A cell-wall protein SRPP provides physiological integrity to the Arabidopsis seed.

Seed and root hair protective protein (SRPP) is expressed in seeds and root hairs, localized in the cell wall, and involved in cell wall integrity. We analyzed a loss-of-function mutant of SRPP, focusing on siliques and seeds. The srpp-1 plants generated dark brown shrunken seeds at a high rate. The germination rate of these defect seeds of srpp-1 was less than 6%, although apparently normal srpp-1 seeds germinated at a rate of 83%. The production ratio of severe phenotypic seeds was dependent on the growth conditions. When the srpp-1 plants were cultivated at low humidity, the defect ratio was 73%, which was significantly higher than that at normal humidity. Defects of the silique and seeds could be detected on day 7 after pollination and the apical region of the siliques displayed a severe phenotype at a high frequency. Complementation with an SRPP gene under the control of promoters specific to the embryo, seed coat, or valve (carpel) partially rescued the phenotype, and complementation using the SRPP promoter fully rescued the phenotype. Furthermore, overexpression of SRPP enhanced the thermotolerance. After the treatment of seeds at 50 °C for 2 h, the germination rate of the seeds from overexpression with the 35S promoter increased to levels twice that of the wild-type seeds. Under the same conditions, no srpp-1 seeds germinated. These results indicate that SRPP is essential for the production of normal viable seeds in siliques under stress conditions. It is possible that modification of the SRPP gene improves seed integrity.

[A CASE OF A 7-YEAR-OLD GIRL WITH ANAPHYLAXIS CAUSED BY PECTIN IN ALBEDO OF CITRUS UNSHIU BUT NOT BY THE FRUIT ITSELF].

Pectin is used in several foods as an additive and a thickner. But some cases of anaphylaxis have been reported. Most of these are induced by occasional exposures; however, no cases of anaphylaxis after eating a Citrus unshiu, the albedo of which is rich in pectin, have been reported.A 7-year-old girl developed barking cough and pruritus approximately two hours after eating a frozen Citrus unshiu. She had a history of anaphylaxis induced by consuming cashew nuts. Skin testing and basophil activation tests were performed using a commercially available pectin product. Both tests were positive. In an oral food challenge test, she felt abdominal pain and nausea only after eating fruit, along with the albedo, of Citrus unshiu. We concluded that this case was induced by pectin present in the albedo of Citrus unshiu, but not by the fruit itself. We should consider that patients with cashew nut allergies have a possibility of pectin allergies as well, and that pectin in the albedo of Citrus unshiu may induce anaphylaxis.

Enhancement of cell wall protein SRPP expression during emergent root hair development in Arabidopsis.

SRPP is a protein expressed in seeds and root hairs and is significantly induced in root hairs under phosphate (Pi)-deficient conditions. Root hairs in the knockout mutant srpp-1 display defects, i.e., suppression of cell growth and cell death. Here, we analyzed the expression profile of SRPP during cell elongation of root hairs and compared the transcript levels in several mutants with short root hairs. The mRNA level was increased in wild-type plants and decreased in mutants with short root hairs. Induction of SRPP expression by Pi starvation occurred one or two days later than induction of Pi-deficient sensitive genes, such as PHT1 and PHF1. These results indicate that the expression of SRPP is coordinated with root hair elongation. We hypothesize that SRPP is essential for structural robustness of the cell walls of root hairs.

SRPP, a Cell Wall Protein is Involved in Development and Protection of Seeds and Root Hairs in Arabidopsis thaliana.

Enhancement of root hair development in response to phosphate (Pi) deficit has been reported extensively. Root hairs are involved in major root functions such as the absorption of water, acquisition of nutrients and secretion of organic acids and enzymes. Individual root hair cells maintain these functions and appropriate structure under various physiological conditions. We carried out a study to identify protein(s) which maintain the structure and function of root hairs, and identified a protein (SEED AND ROOT HAIR PROTECTIVE PROTEIN, SRPP) that was induced in root hairs under Pi-deficient conditions. Promoter assay and mRNA quantification revealed that SRPP was expressed in root hairs and seeds. A knockout mutant, srpp-1, consistently displayed defects in root hairs and seeds. Root hairs in srpp-1 were short and the phenotypes observed under Pi-deficient conditions were also detected in ethylene-treated srpp-1 plants. Propidium iodide stained most root hairs of srpp-1 grown under Pi-deficient conditions, suggesting cell death. In addition to root hairs, most srpp-1 seeds were withered and their embryos were dead. SRPP tagged with green fluorescent protein was detected in the cell wall. Electron microscopy showed abnormal morphology of the cell wall. Wild-type phenotypes were restored when the SRPP gene was expressed in srpp-1. These data strongly suggest that SRPP contributes to the construction of robust cell walls, whereby it plays a key role in the development of root hairs and seeds.

