Practical use of the central venous access port for contrast-enhanced CT: comparison with peripheral intravenous access regarding enhancement and safety.

AIM: To evaluate the efficacy of using the central venous (CV) port compared with peripheral intravenous access for contrast-material injection for contrast enhancement during the portal venous phase. MATERIALS AND METHODS: Patients were divided into three groups: CV delay, CV routine, and peripheral access (PA) groups. Patients in the CV delay group underwent injection in the arm-down position with an additional delay, while those in the CV routine and PA groups underwent injections with the routine injection protocol for portal venous phase imaging. Contrast enhancement was evaluated by measuring the mean radiodensity (Hounsfield units) values for the aortic arch, abdominal aorta, inferior vena cava, portal vein, and spleen. The peak injection pressure was recorded and compared among the three groups. RESULTS: No complications related to power injection were observed during 119 contrast-material injections performed using the CV port device. The CV delay group showed significantly lower radiodensity values than the PA group (165.7 ± 20.1 versus 181 ± 19 HU [p<0.01] for the portal vein); however, no significant differences in mean radiodensity values were observed between the CV routine and PA groups (p>0.05). The median peak injection pressure was 73.5, 67, and 47 psi in the CV delay, CV routine, and PA groups, respectively (p<0.01). CONCLUSION: The CV port can be used for safe contrast-material injection while maintaining contrast enhancement on portal venous phase comparable to that achieved with peripheral intravenous access.

Metabolic shifts toward fatty-acid usage and increased thermogenesis are associated with impaired adipogenesis in mice expressing human APOE4.

BACKGROUND: The Apolipoprotein E (APOE) gene encodes for three isoforms in the human population (APOE2, APOE3 and APOE4). Whereas the role of APOE in lipid metabolism is well characterized, the specific metabolic signatures of the APOE isoforms during metabolic disorders, remain unclear. OBJECTIVE: To elucidate the molecular underpinnings of APOE-directed metabolic alterations, we tested the hypothesis that APOE4 drives a whole-body metabolic shift toward increased lipid oxidation. METHODS: We employed humanized mice in which the Apoe gene has been replaced by the human APOE*3 or APOE*4 allele to produce human APOE3 or APOE4 proteins and characterized several mechanisms of fatty-acid oxidation, lipid storage, substrate utilization and thermogenesis in those mice. RESULTS: We show that, whereas APOE4 mice gained less body weight and mass than their APOE3 counterparts on a Western-type diet (P<0.001), they displayed elevated insulin and homeostatic model assessment, markers of insulin resistance (P=0.004 and P=0.025, respectively). APOE4 mice also demonstrated a reduced respiratory quotient during the postprandial period (0.95±0.03 versus 1.06±0.03, P<0.001), indicating increased usage of lipids as opposed to carbohydrates as a fuel source. Finally, APOE4 mice showed increased body temperature (37.30±0.68 versus 36.9±0.58 °C, P=0.039), augmented cold tolerance and more metabolically active brown adipose tissue compared with APOE3 mice. CONCLUSION: These data suggest that APOE4 mice may resist weight gain via an APOE4-directed global metabolic shift toward lipid oxidation and enhanced thermogenesis, and may represent a critical first step in the development of APOE-directed therapies for a large percentage of the population affected by disorders with established links to APOE and metabolism.

Validation of the optimal site in the neck region for detecting swallowing sounds.

