Menin Reduces Parvalbumin Expression and is Required for the Anti-Depressant Function of Ketamine.

Dysfunction of parvalbumin (PV) neurons is closely involved in depression, however, the detailed mechanism remains unclear. Based on the previous finding that multiple endocrine neoplasia type 1 (Protein: Menin; Gene: Men1) mutation (G503D) is associated with a higher risk of depression, a Menin-G503D mouse model is generated that exhibits heritable depressive-like phenotypes and increases PV expression in brain. This study generates and screens a serial of neuronal specific Men1 deletion mice, and found that PV interneuron Men1 deletion mice (PcKO) exhibit increased cortical PV levels and depressive-like behaviors. Restoration of Menin, knockdown PV expression or inhibition of PV neuronal activity in PV neurons all can ameliorate the depressive-like behaviors of PcKO mice. This study next found that ketamine stabilizes Menin by inhibiting protein kinase A (PKA) activity, which mediates the anti-depressant function of ketamine. These results demonstrate a critical role for Menin in depression, and prove that Menin is key to the antidepressant function of ketamine.

Neuroprotective effect of mesenchymal stem cell-derived extracellular vesicles on optic nerve injury in chronic ocular hypertension.

Mesenchymal stem cells have neuroprotective effects that limit damage to the retina and photoreceptors, and which may be mediated by extracellular vesicles (or exosomes) released by mesenchymal stem cells. To investigate the neuroprotective effect of extracellular vesicles derived from umbilical cord mesenchymal stem cells on glaucoma, we established rat models of chronic ocular hypertension by injecting conjunctival fibroblasts into the anterior chamber to mimic optic nerve injury caused by glaucoma. One week after injury, extracellular vesicles derived from umbilical cord-derived mesenchymal stem cells were injected into the vitreous cavity. We found that extracellular vesicles derived from mesenchymal stem cells substantially reduced retinal damage, increased the number of retinal ganglion cells, and inhibited the activation of caspase-3. These findings suggest that mesenchymal stem cell-derived extracellular vesicles can help alleviate optic nerve injury caused by chronic ocular hypertension, and this effect is achieved by inhibiting cell apoptosis.

Ghrelin improves cognition via activation of the cAMP- CREB signalling pathway in depressed male C57BL/6J mice.

BACKGROUND: Depression leads to a cognitive decline and decreases in ghrelin are observed in depression. Ghrelin affects the level of Brain-derived nerve growth factor (BDNF) through the cAMP-CREB signalling pathway, and lower BDNF levels lead to cognitive decline. Therefore, it is reasonable to assume that in depression, lower ghrelin causes a decrease in BDNF levels and cognitive decline though the cAMP- CREB signalling pathway. METHODS: A total of 120 C57BL/6J male mice were randomly divided into six groups of 20 mice: non-depression groups (sham group, ghrelin group, and ghrelin + (D-lys3)-GHRP-6 group) and depression groups (depression group, depression + ghrelin group and depression + ghrelin + (D-lys3)-GHRP group). A depression mouse model was established by injecting normal saline, ghrelin or ghrelin + (D-lys3) -GHRP-6 into the lateral ventricle of each group. Cognition, hippocampal long-term potentiation (LTP), ghrelin mRNA and protein level, BDNF level and CREB level in the hippocampus were detected. RESULTS: In the depression mouse model groups, all comparison indexes (cognition and hippocampal levels of LTP, ghrelin mRNA and proteins, and BDNF and CREB) had significant negative changes. In the mice with depression, ghrelin or ghrelin + (D-lys3)-GHRP-6 was injected, and all the comparison indicators showed significant positive changes. Supplementation of ghrelin+(D-lys3))-GHRP-6 resulted in more significant positive changes in all comparison indexes than those of ghrelin alone. CONCLUSIONS: In the depression model, lower ghrelin causes hippocampal BDNF to decrease and results in cognitive decline via the cAMP-CREB signalling pathway.

Protective effect of leukemia inhibitory factor on the retinal injury induced by acute ocular hypertension in rats.

