Effect of peak power enhancement of ferrite phase shifter from full-height to increased-height rectangular waveguide.

In order to enhance the high-power performance of the ferrite phase shifter (PS), a method of increasing waveguide height is proposed and experimentally demonstrated. Dual-toroid geometry is utilized as a high-power structure. Two configurations of X-band PSs with full-height (FH) and increased-height (IH) waveguides are designed and fabricated while keeping other parameters consistent. Comparative analysis based on simulation and high-power experiments is conducted. The simulation results agree well with experiments. Compared with the FHPS, the IHPS can enhance the peak-power-capacity from 90 kW to 140 kW while maintaining almost the same insertion loss of 0.5 dB with a slight increase in differential phase shift from 360° to 380°.

Effect of RMT1-10 on the immunological characteristics of dendritic cells cultured in vitro and corneal transplantation in vivo.

OBJECTIVE: Corneal allograft rejection is an immunological hypersensitive reaction caused by the antigenicity of the donor cornea. This study aimed to explore the effects of RMT1-10 on the prevention of corneal graft rejection by modifying immunological characteristics of dendritic cells (DCs). MATERIALS AND METHODS: DCs and CD4+T cells were sorted using flow cytometry and used for in vitro mixed lymphocyte culture. The cultured cells were prepared for the characterization of the DC cell phenotypes using the markers CD11c, CD80, MHC II, CD54, and TIM-4. Cytokine concentrations of IL-4, IL-12, and IL-10 of supernatants were measured by the enzyme-linked immunosorbent assay. CD4+T cells were examined by flow cytometry for apoptosis and proliferation. We also investigated the effect of RMT1-10 in the prevention and treatment of high-risk corneal graft rejection using a mouse model of corneal transplantation. RESULTS: DCs were identified as the CD11c+MHC-II-expressing subset. RMT1-10 suppressed the expression of CD11c, CD80, MHC II, CD54, and TIM-4 of DCs using the blockade of TIM-1 signaling. Moreover, TIM-1 blockade inhibited the production of IL-12 and IL-10 in a mixed lymphocyte culture system. However, a TIM-1 blockade had no effect on the apoptosis of CD4+T cells. RMT1-10 suppressed DC maturation, inhibiting the proliferation of CD4+T cells. CONCLUSIONS: RMT1-10 significantly improved the survival rate of the corneal allografts in mice compared with saline-injected controls. This clinical improvement from RMT1-10 occurred through the inhibition of CD4+T cell proliferation. Moreover, RMT1-10 induced antigen-specific detection of receptor immune tolerance. The cross-linking of TIM-1 on CD4+T cells with the agonist mAb provided a costimulatory inhibition signal for T cell activation or proliferation.

Late-onset Becker-type muscular dystrophy in a Border terrier dog.

A 9-year-old Border terrier was presented to a referral hospital after a 1-year history of progressive stiffness and exercise intolerance. Neurological examination was consistent with a neuromuscular disorder. Serum creatine kinase activity was mildly elevated. A myopathy was suspected based on MRI findings and electrophysiological examination. Muscle histopathology was consistent with a severe non-inflammatory myopathy of a dystrophic type. Immunofluorescence and western blotting confirmed a dystrophinopathy with an 80-kDa truncated dystrophin fragment similar to Becker muscular dystrophy in people. To our knowledge, this is the first description of a late-onset Becker-type muscular dystrophy in a dog, and the first description of a dystrophinopathy in a Border terrier. Muscular dystrophy in dogs should not be ruled out based on late onset clinical signs and only mildly elevated creatine kinase.

Clinical Phenotype of Musladin-Lueke Syndrome in 2 Beagles.

Musladin-Lueke syndrome (MLS), previously termed Chinese Beagle syndrome, is an autosomal-recessive connective tissue disorder characterized by extensive fibrosis of the skin and joints that was first identified in Beagles in the 1970s. Recent research identified a founder mutation (c.660C>T; p.R221C) in the ADAMTSL2 gene in Beagles with MLS. Here, we report the detailed clinical phenotype and laboratory findings in 2 Beagles affected with MLS. We discuss these findings in relation to the human disorder geleophysic dysplasia (GD), which also arises from recessive ADAMTSL2 mutations, and recent findings in Adamtsl2-deficient mice.

A novel high power X-band ferrite phase shifter.