Recently, the swallowing sound has been used to detect swallowing events non-invasively. A previous study, using an accelerometer, showed that the site over the lateral border of the trachea immediately inferior to the cricoid cartilage was the optimal site for detecting swallowing sounds. However, the optimal site for detection of the swallowing sound using a microphone remains undetermined. To validate the optimal site in the neck region for detecting swallowing sounds. Fourteen healthy subjects (mean age, 27·6 ± 2·2 years; seven male and seven female) participated in this study. Twenty condenser microphones were attached to 20 sites on the left neck surface to detect swallowing sounds. Participants were instructed to swallow five different stimuli three times as follows: Resting saliva, 1 and 5 mL of Japanese tea, and 1 and 5 mL of yoghurt. Mean relative peak intensity was used to indicate the magnitude of the swallowing sound. Sound spectrograms were used to illustrate differences in the properties of swallowing sounds. Mean relative peak intensity number was highest in sites at the inferior border of the mandible just above the sternocleidomastoid muscle (site 11) and sites over the lateral border of the trachea immediately inferior to the cricoid cartilage (site 8). Comparison of spectrograms showed a greater density distribution of higher frequency components at site 11 compared with site 8. These results indicate that the inferior border of the mandible just above the sternocleidomastoid muscle is the optimal site for the detection of swallowing sounds.

New method of neck surface electromyography for the evaluation of tongue-lifting activity.

Elevation of the posterior part of the tongue is important for normal deglutition and speech. The purpose of this study was to develop a new surface electromyography (EMG) method to non-invasively and objectively evaluate activity in the muscles that control lifting movement in the posterior tongue. Neck surface EMG (N-EMG) was recorded using differential surface electrodes placed on the neck, 1 cm posterior to the posterior border of the mylohyoid muscle on a line orthogonal to the lower border of the mandible. Experiment 1: Three healthy volunteers (three men, mean age 37·7 years) participated in an evaluation of detection method of the posterior tongue lifting up movement. EMG recordings from the masseter, temporalis and submental muscles and N-EMG revealed that i) N-EMG was not affected by masseter muscle EMG and ii) N-EMG activity was not observed during simple jaw opening and tongue protrusion, revealing the functional difference between submental surface EMG and N-EMG. Experiment 2: Seven healthy volunteers (six men and one woman, mean age 27·9 years) participated in a quantitative evaluation of muscle activity. Tongue-lifting tasks were perfor-med, exerting a prescribed force of 20, 50, 100 and 150 gf with visual feedback. For all subjects, a significant linear relationship was observed bet-ween the tongue-lifting force and N-EMG activity (P < 0·01). These findings indicate that N-EMG can be used to quantify the force of posterior tongue lifting and could be useful to evaluate the effect of tongue rehabilitation in future studies.

Effect of nasal speaking valve on speech intelligibility under velopharyngeal incompetence: a questionnaire survey.

Velopharyngeal incompetence is known as a contributing factor to speech disorders. Suwaki et al. reported that nasal speaking valve (NSV) could improve dysarthria by regulating nasal emission utilising one-way valve. However, disease or condition which would be susceptible to treatment by NSV has not been clarified yet. This study aimed to evaluate the effect of NSV by questionnaire survey using ready-made NSV. Subjects were recruited through the internet bulletin, and NSV survey set was sent to the applicant. Sixty-six participants, who agreed to participate in this study, used NSV and mailed back the questionnaire which included self-evaluation and third-party evaluation of speech intelligibility. Statistical analysis revealed that the use of NSV resulted in significant speech intelligibility improvement in both self-evaluation and third-party evaluation (P < 0·01). Regarding the type of underlying disease of dysarthria, significant effect of NSV on self-evaluation of speech intelligibility could be observed in cerebrovascular disease and neurodegenerative disease (P < 0·01) and that on third-party evaluation in neurodegenerative disease (P < 0·01). Eighty-six percent of subjects showed improvement of speech intelligibility by shutting up nostrils by fingers, and the significant effect of NSV on both self-evaluation and third-party evaluation of speech intelligibility was observed (P < 0·001). From the results of this study, it was suggested that NSV would be effective in cerebrovascular disease and neurodegenerative disease, as well as in subjects whose speech intelligibility was improved by closing nostrils.

A novel automated detection system for swallowing sounds during eating and speech under everyday conditions.

