This article reviews the responses of plant roots to elevated rhizosphere cadmium (Cd) concentrations. Cadmium enters plants from the soil solution. It traverses the root through symplasmic or apoplasmic pathways before entering the xylem and being translocated to the shoot. Leaf Cd concentrations in excess of 5-10 μg g(-1) dry matter are toxic to most plants, and plants have evolved mechanisms to limit Cd translocation to the shoot. Cadmium movement through the root symplasm is thought to be restricted by the production of phytochelatins and the sequestration of Cd-chelates in vacuoles. Apoplasmic movement of Cd to the xylem can be restricted by the development of the exodermis, endodermis, and other extracellular barriers. Increasing rhizosphere Cd concentrations increase Cd accumulation in the plant, especially in the root. The presence of Cd in the rhizosphere inhibits root elongation and influences root anatomy. Cadmium concentrations are greater in the root apoplasm than in the root symplasm, and tissue Cd concentrations decrease from peripheral to inner root tissues. This article reviews current knowledge of the proteins involved in the transport of Cd across root cell membranes and its detoxification through sequestration in root vacuoles. It describes the development of apoplastic barriers to Cd movement to the xylem and highlights recent experiments indicating that their maturation is accelerated by high Cd concentrations in their immediate locality. It concludes that accelerated maturation of the endodermis in response to local Cd availability is of functional significance in protecting the shoot from excessive Cd loads.

Background: New onset or worsening of psoriasis has been reported in patients treated with tumor necrosis factor ␣ (TNF-␣) inhibitors for a variety of rheumatologic conditions. There is mounting evidence that a key innate immune pathway for triggering common human autoimmune disease, including psoriasis, involves plasmacytoid dendritic cell precursors (PDCs) and type 1 interferon (IFN) production. We present herein a case series with clinical and histopathologic evidence of psoriasis in patients with rheumatologic disease treated with TNF-␣ inhibitors. We propose that the cross regulation between TNF-␣ and IFN may have a role in the pathogenesis of this reaction. Observations:We observed new-onset psoriasis (n=13) or severe exacerbation of psoriasis (n = 2) in 15 patients with a variety of rheumatologic conditions-rheumatoid arthritis (n=13), psoriatic arthritis (n=1), and seronegative arthritis (n=1)-during treatment with etanercept (n=6), infliximab (n=5), and adalimumab (n=4). Immunohistochemical staining of skin biopsy specimens for myxovirus-resistance protein A (MxA, a surrogate marker for lesional type 1 IFN activity) showed increased staining in TNF-␣ inhibitor-induced psoriasis compared with psoriasis vulgaris.Conclusions: New onset or severe exacerbation of psoriasis is a rare complication of TNF-␣ inhibitor therapy. The finding of increased production of IFN-␣ in TNF-␣ inhibitor-induced psoriasis is a possible pathophysiologic explanation for this reaction.

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The expression of p-Akt increases dramatically with melanoma invasion and progression and is inversely correlated with patient survival. In addition, p-Akt may serve as an independent prognostic marker and help to identify those patients with low-risk melanomas who are at increased risk of death.

The histologic changes in cutaneous sarcoidosis are more diverse than previously recognized. In sarcoidosis, foreign material may be a frequent nidus for cutaneous granuloma formation. Histologic examination without the clinical history could lead to a misdiagnosis of leprosy, syphilis, other infectious granulomas, rosacea, granuloma annulare, necrobiosis lipoidica, and foreign body reaction in selected cases from this series.

Melanoma is one of the most aggressive cancers affecting humans. Although early melanomas are curable with surgical excision, metastatic melanomas are associated with high mortality. The mechanism of melanoma development, progression, and metastasis is largely unknown. In order to uncover genes unique to melanoma cells, we used high-density DNA microarrays to examine the gene expression profiles of metastatic melanoma nodules using benign nevi as controls. Over 190 genes were significantly overexpressed in metastatic melanomas compared with normal nevi by at least 2-fold. One of the most abundantly expressed genes in metastatic melanoma nodules is osteopontin (OPN). Immunohistochemistry staining on tissue microarrays and individual skin biopsies representing different stages of melanoma progression revealed that OPN expression is first acquired at the step of melanoma tissue invasion. In addition, blocking of OPN expression by RNA interference reduced melanoma cell numbers in vitro. Our observations suggest that OPN may be acquired early in melanoma development and progression, and may enhance tumor cell growth in invasive melanoma.

The objective of this study was to determine the influence of low-temperature plasma (LTP) on seed surface modification, water uptake by seeds, seed germination and vigor of seedlings, as well as changes in the content of endogenous hormones in pea, (Pisum sativum L. var. Prophet). The study's authors used diffuse coplanar surface barrier discharge as the source of LTP in various duration times of treatment (from 60 to 600 s). The SEM analysis showed that LTP induced significant changes on the seeds' surface, which was related to water permeability into the seeds. LTP increased the germination percentage of pea seeds as well as the growth parameters (root and shoot length, dry weight), and the vigor of seedlings and the effects of LTP also depended on exposure time. The LTP-pretreatment produced changes in endogenous hormones (auxins and cytokinins and their catabolites and conjugates), which correlated with increased growth of the pea seedlings. The results suggested an interaction among the modification of seed structure demonstrated by LTP in the induction of faster germination and hormonal activities related to plant signaling and development during the early growth of pea seedlings.

Purpose: The collagen triple helix repeat containing 1 (CTHRC1) is a promigratory protein first found to be expressed during rat tissue repair process. Recent preliminary results revealed CTHRC 1 mRNA in melanoma and breast cancer. However, the full significance of CTHRC1 to human carcinogenesis remains unclear. This study is to further characterize the clinical and functional relevance of CTHRC1in melanoma and other human solid cancers. Experimental Design: First, semiquantitative immunohistochemistry analysis was done on 304 clinically annotated, paraffin-embedded biopsies representing different stages of melanoma progression. Then, short interfering RNA was used to inhibit expression of CTHRC1 protein for migration analysis on cultured melanoma cells. Finally, the CTHRC1 expression was surveyed in 310 samples representing 19 types of human solid cancers. Results: In benign nevi and noninvasive melanoma biopsies, there was little CTHRC1 protein expression. In contrast, in invasive primary melanomas, there was a significant increase of CTHRC1protein (P < 0.01, m 2 test). There was a further increase of CTHRC1protein in metastatic melanoma specimens compared with nonmetastatic lesions (P < 0.01, m 2 test). In addition, inhibition of CTHRC1 expression resulted in decreased cell migration in vitro. Finally, transcription survey in 19 types of human solid cancers revealed aberrant CTHRC1 expression in 16 cancer types, especially cancers of the gastrointestinal tract, lung, breast, thyroid, ovarian, cervix, liver, and the pancreas. Conclusions: Aberrant expression of CTHRC1 is widely present in human solid cancers and seems to be associated with cancer tissue invasion and metastasis. It potentially plays important functional roles in cancer progression, perhaps by increasing cancer cell migration.