Rab11a drives adhesion molecules to the surface of endometrial epithelial cells.

STUDY QUESTION: Is Rab11a GTPase, a regulator of intracellular trafficking, of significance in endometrial functions? SUMMARY ANSWER: Rab11a is an important component of the cascades involved in equipping the endometrial epithelium (EE) with 'adhesiveness' and 'cohesiveness'. WHAT IS KNOWN ALREADY: Cell adhesion molecules (CAMs) have been investigated extensively for modulation in their endometrial expression during the peri-implantation phase. However, the mechanisms by which CAMs are transported to the EE surface have not received the same attention. Rab11a facilitates transport of specific proteins to the plasma membrane in endothelial cells, fibroblasts, embryonic ectodermal cells, etc. However, its role in the transport of CAMs in EE remains unexplored. STUDY DESIGN, SIZE, DURATION: In-vitro investigations were directed towards deciphering the role of Rab11a in trafficking of CAMs (integrins and E-cadherin) to the cell surface of Ishikawa, an EE cell line. Towards this, Rab11a stable knockdown (Rab-kd) and control clones of Ishikawa were generated. JAr (human trophoblastic cell line) cells were used to form multicellular spheroids. Pre-receptive (n = 6) and receptive (n = 6) phase endometrial tissues from women with proven fertility and receptive phase (n = 6) endometrial tissues from women with unexplained infertility were used. PARTICIPANTS/MATERIALS, SETTING, METHODS: Rab-kd and control clones were used for in-vitro assays. Live cells were used for biotinylation, JAr spheroid assays, flow cytometry, trans-epithelial electrical resistance assays and wound-healing assays. Lysosome and Golgi membranes were isolated by ultracentrifugation. Confocal microscopy, immunoblotting, qRT-PCR and immunohistochemistry were employed for assessing the expression of Rab11a, integrins and E-cadherin. MAIN RESULTS AND THE ROLE OF CHANCE: shRNA-mediated attenuation of Rab11a expression led to a significant (P < 0.01) decline in the surface localization of αVß3 integrin. Cell surface protein extracts of Rab-kd clones showed a significant (P < 0.05) reduction in the levels of αV integrin. Further, a significant (P < 0.01) decrease was observed in the percent JAr spheroids attached to Rab-kd clones, compared to control clones. Rab-kd clones also showed a significant (P < 0.001) decline in the total levels of E-cadherin. This was caused neither by reduced transcription nor by increased lysosomal degradation. The role of Rab11a in maintaining the epithelial nature of the cells was evident by a significant increase in the migratory potential, presence of stress-fibres and a decrease in the trans-epithelial resistance in Rab-kd monolayers. Further, the levels of endometrial Rab11a and E-cadherin in the receptive phase were found to be significantly (P < 0.05) lower in women with unexplained infertility compared to that in fertile women. Taken together, these observations hint at a key role of Rab11a in the trafficking of αVß3 integrin and maintenance of E-cadherin levels at the surface of EE cells. LARGE-SCALE DATA: N/A. LIMITATIONS, REASONS FOR CAUTION: The in-vitro setting of the study is a limitation. Further immunohistochemical localizations of Rab11a and CAMs were conducted on a limited number of human endometrial samples. WIDER IMPLICATIONS OF THE FINDINGS: Rab11a-mediated trafficking of endometrial CAMs in EE cells can be explored further for its potential as a target for fertility regulation or infertility management. STUDY FUNDING/COMPETING INTEREST(S): This study was funded by the Indian Council of Medical Research (ICMR), the Department of Science and Technology (DST), the Council of Scientific and Industrial Research (CSIR), Government of India. No competing interests are declared.

HbAHP-25 attenuates HIV-1 gp120 mediated inflammation and barrier dysfunction.

