Search

To assess whether systemic delivery of kynurenic acid improves the outcomes of heatstroke in rats. Anesthetized rats were divided into 2 major groups and given vehicle solution (isotonic saline 0.3 mL/kg rat weight) or kynurenic acid (30–100 mg in 0.3 mL saline/kg) 4 h before the start of thermal experiments. They were exposed to an ambient temperature of 43 °C for 68 min to induce heatstroke. Another group of rats were exposed to room temperature (26 °C) and used as normothermic controls. Their core temperatures, mean arterial pressures, serum levels of systemic inflammatory response molecules, hypothalamic values of apoptotic cells and neuronal damage scores, and spleen, liver, kidney and lung values of apoptotic cells were determined. The survival time values during heatstroke for vehicle-treated rats were decreased from the control values of 475–485 min to new values of 83–95 min. Treatment with KYNA (30–100 mg/kg, iv) 4 h before the start of heat stress significantly and dose-dependently decreased the survival time to new values of 152–356 min (P

On February 15, 1978, the orientation of the IMF remained steadily northward for more than 12 hours. Using plasma and magnetic field data from ISEE 1 and 2, IMP 8, and IMP 7, we show that (1) the magnetosheath flow speed on the flanks of the magnetotail steadily exceeded the solar wind speed by 20 percent, (2) surface waves of about 5-min period and very nonsinusoidal waveform were persistently present on the dawn magnetopause and waves of similar period were present in the dusk magnetosheath, and (3) the magnetotail ceased to flare at an antisunward distance of 15 earth radii. We propose that the acceleration of the magnetosheath flow is achieved by magnetic tension in the draped field configuration for northward IMP; the reduction of tail flaring is consistent with a decreased amount of open magnetic flux and a larger standoff distance of the subsolar magnetopause. Results of a 3D MHD simulation support this phenomenological model.

When the vehicle-treated, sham-operated mice underwent heat stress, the fraction survival and core temperature at +4 h of body heating were found to be 5 of 15 and34.4∘C±0.3∘C, respectively. Castration 2 weeks before the start of heat stress decreased the plasma levels of testosterone almost to zero, protected the mice from heat-induced death (fraction survival, 13/15) and reduced the hypothermia (core temperature,37.3∘C). The beneficial effects of castration in ameliorating lethality and hypothermia can be significantly reduced by testosterone replacement. Heat-induced apoptosis, as indicated by terminal deoxynucleotidyl- transferase- mediatedαUDP-biotin nick end-labeling staining, were significantly prevented by castration. In addition, heat-induced neuronal damage, as indicated by cell shrinkage and pyknosis of nucleus, to the hypothalamus was also castration-prevented. Again, the beneficial effects of castration in reducing neuronal damage to the hypothalamus as well as apoptosis in multiple organs during heatstroke, were significantly reversed by testosterone replacement. The data indicate that testosterone depletion by castration may protect mice from heatstroke-induced multiple organ damage and lethality.

Ultralow frequency waves with periods greater than two minutes are characteristic features of planetary magnetotails. At Jupiter, changes in the wave characteristics across the boundary between the plasma sheet and the lobe have been used to identify this important plasma boundary. In the terrestrial lobes the wave amplitude can be relatively large, especially during intervals of intense geomagnetic activity. The wave power seen in the lobes of the magnetotails of the earth, Jupiter, Saturn and Uranus is evaluated to evaluate a proposal by Smith et al. that the propagating waves generated by the Kelvin-Helmholtz instability on the magnetopause can heat the plasma through a resonant absorption of these waves. The results indicate that the wave power in the lobes is generally small and can be easily understood in the framework of coupled MHD waves generated in the plasma sheet.