The wave analysis of swallowing sounds has been receiving attention because the recording process is easy and non-invasive. However, up until now, an expert has been needed to visually examine the entire recorded wave to distinguish swallowing from other sounds. The purpose of this study was to establish a methodology to automatically distinguish the sound of swallowing from sound data recorded during a meal in the presence of everyday ambient sound. Seven healthy participants (mean age: 26·7 ± 1·3 years) participated in this study. A laryngeal microphone and a condenser microphone attached to the nostril were used for simultaneous recording. Recoding took place while participants were taking a meal and talking with a conversational partner. Participants were instructed to step on a foot pedal trigger switch when they swallowed, representing self-enumeration of swallowing, and also to achieve six additional noise-making tasks during the meal in a randomised manner. The automated analysis system correctly detected 342 out of the 352 self-enumerated swallowing events (sensitivity: 97·2%) and 479 out of the 503 semblable wave periods of swallowing (specificity: 95·2%). In this study, the automated detection system for swallowing sounds using a nostril microphone was able to detect the swallowing event with high sensitivity and specificity even under the conditions of daily life, thus showing potential utility in the diagnosis or screening of dysphagic patients in future studies.

Expression of B7-H3, a potential factor of tumor immune evasion in combination with the number of regulatory T cells, affects against recurrence-free survival in breast cancer patients.

BACKGROUND: In the tumor microenvironment, factors inhibiting the targeting of cancer cells by activated T cells have recently been noted. B7-H3 belongs to the B7 superfamily of immune regulatory ligands and plays an important role in the adaptive immune response of co-inhibitory/stimulatory factors in regulating T cells. However, the degree to which B7-H3 directly affects tumor immune evasion mechanisms remains unclear, particularly in patients with breast cancer. Regulatory T cells (Tregs) are known as a key player in the inhibition of immune mechanisms. The present study demonstrated that expression of B7-H3 on tumor cells and the number of Tregs in the tumor microenvironment independently affected prognosis in breast cancer patients. METHODS: We immunohistochemically investigated the presence of B7-H3 and forkhead box P3 (Foxp3)-positive Tregs in pathological specimens from 90 patients with breast cancer. RESULTS: Positive B7-H3 expression was associated with shorter recurrence-free survival (RFS) (p = 0.014). A higher percentage of Foxp3-positive cells also correlated with shorter RFS (p = 0.039). Multivariate analysis showed B7-H3 as an independent factor on RFS. Foxp3 expression in tumor-infiltrating lymphocytes (TILs) correlated significantly with larger tumor size (>2 cm), expression of human epidermal growth factor receptor 2 (HER2), and higher nuclear grade (p = 0.003, p < 0.001, p = 0.001, respectively). No correlation was identified between expression of B7-H3 and the percentage of Foxp3-positive TILs. CONCLUSIONS: B7-H3 and Foxp3 can be regarded as markers of poor prognosis in breast cancer. These expressions were not correlated, suggesting that B7-H3 expression plays an independent role in tumor immune evasion, regardless of Tregs.

Terminal RFLP analysis to determine the oral microbiota with hyposalivation.

Previous studies of oral microbiota by culture-dependent or targeted DNA approaches demonstrated that hyposalivation, a reduction in salivary secretions, might increase the amount of certain oral pathogens. However, the relationship between hyposalivation and the balance of oral microbiota, especially uncultivable bacteria, remains still unclear. The aim of this study was to elucidate the relationship between hyposalivation and oral microbiota by analyzing terminal restriction fragment length polymorphism (T-RFLP) of 16S rDNA. The 61 subjects were divided into two groups, hyposalivation group and normo-salivation group. The microbiota of tongue-coating samples was analyzed by T-RFLP. The amount of saliva, the number of Candida albicans, and also the dental status including plaque index, gingival index, bleeding on probing, probing pocket depth and decayed, missing, and filled teeth (DMFT) were assessed. Regarding the dental status, none of the evaluated factors were significantly different between the groups except the number of DMFT. According to the T-RFLP profiles, the patterns of microbiota in the tongue coating were classified into two groups, Clusters I and II. Cluster I is made up 76% of subjects with hyposalivation, while Cluster II is made up 61% of subjects with normo-salivation (p<0.001). Compared with the microbiota found in Cluster II, that in Cluster I had higher proportions of T-RFs corresponding to genera Veillonella, Dialister, Prevotella, Fusobacterium, and Streptococcus. T-RFLP analysis showed a significant role of salivary volume in determining the composition of the microbial community, regardless of the cultivability of the bacteria.

