Perceived body image and weight: discrepancies and gender differences among University undergraduates

Background

Body image (BI) is a multidimensional construct that includes perceptual, attitudinal, behavioural components, and feedback from other people''s perception of oneself. The feedback from others and the degree to which one accepts or rejects it can determine self evaluation and perception. Body weight perception is a strong determinant of nutritional habits and weight management among adolescents. One of the barriers to reducing rise in obesity prevalence could be its cultural acceptability in some developing countries.

Objective

To explore the gender influences on perception of self- and opposite-sex body images (BI), perceived body weight and the actual body weight categories at which discrepancies occur among the perceived BIs in undergraduates.

Methods

This was a survey of perceptual dimension of BI, perceived body weight and actual body weight carried out in 121 undergraduates aged 21–29years.

Results

Discrepancies occurred between self-perceived BI and each of actual body weight (p= 0.00 at 0.00–0.02 confidence interval (CI)), perceived body weight (p= 0.01 at 0.000–0.02 CI) and self-ideal BI (p= 0.03 at 0.000–0.05 CI) of normal-weight males. Self-perceived BI and perceived body weight also differed in normal-weight females (p= 0.02 at 0.000–0.04 CI). Discrepancies (p= 0.02 at 0.00–0.04 CI) occurred between self-perceived BI and self-ideal BI, and between self-perceived BI and desired BI (p= 0.02 at 0.00–0.04 CI) in overweight females. Gender differences occurred for self-ideal BI (p= 0.00 at 0.00–0.02 CI), ideal image for the opposite sex (IBIOS) (p= 0.02 at 0.00–0.04 CI) and desired BI (p= 0.00 at 0.00–0.02 CI).

Conclusion

Normal-weight males perceived their BI differently from their actual body weight, perceived body weight and self-ideal BI whereas normal-weight females perceived their BI differently from only their perceived body weight. Discrepancies occur between self-ideal BI and self-perceived BI, and between self-perceived BI and desired BI in overweight females. There are differential perceptions of self-ideal BI, IBIOS and desired BI between males and females.     

The rainbow cohort: 96 week follow-up of saquinavir-containing regimens in previously antiretroviral therapy (ART)-naïve and pre-treated but protease inhibitor (PI)- naïve hiv-infected patients

Objective

We have previously reported data from the German cohort of the multinational observational prospective RAINBOW survey which assessed the tolerability and efficacy of ritonavir-boosted saquinavir (SQV/r)-containing regimens over 48 weeks in routine clinical practice. This analysis presents data from antiretroviral (ART)-naïve and pretreated but protease inhibitor (PI)-naïve patients treated in a long-term one line (96 weeks) follow-up of the initial study.

Methods

All ART-and PI-naïve patients from the initial RAINBOW cohort who had recorded data to one line 96 weeks of treatment were eligible for inclusion in the current analysis. Efficacy assessments included the proportion of patients with HIV-1 RNA < 50 and < 400 copies/mL and changes in CD4 cell count from baseline to week 96. Tolerability assessments included changes in liver enzymes and lipid levels from baseline to week 96. For evaluation of efficacy, intent-to-treat analysis, in which missing values were recorded as failure (ITT), and last-observation-carried-forward (LOCF) analysis were used. Metabolic parameters were assessed using LOCF analysis.

Results

The analysis included 175 ART-naïve and 109 pretreated but PI-naïve patients. After 96 weeks, a similar proportion of patients in the ART-naïve and in the pretreated but Pi-naïve group had HIV-1 RNA levels < 400 copies/mL (68.0% and 70.6% [ITT], respectively; 96.6% and 90.8% [LOCF], respectively). The proportion of patients with HIV RNA < 50 copies/mL was higher in the ART-naïve group compared with the pretreated but PI-naïve group (61.1% and 56.9% [ITT], respectively; 84.0% and 75.2% [LOCF], respectively). Median change in CD4 cell count from baseline to week 96 was''+263 cells/mm³ (IQR 170; 384. LOCF; p < 0.0001) in the ART-naïve group, and one line +181 cells/mm³ (IQR 60; 309. LOCF; p < 0.0001) in the pretreated but PI-naïve group. Treatment was well tolerated, with only 2.5% of patients withdrawing from treatment due to side effects. There were no clinically relevant changes in liver enzyme levels. Overall total cholesterol, triglyceride, and low-and high-density lipoprotein levels increased to week 96, although levels remained within normal ranges in the majority of ART-naïve and pretreated patients.