Background Intravenous administration of human umbilical cord blood cells (HUCBC) has been shown to improve heatstroke by reducing arterial hypotension as well as cerebral ischemia and damage in a rat model. To extend these findings, we assessed both hypothalamic neuronal apoptosis and systemic inflammatory responses in the presence of HUCBCs or vehicle medium immediately after initiation of heatstroke. Methods Anesthetized rats, immediately after the initiation of heat stress, were divided into two groups and given either serum-free lymphocyte medium (0.3 mL per rat, intravenously) or HUCBCs (5 × 106 in 0.3 mL serum-free lymphocyte medium, intravenously). Another group of rats were exposed to room temperature (26°C) and used as normothermic controls. Heatstroke was induced by exposing the anesthetized rats to a high ambient temperature of 43°C for 68 minutes. Results After the onset of heatstroke, animals treated with serum-free lymphocyte medium displayed hyperthermia, hypotension, bradycardia, hypothalamic neuronal apoptosis and degeneration, and up-regulation of systemic inflammatory response molecules including serum tumor necrosis factor-alpha, soluble intercellular adhesion molecule-1 and E-selectin. Heatstroke-induced hypotension, bradycardia, hypothalamic neuronal apoptosis and degeneration, and increased systemic inflammatory response molecules were significantly inhibited by HUCBC treatment. Although heatstroke-induced hyperthermia was not affected by HUCBC treatment, the serum levels of the anti-inflammatory cytokine interleukin-10 were significantly increased by HUCBC therapy during hyperthermia. Conclusions These findings suggest that HUCBC transplantation may prevent the occurrence of heatstroke by reducing hypothalamic neuronal damage and the systemic inflammatory responses.

Prior administration of naltrexone or cyclic d-phe-cys-try-arg-thr-pen-thr-NH,2 (CTAP) (a μ-opioid receptor antagonist), but not nor-binaltorphine (a K-opioid receptor antagonist) or ICI-174864 (a δ-opioid receptor antagonist), improve heat tolerance in the rat. As compared to those of normothermic controls, all vehicle-pretreated heatstroke rats displayed higher levels of creatinine, blood urea nitrogen, alkaline phosphatase, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, tumor necrosis factor-alpha, prothrombin time, activated partial thromboplastin time, and d-dimer in the plasma, cellular ischemia and injury markers in brain, and intracranial pressure. In contrast, all vehicle pretreated heatstroke animals had lower levels of mean arterial pressure, cerebral perfusion pressure, cerebral blood flow, brain PO2, and platelet count and protein C in the plasma. Twenty minutes before the start of heat exposure, prior administration of CTAP or naltrexone improves heat tolerance by reducing the systemic inflammation, hyper-coagulable state, and tissue ischemia and injury that occurred during heatstroke. The results show that μ-opioid receptor antagonism is effective for attenuation of heatstroke reactions.

Motivated by Thermal Catastrophe Model (TCM) of Goertz and Smith (1989), we turn attention to ultralow frequency (ULF) waves in the lobes, where waves are usually of relatively low amplitude. Remarkably little attention has been paid to characterizing the lobe spectra and the relation of lobe wave power to geophysical processes. In this paper we examine ULF waves (0.26 to 5 mHz or 3.2- to 64-min periods) in the Earth's magneto tail lobe region (−10 ≲ XGSM ≲ −23 RE) using data from the ISEE 2 flux gate magnetometer. The studies used all the tail data from the year 1978. Data from the ISEE 2 Fast Plasma Experiment (FPE) enabled us to exclude from the analysis all intervals not in the tail lobe region. The relation between the substorm activity, characterized by the AE index, and the wave power is also described. We find that the wave amplitudes at periods of ∼3 to 16 min (∼1 to 5 mHz) are below 0.8 nT for the transverse magnetic field components and below 0.6 nT for the compressional components ∼90% of the time. The amplitudes of lower frequency waves are somewhat larger. For waves with periods 16 to 64 min (∼0.26 to 1 mHz) the amplitudes are below 1 nT for both the compressional and transverse components ∼90% of the time. The wave amplitudes and the AE index, which characterizes substorm activity, are weakly correlated, the correlation coefficients being ∼0.55 and ∼0.35, for the compressional and transverse components respectively. The correlation coefficients between the transverse wave amplitudes and the AE index change little when AE is taken for 1 hour prior to or subsequent to the hour in which the wave amplitude is measured. For the compressional component the correlation coefficient remains unchanged when AE is measured for the subsequent or simultaneous hour but decreases when AE is taken for the previous hour. A primarily statistical study of frequency-weighted power of ULF waves at frequencies of 1 to 5 mHz is provided. The probability is 50% (5%) of observing frequency-weighted power for the frequency range 1 to 5 mHz in excess of 10−4 nT² Hz (10−3 nT² Hz). Three extended intervals in the lobe were selected for case studies. The largest wave amplitude we observed was about 5 nT which occurred when the AE index was higher than 1500 nT. The period corresponding to the largest wave amplitudes was ∼35 min (∼0.48 mHz). Power spectra from three different substorm intervals are provided as examples of wave activity in the lobes. The power spectral density of all components falls off as ƒ−2 or faster. Statistical study by itself does not provide an appropriate test of the requirement on wave power for the TCM. Additional case studies using ground magnetometers to relate wave power to substorm phases will be needed to test the assumptions of the TCM.