Does shoulder impingement syndrome affect the shoulder kinematics and associated muscle activity in archers?

BACKGROUND: Archery related injuries, such as shoulder impingement syndrome are caused by repeated motion of the shoulder. The aim of this study was to analyze differences in the shoulder kinematics and the associated muscle activity between archers with shoulder impingement and uninjured archery players. METHODS: Thirty male archers, who were divided into an impingement group and an uninjured group, were included in this study. The angle of scapular elevation, shoulder joint abduction, horizontal extension, and elbow joint flexion as well as the electromyographic activity of the upper trapezius, lower trapezius, deltoid middle, deltoid posterior, biceps brachii, and triceps brachii muscles at the point of stabilization during shooting were measured. Variables differing between impingement and uninjured groups were identified, and a stepwise regression analysis was performed to identify a combination of variables that effectively impingement syndrome. RESULTS: The results indicated that the angle of scapular elevation was significantly greater than that uninjured group (P<0.05). The angle of horizontal extension in the impingement group was significantly smaller than that in the uninjured group (P<0.05). The angle of elbow flexion in the impingement group was significantly smaller than that in the uninjured group (P<0.05). The levels of upper trapezius and deltoid middle muscle activity were significantly higher in the impingement group, while the level of lower trapezius muscle activity was significantly lower (P<0.05) when compared to the uninjured group. The impingement group had a greater angle of scapular elevation, smaller angle of horizontal extension, smaller angle of elbow flexion, higher the levels of upper trapezius, lower the levels of lower trapezius, higher deltoid middle muscle activity and higher UT/LT ratio (all differences were significant). A logistic model for predicting impingement syndrome showed that UT/LT ratio was significantly related impingement syndrome (P<0.05). CONCLUSION: The authors concluded that archers with shoulder impingement syndrome exhibit different kinematics and muscle activity compared to uninjured archers. Therefore, in order to prevent shoulder joint impingement during archery, training is necessary what can make lower trapezius muscle activity increased to decrease the UT/LT ratio.

Macular corneal dystrophy type I and type II are caused by distinct mutations in a new sulphotransferase gene.

Macular corneal dystrophy (MCD; MIM 217800) is an autosomal recessive hereditary disease in which progressive punctate opacities in the cornea result in bilateral loss of vision, eventually necessitating corneal transplantation. MCD is classified into two subtypes, type I and type II, defined by the respective absence and presence of sulphated keratan sulphate in the patient serum, although both types have clinically indistinguishable phenotypes. The gene responsible for MCD type I has been mapped to chromosome 16q22, and that responsible for MCD type II may involve the same locus. Here we identify a new carbohydrate sulphotransferase gene (CHST6), encoding an enzyme designated corneal N-acetylglucosamine-6-sulphotransferase (C-GlcNAc6ST), within the critical region of MCD type I. In MCD type I, we identified several mutations that may lead to inactivation of C-GlcNAc6ST within the coding region of CHST6. In MCD type II, we found large deletions and/or replacements caused by homologous recombination in the upstream region of CHST6. In situ hybridization analysis did not detect CHST6 transcripts in corneal epithelium in an MCD type II patient, suggesting that the mutations found in type II lead to loss of cornea-specific expression of CHST6.

Functions of chondroitin sulfate and heparan sulfate in the developing brain.