OBJECTIVES: Development of HbAHP-25, a peptide that prevents HIV-1 entry into cells by blocking gp120-CD4 interaction, as a topical anti-HIV drug, necessitates that it is first tested for toxic or abrasive effects on genital epithelial cells and also on the vaginal microbiome. The present study was, therefore, undertaken to investigate whether: (1) HbAHP-25 has any adverse effect on growth and membrane integrity of various cell lines, and (2) HbAHP-25 neutralizes gp120 mediated insults on genital epithelial cells. METHODS: MTT and trans-epithelial resistance (TER) assays were performed to assess the viability and integrity of epithelial cells. Real-time PCR and Immunofluorescence/Western blotting were used to decipher the expression of tight junction proteins, at the mRNA and protein levels, respectively. A multiplex cytokine assay was performed to quantify the cytokines. RESULTS: HbAHP-25 had no adverse effect on the viability of VK2/E6E7, End1/E6E7, Ect1/E6E7 and HEC-1A cells, and also on growth of lactobacilli. The barrier integrity of HbAHP-25-treated cells remained unaltered. Expression of tight junction proteins, Claudin-1 and ZO-1, at transcript and protein levels, remained unaltered in HbAHP-25-treated HEC-1A cells. Interestingly, HbAHP-25 treatment prevented the breach of barrier integrity caused by gp120. Further, HbAHP-25 did not elicit the expression of inflammatory cytokines. Instead, the in vitro induction of inflammatory cytokines by gp120 was also abrogated in the presence of HbAHP-25. CONCLUSION: HbAHP-25 is exceedingly safe to genital epithelial cells and attenuates HIV-1 gp120-mediated barrier dysfunction by limiting excessive inflammation. This study provides significant evidences in the favor of HbAHP-25's potential as a topical anti-HIV agent.

mTORC2/AKT/HSF1/HuR constitute a feed-forward loop regulating Rictor expression and tumor growth in glioblastoma.

Overexpression of Rictor has been demonstrated to result in increased mechanistic target of rapamycin C2 (mTORC2) nucleation and activity leading to tumor growth and increased invasive characteristics in glioblastoma multiforme (GBM). However, the mechanisms regulating Rictor expression in these tumors is not clearly understood. In this report, we demonstrate that Rictor is regulated at the level of mRNA translation via heat-shock transcription factor 1 (HSF1)-induced HuR activity. HuR is shown to directly bind the 3' untranslated region of the Rictor transcript and enhance translational efficiency. Moreover, we demonstrate that mTORC2/AKT signaling activates HSF1 resulting in a feed-forward cascade in which continued mTORC2 activity is able to drive Rictor expression. RNAi-mediated blockade of AKT, HSF1 or HuR is sufficient to downregulate Rictor and inhibit GBM growth and invasive characteristics in vitro and suppress xenograft growth in mice. Modulation of AKT or HSF1 activity via the ectopic expression of mutant alleles support the ability of AKT to activate HSF1 and demonstrate continued HSF1/HuR/Rictor signaling in the context of AKT knockdown. We further show that constitutive overexpression of HuR is able to maintain Rictor expression under conditions of AKT or HSF1 loss. The expression of these components is also examined in patient GBM samples and correlative associations between the relative expression of these factors support the presence of these signaling relationships in GBM. These data support a role for a feed-forward loop mechanism by which mTORC2 activity stimulates Rictor translational efficiency via an AKT/HSF1/HuR signaling cascade resulting in enhanced mTORC2 activity in these tumors.

Hypoglycemic and antidiabetic profile of the aqueous root extracts of Leptadenia hastata in albino rats.

This study was designed to evaluate the antidiabetic profile and the hypoglycaemic activity of aqueous root extracts of L. hastata in normal and alloxan-induced diabetic rats model. Eighty five albino rats were used for this study out of this thirty five were used subjected to experimental diabetes by the use of alloxan at a dose of 160 mg kg(-1) body weight. Seven experimental groups of five rats per group (A-G) were used for this study. A standard antidiabetic drug (insulin) group (B) and normal saline group (G) serves as positive control. The blood glucose lowering activity of the extract, insulin and normal saline groups were monitored at 0, 1, 3, 6, 12 and 18 hpost extract administration. On the other hand the remaining fifty albino rats were used to determine the acute toxicity and the hypoglycemic activity of the extract. The blood glucose levels of the rats were monitored at 0, 7, 14, 21 and 28 days post extract administration. Oral administration of aqueous root extract at 600 and 800 mg kg(-1) b.wt have significantly (p < 0.05) decreased the blood glucose in diabetic albino rats. On the other hand the hypoglycemic activity of the aqueous root extract on normal rats at dose of 1000 mg kg(-1) b.wt have significantly (p < 0.05) decreases blood glucose level in normal albino rats. The results of the current study have demonstrated the antidiabetic and hypoglycaemic effects of L. hastata aqueous root extracts and underscore its potentials in the management of diabetes mellitus especially following prolonged use in days.

Central nervous system sites of the sleep promoting effects of eszopiclone in rats.

