Chemical Pleurodesis Could Exacerbate Lymphedema of Yellow Nail Syndrome

Chemical pleurodesis is sometimes performed for the management of intractable pleural effusion. We describe a woman with yellow nail syndrome (YNS), which is characterized by yellow discoloration of the nails, lymphedema, and pleural effusion. At the age of 43, she was hospitalized with edema of the lower limbs. Despite a number of medical treatments, massive lymphedema of lower limbs developed over a period of three years, resulting in skin cracks and subsequent infection, septicemia and multiple organ failure. At autopsy, abnormally dilated lymph and blood vessels were evident in soft tissue throughout the whole body. She had undergone chemical pleurodesis at 36 years of age for reduction of pleural effusion associated with YNS. Our case illustrates possible complication of chemical pleurodesis to YNS, which resulted in accumulation of lymph flow into the lower half of the body

Neuroprotective effect of a new DJ-1-binding compound against neurodegeneration in Parkinson's disease and stroke model rats

<p>Abstract</p> <p>Background</p> <p>Parkinson's disease (PD) and cerebral ischemia are chronic and acute neurodegenerative diseases, respectively, and onsets of these diseases are thought to be induced at least by oxidative stress. PD is caused by decreased dopamine levels in the substantia nigra and striatum, and cerebral ischemia occurs as a result of local reduction or arrest of blood supply. Although a precursor of dopamine and inhibitors of dopamine degradation have been used for PD therapy and an anti-oxidant have been used for cerebral ischemia therapy, cell death progresses during treatment. Reagents that prevent oxidative stress-induced cell death are therefore necessary for fundamental therapies for PD and cerebral ischemia. DJ-1, a causative gene product of a familial form of PD, PARK7, plays roles in transcriptional regulation and anti-oxidative stress, and loss of its function is thought to result in the onset of PD. Superfluous oxidation of cysteine at amino acid 106 (C106) of DJ-1 renders DJ-1 inactive, and such oxidized DJ-1 has been observed in patients with the sporadic form of PD.</p> <p>Results</p> <p>In this study, a compound, comp-23, that binds to DJ-1 was isolated by virtual screening. Comp-23 prevented oxidative stress-induced death of SH-SY5Y cells and primary neuronal cells of the ventral mesencephalon but not that of DJ-1-knockdown SH-SY5Y cells, indicating that the effect of the compound is specific to DJ-1. Comp-23 inhibited the production of reactive oxygen species (ROS) induced by oxidative stress and prevented excess oxidation of DJ-1. Furthermore, comp-23 prevented dopaminergic cell death in the substantia nigra and restored movement abnormality in 6-hydroxyldopamine-injected and rotenone-treated PD model rats and mice. Comp-23 also reduced infarct size of cerebral ischemia in rats that had been induced by middle cerebral artery occlusion. Protective activity of comp-23 seemed to be stronger than that of previously identified compound B.</p> <p>Conclusions</p> <p>The results indicate that comp-23 exerts a neuroprotective effect by reducing ROS-mediated neuronal injury, suggesting that comp-23 becomes a lead compound for PD and ischemic neurodegeneration therapies.</p

Renal Outcome of Immunoglobulin A Nephropathy With Mild Proteinuria

We determined the natural history of immunoglobulin A nephropathy (IgAN) among patients who presented with mild proteinuria (0.2 to 0.4 g/day), and factors associated with development of adverse clinical events, defined as proteinuria 竕ｧ 1.0g/day, blood pressure > 130/80mmHg, serum creatinine 竕ｧ 1.4mg/dl. We did analyzed data from 27 patients(mean age 30 ﾂｱ 12 years) with IgAN accompanied by mild proteinuria between 1990 and 1998. We also evaluated semiquantitave scores of glomerulosclerosis, tubulointerstitial injury, hyaline arteriosclerosis, and IgAN classification. The median duration of follow-up was 51 months. During followup, at least one adverse clinical event affected 15 patients (56%): among who eight (53%) developed proteinuria. And one of 8 developed impaired renal function and 7 (47%) became hypertensive. Another 12 patients (44%) were not affected by adverse clinical events. The clinical findings were not significantly different between the adverse events and no evens group. The scores of glomerulosclerosis and tubulointerstitial injury reveled significant differences between events. The only renal histological parameters of glomerulosclerosis and adverse clinical events were statistically correlated with renal survival. We concluded that IgAN with mild proteinuria frequently follows a slow by progressive course and that the severity of glomerulosclerosis may be predictable prognostic factor in patients who have IgAN with by mild proteinuria