Chondroitin sulfate and heparan sulfate proteoglycans are major components of the cell surface and extracellular matrix in the brain. Both chondroitin sulfate and heparan sulfate are unbranched highly sulfated polysaccharides composed of repeating disaccharide units of glucuronic acid and N-acetylgalactosamine, and glucuronic acid and N-acetylglucosamine, respectively. During their biosynthesis in the Golgi apparatus, these glycosaminoglycans are highly modified by sulfation and C5 epimerization of glucuronic acid, leading to diverse heterogeneity in structure. Their structures are strictly regulated in a cell type-specific manner during development partly by the expression control of various glycosaminoglycan-modifying enzymes. It has been considered that specific combinations of glycosaminoglycan-modifying enzymes generate specific functional microdomains in the glycosaminoglycan chains, which bind selectively with various growth factors, morphogens, axon guidance molecules and extracellular matrix proteins. Recent studies have begun to reveal that the molecular interactions mediated by such glycosaminoglycan microdomains play critical roles in the various signaling pathways essential for the development of the brain.

Propofol infusions using a human target controlled infusion (TCI) pump in chimpanzees (Pan troglodytes).

Chimpanzees are genetically and physiologically similar to humans. Several pharmacokinetic models of propofol are available and target controlled infusion (TCI) of propofol is established in humans, but not in chimpanzees. The purpose of this study was to investigate if human pharmacokinetic models can accurately predict propofol plasma concentration (Cp) in chimpanzees and if it is feasible to perform TCI in chimpanzees. Ten chimpanzees were anaesthetized for regular veterinary examinations. Propofol was used as an induction or maintenance agent. Blood samples were collected from a catheter in a cephalic vein at 3-7 time points between 1 and 100 min following the propofol bolus and/or infusion in five chimpanzees, or TCI in six chimpanzees. Cp was measured using high-performance liquid chromatography. The Marsh, Schnider and Eleveld human pharmacokinetic models were used to predict Cp for each case and we examined the predictive performances of these models using the Varvel criteria Median PE and Median APE. Median PE and Median APE for Marsh, Schnider and Eleveld models were within or close to the acceptable range. A human TCI pump was successfully maintained propofol Cp during general anesthesia in six chimpanzees. Human propofol pharmacokinetic models and TCI pumps can be applied in chimpanzees.

Vascular endothelial growth factor can substitute for macrophage colony-stimulating factor in the support of osteoclastic bone resorption.

We demonstrated previously that a single injection of recombinant human macrophage colony-stimulating factor (rhM-CSF) is sufficient for osteoclast recruitment and survival in osteopetrotic (op/op) mice with a deficiency in osteoclasts resulting from a mutation in M-CSF gene. In this study, we show that a single injection of recombinant human vascular endothelial growth factor (rhVEGF) can similarly induce osteoclast recruitment in op/op mice. Osteoclasts predominantly expressed VEGF receptor 1 (VEGFR-1), and activity of recombinant human placenta growth factor 1 on osteoclast recruitment was comparable to that of rhVEGF, showing that the VEGF signal is mediated through VEGFR-1. The rhM-CSF-induced osteoclasts died after injections of VEGFR-1/Fc chimeric protein, and its effect was abrogated by concomitant injections of rhM-CSF. Osteoclasts supported by rhM-CSF or endogenous VEGF showed no significant difference in the bone-resorbing activity. op/op mice undergo an age-related resolution of osteopetrosis accompanied by an increase in osteoclast number. Most of the osteoclasts disappeared after injections of anti-VEGF antibody, demonstrating that endogenously produced VEGF is responsible for the appearance of osteoclasts in the mutant mice. In addition, rhVEGF replaced rhM-CSF in the support of in vitro osteoclast differentiation. These results demonstrate that M-CSF and VEGF have overlapping functions in the support of osteoclastic bone resorption.

Interleukin 3 prevents delayed neuronal death in the hippocampal CA1 field.

