／L of apatinib in KYSE?150 cells, the relative levels of VEGF mRNA were (42.57± 10.43)% and ( 25.69± 1.24)%, and those of VEGF?2 mRNA were (36.09±10.82)% and (13.99±6.54)%, which were all significantly decreased compared to control group (100.00±0.00, P＜0.05 for all). For ECA?109 cells, the relative expression of VEGF and VEGFR2 showed similar tendency (P＜0.05 for all). Moreover, after treatment with 20 μmol／L and 40 μmol／L of apatinib in KYSE?150 cells, the VEGF concentrations were ( 766.48± 114.27) pg／ml and ( 497.40± 102.18) pg／ml, which were significantly decreased compared to control group [(967.41± 57.75) pg／ml, P＜0.05)]. The results in ECA?109 were consistent (P＜0.05). Furthermore, after treatment with 40 μmol／L of apatinib in KYSE?150 and ECA?109, the relative expression of p?MEK and p?ERK were 0.49±0.05 and 0.28±0.03 as well as 0.63±0.03 and 1.22±0.15, which were significantly lower than control group (1.23±0.19 and 0.66± 0.07 as well as 1.03±0.20 and 1.76±0.20; P＜0.05). The relative expression of STAT3, p?STAT3 in control group and experimental group were 0.96 ± 0.15 and 0.85 ± 0.16 as well as 0.62 ± 0.09 and 0.36 ± 0.13, respectively. The results showed that the protein levels of STAT3 and p?STAT3 were significantly lower than the control group (P＜0.05 for all). The inhibition rates of apatinib in xenograft nude mice were 29.25% and 19.96% for 250 mg and 500 mg treatment groups. The concentration of VEGF were (25.11±4.12) pg／ml, (16.40 ± 2.81) pg／ml and ( 15.04 ± 4.88) pg／ml for control, 250 mg and 500 mg treatment groups, respectively. Conclusions Apatinib can inhibit cell proliferation, induce apoptosis and suppress migration of esophageal cancer cells in vitro and in vivo. This effect was mainly mediated via the alterations of Ras／Raf／MEK／ERK pathway and JAK2／STAT3 pathway.

Overexpressing of ATP-binding cassette (ABC) transporters is the essential cause of multidrug resistance (MDR), which is a significant hurdle to the success of chemotherapy in many cancers. Therefore, inhibiting the activity of ABC transporters may be a logical approach to circumvent MDR. Olmutinib is an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), which has been approved in South Korea for advanced EGFR T790M-positive non-small cell lung cancer (NSCLC). Here, we found that olmutinib significantly increased the sensitivity of chemotherapy drug in ABCG2-overexpressing cells. Furthermore, olmutinib could also increase the retention of doxorubicin (DOX) and rhodamine 123 (Rho 123) in ABC transporter subfamily G member 2 (ABCG2)-overexpressing cells. In addition, olmutinib was found to stimulate ATPase activity and inhibit photolabeling of ABCG2 with [I]-iodoarylazidoprazosin (IAAP). However, olmutinib neither altered ABCG2 expression at protein and mRNA levels nor blocked EGFR, Her-2 downstream signaling of AKT and ERK. Importantly, olmutinib enhanced the efficacy of topotecan on the inhibition of S1-MI-80 cell xenograft growth. All the results suggest that olmutinib reverses ABCG2-mediated MDR by binding to ATP bind site of ABCG2 and increasing intracellular chemotherapeutic drug accumulation. Our findings encouraged to further clinical investigation on combination therapy of olmutinib with conventional chemotherapeutic drugs in ABCG2-overexpressing cancer patients.

