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OBJECTIVES: To assess plasma vitamin D status and its association with dietary intake and body mass index (BMI) in primary gravida women. METHODS: This cross-sectional study was carried out in the Department of Gynecology, Lady Reading Hospital (LRH) and Institute of Basic Medical Sciences, Khyber Medical University, Peshawar from January to March 2016. Primary gravida women (n=88) in their first trimester attending antenatal clinic at LRH were included. Socio-demographic and anthropometric measures were recorded using standard methods. Nutritional intake was assessed using 24-hours dietary recall. Blood samples were collected to assess plasma vitamin D status through ELISA. RESULTS: Median plasma 25-OH vitamin D levels were 41.71 ηg/mL (IQR=17.29). Only 8 (9.09%) women had vitamin D deficiency (30 ηg/mL) levels of plasma vitamin D. Dietary intake of vitamin A and thiamine were significantly different between the three groups (sufficient/insufficient/deficient). No significant correlation was found between plasma vitamin D and anthropometric and dietary variables. Only socioeconomic status (p=0.03) was significantly associated with plasma vitamin D status. CONCLUSION: In our study, plasma vitamin D status was not significantly associated with dietary intake and BMI in primary gravida women. However, due to relatively small sample size, results may be taken with caution and large-scale study is recommended to establish the relationship of plasma vitamin D status with dietary intake and BMI in antenatal women.

To compare key thoracic anatomical surface landmarks between healthy and patient adult populations using Computed Tomography (CT). Sixteen slice CT images of 250 age and gender matched healthy individuals and 99 patients with lung parenchymal disease were analyzed to determine the relationship of 17 thoracic structures and their vertebral levels using a 32-bit Radiant DICOM viewer. The structures studied were: aortic hiatus, azygos vein, brachiocephalic artery, gastroesophageal junction (GEJ), left and right common carotid arteries, left and right subclavian arteries, pulmonary trunk bifurcation, superior vena cava junction with the right atrium, carina, cardiac apex, manubriosternal junction, xiphisternal joint, inferior vena cava (IVC) crossing the diaphragm, aortic arch and junction of brachiocephalic veins. The surface anatomy of all structures varied among individuals with no significant effect of age. Binary logistic regression analysis showed a significant association between individual health status and vertebral level for brachiocephalic artery (P = 0.049), GEJ (P = 0.020), right common carotid (P = 0.009) and subclavian arteries (P = 0.009), pulmonary trunk bifurcation (P = 0.049), carina (P = 0.004), and IVC crossing the diaphragm (P = 0.025). These observations differ from those reported in a healthy white Caucasian population and from the vertebral levels of the IVC, esophagus, and aorta crossing the diaphragm in an Iranian population. The differences observed in this study provide insight into the effect of lung pathology on specific thoracic structures and their vertebral levels. Further studies are needed to determine whether these are general changes or pathology-specific. Clin. Anat. 30:227-236, 2017. © 2017 Wiley Periodicals, Inc.

Despite the availability of plasmapheresis and intravenous immunoglobulin, the mortality and long-term morbidity from Guillain–Barré Syndrome (GBS) remains significant. This study aimed to determine the short-term outcomes in patients with GBS admitted to an intensive care unit. A total of 27 patients with a mean age of 31.67 ± 15.88 years were prospectively followed for 4 weeks after admission. Overall muscle power was graded using Medical Research Council (MRC) score 0–5, GBS disability was graded according to the Hughes scale, and tendon reflexes and features of dysautonomia were also noted. Plasma and cerebrospinal fluid biochemical parameters were analysed. Plasmapheresis sessions were done in all except one patient. Seven patients (26%) who died during follow-up showed a significantly higher proportion of dysautonomia features compared to those who survived. However, muscle power and plasma and cerebrospinal fluid biochemical features were similar between the two groups. Increasing age was associated with poor outcome [Unadjusted odds ratio (OR) 0.9270, 95% confidence interval (CI) 0.8598–0.9995, p = 0.027]. Plasmapheresis had no impact on the improvement of overall MRC score. Platelet count reduced significantly with plasmapheresis sessions (p = 0.014). Survival rate of patients decreased with prolonged preceding illness, hospital stay, and duration of mechanical ventilation >10 days. Only three patients were capable of independent survival at the end of 4 weeks’ follow-up. Plasmapheresis-only treatment does not improve overall MRC score in the short term in patients presenting with low MRC score.