A novel high power X-band ferrite phase shifter (PS) employing the structure of several waveguides connected in parallel is proposed. Each of the waveguides is a phase shift unit utilizing a dual-toroid structure. First, the phase shift unit is designed, manufactured, and tested. The results indicate that the power capacity reaches 115 kW. At this power, the maximum magnetic field strength of ferrite is 7.9 kA/m, beyond which the nonlinear effect of ferrite will occur. On this basis, the PS that consists of four units connected in parallel is designed. According to the threshold of ferrite, the power capacity of the PS can theoretically reach 430 kW. Limited by the maximum output power of the microwave source, the preliminary high-power test results demonstrate that the PS can operate properly at 270 kW. The PS exhibits an insertion loss of 0.82 dB and a maximum differential phase shift of approximately 300° at 9.3 GHz. The return loss of the PS is more than 16 dB from 9.0 to 9.5 GHz.

Major Histocompatibility Complex I and II Expression and Lymphocytic Subtypes in Muscle of Horses with Immune-Mediated Myositis.

BACKGROUND: Major histocompatibility complex (MHC) I and II expression is not normally detected on sarcolemma, but is detected with lymphocytic infiltrates in immune-mediated myositis (IMM) of humans and dogs and in dysferlin-deficient muscular dystrophy. HYPOTHESIS/OBJECTIVES: To determine if sarcolemmal MHC is expressed in active IMM in horses, if MHC expression is associated with lymphocytic subtype, and if dysferlin is expressed in IMM. ANIMALS: Twenty-one IMM horses of Quarter Horse-related breeds, 3 healthy and 6 disease controls (3 pasture myopathy, 3 amylase-resistant polysaccharide storage myopathy [PSSM]). METHODS: Immunohistochemical staining for MHC I, II, and CD4+, CD8+, CD20+ lymphocytes was performed on archived muscle of IMM and control horses. Scores were given for MHC I, II, and lymphocytic subtypes. Immunofluorescent staining for dysferlin, dystrophin, and a-sarcoglycan was performed. RESULTS: Sarcolemmal MHC I and II expression was detected in 17/21 and 15/21 of IMM horses, respectively, and in specific fibers of PSSM horses, but not healthy or pasture myopathy controls. The CD4+, CD8+, and CD20+ cells were present in 20/21 IMM muscles with CD4+ predominance in 10/21 and CD8+ predominance in 6/21 of IMM horses. Dysferlin, dystrophin, and a-sarcoglycan staining were similar in IMM and control muscles. CONCLUSIONS AND CLINICAL IMPORTANCE: Deficiencies of dysferlin, dystrophin, and a-sarcoglycan are not associated with IMM. Sarcolemmal MHC I and II expression in a proportion of myofibers of IMM horses in conjunction with lymphocytic infiltration supports an immune-mediated etiology for IMM. The MHC expression also occured in specific myofibers in PSSM horses in the absence of lymphocytic infiltrates.

Compact high-power microwave divider and combiner.

A novel, compact, TM01-TE10 mode power divider and a novel, compact, four-way TE10-TM01 mode power combiner were theoretically designed and experimentally tested as a proof of principle. The theoretical and experimental S parameters are consistent with each other. High-power experiments show that their power capacities are no less than 1.5 GW and 3 GW, respectively. The devices have the merits of high power capacities and low insertion losses.

CLINICAL DIAGNOSIS OF CAROTID ATHEROSCLEROSTIC PLAQUE IN HYPERTENSIVE PATIENTS WITH HIGH RESOLUTION MAGNETIC RESONANCE ANGIOGRAPHY.

As the incidence of ischemic cerebrovascular disease increases continuously over the years, carotid atherosclerosis as an important dangerous factor has drawn a lot of attention from many experts and scholars. To explore the clinical significance of high resolution magnetic resonance angiography (MRA) in carotid atherosclerosis and ischemic cerebrovascular disease, a group contrasting method was adopted. One hundred patients with ischemic cerebrovascular disease and 100 patients without ischemic cerebrovascular disease were taken as observation group and control group, respectively. High resolution MRA was used for examining and observing the development of carotid atherosclerostic plaque in patients in the two groups. We found that the proportion of carotid atherosclerostic plaque in the experimental group and control group had statistical difference (P<0.05); and the proportion of carotid atherosclerostic plaque in patients over 60 years of age was higher than in patients under 60 years, and the difference was statistically significant (P<0.05). The proportion of carotid atherosclerostic plaque in patients with high blood pressure was also higher than in patients without high blood pressure, and the difference was statistically significant (P<0.05). Moreover, the proportion of carotid atherosclerostic plaque in patients with hyperlipidemia was higher than in patients without hyperlipidemia, and the differences were statistically significant (P<0.05). We can therefrore draw a conclusion that the development of carotid atherosclerostic plaque affects the occurrence of ischemic cerebrovascular disease, which is related to patient’s age, level of blood pressure and blood lipids. In addition, high resolution MRA is helpful to early discovery of the formation of carotid atherosclerostic plaque.

The effectiveness of psychoeducational family intervention for patients with schizophrenia in a 14-year follow-up study in a Chinese rural area.

