Gelatin Blending Improves the Performance of Poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) Films for Biomedical Application.

To improve the performance of poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) (PHBHHx), gelatin was blended with PHBHHx at different ratios. With increasing gelatin content, the weight loss of gelatin/PHBHHx blend in simulated body fluid at 37 degrees C was accelerated. After 2 months, there was about 15% weight loss in PHBHHx blending with 30% gelatin. Scanning electron microscopy and X-ray diffraction results showed that gelatin blending increased the surface porosity and decreased the crystallinity, which may be responsible for the acceleration of the weight loss. Second harmonic generation results indicated that 10% gelatin blending had less disruption to PHBHHx spatial structure, resulting in better tensile mechanical properties. At the same time, increased surface porosity and decreased crystallinity caused by gelatin incorporation may be beneficial for cell growth compared with pure PHBHHx. All these indicated that gelatin incorporation may improve the performances of PHBHHx to meet the need of different situations during medical implantation.

Body image evaluations in obese females with binge eating disorder.

Dimensions of body image in a sample of obese women diagnosed with binge eating disorder (BED; N=42) were compared with a sample of obese women without BED (non-BED; N=42), matched on age and BMI. Additionally, the relationship between BED, body image and several dimensions of treatment response was examined. Results indicated BED women were more likely to negatively evaluate their global physical appearance and have less satisfaction with specific areas of the body than were non-BED women, even after controlling for depression scores. While BED women were significantly more likely to endorse depressive symptoms, depression scores were negatively correlated with body satisfaction in non-BED women only. BED women did not fare worse in formal weight-loss treatment, as measured by length of time in treatment, group-therapy attendance, or BMI at posttreatment. The role of body image in women with BED seeking weight-loss treatment is discussed relevant to the context of potential impact of BED and negative body image on active weight-loss treatment and maintenance.

Nutritionally induced body weight loss and ovarian quiescence in Shiba goats.

Four female Shiba goats were used to determine the influence of body weight loss by dietary restriction on estrous cyclicity. The dietary restriction was started on the day following ovulation. The goats were fed hay cube and straw at an amount of 30% of energy requirement based on weekly body weight measurement. The ovaries were monitored daily by transrectal ultrasonography and blood samples were collected daily by jugular venipuncture for ovarian steroids analysis. After the start of food restriction, all animals lost body weight and entered ovarian quiescence. Intervals to the onset of ovarian quiescence tended to depend on the body weight of each animal at the start of food restriction. The mean concentration of progesterone during the mid-luteal phase (from 7 to 13 days after ovulation) in the last estrous cycle before ovarian quiescence was significantly lower than that in normal estrous cycle of the control period (19.7 +/- 2.8 vs 12.3 +/- 2.2 ng/ml, P<0.05), whereas there was no significant difference in the length of the luteal phase, determined as the period when corpora lutea existed and concentrations of progesterone were equal to or greater than 1 ng/ml (15.8 +/- 1.5 vs 15.0 +/- 2.8 days, P>0.1). A rise of estradiol concentration and follicular growth in the follicular phase following a decline of progesterone level after luteal regression tended to be suppressed at the onset of ovarian quiescence. It seems that the present results are consistent with previous findings that nutritionally induced body weight loss influences the secretion of ovarian steroids and eventually induces ovarian quiescence.

Attaining successful weight loss with an ideal macronutrient balance.

A dramatic increase in the number of people who are overweight or obese in this country presents a growing public health problem. Successful weight loss requires diet, physical activity, and behavior modification interventions. weight loss diets with distinctively different macronutrient profiles have resulted in short-term weight loss. There is great interest in identifying the most effective strategies to achieve long-term weight loss. Individualizing weight loss interventions, including diet, will be important to facilitate significant weight loss on a population basis. Nurses and nurse practitioners can play an integral role in supporting their patient's weight loss efforts.

Activation of the hypothalamic arcuate nucleus predicts the anorectic actions of ciliary neurotrophic factor and leptin in intact and gold thioglucose-lesioned mice.