[A case of tracheal intubation for apnea with epidural opioid in recovery room after operation under general anesthesia].

We report a 68-year-old, American Society of Anesthesiologists Class I (ASA I), female patient scheduled for malignant uterine adnexal tumor surgery and revascularization for ovarian cancer. An epidural catheter was inserted at T12-L1 for 5 cm. Anesthesia was induced with remifentanil (0.25 microg x kg(-1) x min(-1)), sevoflurane (5%) and rocuronium (30 mg). Anesthesia was satisfactorily maintained after intubation with sevoflurane (1.5%) and remifentanil (0.2 microg x kg(-1) x min(-1)). We extubated the patient because spontaneous breathing and consciousness were observed. We intubated the patient immediately for apnea that occurred after extubation. The patient made an uneventful recovery after naloxone administration. In pharmacokinetic simulation, on the assumption that epidural administrated fentanyl was carried to blood content promptly, effect concentration to cause respiratory depression was not reached. Postoperative apnea was rationalized as follows; tardy respiratory depression with the epidural administration, and unexpected dosage of the residual fentanyl in the catheter.

[Application of video laryngoscope for vocal cord synechiotomy in a patient with recurrent laryngeal nerve paralysis].

Vocal cord synechia causes respiratory disturbance and severe pneumonia. A 63-year-old woman with recurrent laryngeal nerve paralysis caused by translaryngeal intubation after resection of acoustic tumor and by thyroid surgery in her history and progressive dyspnea, had received vocal cord synechiotomy under general anesthesia. Preoperative endoscopic examination revealed edematous larynx, immobility of left unilateral vocal fold, insufficient mobility of right vocal fold, left arytenoid cartilage dislocation and a posterior glottic adhesion. Anesthesia was induced by propofol administration, and a muscle relaxant was administered following confirmation of effective face mask ventilation. Trachea was cannulated immediately after incision of the scar under indirect video laryngoscopy. Vocal cord synechiotomy was completed without any respiratory complication. The case indicated that recurrent laryngeal nerve paralysis has a potential for vocal cord synechia and difficulty of tracheal intubation, and visibility of the surgical field among anesthesiologists and surgeons by indirect video laryngoscopy for vocal cord synechiotomy contributes to establish prompt surgical manipulation and tracheal intubation as to vocal cord synechiotomy.

[How much should be done for better thromboprophyraxis?].

How much should be done for better managements of the perioperative thromboprophylaxis? In Japan, the guideline for prevention of venous thromboembolism (VTE) was established for the first time in February, 2004. Our academic medical center formed a committee for prevention of thrombosis for all departments using operating rooms in October, 2002 and began to make the database of symptomatic pulmonary thromboembolism (PTE). From the end of September, 2003, we asked the surgeons to indicate the PTE risk grades when ordering surgical operations. The prevention team of VTE prepared VTE risk tables and recommended prevention methods for perioperative period. If surgeons did not choose prevention methods, the team took the consultation. Also, we made a manual how to make emergency calls and a flow chart for the diagnosis and therapy cooperating with cardiologists and anesthesiologists. We founded another meeting of Kinki Clinical Thrombosis Research Association for the study and education. We assessed the incidence of symptomatic PTE every year. The incidences of symptomatic PTE were 14 of 4101 (0.34%) in the first year, 2 of 3796 (0.053%) in the second year; 2 of 4002 cases (0.049%) in the third year under general anesthesia, respectively. Cases of fatal PTE were 2 (0.34%), 1 (0.049%) and 0 (0%), respectively. The multidisciplinary thromboprophylaxis effort that we had adopted was very important to prevent aggravation of VTE.

Volatile anesthetics constrict pulmonary artery in rabbit lung perfusion model.