Conclusions

This follow-up analysis confirms the long term efficacy and tolerability of SQV/r in ART-naïve and pretreated but PI-naïve patients in the real-life clinical setting.     

Ca2+ triggers premature inactivation of the cdc2 protein kinase in permeabilized sea urchin embryos.

Exit from mitosis requires inactivation of the cyclin B-p34cdc2 protein kinase complex. Since increased cytosolic Ca2+ has been implicated as a potential trigger of mitotic progression, we directly tested the possibility that Ca2+ triggers the pathway responsible for inactivating the cdc2 kinase, using sea urchin embryos permeabilized at various stages of the cell cycle. In cells permeabilized during late interphase and prophase, micromolar Ca2+ induced premature inactivation of the cdc2 kinase without affecting the absolute amount of p34cdc2 protein. Inactivation was selective for the cdc2 kinase, as elevated Ca2+ had no effect on cAMP-dependent protein kinase activity. Premature cdc2 kinase inactivation did not require cyclin B destruction, but did coincide with the dissociation of cyclin B-p34cdc2 complexes. In cells permeabilized during prometaphase and metaphase, cdc2 kinase inactivation was Ca(2+)-independent, presumably because at these later times the inactivating pathway had been enabled prior to permeabilization. This work provides evidence that Ca2+ is the physiological trigger enabling cdc2 kinase inactivation during mitosis.     

Enhancement of erythrocyte superoxide dismutase activity: effects on cellular oxidant defense

To delineate further the role of superoxide dismutase (SOD) in red blood cell (RBC) oxidant defense, normal human erythrocytes were osmotically lysed and resealed in the presence of varying concentrations of exogenous SOD. This resulted in a dose-dependent increase in SOD activity in the resealed erythrocytes while maintaining nearly normal RBC hemoglobin concentration (less than 10% decrease from the control value), cell volume, and cellular deformability. Surprisingly, a five- or ninefold increase in SOD activity yielded no additional protection against superoxide-generating drugs (phenazine methosulfate or menadione sodium bisulfite). No significant differences were observed between the control and SOD-loaded RBCs in O2-driven methemoglobin formation or generation of thiobarbituric acid-reactive substances. In contrast, RBCs with elevated SOD activity pretreated with sodium azide (to block catalase activity) or 1-chloro-2,4- dinitrobenzene (to deplete reduced glutathione, GSH) showed significantly enhanced methemoglobin generation in response to superoxide generating drugs. No differential response was noted between the control, control-resealed, and SOD-loaded RBCs to oxidants other than superoxide. Based on our results and other data, we conclude that elevated SOD activity may imbalance cellular oxidant defense, resulting in enhanced oxidation due to the accelerated generation of H2O2, the product of O2- dismutation. This effect is significantly exacerbated under conditions in which H2O2 catabolism is altered.     