Similar to leptin, ciliary neurotrophic factor (CNTF) suppresses appetite and selectively reduces body fat in leptin-deficient ob/ob mice. To assess the relative importance of specific regions of the hypothalamus in mediating these effects, we administered a CNTF analogue (CNTFAx15) or leptin to mice made obese by administration of gold thioglucose (GTG), which destroys a well-defined portion of the medial basal hypothalamus. CNTFAx15 treatment reduced appetite and body weight in obese GTG-lesioned C57BL/6 mice, whereas leptin failed to effect similar changes regardless of whether treatment was initiated before or after the lesioned mice had become obese. Because leptin does not reduce food intake or body weight in most forms of obesity (a condition termed 'leptin resistance'), we also investigated the actions of leptin in GTG-lesioned leptin-deficient (ob/ob) mice. By contrast to C57BL/6 mice, leptin treatment reduced food intake and body weight in GTG-lesioned ob/ob mice, although the effect was attenuated. To further compare the neural substrates mediating the anorectic actions of leptin and CNTF, we determined the patterns of neurone activation induced by these proteins in the hypothalamus of intact and GTG-lesioned mice by staining for phosphorylated signal transducer and activator of transcription 3 (pSTAT3). CNTFAx15 stimulated robust pSTAT3 signalling in neurones of the medial arcuate nucleus in both intact and lesioned C57BL/6 and ob/ob mice. Leptin administration stimulated pSTAT3 signalling in only a few neurones of the medial arcuate nucleus in intact or lesioned C57BL/6 mice, but elicited a robust response in intact or lesioned ob/ob mice. By contrast to CNTFAx15, leptin treatment also resulted in prominent activation of STAT3 in several areas of the hypothalamus outside the medial arcuate nucleus. This leptin-induced pSTAT3 signal was at least as prominent in intact and GTG-lesioned C57BL/6 mice as it was in ob/ob mice, and thus was not correlated with appetite suppression or weight loss. These results indicate that the medial arcuate nucleus is a key mediator of appetite suppression and weight loss produced by CNTF and leptin, whereas GTG-vulnerable regions play a role only in leptin-induced weight loss. Other regions of hypothalamus in which pSTAT3 signal is induced by leptin may regulate energy metabolism through mechanisms other than appetite reduction.

Cerebrospinal fluid and plasma concentrations of leptin, NPY, and alpha-MSH in obese women and their relationship to negative energy balance.

Leptin and its principal mediators, NPY and alpha-MSH are postulated to play a pivotal role in energy balance. To determine the possibility of the disturbance in neuropeptides in human obesity and their consequent changes in response to negative energy balance, we evaluated plasma and cerebrospinal fluid (CSF) leptin, NPY, and alpha-MSH levels in obese women before and after weight loss in comparison with normal control women. Subjects included 16 obese women [mean body mass index (BMI), 35.6 kg/m(2)] before and after weight loss induced by a 2-wk very low caloric diet (800 kcal/d) and 14 normal weight women (mean BMI, 20.4 kg/m(2)). The CSF to plasma leptin ratio in normal weight subjects was 2.3-fold higher than that in obese subjects. After weight loss in obese subjects, plasma leptin levels decreased by 40% and CSF levels decreased by 51%. There was a positive linear correlation between CSF and plasma leptin levels at baseline in obese subjects (r = 0.74, P < 0.05) and a positive logarithmic correlation in normal weight subjects (r = 0.89, P < 0.05) and in obese subjects after weight loss (r = 0.64, P < 0.05). The BMI was negatively correlated with the CSF to plasma leptin ratio (r = -0.86, P < 0.05) in all subjects. Neither the baseline plasma levels nor the baseline CSF levels of NPY were different between normal weight subjects and obese subjects. After weight loss, the CSF NPY level decreased significantly compared with baseline values in obese subjects. The alpha-MSH levels in plasma and CSF did not differ significantly from controls in obese subjects at baseline or after weight loss. Baseline CSF leptin level correlated with neither the baseline CSF NPY level nor the baseline CSF alpha-MSH level. In conclusion, this study demonstrated that the efficiency of brain leptin delivery is reduced in human obesity and central nervous system leptin uptake involves a combination of a saturable and an unsaturable mechanism. CSF NPY and alpha-MSH did not differ from controls in human obesity, and the CSF NPY level decreased significantly whereas alpha-MSH did not differ after weight loss in obese subjects compared with baseline. There was no significant correlation between CSF leptin and CSF NPY or alpha-MSH. This could be the result of leptin resistance present in human obesity and/or the more complex mechanisms involved in modulating appetite and regulating energy balance in human obesity.

Skeletal muscle enzymes as predictors of 24-h energy metabolism in reduced-obese persons.

