GeSn-on-Si normal incidence photodetectors with bandwidths more than 40 GHz.

GeSn (Sn content up to 4.2%) photodiodes with vertical pin structures were grown on thin Ge virtual substrates on Si by a low temperature (160 °C) molecular beam epitaxy. Vertical detectors were fabricated by a double mesa process with mesa radii between 5 µm and 80 µm. The nominal intrinsic absorber contains carrier densities from below 1 · 10(16) cm(-3) to 1 · 10(17) cm(-3) for Ge reference detectors and GeSn detectors with 4.2% Sn, respectively. The photodetectors were investigated with electrical and optoelectrical methods from direct current up to high frequencies (40 GHz). For a laser wavelength of 1550 nm an increasing of the optical responsivities (84 mA/W -218 mA/W) for vertical incidence detectors with thin (300 nm) absorbers as function of the Sn content were found. Most important from an application perspective all detectors had bandwidth above 40 GHz at enough reverse voltage which increased from zero to -5 V within the given Sn range. Increasing carrier densities (up to 1 · 10(17) cm(-3)) with Sn contents caused the depletion of the nominal intrinsic absorber at increasing reverse voltages.

Treatment of sicca symptoms with hydroxychloroquine in patients with Sjogren's syndrome.

OBJECTIVE: There is no established disease-modifying treatment of xerostomia and xerophthalmia in SS. This retrospective study was performed in order to evaluate the efficacy of HCQ for glandular function, i.e. saliva and tear production. METHODS: Fourteen patients with primary SS (pSS) were included (Group A). All patients were anti-Ro and/or -La antibody positive except one. Patients were treated with HCQ for a period of up to 6 months. Glandular function was determined by Saxon's and Schirmer's tests for the dominant eye at baseline and at the end of the treatment. We included a control group of 21 patients with objective sicca symptoms and positive alpha-fodrin antibodies (Group B). RESULTS: In patients with pSS (Group A), a significant increase in saliva production after HCQ treatment (P = 0.022) was observed. A subanalysis revealed that particularly the alpha-fodrin-positive patients responded to HCQ (P = 0.017 alpha-fodrin positive vs P = 0.4 alpha-fodrin negative). Interestingly, patients with sicca symptoms and alpha-fodrin antibodies (Group B) showed a significant increase in tear production (P = 0.001). In addition, there was a positive correlation between the alpha-fodrin IgA antibody concentration and the Schirmer's test at baseline (r = 0.66; P = 0.001) and after treatment (r = 0.6; P = 0.004) in this group. CONCLUSIONS: HCQ treatment led to a beneficial effect on xerostomia in patients with pSS who lack severe organ manifestations. The response was greater in alpha-fodrin-positive patients.

Successful treatment of post-kala-azar dermal leishmaniasis (PKDL) in a HIV infected patient with multiple relapsing leishmaniasis from Western Europe.

We present a 42-year-old man who was admitted with worsening of his general condition and facial skin lesions. He had previously been diagnosed with HIV infection and visceral leishmaniasis (VL). Diagnostic work-up revealed a new relapse of VL paralleled by the diagnosis of post-kala-azar dermal leishmaniasis (PKDL). The patient was treated with IV liposomal amphotericin B as well as sodium stibogluconate followed by oral hexadecylphosphocholine (miltefosine) over a period of 9 months. PKDL lesions began to disappear after 8 months of treatment. In addition, severe and relapsing VL so far remains in remission. This case demonstrates successful treatment of PKDL and relapsing VL in a Western European patient with HIV infection.

Successful tumor necrosis factor alpha blockade treatment in therapy-resistant sarcoidosis.

Sarcoidosis is a multisystemic disorder histologically characterized by a noncaseating granulomatous inflammatory process. The etiology remains unclear, but tumor necrosis factor alpha seems to play a crucial role. Herein we describe a patient with severe sarcoidosis involving the lung and liver. Various treatment regimens with azathioprine, methotrexate, cyclophosphamide, and pentoxifylline failed to control the disease. Therefore, salvage therapy with infliximab was commenced. Arthritis and pulmonary and liver involvement improved. We were then able to taper the corticosteroid treatment to a lower-dose regimen with no need for additional immunosuppressive treatment. To our knowledge, this is the first reported case of successful treatment of multiorgan sarcoidosis that was previously resistant to conventional therapy.

Antibodies against alpha-fodrin in Sjögren's syndrome.

Alpha-fodrin is a part of the membrane skeleton and expressed in the majority of mammalian cells. It is cleaved in apoptosis by caspase 3. One of the cleavage products, a 120-kDa protein, represents a neoantigen. Antibodies against that cleavage product of alpha-fodrin have originally been described in a murine model of Sjögren's syndrome. In addition, they are also present in up to 93% of patients with Sjögren's syndrome, depending on the stringency of the classification used. Although antibodies against alpha-fodrin are observed in other diseases characterized by chronic apoptosis, they are a valuable laboratory marker in the evaluation of Sjögren's syndrome.