We examined the effects of eszopiclone (ESZ), a GABA-A receptor agonist in current clinical use as a hypnotic medication, on the activity of subcortical wake- and sleep-active neuronal populations in the rat brain. Sleep-wake states were quantified after i.p. injections of ESZ (3 and 10 mg/kg) or vehicle administered early in the dark phase, when rats are spontaneously awake. Rats were euthanized 2 h post-injection and brain tissue was processed for c-Fos protein immunoreactivity (IR) and for neurotransmitter markers. ESZ at 3 and 10 mg/kg increased time spent in non-rapid-eye-movement (nonREM) sleep, but had no significant effect on Fos-IR in GABAergic neurons in the preoptic hypothalamus that normally express c-Fos during sleep. Among wake-active cell types examined, Fos-IR in hypocretin (HCRT) neurons in the perifornical lateral hypothalamus (LH) was reduced following 3 and 10 mg/kg ESZ. At 10 mg/kg, ESZ suppressed Fos-IR in cholinergic and noncholinergic neurons in the basal forebrain and in serotonergic and nonserotonegic neurons in the dorsal raphe. Having determined that HCRT neurons were responsive to the low dose of systemic ESZ, we unilaterally perfused ESZ directly into the LH of awake rats, using reverse microdialysis. Perfusion of ESZ at 50 µM into the LH for 2 h suppressed waking-related Fos-IR in HCRT neurons, but not in nonHCRT neurons ipsilateral to the dialysis probe. Bilateral LH perfusion of ESZ at 50 µM for 2 h early in the dark phase significantly increased sleep. These findings demonstrate that sleep induction by ESZ does not require activation of GABAergic sleep-regulatory neurons in the preoptic hypothalamus, and identify suppression of HCRT neurons in the LH and suppression of basal forebrain and dorsal raphe neurons as potential mechanisms underlying the sleep-promoting effects of ESZ.

Sustained sleep fragmentation results in delayed changes in hippocampal-dependent cognitive function associated with reduced dentate gyrus neurogenesis.

Sleep fragmentation (SF) is prevalent in human sleep-related disorders. In rats, sustained SF has a potent suppressive effect on adult hippocampal dentate gyrus (DG) neurogenesis. Adult-generated DG neurons progressively mature over several weeks, and participate in certain hippocampal-dependent cognitive functions. We predicted that suppression of neurogenesis by sustained SF would affect hippocampal-dependent cognitive functions in the time window when new neurons would reach functional maturity. Sprague-Dawley rats were surgically-prepared with electroencephalogram (EEG) and electromyogram (EMG) electrodes for sleep state detection. We induced sleep-dependent SF for 12 days, and compared SF animals to yoked sleep fragmentation controls (SFC), treadmill controls (TC) and cage controls (CC). Rats were injected with bromodeoxyuridine on treatment days 4 and 5. Rats were returned to home cages for 14 days. Cognitive performance was assessed in a Barnes maze with 5 days at a constant escape position followed by 2 days at a rotated position. After Barnes maze testing rats were perfused and DG sections were immunolabeled for BrdU and neuronal nuclear antigen (NeuN), a marker of mature neurons.SF reduced BrdU-labeled cell counts by 32% compared to SFC and TC groups. SF reduced sleep epoch duration, but amounts of rapid eye movement (REM) sleep did not differ between SF and SFC rats, and non-rapid eye movement (NREM) was reduced only transiently. In the Barnes maze, SF rats exhibited a progressive decrease in escape time, but were slower than controls. SF animals used different search strategies. The use of a random, non-spatial search strategy was significantly elevated in SF compared to the SFC, TC and CC groups. The use of random search strategies was negatively correlated with NREM sleep bout length during SF. Sustained sleep fragmentation reduced DG neurogenesis and induced use of a non-spatial search strategy, which could be seen 2 weeks after terminating the SF treatment. The reduction in neurogenesis induced by sleep fragmentation is likely to underlie the delayed changes in cognitive function.

GABAergic regulation of the perifornical-lateral hypothalamic neurons during non-rapid eye movement sleep in rats.

