Effects of Japan Sea Proper Water on the growth ofLegionella pneumophila, Escherichia coli, andStaphylococcus aureus

Objective To assess whetherLegionella pneumophila serogroup 1 and serogroup 6,Escherichia coli, andStaphylococcus aureus can survive in Japan Sea Proper Water (JSPW). Methods The inhibitory effects of JSPW, surface seawater (SSW), phosphate buffer solution with 3.5% NaCl of pH 7.0 (3.5% NaCIPBS), and the 10²- and 10⁴-fold dilute solutions with purified water or phosphate buffer solution of pH 7.0, and purified water were investigated. Survival cells were counted immediately after the water and the bacteria were mixed, and at 1,3,5, and 7 days after incubation at 37°C. If the number of surviving cells was decreased more than 2 log units compared with the starting value, we judged the medium to have had an inhibitory effect on the growth of the bacteria. Results The survival cells of the bacteria in JSPW had decreased more than 2 log units compared with the starting value at 1 day after incubation. After 1 day of incubation, the cells ofLegionella pneumophila serogroup 6 andStaphylococcus aureus were found to have decreased more than 2 log units in purified water (PW) used as a control. Furthermore,Legionella pneumophila serogroup 1 in the 10²-fold dilute solution of JSPW was only 1.04 log units lower than the starting value at 7 days after incubation. In the 10²- and 10⁴-fold dilute solutions of JSPW,Escherichia coli survived for 7 days after incubation. These results were almost similar to the results in SSW and 3.5% NaCIPBS. Conclusions The present findings demonstrate thatLegionella pneumophila serogroup 1 andEscherichia coli cannot survive in undiluted JSPW for over a day at 37°C, suggesting the inhibitory effects may be due to the sodium chloride contained in JSPW.     

Cartilage change after arthroscopic repair for an isolated meniscal tear

To investigate the direct effect to the cartilage caused by the meniscal repair, we examined patients who underwent an isolated meniscal repair without any other abnormalities by arthroscopic examination. A total of 17 patients were examined by second-look arthroscopy after an average interval of 9 months from the meniscal repair, and have been evaluated the status of the repaired meniscus and of the relative femoral condylar cartilage. Changes in the severity of the cartilage lesion between at the time of meniscal repair and the time of the second-look arthroscopy were considered based on the status of the repaired meniscus. Regardless of the healing status of the repair site, it was possible to prevent degeneration in the cartilage in 9 of the 10 patients who demonstrated no degeneration in the meniscal body. Of the 7 patients who demonstrated degeneration in the meniscal body, progression in cartilage degeneration was noted as 1 grade in 2 patients and 2 grades in another 3 patients. Even in those in which stable fusion of the repair site was achieved, the condition of the inner meniscal body was not necessarily maintained favorably in all cases, indicating that degeneration in the meniscal body was a risk factor for cartilage degeneration. It was concluded that recovery could not be expected even at 9 months after the repair if the lesion had already demonstrated degeneration in the meniscal body at the time of repair.     

A review of hazardous chemical toxicity studies utilizing genetically-modified animals--their applications for risk assessment

Studies on the mechanisms of chemical toxicity carried out using knockout mice lacking genes of enzymes for drug metabolism or nuclear receptor proteins were reviewed, and the studies were compared with the respective conventional mechanistic studies. While the toxicity of many hazardous chemicals was observed only in wild-type or knockout mice, which clearly showed that their toxicity was involved in the enzyme or receptor, some chemicals exhibited the same degree of toxicity in two genotypes, i.e., in both the wild strain and knockout mice, demonstrating that the enzymes or receptors are not involved in their toxicity. The use of genetically-modified animals presents not only the advantage of simultaneous evaluation of toxicity endpoints and mechanisms, but also suggests significant benefits over conventional methods using several chemicals to elucidate toxicity mechanisms. Elucidation of the mechanism of toxicity will provide useful information for risk assessment, and the use of genetically-modified animals for this purpose will lead to the advancement of this assessment.     

Platypnea-orthodeoxia syndrome combined with multiple congenital heart anomalies

A 71-year-old woman was admitted for paralysis on the left side of her body. She developed dyspnea and hypoxemia after admission. Although pulmonary embolism was suspected, hypoxemia and dyspnea occurred repeatedly in spite of anticoagulation therapy. Transesophageal echocardiography revealed a patent foramen ovale (PFO), an atrial septal aneurysm (ASA), and a right-to-left shunt that appeared in an upright position. She was diagnosed with platypnea-orthodeoxia syndrome. Moreover, cardiac catheterization showed congenital anomalies, such as unroofed coronary sinus, partial anomalous pulmonary venous return and persistent left superior vena cava. Simple surgical closure of the ASA and PFO improved all of her symptoms.     