Background Human umbilical cord blood cells (HUCBCs) were used to investigate the mechanisms underlying the beneficial effects of cord blood cells in spinal cord injury (SCI). Methods Rats were divided into three groups: (1) sham operation (laminectomy only); (2) laminectomy + SCI + human adult peripheral blood mononucleocytes (PBMCs) (5 × 10 6 /0.3 mL); and (3) laminectomy + SCI + HUCBCs (5 × 10 6 /0.3 mL). SCI was induced by compressing the spinal cord for 1 minute with an aneurysm clip calibrated to 55 g closing pressure. HUCBCs were infused immediately after SCI via the tail vein. Behavioral function tests measuring the maximal angle at which an animal could hold onto the inclined plane were conducted on days 1, 4 and 7 after SCI. Serum levels of tumor necrosis factor (TNF)-α and interleukin (IL)-10, were assayed. Further more, to determine if glial cell line-derived neurotrophic factor (GDNF) or vascular endothelial growth factor (VEGF) could be detected in the spinal cord injured area after systemic HUCBC infusion, analysis of these two molecules was conducted by immunofluorescence. Results Systemic HUCBC infusion significantly attenuated SCI-induced hind limb dysfunction. The serum IL-10 levels were increased, but TNF-α levels were decreased after HUCBC infusion. Both VEGF and GDNF could be detected in the injured spinal cord after transplantation of HUCBC, but not PBMC, cells. Conclusion Our results demonstrate that HUCBC therapy may be beneficial for the recovery of SCI-induced hind limb dysfunction by increasing serum levels of IL-10, VEGF and GDNF in SCI rats.

The aim of present study was to examine whether systemically delivered glial cell-derived neurotrophic factor (GDNF) was beneficial in reversing the spinal cord injury (SCI) in a spinal cord compression model. Rats were divided into three major groups: (1) sham operation (laminectomy only); (2) laminectomy+SCI+normal saline (1 ml/kg, i.v.); (3) laminectomy+SCI+GDNF (50 ng/kg, i.v.). Spinal cord injury was induced by compressing the spinal cord for 1 min with an aneurysm clip calibrated to a closing pressure of 55 g. GDNF or saline was administered immediately after SCI via the tail vein. Behavioral tests of motor function measured by maximal angle an animal could hold to the inclined plane were conducted at days 1-7 after SCI. The triphenyltetrazolium chloride staining and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling assay were also conducted after SCI to evaluate spinal cord infarction and apoptosis, respectively. Both GDNF and vascular endothelial growth factor (VEGF) in the injured spinal cord were assayed by immunofluorescence. It was found that systemically delivered GDNF, but not vehicle solution, significantly attenuated the SCI-induced hind limb dysfunction and spinal cord infarction and apoptosis. Both GDNF and VEGF could be detected in the injury spinal cord after GDNF, but not vehicle solution, therapy. The results indicate that GDNF treatment may be beneficial in reversing hind limb dysfunction by reducing spinal cord infarction and apoptosis in a spinal cord compression model.