BACKGROUND: It is unclear if the impact of psychoeducational family intervention for patients with schizophrenia can be sustained over 10 years. In this study, we explored the 14-year effect of psychoeducational family intervention for patients with schizophrenia in a Chinese rural area. METHOD: The data from a cluster randomized control trial (CRCT) study of psychoeducational family intervention in a 14-year follow-up was analyzed. All patients with schizophrenia (n = 326) who participated in the CRCT drawn from six townships in Xinjin County of Chengdu in 1994, of whom 238 (73.0%) who were still alive, and their informants were followed up in 2008. The Patients Follow-up Scale, the Positive and Negative Syndrome Scale (PANSS) and the Global Assessment of Functioning were used in the follow-up study. RESULTS: There were no significant differences of marital status, mean scores of PANSS positive symptoms, negative symptoms, general mental health, and total scores among the psychoeducational family intervention, medication, and control groups in 2008. The psychoeducational family intervention group had a significantly higher rate of antipsychotic medication and a higher level of work ability than other two groups. The control group had a significantly higher rate of never-treated (26.0%) than psychoeducational family intervention group (6.5%). CONCLUSION: Psychoeducational family intervention might be still effective in the 14-year follow-up, especially in patients' treatment adherence/compliance and social functioning. Psychoeducational family intervention might be more effective in places where family members frequently participated in patients' care and had a lower level of knowledge on mental illness. Family intervention should be considered when making mental health policy and planning mental health services.

Dystrophin-deficient muscular dystrophy in two lurcher siblings.

Two cases of dystrophin-deficient muscular dystrophy in 16-week-old male lurcher siblings are reported. The myopathies were characterised by regurgitation, progressive weakness and muscle wastage. The dogs had generalised weakness in all four limbs, with more pronounced weakness in the pelvic limbs. Reduced withdrawal in all limbs, muscle contracture and lingual hypertrophy were noted. Serum creatine kinase activities were markedly elevated. Electromyographic abnormalities included fibrillation potentials. Histopathological and immunohistochemical staining were consistent with dystrophin-deficient muscular dystrophy. Clinical improvement was noted in one of the cases with L-carnitine supplementation and supportive therapy. Genetic transmission of the disease was postulated as the dogs were siblings.

Dystrophin-deficient muscular dystrophy in a Norfolk terrier.

A six-month-old male entire Norfolk terrier was presented with a 3-month history of poor development, reluctance to exercise and progressive and diffuse muscle atrophy. Serum creatine kinase concentration was markedly elevated. Magnetic resonance imaging of the epaxial muscles revealed asymmetrical streaky signal changes aligned within the muscle fibres (hyperintense on T2-weighted images and short-tau inversion recovery with moderate contrast enhancement on T1-weighted images). Electromyography revealed pseudomyotonic discharges and fibrillation potentials localised at the level of the supraspinatus, epaxial muscles and tibial cranialis muscles. Muscle biopsy results were consistent with dystrophin-deficient muscular dystrophy. The dog remained stable 7 months after diagnosis with coenzyme Q10 and l-carnitine; however after that time, there was a marked deterioration and the owners elected euthanasia. This case report describes the clinical presentation, magnetic resonance imaging, electrodiagnostic and histopathological findings with immunohistochemical analysis in a Norfolk terrier with confirmed dystrophin-deficient muscular dystrophy, which has not been previously described in this breed.

A compact two-way high-power microwave combiner.

A compact 2-way high-power microwave (HPM) waveguide combiner as an important equipment to realize the coherent microwave combination was theoretically designed, built, and proof-of-principle experimentally tested. The theoretical and experimental S-parameters are basically consistent with each other: return loss <-25 dB, and the isolation degree between 2-channels of the HPM combiner >25 dB to avoid the inter-modulating between the HPM sources. The C-band HPM experiment was carried out, and the power capacity of the HPM combiner was demonstrated to reach multi-gigawatts.

Myopathy associated with congenital fibre type disproportion in a young dog.

A 4-month-old, female collie-cross dog was presented for evaluation of slowly progressive weakness, exercise intolerance and muscle atrophy. Neurological examination and electrodiagnostic testing were consistent with a generalized myopathy or, less likely, an axonal polyneuropathy. Muscle biopsy samples revealed marked variability in myofibre size with scattered or clustered atrophic or hypotrophic type 1 fibres. Type 1 fibres were 65% smaller than type 2A fibres and the percentage of type 1 fibres exceeded reference values for both limb muscles examined. On the basis of the clinical evaluation, pathological changes and the absence of another defined congenital or acquired myopathy, a diagnosis of a myopathy associated with congenital fibre type disproportion was made. Three months later the animal was humanely euthanized because of worsening clinical signs.