The perifornical-lateral hypothalamic area (PF-LHA) has been implicated in the regulation of behavioral arousal. The PF-LHA predominantly contains neurons that are active during behavioral and cortical activation and quiescent during non-rapid eye movement (nonREM) sleep, that is, are nonREM-off neurons. Some in vitro and in vivo studies indicate that PF-LHA neurons, including hypocretin-expressing neurons, are under GABAergic control. However, a role of GABA in suppressing the discharge of PF-LHA neurons during spontaneous nonREM sleep has not been confirmed. We recorded the sleep-wake discharge profiles of PF-LHA neurons and simultaneously assessed the contributions of local GABA(A) receptor activation and blockade on their wake- and nonREM sleep-related discharge activities by delivering GABA(A) receptor agonist, muscimol (500 nm, 5 microM, and 10 microM) and its antagonist, bicuculline (5 microM, 10 microM, and 20 microM), adjacent to the recorded neurons via reverse microdialysis. Muscimol dose-dependently decreased the discharge of PF-LHA neurons including nonREM-off neurons. Muscimol-induced suppression of discharge during nonREM sleep was significantly weaker than the suppression produced during waking. In the presence of bicuculline, PF-LHA neurons, including nonREM-off neurons, exhibited elevated discharge, which was dose-dependent and was significantly higher during nonREM sleep, compared to waking. These results suggest that GABA(A) receptor mediated increased GABAergic tone contributes to the suppression of PF-LHA neurons, including nonREM-off neurons, during spontaneous nonREM sleep.

Administration of the protein synthesis inhibitor, anisomycin, has distinct sleep-promoting effects in lateral preoptic and perifornical hypothalamic sites in rats.

Although a robust relationship between sleep and increased brain protein synthesis is well-documented, there have been few reports of the effects of local application of a protein synthesis inhibitor (PSI) on sleep. In this study, we compared the effects of local microdialytic administration of the protein synthesis inhibitor, anisomycin (ANI) into the lateral preoptic area (LPOA), a sleep promoting area vs. the perifornical/lateral hypothalamus (PF/LH), a wake and rapid eye movement (REM) sleep-promoting area. ANI administered to the LPOA at night resulted in an increase in stage 2 of rat non-REM sleep, whereas ANI delivered into the PF/LH during the daytime increased REM sleep. ANI microdialysis into hippocampus did not affect sleep or waking. These differential effects of local protein synthesis inhibition on sleep support a hypothesis that mechanisms controlling protein synthesis are critically involved in the regulation of both NREM sleep and REM sleep.

Hippocampal neurogenesis is reduced by sleep fragmentation in the adult rat.

The adult hippocampal dentate gyrus (DG) is a site of continuing neurogenesis. This process is influenced by a variety of physiological and experiential stimuli including total sleep deprivation (TSD). In humans, sleep fragmentation (SF) is a more common sleep condition than TSD. SF is associated with several prevalent diseases. We assessed a hypothesis that SF would suppress adult neurogenesis in the DG of the adult rat. An intermittent treadmill system was used; the treadmill was on for 3 s and off for 30 s (SF). For sleep fragmentation control (SFC), the treadmill was on for 15 min and off for 150 min. SF was conducted for three durations: 1, 4 and 7 days. To label proliferating cells, the thymidine analog, 5-bromo-2-deoxyuridine (BrdU), was injected 2 h prior to the end of each experiment. Expression of the intrinsic proliferative marker, Ki67, was also studied. SF rats exhibited an increased number of non-rapid eye movement (NREM) sleep bouts with no change in the percent of time spent in this stage. The numbers of both BrdU-positive cells and Ki67-positive cells were reduced by approximately 70% (P<0.05) in the SF groups after 4 and 7 days of experimental conditions whereas no differences were observed after 1 day. In a second experiment, we found that the percentage of new cells expressing a neuronal phenotype 3 weeks after BrdU administration was lower in the SF in comparison with the SFC group for all three durations of SF. We also examined the effects of SF on proliferation in adrenalectomized (ADX) animals, with basal corticosterone replacement. ADX SF animals exhibited a 55% reduction in the number of BrdU-positive cells when compared with ADX SFC. Thus, elevated glucocorticoids do not account for most of the reduction in cell proliferation induced by the SF procedure, although a small contribution of stress is not excluded. The results show that sustained SF induced marked reduction in hippocampal neurogenesis.

FIGO Save the Mothers Initiative: the Pakistan-UK collaboration.

The pilot study in Punjab, Pakistan was one of the five paired demonstration projects sponsored by FIGO in the "Save the Mothers" maternal mortality project. The goal of the project was to bring basic and comprehensive emergency obstetric care (EmOC) to a semiurban and rural area some 30 km from Lahore, where effectively there was none. The aim was to achieve this by using the existing facilities within the rural health system without the deployment of extra specialist staff other than as initial facilitators. This report shows trebling of some performance indicators and an improvement in met need. There is coincidentally a similar increase in the uptake of general medical services. Reducing maternal mortality requires building local capacity for EmOC; the essential components being the premises, trained personnel, equipment, and availability of drugs and blood. Availability and provision of EmOC coupled with changes in the attitude of the population resulted in marked improvement of process indicators.