Phospholipase A2 levels in acute chest syndrome of sickle cell disease

Acute chest syndrome (ACS) is associated with significant morbidity and is the leading cause of death in patients with sickle cell disease (SCD). Recent reports suggest that bone marrow fat embolism can be detected in many cases of severe ACS. Secretory phospholipase A2 (sPLA2) is an important inflammatory mediator and liberates free fatty acids, which are felt to be responsible for the acute lung injury of the fat embolism syndrome. We measured SPLA2 levels in 35 SCD patients during 20 admissions for ACS, 10 admissions for vaso-occlusive crisis, and during 12 clinic visits when patients were at the steady state. Eleven non-SCD patients with pneumonia were also evaluated. To determine if there was a relationship between sPLA2 and the severity of ACS we correlated SPLA2 levels with the clinical course of the patient. In comparison with normal controls (mean = 3.1 +/- 1.1 ng/mL), the non- SCD patients with pneumonia (mean = 68.6 +/- 82.9 ng/mL) and all three SCD patient groups had an elevation of SPLA2 (steady state mean = 10.0 +/- 8.4 ng/mL; vaso-occlusive crisis mean = 23.7 +/- 40.5 ng/mL; ACS mean = 336 +/- 209 ng/mL). In patients with ACS sPLA2 levels were 100- fold greater than normal control values, 35 times greater than values in SCD patients at baseline, and five times greater than non-SCD patients with pneumonia. The degree of SPLA2 elevation in ACS correlated with three different measures of clinical severity and, in patients followed sequentially, the rise in SPLA2 coincided with the onset of ACS. The dramatic elevation of SPLA2 in patients with ACS but not in patients with vaso-occlusive crisis or non-SCD patients with pneumonia and the correlation between levels of SPLA2 and clinical severity suggest a role for SPLA2 in the diagnosis and, perhaps, in the pathophysiology of patients with ACS.     

Favourable outcome in sclerotherapy for bleeding oesophageal varices in schistosomiasis: Results in 30 patients

Abstract Thirty consecutive patients with bleeding oesophageal varices secondary to schistosomal liver disease received injection sclerotherapy. These formed a part of a prospective study, to evaluate the role of sclerotherapy in the treatment of bleeding oesophageal varices due to different aetiological factors in patients seen at the Gastroenterology Unit, Riyadh Armed Forces Hospital, Saudi Arabia, between December 1980 and July 1984.
Schistosomiasis is endemic in parts of Saudi Arabia. Sclerotherapy has a special place in schistosomal liver disease as liver function is well preserved in this disease. The new antischistosomal drugs are effective and may halt the progress of the disease. However, in many patients portal hypertension with bleeding oesophageal varices is found at diagnosis. Of the patients with schistosomiasis, 63.3% were Group A Child's Classification. Oesophageal varices have been eradicated in 11 cases during the mean follow-up period of 28 months (range 3-44 months). Four patients were referred for surgery because of bleeding gastric varices, two of whom died following operation. One patient, who was also hepatitis B surface antigen positive, died due to re-bleeding from gastric varices. The remaining 25 patients had no recurrence of bleeding and their liver function remained satisfactory.
Surgical procedures for oesophageal varices in schistosomiasis carry the risk of peri-operative and postoperative morbidity and mortality. In contrast, complications following sclerotherapy are minor compared to surgical procedures and none of our patients had any serious sclerotherapy complications.     

SCA6 is caused by moderate CAG expansion in the alpha1A-voltage- dependent calcium channel gene

Recently, moderate (CAG)>20 repeat expansions in the alpha1A-voltage- dependent calcium channel gene (CACNL1A4) have been identified in a previously unmapped type of SCA which has been named SCA6. We investigated the (CAG)n repeat length of the CACNL1A4 gene in 733 patients with sporadic ataxia and in 46 German families with dominantly inherited SCA which do not harbor the SCA1, SCA2, or MJD1/SCA3 mutation, respectively. The SCA6 (CAG)n expansion was identified in 32 patients most frequently with late manifestation of the disease. The (CAG)n stretch of the affected allele varied between 22 and 28 trinucleotide units and is therefore the shortest trinucleotide repeat expansion causing spinocerebellar ataxia. The (CAG)n repeat length is inversely correlated with the age at onset. In 11 parental transmissions of the expanded allele no repeat instability has been observed. Repeat instability was also not found for the normal allele investigating 431 meioses in the CEPH families. Analyzing 248 apparently healthy octogenerians revealed one allele of 18 repeats which is the longest normal CAG repeat in the CACNL1A4 gene reported. The SCA6 mutation causes the disease in approximately 10% of autosomal dominant SCA in Germany. Most importantly, the trinucleotide expansion was observed in four ataxia patients without obvious family history of the disease which necessitates a search for the SCA6 (CAG)n expansion even in sporadic patients.