In the central nervous system, interleukin (IL)-3 has been shown to exert a trophic action only on septal cholinergic neurons in vitro and in vivo, but a widespread distribution of IL-3 receptor (IL-3R) in the brain does not conform to such a selective central action of the ligand. Moreover, the mechanism(s) underlying the neurotrophic action of IL-3 has not been elucidated, although an erythroleukemic cell line is known to enter apoptosis after IL-3 starvation possibly due to a rapid decrease in Bcl-2 expression. This in vivo study focused on whether IL-3 rescued noncholinergic hippocampal neurons from lethal ischemic damage by modulating the expression of Bcl-xL, a Bcl-2 family protein produced in the mature brain. 7-d IL-3 infusion into the lateral ventricle of gerbils with transient forebrain ischemia prevented significantly hippocampal CA1 neuron death and ischemia-induced learning disability. TUNEL (terminal deoxynucleotidyltransferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling) staining revealed that IL-3 infusion caused a significant reduction in the number of CA1 neurons exhibiting DNA fragmentation 7 d after ischemia. The neuroprotective action of IL-3 appeared to be mediated by a postischemic transient upregulation of the IL-3R alpha subunit in the hippocampal CA1 field where IL-3Ralpha was barely detectable under normal conditions. In situ hybridization histochemistry and immunoblot analysis demonstrated that Bcl-xL mRNA expression, even though upregulated transiently in CA1 pyramidal neurons after ischemia, did not lead to the production of Bcl-xL protein in ischemic gerbils infused with vehicle. However, IL-3 infusion prevented the decrease in Bcl-xL protein expression in the CA1 field of ischemic gerbils. Subsequent in vitro experiments showed that IL-3 induced the expression of Bcl-xL mRNA and protein in cultured neurons with IL-3Ralpha and attenuated neuronal damage caused by a free radical-producing agent FeSO4. These findings suggest that IL-3 prevents delayed neuronal death in the hippocampal CA1 field through a receptor-mediated expression of Bcl-xL protein, which is known to facilitate neuron survival. Since IL-3Ralpha in the hippocampal CA1 region, even though upregulated in response to ischemic insult, is much less intensely expressed than that in the CA3 region tolerant to ischemia, the paucity of IL-3R interacting with the ligand may account for the vulnerability of CA1 neurons to ischemia.

Critical contribution of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) to apoptosis of human CD4+ T cells in HIV-1-infected hu-PBL-NOD-SCID mice.

Apoptosis is a key for CD4+ T cell destruction in HIV-1-infected patients. In this study, human peripheral blood lymphocyte (PBL)-transplanted nonobese diabetic (NOD)-severe combined immunodeficient (SCID) (hu-PBL-NOD-SCID) mice were used to examine in vivo apoptosis after HIV-1 infection. As the hu-PBL-NOD-SCID mouse model allowed us to see extensive infection with HIV-1 and to analyze apoptosis in human cells in combination with immunohistological methods, we were able to quantify the number of apoptotic cells with HIV-1 infection. As demonstrated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), massive apoptosis was predominantly observed in virus-uninfected CD4+ T cells in the spleens of HIV-1-infected mice. A combination of TUNEL and immunostaining for death-inducing tumor necrosis factor (TNF) family molecules indicated that the apoptotic cells were frequently found in conjugation with TNF-related apoptosis-inducing ligand (TRAIL)-expressing CD3+CD4+ human T cells. Administration of a neutralizing anti-TRAIL mAb in HIV-1-infected mice markedly inhibited the development of CD4+ T cell apoptosis. These results suggest that a large number of HIV-1-uninfected CD4+ T cells undergo TRAIL-mediated apoptosis in HIV-infected lymphoid organs.

Insulin-mediated regulation of decidual protein induced by progesterone (DEPP) in adipose tissue and liver.

