The water-energy-food nexus: a systematic bibliometric analysis.

Adequate water, electricity, and food are essential for sustainable development. Regional conflicts intensified by global water, energy, and food shortages necessitate a rethinking of the security and interdependence of these resources. However, most earlier scholars concentrated on the subsystems of the water-energy-food nexus (WEF nexus), lacking holistic studies. Therefore, to understand the history and current state of research on the WEF nexus and predict future research directions, this study analyzed 1313 journal articles from the Web of Science database between 2007 and 2022 using the bibliometric analysis and Citespace software. The findings in this study indicate that (1) the progress of the WEF nexus research can be classified into three stages between 2007 and 2022: the early stage (2007-2010), the fast-developing stage (2011-2015), and the steady and in-depth stage (2016-2022). The WEF nexus has become a hot zone for academic research. (2) Map of the network of countries, institutions, and author collaborations implies tight academic collaboration among countries, institutions, and writers. (3) Climate change, integrated WEF nexus, sustainable development, and security are research hotspots in this field. Meanwhile, energy security, circular economy, and resource allocation are advanced subjects in this field. These key findings can provide managers and researchers with valuable information for decision-making.

Note of the methodological flaws in the paper entitled "GSTT1 and GSTM1 polymorphisms predict treatment outcome for breast cancer: a systematic review and meta-analysis".

With great interest, we read the paper "GSTT1 and GSTM1 polymorphisms predict treatment outcome for breast cancer: a systematic review and meta-analysis" (by Hu XY et al.), which has reached important conclusions that GSTM1 null and GSTT1/GSTM1 double null polymorphisms might be significantly associated with an increased tumor response in breast cancer. The result is encouraging. Nevertheless, several methodological flaws in this meta-analysis are worth noticing.

The effects of statins on benign prostatic hyperplasia in elderly patients with metabolic syndrome.

PURPOSE: To evaluate the effects of simvastatin and atorvastatin in elderly male patients with benign prostatic hyperplasia (BPH) accompanied by metabolic syndrome (MetS). METHODS: Eligible patients aged >60 year with BPH accompanied by MetS were randomly assigned to receive 40 mg of simvastatin daily, 20 mg of atorvastatin daily or placebo (control group) treatment for 12 months. Serum lipids, interleukin 6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), prostate-specific antigen, prostate volume (PV) and the International Prostate Symptom Score (IPSS) were tested before and after treatment. RESULTS: The levels of serum total cholesterol (TC), triglycerides, low-density lipoprotein cholesterol, hs-CRP, IL-6 and IPSS was decreased, serum high-density lipoprotein cholesterol (HDL-C) was increased, and PV was reduced in the patients following treatments with statins. The PV of the patients who received simvastatin were reduced more than those of the patients who received atorvastatin. The decrease in PV was more significant in the obesity patients than in the normal weight patients and in the hyperlipidemia patients than in the normal-lipid patients following the statin interventions. The reduction in PV was positively related to the decreases in the levels of TC and IL-6 and to the increase in the level of HDL-C. CONCLUSIONS: Simvastatin and atorvastatin significantly reduced PV, improved lower urinary tract symptoms, and slowed the clinical progression of BPH possibly by lowering cholesterol and anti-inflammatory factors.

Impact of metabolic syndrome on benign prostatic hyperplasia in elderly Chinese men.

OBJECTIVE: The aim of the present study was to evaluate the impact of metabolic syndrome (MetS) on benign prostatic hyperplasia (BPH) in elderly Chinese men. METHODS: A total of 401 elderly BPH patients were divided into the without or with MetS group to assess the associations of MetS and components of MetS with BPH. Urologic evaluation included prostate volume, International Prostate Symptom Score, serum prostate-specific antigen, duration of concomitant lower urinary tract symptoms (LUTS) and maximum flow rate. RESULTS: Body mass index (BMI), waist circumference, fasting glucose, glycosylated hemoglobin, triglyceride, fasting insulin (FINS), insulin resistance assessed by homeostasis model assessment (HOMA-IR) were greater and high-density lipoprotein cholesterol (HDL-C) was lower in BPH patients with MetS than in those without MetS. The patients with MetS showed a significantly larger prostate volume (p = 0.000) and longer duration of LUTS (p = 0.006) than those without MetS. Prostate volume was positively correlated with BMI (p = 0.000), FINS (p = 0.001), HOMA-IR (p = 0.003) and inversely correlated with HDL-C (p = 0.000). Multiple linear regression analysis showed that prostate volume was significantly correlated with HOMA-IR (p = 0.015). CONCLUSIONS: Our results suggest that MetS, BMI, low HDL-C level, increased serum insulin and especially insulin resistance are considered risk factors for prostate enlargement in elderly Chinese men.

