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This article describes the rapid mitigation strategies in addressing the rising number of coronavirus disease 2019 (COVID-19) cases in Singapore. Learning from the severe acute respiratory syndrome experience in 2003, early preparation started in January 2020 when Wuhan was declared as the epicentre of the epidemic. The government had constructed a three-pronged approach which includes travel, healthcare and community measures to curb the spread of COVID-19.

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Acute scrotal pain is a common complaint in emergency or primary care practice. A myriad of pathologies need to be considered, and while the clinical history often leads the clinician to the correct diagnosis, radiologists are often called upon to provide further diagnostic information through ultrasonography. Here, we present the sonographic features of various scrotal emergencies, as well as a few pitfalls. Through this, we explore the breadth of urgent pathologies that may be encountered, both traumatic and non-traumatic. For the clinician who performs point-of-care ultrasound, whether in clinic or in the emergency department, we hope that this pictorial article will lay a good foundation for confident and accurate image interpretation.

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We recruited 144 women of whom 131 underwent scheduled caesarean section and were allocated to intrathecal bupivacaine without (46) or with (47) morphine and postoperative rectus sheath bupivacaine; or intrathecal bupivacaine with morphine and postoperative rectus sheath saline (38). We measured postoperative pain with a 10-point numeric rating scale. The mean (SD) areas under the curve for pain on movement during 48 postoperative hours were 273.5 (63.6), 223.8 (80.7) and 223.8 (80.7), respectively, p = 0.008. There was no difference between women who had intrathecal morphine with or without rectus sheath bupivacaine, p = 1. The equivalent values for pain at rest were 160.8 (64.7), 85.8 (79.4) and 82.8 (74.3), respectively, p < 0.001. There was no difference between women who had intrathecal morphine with or without rectus sheath bupivacaine, p = 0.98.

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Uniform SnO(2) nanorod arrays were deposited on a 4 inch SiO(2)/Si wafer by plasma-enhanced chemical vapor deposition (PEVCD) at low deposition temperature of around 300 degrees C. The SnO(2) nanorods were connected at the roots, thus the nanorod sensors could be fabricated by a feasible way compatible with microelectronic processes. The surface of the sensors was modified by Pt nanoparticles deposited by dip coating and sputtering, respectively. The sensing properties of the Pt-modified SnO(2) nanorod sensors to CO and H(2) gases were comparatively studied. After surface modification of Pt, the sensing response to CO and H(2) gases increased dramatically. The 2 nm Pt-modified SnO(2) nanorod sensors by sputtering showed the best sensing performance. By increasing Pt thickness from 2 nm up to 20 nm, the optimal working temperature decreased by 30 degrees C while the sensing response also decreased by about 4 times. Comparing these two Pt modification approaches by dip coating and sputtering, both could achieve comparable promotion effect if the Pt thickness can be controlled around its optimal value. The deposition technique of SnO(2) nanorod arrays by PECVD has good potential for scale-up and the fabrication process of nanorod sensors possesses simplicity and good compatibility with contemporary microelectronics-based technology.