Glaucoma is one of the leading causes of irreversible blindness worldwide. As such, neuroprotective therapy is essential for the treatment of this disease. Leukemia inhibitory factor (LIF) is a member of the IL-6 cytokine family and the LIF signaling pathway is considered to be one of the major endogenous factors mediating neuroprotection in the retina. Therefore, the present study aimed to investigate the possible effects of LIF in acute ocular hypertension (AOH). The intraocular pressure in rat eyes was raised to 110 mmHg for 1 h by infusing the anterior chamber with normal saline to establish the AOH model. In the treatment group, LIF was then injected into the vitreous cavity after AOH was ceased. The retinal tissues were obtained after the termination of AOH, and H&E staining was conducted to assess the morphological damage. The number of retinal ganglion cells (RGCs) was counted using the Fluoro-Gold retrograde staining method. TUNEL staining was used to determine the extent of apoptosis among the retinal cells. In addition, the protein expression levels of cleaved caspase-3, poly (ADP-ribose) polymerase (PARP), STAT3 and components of the AKT/mTOR/70-kDa ribosomal protein S6 kinase (p70S6K) signaling pathway were examined by western blotting. The results showed that AOH induced tissue swelling and structural damage in the retina, which were reversed by LIF injection. In the LIF treatment group, RGC loss was significantly inhibited and the quantity of TUNEL-stained cells was also significantly reduced, whereas the expression of cleaved caspase-3 and PARP was decreased. Furthermore, increased phosphorylation of STAT3, AKT, mTOR and p70S6K was observed after LIF treatment. By contrast, pretreatment with the STAT3 inhibitor C188-9 or the PI3K/AKT/mTOR inhibitor LY3023414 reversed the LIF-induced inhibition of RGC loss. These results suggested that exogenous LIF treatment inhibited the retinal damage induced by AOH, which was associated with the activation of STAT3 and mTOR/p70S6K signaling. Therefore, LIF may serve a role in neuroprotection for glaucoma treatment.

The association of nonalcoholic fatty liver disease with bone mineral density in type 2 diabetes.

OBJECTIVE: We examined the association between nonalcoholic fatty liver disease and lumbar spine bone mineral density in individuals with and without type 2 diabetes. METHODS: The lumbar BMD of 1088 subjects was measured using dual-energy X-ray absorptiometry (DXA). Liver fat content was quantified via B-mode ultrasound. Multivariable linear regression was used to study the association between NAFLD and lumbar BMD in participants with and without T2DM. RESULTS: The lumbar BMD in the T2DM group and the non-diabetes group was higher in the NAFLD group than in the non-NAFLD group (P < 0.001). Multivariate regression analysis in the T2DM group showed that after adjusting for confounders, the positive association between lumbar spine BMD and NAFLD remained (P = 0.027). In the non-diabetes group, after adjusting for confounders, the association between NAFLD and lumbar spine BMD disappeared. CONCLUSIONS: The relationship between nonalcoholic fatty liver disease and lumbar bone mineral density may differ in individuals with and without diabetes. The effect of nonalcoholic fatty liver disease on bone mineral density needs to be evaluated in different clinical contexts.

A Machine Learning Method for the Quantitative Detection of Adulterated Meat Using a MOS-Based E-Nose.

Meat adulteration is a global problem which undermines market fairness and harms people with allergies or certain religious beliefs. In this study, a novel framework in which a one-dimensional convolutional neural network (1DCNN) serves as a backbone and a random forest regressor (RFR) serves as a regressor, named 1DCNN-RFR, is proposed for the quantitative detection of beef adulterated with pork using electronic nose (E-nose) data. The 1DCNN backbone extracted a sufficient number of features from a multichannel input matrix converted from the raw E-nose data. The RFR improved the regression performance due to its strong prediction ability. The effectiveness of the 1DCNN-RFR framework was verified by comparing it with four other models (support vector regression model (SVR), RFR, backpropagation neural network (BPNN), and 1DCNN). The proposed 1DCNN-RFR framework performed best in the quantitative detection of beef adulterated with pork. This study indicated that the proposed 1DCNN-RFR framework could be used as an effective tool for the quantitative detection of meat adulteration.

Human Umbilical Cord-Mesenchymal Stem Cells Survive and Migrate within the Vitreous Cavity and Ameliorate Retinal Damage in a Novel Rat Model of Chronic Glaucoma.