Prostate volume correlates with diabetes in elderly benign prostatic hyperplasia patients.

BACKGROUND: To evaluate the relationship between prostate volume (PV) and diabetes mellitus (DM) in geriatric benign prostatic hyperplasia (BPH) patients. METHODS: One hundred and seventeen geriatric patients with BPH were retrospectively studied between 2008 and 2009. Patients were divided into two groups: BPH and BPH with DM group. The effects of indexes of DM, including fasting blood glucose (FBG), 2-h postprandial blood glucose, glycosylated hemoglobin (HbA1c), fasting insulin (FINS), insulin resistance (IR) index, prostate-specific antigen (PSA), International Prostate Symptom Score (IPSS), and lower urinary tract symptoms (LUTS) were evaluated. RESULTS: The values of PV (P = 0.005), PSA (P = 0.013), and IPSS (P = 0.01) in the BPH patients with DM group were significantly higher than in the BPH group. The values of PV (P = 0.002) and PSA (P = 0.006) in the BPH patients with elevated FBG were significantly higher than in the BPH patients with normal FBG. BPH patients with elevated HbA1c had significantly higher PV than BPH patients with normal HbA1c (P = 0.046). BPH with hyperinsulinemia group showed significantly higher PV (P = 0.017) and longer duration of LUTS (P = 0.031) than BPH patients with normal FINS. Similarly, BPH patients with IR had higher PV (P = 0.004) and longer duration of LUTS (P = 0.036) than BPH patients without IR. The logistic regression analysis showed that FBG and FINS were the risk factors for BPH. CONCLUSIONS: Our study demonstrates that PV is closely correlated with diabetes and diabetes has a direct effect on the occurrence and development of BPH.

Influence and pathophysiological mechanisms of simvastatin on prostatic hyperplasia in spontaneously hypertensive rats.

OBJECTIVE: To explore the effects and mechanisms of simvastatin on prostate hyperplasia in spontaneously hypertensive rats (SHRs). METHODS: Thirty-six male SHRs were randomly divided into three groups: the 10 and the 20 mg/kg/d simvastatin group and the control group. After 6 weeks the ultra-microscopic prostate structures were observed. The serum levels of interleukin-6 (IL-6), insulin-like growth factor (IGF-1) and angiotensin II (Ang-II) were measured by enzyme-linked immunosorbent assays. The endothelium-derived nitric oxide synthase (eNOS) expression was evaluated with immunohistochemistry. RESULTS: Compared to the control group, the 20 mg/kg/d simvastatin group presented with lower absolute (p = 0.005) and relative prostate weight (p = 0.009). The basal cells and columnar cells presented with edema, condensed heterochromatin in interstitial fibroblast nuclei, widened nucleus gaps, and decreased mitochondria and endoplasmic reticulum in the 10 mg/kg/d simvastatin group, these changes were more pronounced in the 20 mg/kg/d simvastatin group. The IL-6 levels in the 10 and 20 mg/kg/d simvastatin groups were lower than those of the controls (p = 0.005 and p = 0.008). The IGF-1 levels of the 20 mg/kg/d simvastatin group were reduced compared to the control group (p = 0.016). CONCLUSIONS: Simvastatin can delay and inhibit prostatic hyperplasia and progression in SHR. These actions may be mediated through the suppression of inflammatory and growth factors.

[Inhibitory effect of losartan on prostatic hyperplasia in spontaneous hypertension rats and its pathophysiological mechanism].