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OBJECTIVES: To assess whether there is a need to correct first-trimester biochemical markers (free beta-hCG and pregnancy-associated plasma protein-A (PAPP-A)) or first-trimester fetal nuchal translucency thickness (NT) in different ethnic groups, when screening for Downs syndrome at 11-14 weeks of gestation. METHODS: Free beta-hCG, PAPP-A and fetal NT were measured at 11-14 weeks of gestation in a group of women presenting for first-trimester screening in two OSCAR centres. The group comprised 61 219 sets of data from Caucasian women (the reference group); 4835 sets of data from South Asian women; 3450 sets of data from Oriental women and 2727 sets of data from Afro-Caribbean women. The Oriental data set was supplemented with a further 480 cases collected in Hong Kong and the Afro-Caribbean data set was supplemented with 216 cases collected from Kings College. The difference in marker values between the reference group and the other ethnic groups was compared before and after weight correction for the biochemical markers using standard statistical techniques. A correction factor for ethnic origin was applied for all three markers and the screen-positive rate before and after correction was assessed for the various groups. RESULTS: After maternal weight correction, in Afro-Caribbean women, the median PAPP-A was increased by 55% and the free beta-hCG increased by 11%. In south Asian women, the PAPP-A was increased by 8% and the free beta-hCG decreased by 7.5%. In Oriental women, the PAPP-A was increased by 9% and the free beta-hCG by 6%. For delta NT in Afro-Caribbean women, the values were 0.064 mm lower on average than in Caucasian women and for south Asian women 0.045 mm lower. The difference of -0.012 for Oriental women was not significant. Before correcting for ethnic origin, these changes resulted in the screen-positive rates being lower in the Afro-Caribbean group (3.7% vs 5.6%), the south Asian group (4.3% vs 5.6%) and Oriental group (4.9% vs 5.6%). After correction, the screen-positive rates were largely similar in the four groups. CONCLUSION: Differences in median PAPP-A, free beta-hCG and, to a lesser extent, in NT exist in Afro-Caribbean, South Asian and Oriental women. In populations where the medians and delta NT reference ranges are established in predominantly Caucasian populations, some correction for ethnicity is appropriate and can redress differences in screen-positive rates between these different groups.

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OBJECTIVE: To investigate whether the reported increase in maternal serum activin A concentration in pre-eclampsia is evident from the first trimester. DESIGN: This was a case-control study carried out in antenatal clinics among singleton pregnancies at 10-14 weeks of gestation. METHODS: Activin A concentration was measured in stored maternal serum samples obtained at 11-14 weeks of gestation from 131 women who subsequently developed pre-eclampsia, 77 who developed non-proteinuric pregnancy-induced hypertension, 141 with fetal growth restriction in the absence of hypertensive complications and from 494 normotensive controls. RESULTS: Compared to the median activin A level in the control group (1.00 MoM), the median MoM in the patients who subsequently developed pre-eclampsia and pregnancy-induced hypertension (1.49 MoM and 1.32 MoM, respectively) was significantly increased (p < 0.001), and in patients with fetal growth restriction (1.02 MoM) it was not significantly different (p = 0.57). In the pre-eclampsia group (n = 131) the disease was considered to be sufficiently severe to necessitate iatrogenic delivery before 35 weeks in 25 patients, and in this group the median MoM was 1.92. CONCLUSION: Maternal serum activin A concentration at 12 weeks of gestation in pregnancies which subsequently develop hypertensive disease is increased, whereas in those complicated by fetal growth restriction it is normal.

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OBJECTIVE: To determine whether the reported decrease in maternal serum placenta growth factor concentration in preeclampsia is evident from the first trimester and before clinical onset of the disease. We also examined levels in pregnancies that subsequently resulted in fetal growth restriction (FGR). METHODS: Placenta growth factor concentration was measured in stored maternal serum samples obtained at 11-14 weeks of gestation from 131 women who subsequently developed preeclampsia, 137 women who subsequently developed FGR, and 400 randomly selected controls who did not develop preeclampsia or FGR. Preeclampsia was defined as diastolic blood pressure of 90 mmHg or more on two occasions 4 hours apart, accompanied by proteinuria (more than 300 mg of total protein in a 24-hour urine collection or a positive test for albumin on reagent strip) in women with no pre-existing hypertensive or renal disease. Fetal growth restriction was considered present if a woman subsequently delivered a live infant with a birth weight below the fifth centile for gestation. RESULTS: In the control group, maternal serum placenta growth factor concentration increased with gestation. Compared with the controls (median multiple of the median 0.98, standard deviation [SD] 0.51), levels in the preeclampsia group (median multiple of the median 1.09, SD 0.52) were not significantly different (t = 1.83, P = .07), but in the FGR group (median multiple of the median 1.57, SD 0.74), levels were significantly increased (t = 10.85, P < .001). CONCLUSION: The previously reported decrease in serum placenta growth factor levels in women with preeclampsia might not precede clinical onset of the disease and is not apparent in the first trimester of pregnancy. Levels are significantly increased in pregnancies resulting in FGR.