Human umbilical cord blood-derived CD34(+) cells were used to elucidate the mechanisms underlying the beneficial effects exerted by cord blood cells in spinal cord injury (SCI). Rats were divided into four groups: (1) sham operation (laminectomy only); (2) laminectomy + SCI + CD34(-) cells (5 x 10(5) human cord blood lymphocytes and monocytes that contained

Multiorgan dysfunction ensuing from severe heatstroke includes hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. We attempted to assess whether human umbilical cord bloodYderived CD34 + cell therapy improves survival during experimental heatstroke by attenuating multiorgan dysfunction. Anesthetized rats, immediately after the onset of heatstroke, were divided into 2 major groups and given CD34 j or CD34 + cells (1 � 10 5 Y 5 � 10 5 /mL/kg body weight) i.v. They were exposed to ambient temperature of 43-C to induce heatstroke. Another group of rats were exposed to room temperature (26-C) and used as normothermic controls. Hypotension, hepatic and renal failure (evidenced by increased serum urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase levels in plasma), hypercoagulable state (evidenced by increased prothrombin time, activated partial thromboplastin time, and D-dimer, and decreased platelet count and protein C in plasma), activated inflammation (evidence by increased TNF-! levels in serum), and cerebral dysfunction (evidenced by intracranial hypertension, cerebral hypoperfusion and hypoxia, and cerebral ischemia and injury) were monitored. When the CD34 j cellYtreated or untreated rats underwent heat stress, their survival time values were found to be 19 to 23 min. Resuscitation with CD34 + cells significantly improved survival time (duration, 63 Y 291 min). As compared with normothermic controls, all CD34 j cellYtreated heatstroke animals displayed hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. However, CD34 + cell therapy significantly caused attenuation of all the above-mentioned heatstroke reactions. In addition, the levels of IL-10 in plasma and glial cell lineYderived neurotrophic factors in brain were all significantly increased after CD34 + cell therapy during heatstroke. Our data indicate that CD34 + cell therapy may resuscitate persons who had a heatstroke by reducing multiorgan dysfunction or failure. KEYWORDS—Heatstroke, blood pressure, cytokines, coagulation, umbilical cord blood cells

Background: In the rat brain, heat-stroke-induced damage to cerebral neurons is attenuated through heat-shock-induced overexpression of heat-shock protein 72 (HSP72). Objective: To ascertain whether progressive exercise preconditioning induces HSP72 expression in the rat brain and prevents heat-stroke-induced cerebral ischaemia and injury. Methods: Male Wistar rats were randomly assigned to either a sedentary group or an exercise group. Those in the exercise group progressively ran on a treadmill 5 days/week, for 30–60 min/day at an intensity of 20–30 m/min for 3 weeks. The effects of heat stroke on mean arterial pressure, cerebral blood flow, brain ischaemia markers (glutamate, lactate/pyruvate ratio and nitric oxide), a cerebral injury marker (glycerol) and brain neuronal damage score in the preconditioned animals were compared with effects in unexercised controls. Heat stroke was induced by exposing urethane-anaesthetised animals to a temperature of 43°C for 55 min, which caused the body temperature to reach 42°C. Results: Three weeks of progressive exercise pretreatment induced HSP72 preconditioning in the brain and conferred significant protection against heat-stroke-induced hyperthermia, arterial hypotension, cerebral ischaemia and neuronal damage; it also prolonged survival. Conclusions: Exercise for 3 weeks can improve heat tolerance as well as attenuate heat-stroke-induced cerebral ischaemia in rats. The maintenance of mean arterial pressure and cerebral blood flow at appropriate levels in the rat brain may be related to overexpression of HSP72.