OBJECTIVE: To investigate the effect of losartan on prostatic hyperplasia in spontaneous hypertension rats (SHRs) and its pathophysiological mechanism. METHODS: We randomly divided 36 male SHRs into three groups of equal number to be treated intragastrically with high-dose losartan (30 mg per kg per d), low-dose losartan (15 mg per kg per d) and distilled water (control group). After 6 weeks of intervention, we measured the body weight and tail artery blood pressure of the rats and compared them with the baseline data. We collected blood from the heart for determination of the levels of serum angiotensin II (Ang II), insulin-like growth factor-1 (IGF-1) and interleukin-6 (IL-6) by enzyme-linked immunosorbent assay (ELISA), and harvested their prostates for measurement of their weight, observation of the tissue ultrastructures under the electron microscope and detection of the expression of endothelial nitric oxide synthase (eNOS) in the prostate tissue by immunohistochemistry. RESULTS: Compared with the control group, the low- and high-dose losartan groups showed significant decreases in systolic blood pressure ([203.75 +/- 10.28] vs [184.54 +/- 16.90] mmHg, P = 0.013; [203.75 +/- 10.28] vs [166.88 +/- 14.74] mmHg, P = 0.001) and diastolic blood pressure ([151.58 +/- 9.96] vs [136.71 +/- 14.28] mmHg, P = 0.022; [151.58 +/- 9.96] vs [122.71 +/- 11.56] mmHg, P < 0.001) of the lower tail artery after treatment, as well as in the prostate weight ([0.73 +/- 0.08] vs [0.64 +/- 0.10] mg, P = 0.011; [0.73 +/- 0.08 ] vs [0.50 +/- 0.17] mg, P < 0.001). Electron microscopy revealed edema of the basal and columnar epithelial cells, concentrated and marginated heterochromatin and widened nuclear gap of interstitial fibroblast nuclei, and reduced mitochondria and endoplasmic reticula in the low-dose losartan group, and even more obvious in the high-dose group. The level of serum Ang II was remarkably higher in the low- and high-dose losartan groups than in the control ([61.32 +/- 2.49] vs [54.85 +/- 7.20] pg/ml, P = 0.021; [65.49 +/- 6.78] vs [54.85 +/- 7.20] pg/ml, P < 0.001]) , that of serum IGF-1 was lower in high-dose losartan than in the control group ([1.50 +/- 0.11] vs [1.60 +/- 0.10] ng/ml, P = 0.03), but the serum IL-6 levels exhibited no significant differences among the three groups. The expression of eNOS in the prostate tissue was significantly higher in the losartan groups than in the controls (P = 0.022), even higher in the high-dose than in the low-dose group. CONCLUSION: Losartan can suppress the progression of prostate hyperplasia in spontaneous hypertension rats by inhibiting RAS, IGF-1 and angiogenesis.

[Reduced expression and secretion of apolipoprotein M in fat-fed, streptozotocin-diabetic rats is partially reversed by an artificial ligand of PPARγ].

OBJECTIVE: To investigate the effect of administration of rosiglitazone, an artificial ligand of PPARγ, on the expression and secretion of apolipoprotein (apoM) in fat-fed, streptozotocin-treated rats, an animal model for type 2-like diabetes. METHODS: Healthy male SD rats were divided into 4 groups: a control group (n=7), a high-fat chow group (HF group, n=8), a diabetes mellitus group (DM group, n=7), and a diabetes mellitus group with rosiglitazone intervention group (RSG group, n=7). Fasting blood glucose (FBG), fasting insulin (FINS), triglyceride (TG) and total cholesterol (TC) were measured at the beginning of the study. The diabetic rats model was established by feeding high fat chow and intraperitoneal injection of streprozotocin. Then the randomly selected treatment group was given rosiglitazone by daily gavage for 8 weeks. All the rats were killed at the fifteenth week, at which time blood and tissues (liver, kidney, adipose) were collected and prepared. The levels of FBG, FINS, TG and TC were assayed. The level of apoM in serum was measured by enzyme-linked immunosorbent assay (ELISA). Reverse transcription polymerase chain reaction (RT-PCR) was used to determine apoM mRNA expression in liver, kidney, and adipose tissues. RESULTS: Compared with either control group or HF group, serum apoM concentration in the DM group was reduced significantly (P<0.05); compared with the DM group, however, serum apoM concentrations in RSG group were increased (P<0.05). The expression of apoM mRNA in liver was highest, in kidney medium, and in adipose tissue extremely low (P<0.05). ApoM mRNA expression in liver and kidney was decreased in both DM and HF groups compared to control group (P<0.05). But, as with serum apoM concentration, apoM mRNA in the liver, kidney and adipose tissues of the RSG group were all increased markedly (P<0.05). The level of serum apoM in SD rats correlated negatively with TG (r=-0.466, P=0.011), TC (r=-0.568, P= 0.001), FBS (r =-0.371, P<0.001), and FINS(r=-0.768, P= 0.048 ). CONCLUSION: These results suggest that apoM may participate in the glucose and lipid metabolism by the regulation of PPARγ.