Adoptive transfer of antithyrotropin receptor (TSHR) autoimmunity from TSHR knockout mice to athymic nude mice

We have recently shown that wild type mice are highly tolerant, whereas thyrotropin receptor (TSHR) knockout (KO) mice are susceptible to immunization with the mouse TSHR, the autoantigen in Graves\u27 disease. However, because TSHR KO mice lack the endogenous TSHR, Graves-like hyperthyroidism cannot be expected to occur in these mice. We therefore performed adoptive transfer of splenocytes from TSHR KO mice into nude mice expressing the endogenous TSHR. Anti-TSHR autoantibodies were detected in approximately 50% recipient mice 4 wk after adoptive transfer of splenocytes (5 × 10 7/mouse) from TSHR KO mice immunized with adenovirus expressing mTSHR A subunit and persisted for 24 wk. Depletion of regulatory T cells by anti-CD25 antibody in the donor mice increased successful transfer rates without increasing antibody levels. Some recipient mice showed transient increases in thyroid-stimulating antibodies and T4 levels 4-8 wk after transfer, but many became thyroid-blocking antibody positive and hypothyroid 24 wk later. Adoptive transfer of splenocytes from naïve TSHR KO mice transiently induced very low antibody titers when the recipient mice were treated with anticytotoxic lymphocyte antigen 4 and antiprogrammed cell death 1 ligand 1 antibodies for 8 wk after transfer. Histologically, macrophages infiltrated the retrobulbar adipose tissues and extraocular muscles in a small fraction of the recipients. Our findings demonstrate successful adoptive transfer of anti-TSHR immune response from TSHR KO mice to nude mice. Although the recipient mice developed only transient and infrequent hyperthyroidism, followed by eventual hypothyroidism, induction of orbital inflammation suggests the possible role of anti-TSHR immune response for Graves\u27 orbitopathy

Postnatal Expression of BRAFV600E Does Not Induce Thyroid Cancer in Mouse Models of Thyroid Papillary Carcinoma

The mutant BRAF (BRAFV600E) is the most common genetic alteration in papillary thyroid carcinomas (PTCs). The oncogenicity of this mutation has been shown by some genetically engineered mouse models. However, in these mice, BRAFV600E is expressed in all the thyroid cells from the fetal periods, and suppresses thyroid function, thereby leading to TSH elevation, which by itself promotes thyroid tumorigenesis. To overcome these problems, we exploited 2 different approaches, both of which allowed temporally and spatially restricted expression of BRAFV600E in the thyroid glands. First, we generated conditional transgenic mice harboring the loxP-neoR-loxP-BRAFV600Einternal ribosome entry site-green fluorescent protein sequence [Tg(LNL-BRAFV600E)]. The double transgenic mice (LNL-BRAFV600E;TPO-Cre) were derived from a high expressor line of Tg(LNLBRAFV600E) mice and TPO-Cre mice; the latter expresses Cre DNA recombinase under the control of thyroid-specific thyroid peroxidase (TPO) promoter and developed PTC-like lesions in early life under normal serum TSH levels due to mosaic recombination. In contrast, injection of adenovirus expressing Cre under the control of another thyroid-specific thyroglobulin (Tg) promoter (Ad-TgP-Cre) into the thyroids of LNL-BRAF V600E mice did not induce tumor formation despite detection ofBRAFV600EandpERKin a small fraction of thyroid cells. Second, postnatal expression ofBRAFV600E in a smallnumberof thyroid cellswasalso achieved by injecting the lentivirus expressing loxP-green fluorescent protein-loxP-BRAFV600E into the thyroids of TPO-Cre mice; however, no tumor development was again observed. These results suggest that BRAFV600E does not appear to induce PTC-like lesions when expressed in a fraction of thyroid cells postnatally under normal TSH concentrations

A case of minimal change nephrotic syndrome with immunoglobulin A nephropathy transitioned to focal segmental glomerulosclerosis

