STUDY OF AN ORGANIC CRYSTALLIZATION FOULING PROBLEM

One of the aromatic compound plants in Mitsubishi Chemical Corporation has a heavy crystallization fouling problem. We have been studying the crystallization process using the shell and tube heat-exchanger. In order to solve our fouling problem of the heat exchanger, we developed the specified evaluation equipment (crystallization fouling simulator : CFS) which consists of a single tube heatexchanger (Tube size: ID=10.3mm Length=500mm). The result of the modeling for describing the crystallization fouling rate and the countermeasure of the fouling problem are discussed in this work. It can be possible to describe the fouling rate as one equation which has two parameters, and the fouling rate of the industrial plant and the evaluation equipment agree with each other

Measurement and Modeling for the Mitigation of Organic Crystallization Fouling

One of the aromatic compound plants in Mitsubishi Chemical Corporation has a heavy crystallization fouling problem. In order to solve this problem, using a low power gamma ray sensor, we found the location of heaviest fouling and measured the fouling growth rate. We also made a crystallization fouling laboratory test unit (simulator) to study the effects of some factors, such as temperature, liquid velocity, surface roughness and liquid composition. Fouling rates of the industrial plant cooler and the laboratory fouling test unit were modeled using a combination of Kern-Seaton and Reitzer models. However, the parameters of the plant and test unit did not agree with each other, perhaps because of scale up problems. We also measured the melting process (removal) of the fouling with the test unit. The heat flux necessary to melt the foulant was measured and used for the actual plant melting system. In the industrial plant, a steam trace melting system was installed at the position of heaviest fouling, and the plant now runs better than before

Role of Ribosome Recycling Factor in Natural Termination and Translational Coupling as A Ribosome Releasing Factor

The role of ribosome recycling factor (RRF) of E. coli was studied in vivo and in vitro. We used the translational coupling without the Shine-Dalgarno sequence of downstream ORF (d-ORF) as a model system of the RRF action in natural termination of protein synthesis. For the in vivo studies we used the translational coupling by the adjacent coat and lysis genes of RNA phage GA sharing the termination and initiation (UAAUG) and temperature sensitive RRF. The d-ORF translation was measured by the expression of the reporter lacZ gene connected to the 5\u27-terminal part of the lysis gene. The results showed that more ribosomes which finished upstream ORF (u-ORF) reading were used for downstream reading when RRF was inactivated. The in vitro translational coupling studies with 027mRNA having the junction sequence UAAUG with wild-type RRF were carried out with measuring amino acids incorporation. The results showed that ribosomes released by RRF read downstream from AUG of UAAUG. In the absence of RRF, ribosomes read downstream in frame with UAA. These in vivo and in vitro studies indicate that RRF releases ribosomes from mRNA at the termination codon of u-ORF. Furthermore, the non-dissociable ribosomes read downstream from AUG of UAAUG with RRF in vitro. This suggests that complete ribosomal splitting is not required for ribosome release by RRF in translational coupling. The data are consistent with the interpretation that RRF functions mostly as a ribosome releasing factor rather than ribosome splitting factor. Additionally, the in vivo studies showed that short (less than 5 codons) u-ORF inhibited d-ORF reading by ribosomes finishing u-ORF reading, suggesting that the termination process in short ORF is not similar to that in normal ORF. This means that all the preexisting studies on RRF with short mRNA may not represent what goes on in natural termination step

Temporal bone histopathology in trisomy 18 syndrome: a report of two cases.

Temporal bone histopathological findings of two patients with trisomy 18 syndrome are described. Many of the abnormalities previously described were seen in the present cases; namely, atresia of the external auditory canal, aberrant course of the tensor tympani muscle, malformed stapes, aberrant course of the facial nerve with an obtuse angulation at the first genu and displacement of geniculate ganglion cells into the internal auditory canal, shortened cochlea with decreased spiral ganglion cell population, and vestibular anomalies, such as bony and membranous blockage of the superior semicircular canal. Moreover, an extremely underdeveloped malleus and incus continuous with a persistent Meckel's cartilage were observed.</p