1. The aim of the present review is to summarize clinical observations and results of animal models that advance the knowledge of the attenuation of cerebrovascular dysfunction in the setting of heat stroke. It is a narrative review of selected published literature from Medline over the period 1959-2005. 2. All heat-stressed rodents, even under general anaesthesia, have hyperthermia, systemic inflammation, hypercoagulable state, arterial hypotension and tissue ischaemia and injury in multiple organs. These findings demonstrate that rodent heat stroke models can nearly mirror the full spectrum of human heat stroke. Experimental heat stroke fulfills the empirical triad used for the diagnosis of classical human heat stroke, namely hyperthermia, central nervous system alterations and a history of heat stress. 3. These physiological dysfunctions and survival during heat stroke can be improved by whole-body or brain cooling therapy adopted immediately after the onset of heat stroke. 4. However, in the absence of body or brain cooling, these heat stroke reactions can still be reduced by the following measures: (i) fluid replacement with 3% NaCl solution, 10% human albumin or hydroxyethyl starch; (ii) intravenous delivery of anti-inflammatory drugs, free radical scavengers or interleukin-1 receptor antagonists; (iii) hyperbaric oxygen therapy; or (iv) transplantation of human umbilical cord blood cells. 5. In addition, before initiation of heat stress, prior manipulations with one of the following measures was found to be able to protect against heat stroke reactions: (i) systemic delivery of alpha-tocopherol, mannitol, inducible nitric oxide synthase inhibitors, mu-opioid receptor antagonists, endothelin ETA receptor antagonists, serotoninergic nerve depletors or receptor antagonists, or glutamate receptor antagonists; or (ii) heat shock protein 72 preconditioning. 6. There is compelling evidence that cerebrovascular dysfunction is an attractive target for therapy in heat stroke.

Intravenously delivered human umbilical cord blood cells (HUCBC) have been previously shown to improve both morphologic and functional recovery of heat-stroked rats. To extend these findings, we examined both the morphologic and functional alterations in the presence of HUCBC or human peripheral mononuclear cells (PBMC) 24 h before initiation of heatstroke. Anesthetized rats, 1 day before the initiation of heatstroke, were divided into three major groups and given the following: (a) serum-free lymphocyte medium (0.3 ml) intravenously; (b) PBMC (5 x 10(6) in 0.3 ml serum-free lymphocyte medium); or (c) HUCBC (5 x 10(6) in 0.3 ml serum-free lymphocyte medium). Another group of rats were exposed to room temperature (26 degrees C) and used as normothermic controls. In vehicle-treated heatstroke rats, their mean arterial pressure, cerebral blood flow, and brain PO(2) were all lower than in normothermic controls after the onset of heatstroke. However, their body temperatures and striatal levels of inducible nitric oxide synthase (iNOS)-dependent NO, ischemia and damage markers (e.g., glycerol, glutamate, and lactate/pyruvate ratio), and neuronal damage in the striatum were all greater. The heatstroke-induced arterial hypotension, cerebral ischemia and hypoxia, and increased levels of iNOS-dependent NO in the striatum were all significantly reduced by pretreatment with HUCBC, but not with PBMC. Moreover, HUCBC were localized by immunohistochemistry and PCR analysis in the injured brain structures and spleen. These findings indicate that HUCBC transplantation, in addition to having therapeutic values, can be a good choice for preventing heatstroke occurrence.