A 50-year-old woman with a 1-month history of lower extremity edema and a 5 kg weight increase was admitted to our hospital with suspected nephrotic syndrome in October 1999. Urine protein level was 3.5 g per day, 10-15 erythrocytes in urine per high-power field, and serum albumin level 2.5 g/dl. Furthermore, an accumulation of pleural effusion was confirmed by chest X-ray. The results of a renal biopsy indicated slight mesangial proliferation in the glomeruli by light microscopy, and an immunofluorescence study confirmed the deposition of immunoglobulin (Ig) A and C3 in the mesangial area. Diffuse attenuation of foot processes and dense deposits in the mesangial area were observed by electron microscopy. Treatment with 40 mg/day of prednisolone was effective, and proteinuria was negative 1 month later. Because of this course, we diagnosed minimal change nephrotic syndrome complicated by mild-proliferative IgA nephropathy. In November 2000, there was a relapse of nephrotic syndrome, which was believed to be induced by an influenza vaccination, but response to increased steroid treatment was favorable, and proteinuria disappeared on day 13 of steroid increase. A second relapse in May 2001, showed steroid resistance with renal insufficiency, and an increase in the selectivity index to 0.195. Light microscopy revealed focal sclerotic lesions of the glomeruli, and an immunofluorescence study revealed attenuation of mesangial IgA and C3 deposition. These findings led to the diagnosis that minimal change nephrotic syndrome had transitioned to focal segmental glomerulosclerosis, whereby mesangial IgA deposition was reduced by immunosuppressive treatment. Subsequently, her renal function gradually worsened to the point of end-stage renal failure by 27 months after the second relapse of nephrotic syndrome

In vitro synthesis of polyhydroxyalkanoate (PHA) incorporating lactate (LA) with a block sequence by using a newly engineered thermostable PHA synthase from Pseudomonas sp. SG4502 with acquired LA-polymerizing activity

Recently, we succeeded in isolating a thermotolerant bacterium, Pseudomonas sp. SG4502, which is capable of accumulating polyhydroxyalkanoate (PHA) even at 55℃, as a source of thermostable enzymes. In this study, we cloned a pha locus from the bacterium and identified two genes encoding PHA synthases (PhaC1_[SG] and PhaC2_[SG]). Two mutations, Ser324Thr and Gln480Lys, corresponding to those of a lactate (LA)-polymerizing enzyme (LPE) from mesophilic Pseudomonas sp. 61-3 were introduced into PhaC1_[SG] to evaluate the potential of the resulting protein as a "thermostable LPE". The mutated PhaC1_[SG] [PhaC1_[SG](STQK)] showed high thermal stability in synthesizing P(LA-co-3HB) in an in vitro reaction system under a range of high temperatures. Requirement of 3HBCoA as a priming unit for LA polymerization by the LPE has been suggested in both of the in vitro and in vivo experiments. Based on the finding, the PhaC1_[SG](STQK)-mediated synthesis of a LA-based copolymer with a block sequence was achieved in the in vitro system by sequential feeding of the corresponding two substrates. This in vitro reaction system using the thermostable LPE provides us with a versatile way to synthesize the various types of LA-based copolymers with desired sequence patterns, random or block, depending on the way of supplying hydroxyalkanoates (mixed or sequential feeding)

Phased array active loop antenna for digital television receiver

IEEE Antennas and Propagation Society International Symposium 1999, Orlando, Florida July 11-16, 199

Preoperative segmental embolization of the proper hepatic artery prior to pylorus-preserving pancreaticoduodenectomy: A case report

Introduction: Radical resection of bile duct carcinoma may require resection of hepatic arteries. Preoperative segmental embolization of the hepatic artery for resection of hilar cholangiocarcinoma has been reported. We report a patient with bile duct carcinoma infiltrating the proper hepatic artery. Presentation of case: A 66-year old male with jaundice was diagnosed with mid-distal bile duct carcinoma. A replaced left hepatic artery originated from the left gastric artery. Pylorus-preserving pancreaticoduodenectomy (PPPD) with combined resection of hepatic artery was planned. To promote the development of collateral blood flow after excision of the hepatic artery, preoperative segmental embolization of the proper hepatic artery was performed. The patient underwent PPPD with concurrent resection of the common hepatic, right hepatic, and middle hepatic arteries without arterial reconstruction. He received adjuvant chemotherapy with gemcitabine for six months and is alive three years after surgery without tumor recurrence. Discussion: The growth of collateral vessels after selective embolization of the proper hepatic artery has been used for hilar lesions and bile duct lesions. Resection of the hepatic artery without the need for complex arterial reconstruction, allowing a radical resection, may have contributed to this patient's relatively unremarkable recovery and long-term survival. Retroperitoneal mobilization of the pancreatic head and duodenum must be limited as important collaterals may originate in that area. Conclusion: Preoperative segmental embolization of the hepatic artery before PPPD for a patient with a replaced left hepatic artery encouraged the growth of collateral blood supply, allowing radical resection including the vessels and obviated the need for arterial reconstruction