Glaucoma is the leading cause of irreversible blindness worldwide, and pathologically elevated intraocular pressure (IOP) is the major risk factor. Neuroprotection is one of the potential therapies for glaucomatous retinal damage. Intravitreal mesenchymal stem cell (MSC) transplantation provides a viable therapeutic option, and human umbilical cord- (hUC-) MSCs are attractive candidates for cell-based neuroprotection. Here, we investigated the ability of transplanted hUC-MSCs to survive and migrate within the vitreous cavity and their neuroprotective effects on chronic glaucomatous retina. For this, we developed a chronic ocular hypertension (COH) rat model through the intracameral injection of allogeneic Tenon's fibroblasts. Green fluorescent protein-transduced hUC-MSCs were then injected into the vitreous cavity one week after COH induction. Results showed that a moderate IOP elevation lasted for two months. Transplanted hUC-MSCs migrated toward the area of damaged retina, but did not penetrate into the retina. The hUC-MSCs survived for at least eight weeks in the vitreous cavity. Moreover, the hUC-MSCs were efficient at decreasing the loss of retinal ganglion cells; retinal damage was attenuated through the inhibition of apoptosis. In this study, we have developed a novel COH rat model and demonstrated the prolonged neuroprotective potential of intravitreal hUC-MSCs in chronic glaucoma.

Effects of fastigial nucleus electrostimulation on cardiac nerve regeneration, neurotransmitter release, and malignant arrhythmia inducibility in a post-infarction rat model.

The reduced density of cardiac autonomic nerves plays an important role in malignant arrhythmia after myocardial infarction (MI). Previous studies have shown that there is an interaction between the brain and the heart, and fastigial nucleus electrostimulation (FNS) promotes central nerve regeneration. Whether and how it can promote cardiac nerve regeneration after MI and the underlying mechanisms remain unknown. This study investigated whether FNS promotes cardiac nerve regeneration and reduces malignant arrhythmia inducibility in a post-infarction rat model. Ninety-eight Wistar rats were randomly assigned to Sham control, MI (left anterior descending coronary artery ligation without FNS), FNS (MI plus FNS), and FNL (fastigial nucleus lesion plus FNS plus MI) groups. The frequency of malignant arrhythmia was significantly lower in the FNS group than in the MI and FNL groups. The density of cardiac autonomic nerves was less in the MI group than in the Sham group, which was promoted by FNS. The nerve growth factor (NGF) mRNA expression was downregulated in the MI group compared to the Sham group, which was significantly enhanced by FNS. The expression levels of norepinephrine (NE) and acetylcholine (ACh) were higher and lower respectively in the MI and FNL groups than in the Sham group. After FNS, NE concentration was reduced and Ach level was elevated compared to the MI group. These data suggested that FNS promoted the regeneration of cardiac autonomic nerves and reduced the incidence of malignant arrhythmias in MI rat model. The mechanisms might involve up-regulation of NGF mRNA expression, decrease of NE release and increase of ACh release.

Fibrinogen, fibrin degradation products and risk of sarcopenia.

BACKGROUND & AIMS: Increasing data suggests that chronic low-grade inflammation plays an important role on development of sarcopenia. The present study was designed to identify the association between fibrinogen, fibrin degradation products (FDP) and sarcopenia risk in hospitalized old patients. METHODS: A total of 437 patients were enrolled in this cross-sectional study (148 with sarcopenia and 289 without sarcopenia). Sarcopenia was diagnosed according to the Asian Working Group for Sarcopenia (AWGS) 2019 criteria. Body composition, grip strength and gait speed were performed to participants. Fibrinogen, FDP levels were measured. Logistic regression analyses were carried out to assess the association between fibrinogen and sarcopenia, between FDP and sarcopenia, respectively. RESULTS: Compared to non-sarcopenic patients, fibrinogen and FDP levels were found to be higher in the sarcopenic group (3.07 g/L vs 2.79 g/L, 1.75 µg/mL vs 1.00 µg/mL, respectively, p < 0.05). Multiple linear regression analysis showed a significant negative association between fibrinogen and gait speed (ß: -0.164, p = 0.008), and muscle strength (ß: -0.231, p < 0.001). Multivariable logistic regression analysis showed that fibrinogen and FDP were independently associated with sarcopenia (odds ratio 1.32 [95% confidence interval 1.03, 1.70], p = 0.009; odds ratio 1.07 [95% confidence interval 1.01, 1.19], p = 0.049, respectively). ROC curve revealed that the cutoff values of fibrinogen and FDP to predict sarcopenia risk were 2.54 g/L and 1.15 µg/mL, respectively. CONCLUSIONS: In hospitalized old patients, serum fibrinogen and FDP levels are elevated in sarcopenia patients than those without sarcopenia. Fibrinogen and FDP are associated with sarcopenia in a concentration-dependent manner.