Volatile anesthetics are generally considered to possess a vasodilator action. Some of their actions on pulmonary vessels, however, are not clearly understood. We examined the effects of various volatile anesthetics on pulmonary vessels using an in situ rabbit isolated-lung perfusion model. We prepared a rabbit constant-flow lung-perfusion model by sending blood to the pulmonary artery and removing blood from the left atrium, and observed the changes in pulmonary arterial perfusion pressure caused by inhalation of 0.5, 1, 2, and 3 minimum alveolar concentration (MAC) volatile anesthetics: halothane, enflurane, isoflurane, and sevoflurane, in random order. These volatile anesthetics increased pulmonary arterial perfusion pressure in a dose-dependent manner and caused the pulmonary arteries to constrict. In particular, halothane at all concentrations induced significantly greater pulmonary vasoconstriction than the other volatile anesthetics. Therefore, it is suggested that volatile inhalation anesthetics induce the pulmonary arteries to constrict, and halothane exhibits the most potent pulmonary vasoconstrictor effect among the volatile anesthetics tested.

Anti-inflammatory effects of tacalcitol (1,24(R)(OH)2D3, TV-02) in the skin of TPA-treated hairless mice.

Tacalcitol (1,24(R)(OH)2D3, TV-02) inhibited the TPA-induced inflammatory cell infiltration (largely neutrophils) histopathologically and myeloperoxidase (MPO) activity dose-dependently. Tacalcitol inhibited the mRNA expression and protein production of TPA-induced macrophage inflammatory protein-2 (MIP-2) and KC, the functional analogue of human interleukin (IL)-8, in the skin. Immunohistochemical staining of the TPA-applied skin revealed that mast cells expressed MIP-2, whereas KC was observed in keratinocytes, fibroblasts and outer root sheath of hair follicles. Furthermore, tacalcitol inhibited TPA-induced mast cell degranulation 24 hr after application without influence on the total number of mast cells. In this study, tacalcitol was found to have an inhibitory effect on cutaneous inflammation such as inhibition of neutrophil infiltration, MIP-2 and KC production, and mast cell degranulation in TPA-treated hairless mice. These results suggest that tacalcitol modulates cutaneous inflammation as well as keratinocyte proliferation and differentiation, and the inhibitory effect of tacalcitol on cutaneous inflammation may contribute to clinical the effectiveness in the treatment of psoriasis.

Change in location of cytokine-induced neutrophil chemoattractants (CINCs) in pulmonary silicosis.

Rat cytokine-induced neutrophil chemoattractants (CINCs), which belong to the interleukin-8 family, are known to be induced by treatment with lipopolysaccharide (LPS). Recently, CINCs were grouped into four subtypes-CINC-1, CINC-2alpha, CINC-2beta, and CINC-3-and CINC-1 was considered to be a major isoform among the four CINCs in LPS-induced acute lung inflammation in rats. The purpose of this study was to investigate the change in location of CINCs with chronic inflammation induced by experimental pulmonary silicosis. Administration of silica particles induced lung granulomas. Immunohistochemical staining for CINCs showed that the number of cells positive for CINC-2alpha, CINC-2beta, and CINC-3 was increased, peaking at 1 day after treatment with silica particles, whereas CINC-1 was almost undetectable. We suggest that CINC-2alpha, CINC-2beta, and CINC-3 are the most important chemoattractants in the formation of granulomas in chronic inflammation.

Expression of hepatocyte growth factor mRNA in rat liver cirrhosis induced by N-nitrosodimethylamine as evidenced by in situ RT-PCR.

Hepatocyte growth factor (HGF) is a potent inducer of hepatocyte proliferation and is expressed during liver failure. In this study we used the in situ reverse transcriptase-polymerase chain reaction (RT-PCR) method to detect HGF mRNA expression in normal rat livers and cirrhotic rat livers induced by treatment with N-nitrosodimethylamine (DMN). In normal control livers, in situ RT-PCR detected HGF mRNA expression in Ito cells and Kupffer cells, both of which showed rounded morphologies. However, in the cirrhotic livers induced by DMN, HGF mRNA-positive cells were spindle-shaped and surrounded the hepatocytes located around the sinusoids. These cells appeared to be sinusoidal endothelial cells as well as Ito and Kupffer cells. Because it has been suggested that HGF expression is related to transforming growth factor-beta (TGF-beta) levels that may play an essential role in disease progression in cirrhotic livers, TGF-beta mRNA expression in normal and cirrhotic livers was also compared using in situ RT-PCR. Our results confirmed that expression of TGF-beta mRNA co-localized with HGF mRNA expression in the cirrhotic liver.