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Objective To investigate the relationship between nutritional status and quality of life ( QOL) in patients with nasopharyngeal carcinoma undergoing concurrent chemoradiotherapy, and to identify the optimal indices of body composition for evaluation of malnutrition. Methods Based on the European Society Parenteral and Enteral Nutrition ( ESPEN) consensus on the diagnosis of malnutrition and patient?generated subjective global assessment (PG?SGA), a prospective study was performed in 48 patients with nasopharyngeal carcinoma who received concurrent chemoradiotherapy in our hospital from 2014 to 2015. Changes in body composition and nutritional status were evaluated in those patients. The relationship between nutritional status and QOL was studied. The predictive factors for nutritional status in patients with nasopharyngeal carcinoma were explored. The correlation between datasets was evaluated by the Pearson correlation coefficient. The influencing factors for nutritional status were analyzed by Logistic regression. Results During concurrent chemoradiotherapy, some indices of body composition, including weight, body mass index ( BMI) , fat mass index ( FMI) , fat?free mass index ( FFMI) , body cell mass ( BCM) , skeletal muscle mass ( SM) , and phase angle ( PA) had different degrees of reduction ( P=0?00) , while the PG?SGA score gradually increased. The incidence of malnutrition in patients with nasopharyngeal carcinoma during radiotherapy was 2?1%?39?6% based on 2015 ESPEN consensus on the diagnosis of malnutrition and 12?5%?41?7% based on PG?SGA. These two methods showed good agreement at the fourth and sixth weeks of radiotherapy ( Kappa=0?911;Kappa=0?957) . The changes in QOL score were correlated with changes in FFMI and weight during radiotherapy ( r= 0?805, P= 0?00;r= 0?777, P= 0?00 ) . Logistic regression indicated that age, FMI, and FFMI were influencing factors for nutritional status ( P= 0?035, 0?013, 0?043) . Conclusions Patients with nasopharyngeal carcinoma have substantial nutritional deterioration during chemoradiotherapy. The nutritional status is closely associated with QOL. A prediction model of nutritional status can provide a comprehensive and accurate judgment of nutritional status in patients.
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Objectives To explore the role of hydrogen sulfide(H_(2)S) in lipopolysaccharide(LPS)-induced acute lung injury(ALI) in rats and the underlying mechanisms.Methods Sixty-four Sprague-Dawley rats were randomly divided into four groups: control,LPS(instilled intratracheally to induce ALI),NaHS(H_(2)S donor)+LPS,propargylglycine [inhibitor of cystathionine-?-lyase(CSE),PPG]+LPS.Animals were sacrificed at(4 h) or 8h after agent administration.Lung weight/body weight ratio(LW/BW) was measured and calculated.Morphological changes of lung tissues were observed,H_(2)S concentration and carbon monoxide(CO) level in plasma were tested.Malondialdehyde(MDA) content,CSE activity and heme oxygenase(HO) activity of the lung were determined.Immunohistochemisty technique was performed to examine the expression and the absorbance value of(HO1) protein in lung tissues.Results Compared with control conditions,severe injuries of lung tissues and a raised LW/BW and MDA content were observed in rats treated with LPS.LPS also lead to a drop in plasma H_(2)S concentration and lung CSE activity.The enzyme activity of HO,the protein expression of(HO-1) and plasma CO level increased after LPS instillation. Administration of NaHS before LPS could atten-uated the changes induced by LPS.Pre-administration of PPG exacerbated the injuries induced by LPS,but there was no prominent variation in CO level,HO activity and(HO-1) protein expression compared with those of LPS group.Conclusions Downregulation of H_(2)S/CSE was involved in the pathogenesis of acute lung injury induced by LPS.Exogenous(H_(2)S) provided protection against the lung injuries to some extent,which may be explained by its anti-oxidative effects and the upregulation of CO/(HO-1) system.
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AIM: To examine the effect of cholecystokinin-octapeptide (CCK-8) on focal cerebral ischemia/reperfusion injury and its underlying mechanisms. METHODS: By using the suture model of focal cerebral ischemia and reperfusion, the effects of intracerebroventricular (icv) injection of CCK-8 and proglumide, nonselective CCK receptors antagonist, on the infarct size, regional cerebral blood flow (rCBF), and the levels of nitric oxide (NO), malondialdehyde (MDA) were observed in different brain regions of rats subjected to 1 h focal cerebral ischemia followed by 24 h reperfusion. RESULTS: (1) pretreatment with different doses of CCK-8 (0.3 ?g,1.0 ?g,2.0 ?g or 4.0 ?g) could attenuate the infarct size, but the statistically significant effects of CCK-8 were obtained only at the doses of 1.0 ?g and 2.0 ?g(P
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AIM: To investigate the effect of H_2S on pulmonary artery hypertension during acute lung injury induced by LPS and the interaction between the systems of hydrogen sulfide (H_2S)/cystathionine-?-lyase (CSE) and nitric oxide (NO)/nitric oxide synthase (NOS) in this process. METHODS: Seventy-two adult male rats were randomly divided into four groups: control group, LPS group, LPS+L-NAME group and LPS+propargylglycine (PPG) group. Mean pulmonary artery pressure (mPAP) of each rat was examined at 2 h, 4 h, 6 h and 8 h after treatment. H_2S and NO contents in plasma, NO content, iNOS, cNOS and CSE activity in lung were measured at 4 h or 8 h after treatment, respectively. Expression of iNOS in lung tissue was also detected by immunohistochemistry technique, and the injury of lung was evaluated with morphological changes under microscope. RESULTS: LPS could induce severe lung injury, and mPAP, NO content, iNOS activity and its protein expression in LPS group significantly increased, but cNOS activity, H_2S content and CSE activity decreased compared with those of control group. Administration of L-NAME before LPS could attenuate the changes induced by LPS. Pre-administration of PPG, a CSE inhibitor, exacerbated the injury by LPS, but there was no prominent variation in cNOS activity. CONCLUSION: Reduced endogenous H_2S could increase pulmonary artery hypertension during acute lung injury induced by LPS. There is a negative effect between H_2S/CSE system and NO/NOS system in this process.