We analyzed the profile of the genes expressed in human adipose tissue and identified the fat-derived molecules, adiponectin and aquaporin 7, which modulate glucose and lipid metabolism. The same Bodymap analysis revealed abundant expression of the decidual protein induced by progesterone (DEPP) in the white adipose tissue. Northern blot analysis confirmed that human DEPP mRNA was highly expressed in white adipose tissue. Mouse DEPP mRNA was detected in heart, lung, skeletal muscle, and white adipose tissue under feeding state. In contrast, under fasting state, mouse DEPP mRNA was enhanced in lung, skeletal muscle, and white adipose tissue and it appeared also in the liver and kidney, suggesting up regulation of DEPP by fasting. Because fasting-induced DEPP expression was observed in insulin-sensitive organs, we investigated the regulation of DEPP in white adipose tissue and liver. During adipogenesis of mouse 3T3-L1 cells, DEPP mRNA increased in a differentiation-dependent manner similar to adiponectin and aquaporin 7. Treatment of cultured 3T3-L1 mature adipocytes, rat H4IIE, and human HepG2 hepatoma cells with insulin significantly decreased DEPP mRNA levels in dose- and time-dependent manners. IN VIVO experiments showed significant decrease of hepatic and adipose DEPP mRNA levels in refed mice, compared to fasted animals, and also showed significant increase in DEPP mRNA in streptozotocin-induced insulin-deficient diabetic mice. These results indicate that DEPP is a novel insulin-regulatory molecule expressed abundantly in insulin-sensitive tissues including white adipose tissue and liver.

Tetraparesis resembling acute transverse myelitis in a captive chimpanzee (Pan troglodytes): long-term care and recovery.

BACKGROUND: A 24-year-old, male chimpanzee (Pan troglodytes) developed acute tetraparesis. Magnetic resonance imaging showed a diffuse T2-weighted hyperintensive lesion, indicating inflammation at the C1-2 level. All infective, autoimmune, and vascular investigations were unremarkable. RESULTS AND CONCLUSIONS: The chimpanzee's condition most resembled acute transverse myelitis (ATM) in humans. The chimpanzee was in severe incapacitated neurological condition with bedridden status and required 24-hour attention for 2 months followed by special care for over a year. Initially, corticosteroid therapy was performed, and his neurological symptoms improved to some extent; however, the general condition of the chimpanzee deteriorated in the first 6 months after onset. Pressure ulcers had developed at various areas on the animal's body, as the bedridden status was protracted. Supportive therapy was continued, and the general condition, appetite, mobility, and pressure ulcers have slowly but synergistically recovered over the course of 2 years.

Association between maternal active smoking during pregnancy and placental weight: The Japan environment and Children's study.

INTRODUCTION: Maternal smoking during pregnancy is a well-known risk factor for reduced birthweight. However, research investigating the association between maternal smoking and placental weight is scarce and inconsistent. Our study was conducted to evaluate the association between maternal smoking and placental weight and placental weight/birthweight ratio (PW/BW ratio). METHODS: We used data from a birth cohort study, the Japan Environment and Children's Study (JECS). Main outcome measures were placental weight, PW/BW ratio, and the risk of high PW/BW ratio. High PW/BW ratio was defined as PW/BW ratio above the 90th percentile for gestational age and sex of offspring. The association between maternal smoking and placental weight was estimated as crude and as adjusted beta coefficients by applying linear regression analyses. Logistic regression analyses were also performed to estimate the association between maternal smoking and the risk of high PW/BW ratio. RESULTS: Of the 91,951 pregnant women, the mean placental weight and the mean PW/BW ratio were lowest for the group of women who had never smoked. Smokers had higher odds ratio for high PW/BW ratio compared with non-smokers. Furthermore, among smokers, the mean placental weight and mean PW/BW ratio were lowest in women who smoked less than 5 daily cigarettes, and highest in women who smoked 20 or more daily cigarettes during pregnancy. DISCUSSION: Placental weight was greater and PW/BW ratio was higher among smokers compared with non-smokers. Moreover, the number of daily cigarettes was positively associated with heavy placental weight.