Menin Deficiency Leads to Depressive-like Behaviors in Mice by Modulating Astrocyte-Mediated Neuroinflammation.

Astrocyte dysfunction and inflammation are associated with the pathogenesis of major depressive disorder (MDD). However, the mechanisms underlying these effects remain largely unknown. Here, we found that multiple endocrine neoplasia type 1 (Men1; protein: menin) expression is attenuated in the brain of mice exposed to CUMS (chronic unpredictable mild stress) or lipopolysaccharide. Astrocyte-specific reduction of Men1 (GcKO) led to depressive-like behaviors in mice. We observed enhanced NF-κB activation and IL-1ß production with menin deficiency in astrocytes, where depressive-like behaviors in GcKO mice were restored by NF-κB inhibitor or IL-1ß receptor antagonist. Importantly, we identified a SNP, rs375804228, in human MEN1, where G503D substitution is associated with a higher risk of MDD onset. G503D substitution abolished menin-p65 interactions, thereby enhancing NF-κB activation and IL-1ß production. Our results reveal a distinct astroglial role for menin in regulating neuroinflammation in depression, indicating that menin may be an attractive therapeutic target in MDD.

Neuron-Specific Menin Deletion Leads to Synaptic Dysfunction and Cognitive Impairment by Modulating p35 Expression.

Menin (MEN1) is a critical modulator of tissue development and maintenance. As such, MEN1 mutations are associated with multiple endocrine neoplasia type 1 (MEN1) syndrome. Although menin is abundantly expressed in the nervous system, little is known with regard to its function in the adult brain. Here, we demonstrate that neuron-specific deletion of Men1 (CcKO) affects dendritic branching and spine formation, resulting in defects in synaptic function, learning, and memory. Furthermore, we find that menin binds to the p35 promoter region to facilitate p35 transcription. As a primary Cdk5 activator, p35 is expressed mainly in neurons and is critical for brain development and synaptic plasticity. Restoration of p35 expression in the hippocampus and cortex of Men1 CcKO mice rescues synaptic and cognitive deficits associated with Men1 deletion. These results reveal a critical role for menin in synaptic and cognitive function by modulating the p35-Cdk5 pathway.

Expression of leukemia inhibitory factor in the rat retina following acute ocular hypertension.

The aim of the present study was to investigate the expression of leukemia inhibitory factor (LIF) and its downstream signaling pathways in the rat retina following acute ocular hypertension. The intraocular pressure of the rats was elevated to 110 mmHg for 1 h by infusing the anterior chamber with normal saline. The retinal tissues were obtained 12 h, 24 h, and 2, 3 and 7 days after termination of the ocular hypertension. Hematoxylin and eosin and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were performed to assess the morphological changes and the apoptosis of retinal cells, respectively. Quantification of the retinal ganglion cells (RGCs) was performed using fluorogold retrograde (FG) staining. The expression levels of LIF, LIF receptor (LIFR), signal transducers and activators of transcription 3 (STAT3), phosphorylated STAT3 (P­STAT3), Akt, phosphorylated­Akt (P­Akt), extracellular signal­regulated kinase (ERK) and phosphorylated ERK (P­ERK) were determined at different time­points following acute ocular hypertension using western blot analysis. Reverse transcription­quantitative polymerase chain reaction was performned to detect the mRNA expression levels of LIF and LIFR. The results revealed that 12 h, 24 h, 2, 3 and 7 days after reperfusion, the thickness of the inner nuclear layer and the inner plexiform layer was decreased, with a significant reduction in the number of RGCs, as determined using TUNEL and FG staining. The expression levels of LIF and LIFR were increased following acute ocular hypertension. At 12 h post­retinal reperfusion, the expression levels of P­STAT3 and P­Akt were significantly upregulated, while the expression of P­ERK was decreased. The changes in the expression levels of LIF and LIFR suggested that LIF may be important in the process of degeneration/protection following retinal ischemia induced by acute ocular hypertension, via activation of the Janus kinase/STAT and Akt signaling pathways.

Autophagy in glaucoma: Crosstalk with apoptosis and its implications.