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Placenta growth factor (PIGF), an angiogenic factor belonging to the vascular endothelial growth factor family, pregnancy-associated plasma protein A (PAPP-A) and free beta-human chorionic gonadotrophin (beta-hCG) were measured in maternal serum from 45 pregnancies with trisomy 21, 45 with trisomy 18 and 493 normal controls at 10-13 completed weeks of gestation. In the normal pregnancies maternal serum PIGF levels increased exponentially with gestation. The median multiple of the median (MoM) PIGF concentration in the trisomy 21 group (1.26 MoM) was significantly higher (p<0.0001) than in the control group (1.00 MoM). In the trisomy 18 group the median PIGF was lower (0.889 MoM) but this did not quite reach significance (p=0.064). The corresponding median MoM values for PAPP-A were 1.00 MoM for the controls, 0.49 MoM for trisomy 21 and 0.16 MoM for trisomy 18. The median MoM values for free beta-hCG were 1.00 MoM for the controls, 2.05 MoM for trisomy 21 and 0.38 MoM for trisomy 18. In the control group there was a small but significant correlation of PIGF with free beta-hCG (r=+0.1024) and PAPP-A (r=+0.2288). In the trisomy 18 group there was a significant association between PIGF and free beta-hCG (r=+0.2629) but not with PAPP-A (r=+0.0038). In the trisomy 21 group there was a small but significant association with PAPP-A (r=+0.1028) but not with free beta-hCG (r=+0.0339). The separation of affected and unaffected pregnancies in maternal serum PIGF is small, and therefore it is unlikely that measurement of PIGF would improve screening for these abnormalities provided by the combination of fetal nuchal translucency and maternal serum PAPP-A and free beta-hCG.

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In 45 cases of trisomy 18 and 493 control pregnancies at 10-14 weeks of gestation, maternal serum inhibin A, total activin A, free beta-hCG and PAPP-A were measured. In the trisomy 18 pregnancies the median values were 0.74 MoM for inhibin A, 1.23 MoM for activin A, 0.38 MoM for free beta-hCG and 0.16 MoM for PAPP-A. The degree of deviation from normal in the levels of inhibin and activin is small in comparison with free beta-hCG and PAPP-A and they are therefore unlikely to be of value in improving the sensitivity of 90% for a 1% false-positive rate achieved by screening with fetal nuchal translucency and maternal serum free beta-hCG and PAPP-A.

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Dimeric inhibin A was measured in maternal serum samples from 45 pregnancies affected by trisomy 21 and 493 samples from unaffected pregnancies at 10-14 weeks of gestation. Inhibin A levels in affected pregnancies were compared with levels of free beta-hCG and PAPP-A in the same series. In the trisomy 21 group, the median multiple of the median (MoM) inhibin A was not significantly elevated (1.28 vs 1.00) with only 15.5% being above the 95th centile. In contrast, the median MoM free beta-hCG was significantly increased (2.05 vs 1.00) with 36% above the 95th centile and PAPP-A was significantly reduced (0.49 vs 1.00) with 42% below the 5th centile. Inhibin A levels in the trisomy 21 group were significantly correlated with gestational age such that median levels rose from 1.04 at 11 weeks to 1.30 at 12 weeks and 1.67 at 13 weeks. These findings suggest that first trimester biochemical screening for trisomy 21, which is currently optimised using maternal serum free beta-hCG and PAPP-A and fetal nuchal translucency, will not benefit from the inclusion of inhibin A.

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Maternal serum total activin-A concentration was measured in 45 pregnancies affected by trisomy 21 and 493 control unaffected pregnancies at 10-14 weeks of gestation. In the trisomy 21 pregnancies total activin-A concentration was significantly higher (1.36 MoM of the unaffected pregnancies) and in 16% of cases the level was above the 95th centile of normal. The log10 SD for the control group and the trisomy 21 group were 0.17 and 0.22, respectively. The median pregnancy associated plasma protein-A (PAPP-A) in this trisomy 21 series was 0.49 and for free beta-hCG was 2.05. In the trisomy group there were significant positive associations between total activin-A and PAPP-A (0.6071) and free beta-hCG (0.4255). The low median difference and the high overlap in values between trisomic and unaffected pregnancies make total activin-A of little practical use in first-trimester screening for trisomy 21.