Objective To evaluate the radiosensitivity effects of apatinib on the esophageal cancer cell line ECA-109 and its cancer stem-like cells,and to investigate the underlying mechanism.Methods A serum-free medium (SFM) was used to culture esophageal cancer stem cell line ECA-109 and enrich the esophageal stem-like spheres.ECA-109 and its stem-like cells were divided into control group,drug treatment group,radiation group and drug plus radiation group.Cell proliferations of ECA-109 and its stem-like cells were detected with CCK-8 method.The concentration of vascular endothelial growth factor (VEGF) in the cell culture medium was determined by enzyme linked immunosorbent assay(ELISA).Cell cycle and apoptosis were detected by flow cytometry method.The expressions of CHK2 and P-STAT3 proteins were detected by Western blot assay.Results With the administration with apatinib for 24,48 and 72 h,the half of the inhibitory concentration (IC50) of ECA-109 stem-like cells was significantly higher than that of the parent cells (t =8.17,9.29,18.85,P ＜ 0.05) in a time dependent manner (parental cells:r2 =0.94-0.97,P ＜0.05;stem-like cells:r2 =0.94-0.98,P ＜0.05).After administration with different concentrations of apatinib (parental cells:10 and 20 μmol/L;stem-like cells:30 and 40 μmol/L) combined with different dose of X-rays (6 and 8 Gy),the proliferations of ECA-109 and its stem-like cells were significantly (t =5.20-39.68,P ＜ 0.05) inhibited compared with radiation alone group.VEGF secretion from both ECA-109 cells and its stem like cells were significantly decreased in different manner (t =7.45,P ＜ 0.05).Compared with control group,the cell apoptosis rate and the percentages of cells in G2/M phase were significantly increased in drug plus radiation group (t =8.83,11.59,P ＜ 0.05),and the expressions of CHK2 and P-STAT3 were decreased in drug group (t =3.36,4.10,P ＜ 0.05).Compared with radiation group,the expressions of CHK2 and P-STAT3 were decreased in drug plus radiation group (t =9.05,2.36,P ＜ 0.05).Conclusions Apatinib enhanced the radiosensitivity of ECA-109 cells and its stem-like cells,which was much more effective on ECA-109 cells and may be related to the radiation-induced inhibition of VEGF signal pathway that can further inhibit cell proliferation,promote cell apoptosis and induce cell cycle redistribution.The higher intrinsic level of VEGF protein may contribute to radioresistance of ECA-109 stem-like cells.

Objective To explore the correlation of metabolic syndrome (MS ) with low triiodothyronine(T3)syndrome(LT3S ,or It is known as ESS :euthyroid sick syndrome) ,subclinical hypothyroidism (SCH )and a high serum total homocysteine (tHcy )level (hyperhomocysteinemia )in elderly patients. Methods We retrospectively analyzed thyroid function ,serum glucose ,lipids and homocysteine(Hcy)level in 83 MS patients(MS group) ,30 patients with low T3 syndrome(low T3 group) ,41 patients with SCH (SCH group)and 80 healthy individuals (control group)aged over 60 years from January 2015 to March 2017 in outpatient and inpatient departments of our hospital. The correlations of thyroid function and serum Hcy level with MS components were analyzed by multiple Logistic regression model. Results The incidence of low T3 syndrome and SCH in MS patients was 37.3％ (31/83)and 49.4％ (41/83) ,respectively.Low T3 group versus control group showed the lower levels in free triiodothyronine ,FT4 ,folic acid ,and Hcy ,with statistically significant differences (all P<0.05).SCH group versus control group showed a lower levels of FT 4 ,of Hcy and of folic acid ,but an increased TSH level ,with statistically significant differences (all P<0.05).Patients with TSH >5.5 mU/L had decreased FT3 which occurred later than the rise of TSH (P<0.05) .Univariate correlation analysis showed that FT3 was negatively correlated with Hcy (P< 0.01) ,and TSH was negatively correlated with high-density lipoprotein cholesterol(P<0.01).Multivariate linear regression analysis found linear correlations of TSH with triglyceride ,high-density lipoprotein cholesterol ,and Hcy(all P < 0.05).Logistic regression analysis showed that FT3 ,Hcy and TSH are highly associated with hypertension after adjustment for gender and body mass index (all P< 0.05).Decreased FT3(P<0.01) ,elevated Hcy(P<0.05) ,and increased TSH(P<0.05)were independent risk factors for MS in elderly patients. Conclusions The incidences of low T3 syndrome and SCH are increased with aging. FT3 ,TSH ,and Hcy are independent risk factors for MS in the elderly.