BACKGROUND: Little is known about the effects of weight loss on the relation between skeletal muscle enzymes and energy metabolism. OBJECTIVE: This study was performed retrospectively to investigate the relation between skeletal muscle enzymes and 24-h energy metabolism in obese persons before and after weight loss. DESIGN: Ten women and 9 men [with body mass indexes (in kg/m(2)) > 30] underwent a 15-wk weight-loss program (-700 kcal/d). Body weight and composition, 24-h energy metabolism (whole-body indirect calorimetry), and maximal activities of phosphofructokinase (EC 2.7.1.11), creatine kinase (CK; EC 2.7.3.2), citrate synthase (CS; EC 4.1.3.7), 3-hydroxyacyl-CoA dehydrogenase (HADH; EC 1.1.1.35), and cytochrome-c oxidase (COX; EC 1.9.3.1) were determined from biopsy samples of the vastus lateralis taken before and after weight loss. RESULTS: Before weight loss, fat-free mass (FFM) was the only predictor of 24-h energy expenditure (R(2) = 0.70, P < 0.001), whereas the cumulative variance in sleeping metabolic rate explained by FFM and fat mass (FM) was 83% (P < 0.001). After weight loss, CS (r = 0.45, P = 0.05) and COX (r = 0.65, P < 0.01) were significantly associated with 24-h energy expenditure, whereas CK (r = 0.53, P < 0.05), CS (r = 0.45, P < 0.05), COX (r = 0.64, P < 0.01), and HADH (r = 0.45, P = 0.05) were all significant correlates of sleeping metabolic rate. After weight loss, FFM, FM, and COX explained 84% (P < 0.01) of the variance in 24-h energy expenditure, whereas FFM, FM, and CK all contributed to the cumulative variance in sleeping metabolic rate explained by this model (R(2) = 0.82, P < 0.05). CONCLUSION: Maximal activities of key skeletal muscle enzymes contribute to the variability in 24-h energy metabolism in reduced-obese persons.

Suppression of hepatocellular carcinoma by transplantation of ex-vivo immune-modulated NKT lymphocytes.

NKT cells are a regulatory subset of T lymphocytes with immune modulatory effects and an important role in anti-tumor immunity. The feasibility of "ex-vivo education" of NKT cells has recently been demonstrated. To evaluate the anti-tumor effect of ex-vivo immune-modulated NKT lymphocytes in a murine model of hepatocellular carcinoma. Athymic Balb/C mice were sublethally irradiated and transplanted with human Hep3B HCC. NKT cells prepared from immunocompetent Balb/C mice were pulsed ex vivo with HCC-derived antigens (Group A), Hep3B cells (group B) or BSA (group C), and adoptively transferred into HCC harboring mice (1 x 0(6) NKT cells per mouse). Group D mice did not undergo NKT cell transplantation. Group E mice were transplanted with 1 x 10(6) NKT cells from HBV-immunized donors. Mice were followed for tumor size and weight. To determine the mechanism of the anti-tumor effect, intrasplenic lymphocyte populations were analyzed by FACS for NKT, CD4+ and CD8+ lymphocyte subpopulations; STAT 1, 4 and 6 expression in splenocytes was assessed by Western blot, and serum cytokine levels were measured by ELISA. Adoptive transfer of NKT cells pulsed with HCC-derived antigens (group A) and NKT cells from immunized donors (group E) resulted in complete disappearance of tumors within 4 weeks and attenuated weight loss (6.5% and 7% in groups A and E, respectively). In contrast, mice in groups B, C, and D developed large, necrotic tumors and severe weight loss (21%, 17% and 23% weight loss in groups B, C, and D, respectively). NKT/CD4 and CD8/CD4 ratios were significantly increased in groups A and E (12.3 and 17.6 in groups A and D, respectively, compared to 6.4, 4.8 and 5.6 in groups B, C and D, respectively, for the NKT/CD4 ratio; 41 and 19.8 in groups A and E, respectively, compared to 6.5, 11.8 and 3.2 in groups B, C, and D, respectively, for the CD8/CD4 ratio). Expression of the transcription factor STAT4 was evident in group A, but not in groups B-D. Serum IFNgamma, IL12 and IL4 levels were increased in groups A and E. Adoptive transfer of NKT lymphocytes exposed ex vivo by HCC-derived antigens loaded on dendritic cells and NKT cells from immunized donors led to suppression of HCC in mice. NKT-mediated anti-tumor activity was associated increased NKT and CD8+ T lymphocyte numbers, increased expression of STAT4, a marker for IL-12 activity and elevated serum levels of the proinflammatory cytokines IFNgamma and IL12, and of IL4. Ex-vivo modulation of NKT lymphocytes holds promise as a novel mode of immune therapy for HCC. (c) 2005 Wiley-Liss, Inc.