[Effects of curcumin on secretion of adiponectin and interleukin-6 in human adipose tissues: an in vitro study].

OBJECTIVE: To investigate the effects of different concentrations of curcumin on secretion of adiponectin (APN) and interleukin-6 (IL-6) in human adipose tissues cultivated in vitro. METHODS: Seven male patients with kidney stones were admitted. Abdominal subcutaneous adipose tissue and perirenal adipose tissue were collected from the operating-patients, and were cultivated with different concentrations of curcumin (10 and 100 microg/ml) in vitro. The contents of APN and IL-6 in the culture medium of adipose tissue cells were measured by enzyme-linked immunosorbent assay (ELISA) after they were cultured for 6 and 24 hours. RESULTS: Compared with the blank control group, the content of APN in the adipose tissue culture medium was increased by 100 microg/ml curcumin (P<0.05) after 6-hour culture, and the content of IL-6 was significantly decreased by 100 microg/ml curcumin after 6- and 24-hour culture (P<0.05). CONCLUSION: 100 microg/ml curcumin can increase APN secretion and decrease IL-6 secretion in human adipose tissues cultivated in vitro.

[The study of soluble P-selectin levels and it's correlation to the severity of coronary artery lesions in coronary heart disease].

OBJECTIVE: To investigate the difference of soluble P-selectin levels in different subtype of coronary heart disease and the relationship between soluble P-selectin levels with the severity of coronary artery lesions. METHODS: Enzyme linked immuoserbent assay (ELISA) was used to measure the plasma soluble P-selectin levels in 69 patients with angiocardiography documented coronary heart disease and 19 normal coronary arteries persons without angiocardiography detectable coronary artery disease (control group). The coronary artery lesions score was recorded according to single, double and triple-vessel lesions while the American College of Cardiology and the American Heart Association proposed type A, B, C lesion and Gensini scoring system. The relationships between plasma soluble P-selectin levels and the coronary artery score (the severity of coronary heart disease) were assessed. RESULTS: (1) The level of plasma soluble P-selectin was obviously higher in the coronary heart disease group than in the control group (180.6 +/- 60.5 ng/L vs. 145.3 +/- 21.7 ng/L, P<0.05). (2) The level of plasma soluble P-selectin was significantly higher in the acute coronary syndrome group (191.4 +/- 63.7 ng/L) than in the control group (145.3 +/- 21.7 ng/L, P< 0.01) and in the stable angina pectoris group (141.3 +/- 17.9 ng/L, P<0.01). (3) The level of plasma soluble P-selectin was high in multi-vessel coronary artery lesions group than in single-vessel group (190.1 +/- 64.2 ng/L vs. 157.2 +/- 43.4 ng/L, P < 0.05). The level of plasma soluble P-selectin was positively correlated with the Gensini score (r = 0.391, P = 0.001); the numbers of vessels lesions (rs = 0.349, P = 0.003); Type A, B and C lesions (rs = 0.358, P = 0.002). CONCLUSION: The positive correlation between the level of soluble P-selectin and the coronary artery score may indicate that soluble P-selectin levels might reflect the severity of coronary heart disease. The elevated soluble P-selectin level in acute coronary syndrome suggested the possible relation of P-selectin to the pathogenesis of acute coronary syndrome, which may save as a potential marker of plaque unstability.