Glaucoma is characterized by elevated intraocular pressure that causes progressive loss of retinal ganglion cells (RGCs). Autophagy is a lysosomal degradative process that updates the cellular components and plays an important role in cellular homeostasis. Recent studies have shown that autophagy is involved in the pathophysiological process of glaucoma. The role played by autophagy in glaucoma is complex, and conflicting evidence shows that autophagy promotes both RGC survival and death. The understanding of the major pattern of RGC loss and the crosstalk between autophagy and apoptosis remains limited in glaucoma. This review focuses on the relationship between autophagy and glaucoma, particularly on the influence of autophagy on apoptosis in glaucoma. Further research on autophagy in glaucoma may provide a novel understanding of the glaucoma pathology and novel treatment targets for glaucoma in the future.

Functional CLOCK gene rs1554483 G/C polymorphism is associated with susceptibility to Alzheimer's disease in the Chinese population.

OBJECTIVE: To examine the association between the circadian locomotor output cycles kaput (CLOCK) gene rs1554483 G/C polymorphism and susceptibility to Alzheimer's disease in Chinese people. METHODS: This case-control study determined apolipoprotein E (APOE) and CLOCK rs1554483 G/C genotypes using polymerase chain reaction restriction fragment length polymorphism. RESULTS: Unrelated patients with Alzheimer's disease (n = 130) and healthy controls (n = 188) were analysed for an association between the CLOCK gene rs1554483 G/C polymorphism and susceptibility to Alzheimer's disease. In the whole sample and in APOE ε4 isoform noncarriers, the prevalence of CLOCK gene rs1554483 G allele carriers was significantly higher in patients with Alzheimer's disease than in controls. Among APOE ε4 carriers, the prevalence of CLOCK rs1554483 G allele carriers was not significantly different between patients with Alzheimer's disease and controls. CONCLUSION: Among APOE ε4 noncarriers, but not APOE ε4 carriers, the CLOCK rs1554483 G allele was associated with increased susceptibility to Alzheimer's disease.

Circadian rhythm of TSH levels in subjects with Alzheimer's disease (AD).

OBJECTIVES: The circadian rhythm of serum thyroid stimulating hormone (TSH) levels in patients with Alzheimer's disease was measured by means of a case-control study. METHODS: Serum samples from cases and controls were collected continuously for 2 days, and then once every 2 h (even number time-point during the first day and odd number time-point in the second). TSH was detected by radioimmunoassay. RESULTS: AD patients had no significant circadian rhythm in serum TSH levels, whereas normal controls did. In normal controls, serum TSH levels from 19:00 to 20:00 were the lowest (19:00, 3.89 ± 0.97 mIU/L; 20:00, 3.76 ± 0.84 mIU/L) and those in the period 2:00-4:00 were the highest (2:00, 6.15 ± 0.94 mIU/L; 3:00, 6.32 ± 1.04 mIU/L; 4:00, 6.39 ± 1.13 mIU/L; F = 6.762, df = 23, P = 0.002). However, in AD patients, 24-h serum TSH levels were 3.80-4.03 mIU/L (F = 0.897, df = 23, P = 0.996). At the 24 time-points, except for the four time-points from 16:00 to 19:00, TSH levels in AD patients were significantly lower than those in normal controls. CONCLUSIONS: The circadian rhythm of serum TSH levels in AD patients did not appear, and their serum TSH levels were significantly lower than those in normal controls. SIGNIFICANCE: The circadian rhythm in serum TSH levels in AD patients differs greatly from that of the general population.

Polymorphism of CLOCK gene rs 4580704 C > G is associated with susceptibility of Alzheimer's disease in a Chinese population.

BACKGROUND AND AIMS: The association of polymorphism of circadian locomotor output cycle kaput (CLOCK) gene rs 4580704 C/G with susceptibility of Alzheimer's disease (AD) was examined in the present study. METHODS: This was a case/control study and investigated the association of polymorphism of CLOCK gene rs 4580704 C/G with susceptibility of AD. Genotypes of apolipoprotein E (APOE) and CLOCK gene rs 4580704 C/G were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) detection method. RESULTS: This study was comprised of 296 unrelated AD patients and 423 controls. We performed an analysis the association of polymorphism of CLOCK gene rs 4580704 C/G with susceptibility of AD. In the whole sample or APOEε4 noncarriers, prevalence of C carriers in CLOCK gene rs 4580704 in AD patients was significantly higher than in controls (in the whole sample: χ(2) = 13.773, p <0.0001; in APOEε4 noncarriers: χ(2) = 51.588, p <0.0001). However, among APOEε4 carriers, prevalence of C carriers in CLOCK gene rs 4580704 between patients and controls was not statistically significant (χ(2) = 0.753, p = 0.386). CONCLUSIONS: Among APOEε4 noncarriers, C carriers in CLOCK gene rs 4580704 were associated with a high susceptibility of AD; however, among APOEε4 carriers the functional polymorphism of clock gene rs 4580704 C/G was not associated with AD susceptibility.