The Japanese Clinical Practice Guideline for acute kidney injury 2016

Acute kidney injury (AKI) is a syndrome which has a broad range of etiologic factors depending on different clinical settings. Because AKI has significant impacts on prognosis in any clinical settings, early detection and intervention are necessary to improve the outcomes of AKI patients. This clinical guideline for AKI was developed by a multidisciplinary approach with nephrology, intensive care medicine, blood purification, and pediatrics. Of note, clinical practice for AKI management which was widely performed in Japan was also evaluated with comprehensive literature search

tRNA2Thr Complements Temperature Sensitivity Caused by Null Mutations in the htrB Gene in Escherichia coli

According to the wobble rule, tRNA2Thr is nonessential for protein synthesis, because the codon (ACG) that is recognized by tRNA2Thr is also recognized by tRNA4Thr. In order to investigate the reason that this nonessential tRNA nevertheless exists in Escherichia coli, we attempted to isolate tRNA2Thr-requiring mutants. Using strain JM101F−, which lacks the gene for tRNA2Thr, we succeeded in isolating two temperature-sensitive mutants whose temperature sensitivity was complemented by introduction of the gene for tRNA2Thr. These mutants had a mutation in the htrB gene, whose product is an enzyme involved in lipid A biosynthesis. Although it is known that some null mutations in the htrB gene give a temperature-sensitive phenotype, our mutants exhibited tighter temperature sensitivity. We discuss a possible mechanism for the requirement for tRNA2Thr

Surgery to improve hearing of a preschool child with profound bilateral deafness

Hearing loss in children under school age adversely effects speech and personality development. It is possible to improve conductive hearing loss by surgery, but difficult to improve combined hearing loss. The authors succeeded surgically improving the hearing of a 5 year-old boy suffering from speech retardation due to bilateral congenital combined hearing loss. The improvement in hearing aided speech training. He has graduated from schools for the deaf (primary, middle and senior high school). His I.Q. is 70 or less. The average hearing is in the speech range of 90 dB bilaterally, showing combined hearing loss by play audiometry. At the age of 1.5 years, he was suspected of having congenital aural atresia on the right side, congenital narrow ear canal on the left side and minor anomalies of the auricles bilaterally, including congenital aural fistulas. His mother and younger brother also suffer from bilateral congenital combined hearing loss. The tympanotomy on the left ear revealed severe anomalies, such as omega shaped ossicle composed of the malleus and incus joined to the posterior bony wall of external auditory canal and bony fixation of the stapes footplate. The bulky ossicle was mobilized by cutting the junction to the bony canal wall, and a small fenestra stapedectomy was performed. A tympanotomy on the right ear was also performed, but irregular development of the inner ear prevented the possibility of obtaining hearing improvement. The authors discussed the possibility and significance of surgery to improve hearing even in cases of profound combined hearing loss in preschool children

Role of ribosome recycling factor in natural termination and translational coupling as a ribosome releasing factor.

The role of ribosome recycling factor (RRF) of E. coli was studied in vivo and in vitro. We used the translational coupling without the Shine-Dalgarno sequence of downstream ORF (d-ORF) as a model system of the RRF action in natural termination of protein synthesis. For the in vivo studies we used the translational coupling by the adjacent coat and lysis genes of RNA phage GA sharing the termination and initiation (UAAUG) and temperature sensitive RRF. The d-ORF translation was measured by the expression of the reporter lacZ gene connected to the 5'-terminal part of the lysis gene. The results showed that more ribosomes which finished upstream ORF (u-ORF) reading were used for downstream reading when RRF was inactivated. The in vitro translational coupling studies with 027mRNA having the junction sequence UAAUG with wild-type RRF were carried out with measuring amino acids incorporation. The results showed that ribosomes released by RRF read downstream from AUG of UAAUG. In the absence of RRF, ribosomes read downstream in frame with UAA. These in vivo and in vitro studies indicate that RRF releases ribosomes from mRNA at the termination codon of u-ORF. Furthermore, the non-dissociable ribosomes read downstream from AUG of UAAUG with RRF in vitro. This suggests that complete ribosomal splitting is not required for ribosome release by RRF in translational coupling. The data are consistent with the interpretation that RRF functions mostly as a ribosome releasing factor rather than ribosome splitting factor. Additionally, the in vivo studies showed that short (less than 5 codons) u-ORF inhibited d-ORF reading by ribosomes finishing u-ORF reading, suggesting that the termination process in short ORF is not similar to that in normal ORF. This means that all the preexisting studies on RRF with short mRNA may not represent what goes on in natural termination step