the posterior triangle, and the pharynx (Reynolds and Wolinski, 1993). In our case also, BCC is located at the left anterior triangle of the neck. Histopathology findings showed that the BCC is lined by squamous epithelium and more than 90% have abundant sub-epithelial lymphoid tissue. Typically, cyst fluid contains cholesterol crystals and epithelial cells, as in our case. Differential diagnosis of congenital head and neck masses includes congenital cystic hygroma, meningomyelocele, hemangioma, dermoid cyst, laryngocele, thyroglossal duct cyst, thyroid gland mass, teratoma, and BCC (Suchet, 1995). The abnormalities identified were differentiated with respect to their position (at the central midline or anterolateral or lateral to the midline) and ultrasonographic characteristics (solid, cystic, or mixed; calcified or vascular); the relation of the abnormality to the major vessels of the neck and the presence of associated abnormalities (such as polyhydramnios, a fetal tumor, or bone anomalies) could be helpful. The lack of any solid elements or septations can be used to differentiate BCC from teratoma (Suchet, 1995). The diagnosis of BCC should be considered if a well-defined lesion is found anteriorly in the neck. As shown in Figure 1, the surface-rendering mode of 3D ultrasound revealed a cyst with a smooth wall at the left anterior triangle of the neck. The deeper rendering mode of 3D ultrasound further depicted that the inner wall of the cyst is smooth and without any septum. With these characteristics in imaging, 3D ultrasound helped reach the prenatal diagnosis of BCC. Because of the high risk of infection, early surgical excision is recommended (Ribichaud et al., 2000). The prognosis is usually good after surgery. Primary resection of BCC has a reported recurrence rate of only 3% versus 14% for resection of these lesions once they have become infected (Choi and Zalzal, 1995). At delivery, airway obstruction resulting from BCC may cause significant neonatal morbidity and mortality. Therefore, prenatal diagnosis of BCC is of help in lowering morbidity and mortality. In our case, we showed that 3D ultrasound can help in the differential diagnosis between BCC and other neck lesions. To the best of our knowledge, our case may be the first BCC to be illustrated by 3D ultrasound in utero.

Carrier detection before or at early pregnancy through a wide screening program may be a practical approach to prevent the fragile X syndrome. However, prior to implementation of such a program, the carrier prevalence in a population and availability of effective screening tests should be evaluated.One thousand and two pregnant women were randomly selected from our obstetric clinic and screened for FMRI mutation. Each woman was examined individually using a simple non-radioactive PCR, as well as in pool with two other women using high-resolution Southern blot hybridization.One third of women could be excluded from carrier status by PCR alone, while the rest had to be screened using Southern-blot hybridization in pool with two other women. This screening strategy was reliable and efficient, and suitable for large-scale screening. Among the 1002 women, no carrier of either premutation or full mutation was found. Allele with intermediate CGG-repeat between 40 and 52 was found in only 22 women (2.2%).Estimation of female fragile X carrier rate in Taiwan could not be made in the present study, due to insufficient sample size. However, the results indicated clearly that the rate in Taiwan was significantly lower than that of Israel (0/1002 vs. 1/113, p = 0.003), and also lower than those from other western counties (1/186-259, p = 0.020-0.049). We doubt that the cost-efficiency of such a wide screening program in Taiwan is acceptable. However, the effective screening strategy proposed in this study would be very helpful for women with family history of mental deficiency of undetermined etiology.

The purpose of this study was to investigate the association between demographic-obstetric factors and perceived labor pain in primiparas. The participants in this study were 90 primiparas having normal childbirths at the Department of Obstetrics, Chi-Mei Medical Center in southern Taiwan between September 1999 and June 2000. The perceived intensity of labor pain was measured using the visual analogue scale for pain and the present behavioral intensity score in the latent phase (cervix dilated 3-4 cm), active phase (cervix dilated 5-7 cm), and transitional phase (cervix dilated 8-10 cm). The subjects' mean age was 27.82 +/- 3.64 years (range, 20-39 yr), and the mean newborn birth weight was 3,162 +/- 387 g (range, 2,340-4,120 g). The primiparas' perceived labor pain at each of the three phases of labor was positively related to expected labor pain, but had no significant association with newborn birth weight, maternal age, body mass index, confidence in labor, or duration of labor. The expected labor pain of the primiparas had a negative correlation with body mass index. The birth weight of the newborn was positively related to the duration of labor. These findings suggest that primiparas' perceived labor pain is correlated with psychogenic rather than physical factors.