Depression as a risk factor for dementia and mild cognitive impairment: a meta-analysis of longitudinal studies.

BACKGROUND: This study examined whether depression was a risk factor for onset of dementia including Alzheimer's disease (AD), vascular dementia (VD) and any dementia, and mild cognitive impairment (MCI) by using a quantitative meta-analysis of longitudinal studies. METHODS: EMBASE and MEDLINE were searched for articles published up to February 2011. All studies that examined the relationship between depression and the onset of dementia or MCI were included. Pooled relative risk was calculated using fixed-effects models. RESULTS: Twelve studies met our inclusion criteria for this meta-analysis. All subjects were without dementia or MCI at baseline. Four, two, five, and four studies compared the incidence of AD, VD, any dementia, and MCI between subjects with or without depression, respectively. After pooling all the studies, subjects with depression had higher incidence of AD (relative risk (RR):1.66, 95% confidence interval (CI): 1.29-2.14), VD (RR: 1.89, 95% CI: 1.19-3.01), any dementia (RR: 1.55, 95% CI: 1.31-2.83), and MCI (RR: 1.97, 95% CI: 1.53-2.54) than those without depression. CONCLUSIONS: The quantitative meta-analysis showed that depression was a major risk factor for incidence of dementia (including AD, VD, and any dementia) and MCI.

Age and risk for depression among the elderly: a meta-analysis of the published literature.

OBJECTIVE: The goal of this study was to determine the relationship between age and risk for depression among the old and the oldest old. Method MEDLINE, EMBASE, and the Cochrane Library database were used to identify potential studies. The studies were divided into cross-sectional and longitudinal subsets. For each study, the numbers of the total participants, cases (for cross-sectional study), or incident cases (for longitudinal study) of depression in each age group were extracted and entered into Review Manager 4.2 software. Qualitative meta-analyses of cross-sectional studies and of longitudinal studies were performed. For prevalence and incidence rates of depression, odds risk (OR) and relative risk (RR) were calculated, respectively. RESULTS: The qualitative meta-analyses showed that, compared with younger participants (above vs. below 65 years, above vs. below 70 years, above vs. below 75 years, and above vs. below 80 years), older age groups had a significantly higher risk for depression. (All of the ORs and RRs were significant.) Compared with participants aged 55-89, those aged above 90 years had no higher risk for depression. (Neither the OR nor the RR was significant.) CONCLUSIONS: Despite the methodological limitations of this meta-analysis, older age appears to be an important risk factor for depression in the general elderly population (aged below 80 years), but not in the oldest population (aged above 85 years).

Association of serum uric acid with body mass index among long-lived Chinese.

OBJECTIVES: To examine the individual association between BMI and level of serum uric acid (SUA) among the very elderly Chinese population. METHODS: A survey was conducted on 870 long-lived subjects (aged ≥90years). Subjects were divided into four groups according to quartile of BMI (<16.6, 16.6-18.9, 18.9-21.1, ≥21.1kg/m(2)) and to classification criteria of underweight, normal weight, overweight and obesity in BMI (<18.5, 18.5-23.0, 23.0-27.5, ≥27.5kg/m(2), respectively). Subjects were also divided into hyperuricemia and normal SUA groups. RESULTS: The sample included 661 unrelated Chinese. The mean age was 93.52±3.29years (range 90-108years). The mean level of BMI was 19.16±3.47kg/m(2) and mean SUA was 318.72±87.01. Compared to individuals without hyperuricemia, high level of SUA was associated with a higher level of BMI in both genders (p<0.001). According to the both BMI classification criteria, the group with higher BMI had higher level of SUA (p<0.001). Pearson correlation showed that SUA was significantly correlated with BMI (with coefficients r=0.235, 0.140, in men and women, respectively). Unadjusted and adjusted multiple logistic regressions showed that odds ratios for hyperuricemia were associated with BMI according to quartile of BMI. CONCLUSIONS: We found that among long-lived Chinese subjects, higher levels of SUA may be associated with higher BMI.