Up-regulation of VGLUT2 expression in hypothalamic-neurohypophysial neurons of the rat following osmotic challenge

A second vesicular glutamate transporter (VGLUT2) has been reported to be expressed in neurosecretory neurons of the hypothalamic-neurohypophysial system. To study its role in the neurosecretory neurons, we evaluated the expression of the VGLUT2 gene in the paraventricular (PVN) and supraoptic (SON) nuclei as well as the immunoreactivity in the neurohypophysis under euhydrated and chronic hyperosmotic conditions with in situ hybridization and immunohistochemistry. The intensity of hybridization signals in the PVN, SON and thalamus of rats subjected to water deprivation for 7 days, or drinking 2% NaCl for 4 or 7 days, was compared with that of euhydrated rats (control). The overall intensity in the entire PVN or SON, but not the thalamus, was higher in osmotically stimulated rats than in controls. Within the PVN, a significantly higher intensity of signals than that of controls was found only in the dorsolateral posterior magnocellular region in 4-day salt-loaded rats and in all subregions in water-deprived or 7-day salt-loaded rats. The intensity in the SON was higher in the stimulated rats than in controls, regardless of subregions. In the neurohypophysis, VGLUT2 staining was frequently localized in vasopressin terminals of control rats and was apparently reduced in stimulated rats. These results indicate that VGLUT2 is principally expressed in magnocellular vasopressin neurons, suggesting some local effect of intrinsic glutamate on neurohypophysial hormone secretion.     

Non-gated fetal MRI of umbilical blood flow in an acardiac twin

Currently, the standard method of diagnosis of twin reversed arterial perfusion (TRAP) sequence is ultrasound imaging. The use of MRI for flow visualization may be a useful adjunct to US imaging for assessing the presence of retrograde blood flow in the acardiac fetus and/or umbilical artery. The technical challenge in fetal MRI flow imaging, however, is that fetal electrocardiogram (ECG) monitoring required for flow imaging is currently unavailable in the MRI scanner. A non-gated MRI flow imaging technique that requires no ECG monitoring was developed using the t-test to detect blood flow in 20 slices of phase-contrast MRI images randomly scanned at the same location over multiple cardiac cycles. A feasibility study was performed in a 24-week acardiac twin that showed no umbilical flow sonographically. Non-gated MRI flow images clearly indicated the presence of blood flow in the umbilical artery to the acardiac twin; however, there was no blood flow beyond the abdomen. This study leads us to conjecture that non-gated MRI flow imaging is sensitive in detecting low-range blood flow velocity and can be an adjunct to Doppler US imaging.     

Role of Ser50 phosphorylation in SCG10 regulation of microtubule depolymerization

Members of the stathmin-like protein family depolymerize microtubules (MTs), probably due to the ability of each stathmin monomer to bind two tubulin heterodimers in a complex (T(2)S complex). SCG10, a member of this family, is localized in the growth cone of neurons. It has four identified sites of serine phosphorylation (S50, S63, S73, and S97). Of these, S50 and S97 are phosphorylated by cAMP-dependent protein kinase, an enzyme involved in growth cone guidance. When the equivalent sites in stathmins are phosphorylated, they lose their ability to depolymerize MTs. We investigated the specific role of the two cAMP-dependent protein kinase (PKA) phosphorylation sites in SCG10. A mutant of SCG10 phosphorylated only on S50 retained the ability to depolymerize MTs, but SCG10 phosphorylated on S97 or on both S50 and S97 lost MT-depolymerizing activity. Surface plasmon resonance studies revealed that the phosphorylation of SCG10 at these sites reduced the tubulin heterodimer binding, mainly due to a reduced rate of association. In particular, compared to the two other phosphorylated forms, SCG10 phosphorylated at S50 had a significantly smaller dissociation constant for the binding of the first tubulin heterodimer and larger association and dissociation rate constants for the binding of the second heterodimer. This indicates that the phosphorylation of S50 compensates for the effect of phosphorylation at other sites by modulating T2S complex formation. Furthermore, these results suggest that S50-P maintains MT-depolymerizing activity, which indicates that the biological functions of phosphorylation at S50 and S97 are different.     

Adrenocorticotropic hormone is produced in the ventricle of patients with essential hypertension

OBJECTIVE: Aldosterone is produced in the ventricle of patients with hypertension. The present study was designed to examine whether adrenocorticotropic hormone (ACTH) and cortisol are also produced from the heart in patients with essential hypertension. METHODS: The study population consisted of 57 patients with essential hypertension and 28 control subjects. Plasma levels of ACTH, aldosterone, and cortisol were measured in the aortic root, the anterior interventricular vein and the coronary sinus during cardiac catheterization. RESULTS: The plasma levels of ACTH were significantly higher at the anterior interventricular vein and coronary sinus than at the aortic root (12.7 +/- 1.0 versus 10.7 +/- 0.9 pmol/l, P < 0.001; and 12.3 +/- 1.0 versus 10.7 +/- 0.9 pmol/l, P < 0.001, respectively) in the hypertension group, whereas there were no significant differences in the levels among these sites in the control group. The plasma levels of aldosterone were significantly higher at the anterior interventricular vein and the coronary sinus than at the aortic root (261.7 +/- 16.4 versus 239.1 +/- 15.1 pmol/l, P < 0.001; and 258.8 +/- 17.0 versus 239.1 +/- 15.1 pmol/l, P < 0.01, respectively) in the hypertension group, whereas there were no significant differences in the levels among these sites in the control group. CONCLUSIONS: ACTH as well as aldosterone is produced, but cortisol is not produced, from the ventricle of patients with essential hypertension.