Preventive effects of caffeine on nicotine plus high-fat diet-induced hepatic steatosis and gain weight: a possible explanation for why obese smokers with high coffee consumption tend to be leaner.

Non-alcoholic fatty liver disease (NAFLD) is a prevalent liver disorder, affecting approximately 25 % of the population. Coffee-drinking obese smokers exhibit lower body weights and decreased NAFLD rates, but the reasons behind this remain unclear. Additionally, the effect of nicotine, the main component of tobacco, on the development of NAFLD is still controversial. Our study aimed to explore the possible reasons that drinking coffee could alleviate NAFLD and gain weight and identify the real role of nicotine in NAFLD of obese smokers. A NAFLD model in mice was induced by administering nicotine and a high-fat diet (HFD). We recorded changes in body weight and daily food intake, measured the weights of the liver and visceral fat, and observed liver and adipose tissue histopathology. Lipid levels, liver function, liver malondialdehyde (MDA), superoxide dismutase (SOD), serum inflammatory cytokine levels and the expression of hepatic genes involved in lipid metabolism were determined. Our results demonstrated that nicotine exacerbated the development of NAFLD and caffeine had a hepatoprotective effect on NAFLD. The administration of caffeine could ameliorate nicotine-plus-HFD-induced NAFLD by reducing lipid accumulation, regulating hepatic lipid metabolism, alleviating oxidative stress, attenuating inflammatory response and restoring hepatic functions. These results might explain why obese smokers with high coffee consumption exhibit the lower incidence rate of NAFLD and tend to be leaner. It is essential to emphasise that the detrimental impact of smoking on health is multifaceted. Smoking cessation remains the sole practical and effective strategy for averting the tobacco-related complications and reducing the risk of mortality.

The role of turbulence in internal phosphorus release: Turbulence intensity matters.

Hydrodynamic fluctuations can trigger sediment suspension concomitantly with internal phosphorus release, while the interactive effect of turbulence mixing and sediment suspension on the regulation of phosphorus dynamics is in need of deep understanding. This study addressed the changes in total phosphorus (TP), phosphate (PO43--P) and suspended sediment (SS) in the overlying water, and measured the profile of dissolved oxygen (DO), Fe(II) and soluble reactive phosphorus (SRP) across the sediment-water interface in the simulated environmental turbulence scenario, For a turbulence intensity (ε) of 3.6 × 10-3 m2/s3, the SRP flux increased hence PO43--P showed a 36.36% increase relative to its initial level. Although ε of 1.3 × 10-2 m2/s3 benefited the delivery of oxygen from the bulk aqueous phase to the upper sediment which can trigger the formation of Fe oxides and hydroxides, the turbulence-induced phosphorus diffusion from the sediment exceeded its inactivation and resulted in a large SRP flux. However, a protion of the released PO43--P can be immobilized through SS adsorption and biotic (likely cyanobacteria) assimilation. Higher turbulence intensities (ε of 3.3 × 10-2 and 7.4 × 10-2 m2/s3) led to an approximately 40-fold increase in TP concentration and a significant increase in sediment suspension, which contributed to the immobilization of a majority of the phosphate through adsorption; thus, the PO43--P concentrations in the overlying water displayed 47.75% and 41.67% decline, respectively. This study also confirmed the sequential phosphorus buffer mechanisms associated with increasing turbulence intensities. With an ε of 3.6 × 10-3 m2/s3, bounding to Fe ion had a significant impact on phosphorus inactivation but with an ε of 7.4 × 10-2 m2/s3, the main immobilization mechanism is switched to phosphorus adsorption from the large quantity of suspended sediment.

[Effect of berberin hydrochloride on blood concentration of cyclosporine A in cardiac transplanted recipients].

OBJECTIVE: To observe the clinic effect of combined use of berberin hydrochloride (Ber) with cyclosporine A (CsA) on the blood concentration of CsA in heart transplanted recipients. METHODS: The blood concentration of CsA, liver-renal function and blood lipids in 22 heart transplanted recipients, who received Ber-CsA combined therapy, were measured. RESULTS: The whole blood steady state concentration of CsA, C0 and C2, in recipients after being treated with Ber-CsA significantly increased than those before applying Ber-CsA (P < 0.01), with the mean increment of 26% and 18% respectively; the dosage of CsA used decreased in 21 patients by 25-100 mg/d; and the Ber-CsA showed no significant effect on liver-renal function or blood lipids (P > 0.05). CONCLUSION: Combined use of CsA with Ber could markedly increase the blood concentration of CsA in heart transplanted recipients and reduce the dosage of CsA required, save the fee for medical service, and shows no obvious adverse reaction.

[Effect of Ginkgo biloba extract on neuronal apoptosis in rabbit with kaolin-induced syringomyelia].

OBJECTIVE: To evaluate the effect of Ginkgo biloba extract (GBE) on neuronal apoptosis in rabbits with kaolin-induced syringomyelia. METHODS: Twenty-four of 30 Chinese white rabbits were subjected to injection of 25% kaolin mixed with equal volume (0.6 ml) of cerebrospinal fluid drawn from the cisterna magna under ketamine anesthesia. Twelve of these 24 rabbits then received intravenous injection of 5 ml of GBE (5 ml/days for 14 days, GBE treatment group) while the other 12 were treated with the same amount of saline administered in similar manner (saline group). The 6 rabbits without kaolin treatment received a sham operation to serve as the control group. At different time points after the operation, the rabbits were killed and the spinal cord samples examined by immunohistochemistry. RESULTS: Histologically, ischemia and edema in the cervical cord of rabbits in GBE treatment group were less severe than those in saline group. TUNEL-positive and bax-positive neurons were less numerous in GBE treatment group than in saline group, and the former group showed more Bcl-2-positive neurons. The number of apoptotic neurons reached the peak level on day 7 after kaolin injection. CONCLUSION: GBE can ameliorate kaolin-induced hydrocephalus in the upper cervical cord and inhibit kaolin-induced neuron apoptosis.