Severe myositis associated with Sarcocystis spp. infection in 2 dogs.

BACKGROUND: Dogs are definitive hosts for numerous species of the intracellular protozoan parasite Sarcocystis. Reports of sarcocysts in muscles of dogs most often represent incidental findings. HYPOTHESIS/OBJECTIVES: To report the clinicopathologic, ultrastructural, and molecular findings in 2 dogs with myositis associated with Sarcocystis spp. infection, as well as the response to treatment with antiprotozoal drugs. ANIMALS: Two dogs with severe myositis in association with massive sarcocystosis. METHODS: Retrospective case review. Affected dogs were identified by a diagnostic laboratory. Attending clinicians were contacted, and the medical records reviewed. Immunostaining and electron microscopy were performed on muscle biopsies. Biopsies also were subjected to 18S rRNA gene PCR. RESULTS: Both dogs had fever, lymphopenia, thrombocytopenia, and increased serum alanine aminotransferase (ALT) activity when first evaluated. One dog developed hyperbilirubinemia. Subsequently, both dogs had increased serum creatine kinase activity and clinical signs of myositis, with reluctance to move, generalized pain, and muscle wasting. Histopathology of muscle biopsies showed severe inflammatory and necrotizing myopathy with numerous sarcocysts. Ultrastructural studies and 18S rRNA gene sequence results were consistent with infection with a Sarcocystis spp. other than Sarcocystis neurona. Both dogs initially were treated unsuccessfully with clindamycin and anti-inflammatory drugs. One dog died. The other dog subsequently responded to treatment with decoquinate. CONCLUSIONS AND CLINICAL IMPORTANCE: Sarcocystis spp. infection should be included in the differential diagnosis for dogs that develop fever, thrombocytopenia, increased liver enzyme activities, and clinical and biochemical evidence of myositis. Although additional studies are required, decoquinate holds promise as an effective treatment for the disease.

Laminin alpha2 deficiency and muscular dystrophy; genotype-phenotype correlation in mutant mice.

Deficiency of laminin alpha2 is the cause of one of the most severe muscular dystrophies in humans and other species. It is not yet clear how particular mutations in the laminin alpha2 chain gene affect protein expression, and how abnormal levels or structure of the protein affect disease. Animal models may be valuable for such genotype-phenotype analysis and for determining mechanism of disease as well as function of laminin. Here, we have analyzed protein expression in three lines of mice with mutations in the laminin alpha2 chain gene and in two lines of transgenic mice overexpressing the human laminin alpha2 chain gene in skeletal muscle. The dy(3K)/dy(3K) experimental mutant mice are completely deficient in laminin alpha2; the dy/dy spontaneous mutant mice have small amounts of apparently normal laminin; and the dy(W)/dy(W) mice express even smaller amounts of a truncated laminin alpha2, lacking domain VI. Interestingly, all mutants lack laminin alpha2 in peripheral nerve. We have demonstrated previously, that overexpression of the human laminin alpha2 in skeletal muscle in dy(2J)/dy(2J) and dy(W)/dy(W) mice under the control of a striated muscle-specific creatine kinase promoter substantially prevented the muscular dystrophy in these mice. However, dy(W)/dy(W) mice, expressing the human laminin alpha2 under the control of the striated muscle-specific portion of the desmin promoter, still developed muscular dystrophy. This failure to rescue is apparently because of insufficient production of laminin alpha2. This study provides additional evidence that the amount of laminin alpha2 is most critical for the prevention of muscular dystrophy. These data may thus be of significance for attempts to treat congenital muscular dystrophy in human patients.

Laminin alpha 2 (merosin)-deficient muscular dystrophy and demyelinating neuropathy in two cats.

We report laminin alpha 2 (merosin) deficiency associated with muscular dystrophy and demyelinating neuropathy in two cats. The cats developed progressive muscle weakness, and atrophy. Either hypotonia or contractures resulted in recumbency, necessitating euthanasia. Muscle biopsies showed dystrophic changes including marked endomysial fibrosis, myofiber necrosis, variability of fiber size, and perimysial lipid accumulation. Immunohistochemistry showed that laminin alpha 2 chain was absent or reduced, while dystrophin and all the components of the dystrophin-associated glycoprotein complex were present and normal. One cat was examined in detail. Motor nerve conduction velocity (MNCV) was decreased, and ultrastructurally the peripheral nerves showed Schwann cell degeneration and demyelination. Brain imaging was not performed, but white matter changes were not apparent in the brain at necropsy. The disease in these cats is similar to primary or secondary merosin (laminin alpha 2)-deficient congenital muscular dystrophy (CMD) in humans and to dystrophia muscularis in mice.