Phenotypic plasticity of Rhyzopertha dominica pheromone signaling: the effects of different hosts and presence of conspecific females on male produced aggregation pheromone.

Male Rhyzopertha dominica (F.) (Coleoptera: Bostrichidae) release an aggregation pheromone consisting of a blend of two components, dominicalure 1 (D1) and Dominicalure 2 (D2). Pheromone from single insects, in different contexts, was collected and measured to determine if this signal is phenotypically plastic. Release rates were lowered when males were moved from maize grains to groundnut kernels or when moved from solitary occupation of maize grain to grain occupied by seven females. The pheromone release was increased again once these moves were reversed. The release of D1 was more affected than D2: thus, on groundnuts or in the presence of females, less pheromone was released and the proportion of D1 in the blend was lowered. Possible reasons for the modifications of the signal are discussed.

[Application of computer thermography in diagnosis of chronic focus of inflammation and the definition of indications to the use of antibiotics before operation in patients with post-operative hernia of anterior abdominal wall]. / Primenenie komp'iuternoi termografii v diagnostike ochaga khronicheskogo vospaleniia i opredelenii pokazanii k ispol'zovaniiu antibiotikov do vypolneniia operatsii u bol'nykh s posleoperatsionnoi gryzhei briushnoi stenki.

We studied the informative value of computer thermography in diagnostics of inflammatory changes in hernia region in 53 patients with post-operative hernia of anterior abdominal wall. Four variants of thermogram were obtained depending from temperature gradient in symmetric points of hernia hilus. This was used to substantiate preventive antibiotics prescription according to general scheme in pre-operation period in 25 patients and administration of electrophoresis of cefazoline in further 28 patients. The method was effective to reduce inflammatory changes in hernia hilus region in 88.9% of patients, which was defined based on temperature gradient decrease in symmetric regions of hernia. Post-operative complications rate decreased from 15.7 to 12.3%. The suppuration of post-operative wound was not observed.

In vivo accumulation of cyclin A and cellular replication factors in autonomous parvovirus minute virus of mice-associated replication bodies.

Autonomous parvovirus minute virus of mice (MVM) DNA replication is strictly dependent on cellular factors expressed during the S phase of the cell cycle. Here we report that MVM DNA replication proceeds in specific nuclear structures termed autonomous parvovirus-associated replication bodies, where components of the basic cellular replication machinery accumulate. The presence of DNA polymerases alpha and delta in these bodies suggests that MVM utilizes partially preformed cellular replication complexes for its replication. The recruitment of cyclin A points to a role for this cell cycle factor in MVM DNA replication beyond its involvement in activating the conversion of virion single-stranded DNA to the duplex replicative form.

Cyclin A activates the DNA polymerase delta -dependent elongation machinery in vitro: A parvovirus DNA replication model.

Replication of the single-stranded linear DNA genome of parvovirus minute virus of mice (MVM) starts with complementary strand synthesis from the 3'-terminal snap-back telomere, which serves as a primer for the formation of double-stranded replicative form (RF) DNA. This DNA elongation reaction, designated conversion, is exclusively dependent on cellular factors. In cell extracts, we found that complementary strand synthesis was inhibited by the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) and rescued by the addition of proliferating cell nuclear antigen, arguing for the involvement of DNA polymerase (Pol) delta in the conversion reaction. In vivo time course analyses using synchronized MVM-infected A9 cells allowed initial detection of MVM RF DNA at the G(1)/S phase transition, coinciding with the onset of cyclin A expression and cyclin A-associated kinase activity. Under in vitro conditions, formation of RF DNA was efficiently supported by A9 S cell extracts, but only marginally by G(1) cell extracts. Addition of recombinant cyclin A stimulated DNA conversion in G(1) cell extracts, and correlated with a concomitant increase in cyclin A-associated kinase activity. Conversely, a specific antibody neutralizing cyclin A-dependent kinase activity, abolished the capacity of S cell extracts for DNA conversion. We found no evidence for the involvement of cyclin E in the regulation of the conversion reaction. We conclude that cyclin A is necessary for activation of complementary strand synthesis, which we propose as a model reaction to study the cell cycle regulation of the Pol delta-dependent elongation machinery.

Quantification of human polyomavirus JC in brain tissue and cerebrospinal fluid of patients with progressive multifocal leukoencephalopathy by competitive PCR.