Objective: Progressive hemorrhagic shock (HS) causes splanchnic vasoconstriction and hypo-perfusion together with profound depletions of cellular cytosolic energy phosphates (ATP). Cellular energy failure and the splanchnic hypo-perfusion are critical to the pathogenesis of shock decompensation and the subsequent death from cardiocirculatory arrest. We recently demonstrated post-resuscitation survival benefit for cellular cytosolic ATP replenishment but not for vasopressors use in a rat model of refractory HS. The aim of this study was to determine the effects of progressive HS on the splanchnic microvasculature, and to compare the effects of adjuvant resuscitations with either norepinephrine, vasopressin or lipid vesicles encapsulating ATP (ATPv) on this microvasculature. Methods: 40-male Sprague-Dawley rats were randomized into 4 groups of 10 each: HS/conventionalresuscitation (CR), HS/CR+Norepinephrine, HS/CR+Vasopressin, and HS/CR+ATPv. HS=initial removal of 30% of the calculated blood volume plus subsequent transection of the spleen for uncontrolled haemorrhage until a predefined intervention set-point was achieved; CR=shed blood returned+double the shed blood volume as lactated Ringer’s solution. Four-level intestinal microvascular A1 through A4 arterioles (100–8 μm diameter) in the terminalileum were continuously monitored with intravital-microscopy, and their diameters were measured at baseline, during shock, after completion of resuscitation, and during a 2 h post-resuscitation observation period. In addition, we recorded measurements of the mean arterial pressure, shock index, blood-gas profiles, and complete metabolic panels. Results: Progressive HS caused bimodal arteriole responses with progressive vasoconstriction from baseline of first-order A1 and second-order A2 (-22.1 ± 1.9%), a progressive vasodilation of the third-order A3 and fourth-order A4 arterioles (+22.2 ± 2.8%). Resuscitation initially restored A1 and A2 diameters to near baseline. This was followed by post-resuscitation A1 and A2 vasoconstriction in all groups, except the ATPv group (-8.1 ± 3.4%). The hemorrhage-induced vasodilation of the A3 and A4 arterioles was maintained during the post-resuscitation observation period in the CR (+55.3 ± 6.4%) and the ATPv groups (+39.5 ± 5.2%), but remarkably attenuated in the norepinephrine (+9.6 ± 5.8%) and vasopressin (+9.4 ± 8.8) groups. Conclusions: Severe hemorrhagic shock causes specific splanchnic microvascular bimodal response that is dependent on arteriolar level. First-order A1 and second-order A2 arterioles exhibit progressive vasoconstriction, whereas, third-order A3 and fourth-order A4 arterioles show progressive vasodilation. Temporary administration of either norepinephrine or vasopressin along with conventional resuscitation exerted deleterious effects at all splanchnic microvascular levels by virtue of their peripheral vascular actions. The cellular cytosolic ATP replenishment maintained a better microvascular profile when compared with the two vasopressors.

The aetiology of obesity has been attributed to several factors (environmental, dietary, lifestyle, host, and genetic factors); however none of these fully explain the increase in the prevalence of obesity worldwide. Gut microbiota located at the interface of host and environment in the gut are a new area of research being explored to explain the excess accumulation of energy in obese individuals and may be a potential target for therapeutic manipulation to reduce host energy storage. Several mechanisms have been suggested to explain the role of gut microbiota in the aetiology of obesity such as short chain fatty acid production, stimulation of hormones, chronic low-grade inflammation, lipoprotein and bile acid metabolism, and increased endocannabinoid receptor system tone. However, evidence from animal and human studies clearly indicates controversies in determining the cause or effect relationship between the gut microbiota and obesity. Metagenomics based studies indicate that functionality rather than the composition of gut microbiota may be important. Further mechanistic studies controlling for environmental and epigenetic factors are therefore required to help unravel obesity pathogenesis.

The Routine Use of Fecal Calprotectin in Clinical Pediatric Practice: Almost there or Still Issues to Address?

Objective: We investigated the relationship of body mass index at presentation and pituitary status with long-term changes in BMI over a period of 5 years. Study Design: Craniopharyngioma patients (n = 25) attending a tertiary pediatric endocrine center were divided into three groups based on their BMI at presentation [BMI ≥2 standard deviation scores (SDS), 0-1.99 SDS, and Results: Median (interquartile range) BMI SDS and hypopituitarism at presentation versus at the 5-year follow-up were as follows: BMI SDS ≥2 group (n = 10): 3.55 (0.68), 6/10 versus 3.76 (1.13), 8/10; BMI SDS 0-1.99 group (n = 11): 1.68 (1.05), 3/11 versus 1.64 (2.04), 7/11, and BMI SDS Conclusions: Our data indicate that obesity at presentation, rather than panhypopituitarism either at or after presentation, predicts obesity 5 years after diagnosis. However, obesity at presentation is not always associated with the subsequent development of panhypopituitarism. Pediatric craniopharyngioma subjects who have BMI SDS ≥2 at presentation require early and aggressive intervention to help prevent the complications of obesity.