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OBJECTIVE: To examine the value of first trimester maternal serum free beta human chorionic gonadotrophin (beta hCG) and pregnancy associated plasma protein A (PAPP-A) as predictors of pregnancy complications. DESIGN: Screening study. SETTING: Antenatal clinics. POPULATION: Singleton pregnancies at 10-14 weeks of gestation. METHODS: Maternal serum free beta hCG and PAPP-A were measured at 10-14 weeks of gestation in 5,584 singleton pregnancies. In the 5,297 (94.9%) pregnancies with complete follow up free beta hCG and PAPP-A were compared between those with normal outcome and those resulting in miscarriage, spontaneous preterm delivery, pregnancy induced hypertension or fetal growth restriction and in those with pre-existing or gestational diabetes. RESULTS: Maternal serum PAPP-A increased and beta hCG decreased with gestation. The multiple of median maternal serum PAPP-A was significantly lower in those pregnancies resulting in miscarriage, pregnancy induced hypertension, growth restriction and in those with pre-existing or gestational diabetes mellitus, but not in those complicated by spontaneous preterm delivery. The level was < 10th centile of the reference range in about 20% of the pregnancies that subsequently resulted in miscarriage or developed pregnancy induced hypertension or growth restriction, and in 27% of those that developed gestational diabetes. Maternal serum free beta hCG was < 10th centile of the reference range in about 15% of the pregnancies that subsequently resulted in miscarriage or developed pregnancy induced hypertension or growth restriction, and in 20% of those that developed gestational diabetes. CONCLUSION: Low maternal serum PAPP-A or beta hCG at 10-14 weeks of gestation are associated with subsequent development of pregnancy complications.

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We have studied changes in first trimester fetal nuchal translucency (NT) and maternal serum free beta-hCG and PAPP-A with gravidity and parity in 3252 singleton pregnancies unaffected by chromosomal abnormality or major pregnancy complications. We have shown that gravidity and parity is associated with a small but progressive decrease in fetal NT and a small but progressive increase in free beta-hCG and PAPP-A. None of these small changes with increasing gravidity or parity are statistically significant and hence correction for these variables is not necessary when considering first trimester screening for chromosomal abnormalities.

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In a study of 2923 normal pregnancies and 203 pregnancies affected by trisomy 21 we have shown a significant difference in the median MoM of the markers: fetal nuchal translucency, maternal serum free beta-hCG and PAPP-A in the presence of a female fetus compared with a male fetus. For maternal serum free beta-hCG levels are higher by 15% if the fetus is chromosomally normal and by 11% if the fetus has trisomy 21. For maternal serum PAPP-A the levels in chromosomally normal fetuses are 10% higher in the presence of a female fetus and 13% higher if the fetus has trisomy 21. In contrast, fetal nuchal translucency is 3-4% lower in both chromosomally normal and trisomy 21 female fetuses. The consequence of such changes when screening for trisomy 21 will be a reduction in the detection rate in female fetuses by a factor of 1-2%. Correction of risk algorithms for fetal sex, however, is probably not feasible, since ultrasound detection of fetal sex is only 70-90% accurate in the 10-14 week period.

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In a first trimester study of 5422 Caucasian women, 752 Afro-Caribbean women and 170 Asian women we have shown that the median maternal serum marker MoMs for free beta-hCG and PAPP-A were 19% and 48% higher in Afro-Caribbean women and 19% higher and 35% higher in Asian women, compared to Caucasian women. Correcting for maternal weight made very little difference to the effect in Afro-Caribbeans (21% and 57% higher after weight correction) but reduced the effect in Asians (4% and 17% higher after weight correction ). It is estimated that correcting for maternal weight and ethnicity overall would increase the detection rate by a modest 1.4%. However, the effect on an individual's risk could result in as much as a two-fold increase in the patient specific risk for trisomy 21. The impact of ethnic origin seems to be greater than that observed with second trimester biochemical markers and larger studies are required in order to develop robust algorithms for correcting for ethnic origin in the first trimester.

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