Activation of human polyomavirus JC (JCV) infection is the cause of the central nervous system (CNS) disease progressive multifocal leukoencephalopathy (PML). Previous studies with uncontrolled quantification systems suggested that the virus load in the CNS correlates with the state of disease and might reflect therapeutic effects. Therefore the aim of this study was the development of a competitive system with standard PCR techniques that allowed rapid detection of JCV subtypes, simultaneous differentiation of the two human polyomaviruses JCV and BKV and absolute quantification of the virus burden in initial diagnosis and progressive disease states. Subtype- and species-specificity of the PCR was achieved with the development of a degenerative PCR primer pair that detected JCV DNA in a range regularly found in PML samples, but did not amplify BKV DNA. The accuracy of the system was evaluated by quantification of known amounts of cloned JCV DNA with a competitive JCV-specific template that exhibited a comparable amplification rate to that of the native product. The calibration study demonstrated a linear correlation over a wide range of DNA concentrations on the background of buffer or JCV-negative diagnostic samples. The reliability of the system for PML diagnosis was analysed by calibration and determination of the virus burden in tissue and cerebrospinal fluid (CSF) of 11 PML patients confirming the accuracy in both types of samples under diagnostic conditions. Comparison of the JCV DNA concentration in tissue and CSF by a tightly controlled quantification technique revealed for the first time differences in a range of about four orders of magnitude and a variable virus load in CSF samples taken at comparable states of disease. This pointed to an individual course of virus shedding and demonstrates that a controlled competitive PCR system of high accuracy is essential for reliable quantification of virus DNA either in initial diagnosis, in progressive disease or for the evaluation of therapeutic effects.

Neoplastic transformation-associated stimulation of the in vitro resolution of concatemer junction fragments from minute virus of mice DNA.

Minute virus of mice (MVM) shows an oncotropic behavior reflected by its ability to amplify its genome more efficiently in a number of transformed versus normal cells. In vivo and in vitro studies revealed that the major effect of cell transformation on MVM DNA replication occurs at the level of double-stranded replicative-form amplification. In particular, resolution of MVM DNA concatemers into monomers was found to be highly sensitive to neoplastic transformation.

Mineral content of the forearms of babies born to Asian and white mothers.

Vitamin D deficiency is common in pregnant Asian women. The effect of maternal vitamin D deficiency on fetal skeletal mineralisation was assessed by measuring the bone mineral content of babies born to 45 Asian women, 19 Asian women who had received 1000 units of vitamin D during the last trimester, and 12 white women. The mean cord blood concentrations of 25-hydroxy vitamin D in the three groups were 5.9 +/- SE 0.9 nmol/l (2.4 +/- SE 0.4 ng/ml), 15.2 +/- 3.2 nmol/l (6.1 +/- 1.3 ng/ml), and 33.4 +/- 3.6 nmol/l (13.4 ng/ml), respectively. Despite this wide variation in values there was no significant difference in the bone mineral content (as assessed by photon absorptiometry) of the forearms of babies born to these women. This suggests that mineralization of the fetal skeleton is not impaired in maternal vitamin D deficiency. Craniotabes (skull softening) was present in seven of the 64 Asian babies. The bone mineral content in these babies was not significantly different from that of babies without this sign, and craniotabes should not therefore be taken as an indication of a generalized impairment in skeletal mineralization.

Nutrient intake and associated biochemical status of pregnant Asians in the United Kingdom.

Forty-six women (17 Pakistanis, 19 Indians, ten Bangladeshis) at 8 to 20 weeks of pregnancy were studied during November to January. Dietary intake was assessed by the diet history method. Mean energy intakes (+/- s.d.) for the Pakistanis, Indians and Bangladeshis were 9.80 (1.99), 8.08 (1.59) and 6.95 (1.70) MJ. Intakes of protein, calcium, phosphorus and iron were positively correlated with energy intake. Vitamin D intake was similar in all groups, mean (+/- s.d) = 2.15 (1.39). Mean serum (+/- s.d.) protein, phosphorus and calcium were 70.9 (6.5) g/l; 2.27 (0.12) mmol/l; 1.00 (0.21) mmol/l and fell within the lower normal range. Mean haemoglobin was 12.2 (1.1) g/dl. Mean (+/- s.d.) serum 25-OHD for Pakistanis, Indians and Bangladeshi respectively was 3.80 (2.25), 4.04 (2.64) and 5.22 (2.47) ng/ml. These are within the range found for patients with osteomalacia (less than 10 ng/ml) and substantially lower than values of 14.6 (2.6) ng/l reported by Bashir et al. (1981) for September and October.