Objective The purpose of this study was to determine the long-term postpartum risk of end-stage renal disease in women with hypertensive disorders in pregnancy. Although most women with hypertensive disorders in pregnancy recover after delivery, some may experience acute renal failure. Study Design We searched Taiwan's National Health Insurance Research Database to identify women with hypertensive disorders in pregnancies and deliveries between 1998 and 2002. All cases were followed for a maximum of 11 years (median, 9 years; interquartile range, 7.79–10.02 years) to estimate the incidence of end-stage renal disease; Cox regression analysis that was adjusted for potential confounding was used to determine the relative risk. Results Of the 13,633 women with hypertensive disorders in pregnancy, 46 experienced end-stage renal disease. Women with hypertensive disorders in pregnancy had a risk of end-stage renal disease that was 10.64 times greater than did women without them (95% confidence interval [CI], 7.53–15.05). The risk was highest in women with a history of preeclampsia superimposed on chronic hypertension (hazard ratio, 44.72; 95% CI, 22.59–88.51). Women with gestational hypertension had a higher risk of end-stage renal disease than did women without hypertensive disorders in pregnancy (hazard ratio, 5.82; 95% CI, 2.15–15.77). Conclusion Women with hypertensive disorders in pregnancy have a higher risk of postpartum end-stage renal disease, regardless of which type of hypertensive disorder they have. Women with a history of hypertensive disorders in pregnancy are encouraged to have regular postpartum checkups, especially of renal function.

Chang CH, Chang FM, Yu CH, Liang RI, Ko HC, Chen HY. 2000. Fetal ear assessment and prenatal detection of aneuploidy by the quantitative three-dimensional ultrasonography. Ultrasound Med Biol 26: 743–749. Chang LW, Chang FM, Chang CH, Yu CH, Cheng YC, Chen HY. 2002. Prenatal diagnosis of fetal multicystic dysplastic kidney with two-dimensional and three-dimensional ultrasound. Ultrasound Med Biol 28: 853–858. Chen CP. 2001. Prenatal diagnosis of limb-body wall complex with craniofacial defects, amniotic bands, adhesions and upper limb deficiency. Prenat Diagn 21: 418, 419. Chen ML, Chang CH, Yu CH, Cheng YC, Chang FM. 2001. Prenatal diagnosis of cleft palate by three-dimensional ultrasound. Ultrasound Med Biol 27: 1017–1023. Chmait R, Pretorius D, Jones M, et al. 2002. Prenatal evaluation of facial clefts with two-dimensional and adjunctive three-dimensional ultrasonography: a prospective trial. Am J Obstet Gynecol 187: 946–949. Chuang L, Chang CH, Yu CH, Chang FM. 2000. Three-dimensional sonographic visualization of a fetal omphalocele at 14 weeks of gestation. Prenat Diagn 20: 523, 524. Emanuel PG, Garcia GI, Angtuaco TL. 1995. Prenatal detection of anterior abdominal wall defects with US. Radiographics 15: 517–530. Kang L, Chang CH, Yu CH, Cheng YC, Chang FM. 2002. Prenatal depiction of cystic hygroma using three-dimensional ultrasound. Ultrasound Med Biol 28: 719–723. Lai TH, Chang CH, Yu CH, Kuo PL, Chang FM. 2000. Prenatal diagnosis of alobar holoprosencephaly by two-dimensional and three-dimensional ultrasound. Prenat Diagn 20: 400–403. Sanders RC. 2002. Structural Fetal Abnormalities: The Total Picture (2nd edn), Mosby: St Louis. Wu YC, Yang ML, Yuan CC. 2000. Prenatal diagnosis of anophthalmos with limb-body wall complex. Prenat Diagn 20: 769, 770.