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This paper explains why only optical techniques will be able to provide debug and diagnosis of bulk silicon FinFET technologies. In order to apply optical techniques through a convenient thickness of silicon on the one hand, light is limited to NIR to minimize absorption. To match resolution requirements on the other hand, it becomes mandatory to use shorter wavelengths. Two key issues have to be addressed: First, the penetration depth of visible light is only a few μm. This challenges device preparation and integrity. Our approach makes use of confocal microscopy suppressing back surface reflection and thus relaxing the preparation requirements to around 10 μm. Second, only solid immersion lenses (SIL) enable nanoscale resolution. But instead of silicon, materials transparent to visible light and providing a high refractive index are necessary. Our concept is based on 658 nm/633 nm laser and supports GaP as SIL material. We demonstrate the power of confocal imaging and prove contactless probing through a device thickness of 10 μm. We discuss how confocal optics relax the thickness requirements for visible light imaging and probing and we layout the concept for a GaP SIL. This concept opens the path to the design of nanoscale visible light debug and diagnosis.

Human cycling endometrium displays a series of periodic transitions unique to this mucosal tissue, which includes rapid proliferation, secretory transformation, physiological angiogenesis, interstitial edema, and menstrual shedding. Among these properties of the endometrium are the inflammatory changes that occur dynamically across the menstrual cycle. Immunocompetent cell composition and inflammatory gene expression pattern in the human endometrium drastically fluctuate from the proliferative phase to the secretory phase, particularly at the time of ovulation. These local immune responses are fine-tuned by the direct or indirect action of two representative ovarian steroids, estradiol and progesterone, and are essential for successful blastocyst implantation. Meanwhile, studies have been accumulating the evidence that such physiological endometrial inflammatory status is altered in the presence of certain gynecologic pathologies. Given that blastocysts are semi-allografts for maternal tissue, even subtle alterations in endometrial immunity potentially have a negative impact on implantation process. In this article, we aimed to review and discuss the physiological and pathological mucosal inflammatory conditions that can affect endometrial receptivity.

The morphologic evolution of hepatitis B virus (HBV) liver disease in 45 hepatic allograft recipients who were HBV surface-antigen positive (HBs-Ag+) at the time of liver replacement and who survived for more than 60 days was studied by routine histologic and immunocytochemical analysis of serial pathology specimens. The findings in these patients were compared to a control group of 30 individuals who were immune to the HBV (anti-HBs antibody positive), but required hepatic replacement for other reasons. Eight of the forty-five (18%) HBsAg-positive patients have no serologic evidence of HBV reinfection after transplantation. All 37 remaining patients are reinfected; 21 (47%) developed chronic active hepatitis and/or cirrhosis, 3 (7%) developed submassive necrosis, and 6 (14%) developed chronic lobular hepatitis. One patient lost her graft to chronic rejection, despite reinfection with the B virus. Four other patients (9%) developed a chronic carrier state. No long-term follow-up biopsies were available in the remaining two patients. The histologic features associated with dysfunction related to recurrent HBV infection evolved from an acute to chronic phase and were similar to hepatitis B seen in nonallografted livers. Furthermore HBV-related lesions could be separated from rejection using routine histology alone. The only exception to this conclusion was the occurrence of a peculiar HBV-related lesion in two recipients, described herein. Immunohistochemical analysis demonstrated the presence of viral antigens in almost all cases. Hepatic inflammation also was commonly present during HBV disease and consisted mostly of accessory cells and T lymphocytes. Analysis of the effect of major histocompatibility complex matching revealed no clear association between the number of class I or II matches or mismatches and the development, or pattern, of active hepatitis in the allograft. Peculiar pathologic alterations in several of the biopsies and failed allografts after HBV reinfection suggests that, under special circumstances, the B virus may be cytopathic.

Thoracic duct lymphocytes from patients receiving thoracic duct drainage as a pretransplant therapy were examined for cell surface markers. Patients followed over the drainage time period showed a variable but decreasing percentage of E-rosette-positive cells in the lymph fluid. A substantial percentage of these E-rosette-positive cells also had C3 receptors on their cell surface. Reactions of the whole lymphocytes with a heteroantisera to human B-lymphocyte antigens reflected the increasing proportion of B cells in the samples, but also indicated that a fraction of the T cells have Ia-like antigens on their surface marker characteristics. Significance of these cells with respect to graft survival is discussed.

A micro-latex fixation test (LFT) for the determination of rheumatoid factor (RF) is presented. Its advantages compared to similar tests are greater precision, simplicity, increased sensitivity, lower cost, reproducibility and adaptibility to large-scale testing. Micro-LFT titres are presented from a wide range of sample populations. The majority of normal samples show measureable titres whereas rheumatoid patients show high titres. A large sampling of pre- and post-transplant sera from kidney patients was studied and the micro-LFT titres were in the range of normal persons. The transplant sera were tested for lymphocytotoxic antibodies and no correlation was observed with the micro-LFT titres.

The early events of liver allograft rejection in untreated rats were studied in the DA to BN rejection strain combination and compared with DA and BN liver isograft recipients. In the liver allografts, T-cell infiltration first occurred at 2 days after transplantation and localized to the portal triads and subjacent to the terminal hepatic venules (THV), regions rich in intensely Ia + spindle and dendritic-shaped interstitial cells. Double staining showed distinct 'clustering' between donor Ia-positive dendritic-shaped cells and W3/25+ infiltrating lymphocytes, or to a lesser extent, OX8+ cells. The infiltrating mononuclear cells underwent blastogenesis and proliferated in both the triads and THV regions at 3 and 4 days. Donor Ia-positive cells were also noted in the W3/25+ periarterial lymphatic sheath and marginal zone of the recipient spleen 1 day after transplantation. The number of these cells in the spleen peaked at 3 to 4 days, but were no longer detectable by 10 to 12 days. Mitotic activity became evident in these same regions by days 3 and 4. Paracortical blastogenesis (day 2) and proliferation (days 3 and 4) were also noted in the regional lymph nodes of liver allograft recipients, but no donor Ia+ cells were found in the mesenteric nodes or thymus of the allograft recipients. These results demonstrate that sensitization of the recipient lymphoid tissue to liver allografts can occur both peripherally (intragraft) and centrally (spleen and lymph nodes). Passenger leukocytes (donor dendritic cells) are likely the primary stimulators of the rejection reaction. Still, it is probable that other pathways of sensitization exist.