Beck FWJ et al. (1997) Decreased expression of CD73 (ecto-5′-nucleotidase in the CD8+ subset is associated with zinc deficiency in human patients. J. Lab. Clin. Med. 130:147–56.

(b) xi = 25*24/(24 - 25) = -600. The image a virtual image 600 cm in front of the lens.Its magnification is M = 600/24 = 25. The image is upright and enlarged.

A thin lens has a focal length of 25 cm.  Locate the image when the object is placed(a) 26 cm(b) 24 cmin front of the lens.  Describe the image in each case.

The role of zinc in modulating oxidative stress has recently been recognized. Oxidative stress is an important contributing factor in several chronic human diseases, such as atherosclerosis and related vascular diseases, mutagenesis and cancer, neurodegeneration, immunologic disorders, and the aging process (20–22). Together O2·−, H2O2, and ·OH are known as reactive oxygen species (ROS), and these are produced continuously in vivo under aerobic conditions. The NADPH oxidases are a group of plasma membrane associated enzymes, which catalyze the production of O2·− from oxygen by using NADPH as the electron donor. Zinc is an inhibitor of this enzyme. The dismutation of O2·− to H2O2 is catalyzed by an enzyme super oxide dismutase (SOD), which contains both copper and zinc. Zinc is known to induce the production of metallothionein, which is very rich in cysteine, and is an excellent scavenger of ·OH (6). Iron and copper ions catalyze the production of ·OH from H2O2. Zinc is known to compete with both iron and copper for binding to cell membrane, thus decreasing the production of ·OH (6).

Our data showed that zinc supplementation to normal healthy subjects a) lowers the oxidative stress-related byproducts MDA (malondialdehyde), 4-hydroxyalkenals (HAE), and 8-hydroxy deoxyguanine (8-OHdG) generated by cells and released into the plasma, b) inhibits the induction of TNF-α and IL-1β mRNA in MNCs, and c) exhibits a protective effect against TNF-α-induced NF-κB activation in isolated MNCs (34). In addition, we provided evidence to show that, in the human pro-myelocytic leukemia cell line HL-60 which differentiates to the monocyte-macrophage phenotype by PMA, zinc increased the expression of A20 and the binding of A20 transactivating factor to DNA, thereby enhancing inhibition of induced NF-κB activation (34).

In a large study organized by the National Eye Institute, NIH, (Bethesda, MD, USA) it was reported that zinc and antioxidants (vitamin C, vitamin E, and β carotene) significantly reduced the odds of developing advanced age related macular degeneration (AMD), and prevented blindness in the high-risk group of elderly subjects (37). Also, it was reported that longevity was increased in the zinc supplemented group (38). Although the mechanism of zinc effect was not defined, one may hypothesize that zinc reduced the oxidative stress and thus was beneficial in AMD.

A few investigators have reported that inflammatory cytokines such as TNF-α (tumor necrosis factor-α) and IL-1β, generated by activated monocytes-macrophages, also are known to produce increased amounts of ROS (23,24). Increases in these cytokines are associated with decreased zinc status in patients.

Arima N et al. (1998) IL-2 induced growth of CD8+ T cell prolymphocytic leukemia cells mediated by NF-κB induction and IL-2 receptor a expression. Leuk. Res. 22:265–73.

Prasad AS, Halsted JA, Nadimi M. (1961) Syndrome of iron deficiency anemia, hepatosplenomegaly, hypogonadism, dwarfism and geophagia. Am. J. Med. 31:532–46.

Song HY, Rothe M, Goeddel DV. (1996) The tumor necrosis factor-inducible zinc finger protein A20 interacts with TRAF1/TRAF2 and inhibits NF-κB activation. Proc. Natl. Acad. Sci. U. S. A. 93:6721–5.

Although the essentiality of zinc for plants and animals has been known for many decades, the essentiality of zinc for humans was recognized only 40 years ago in the Middle East. The zinc-deficient patients had severe immune dysfunctions, inasmuch as they died of intercurrent infections by the time they were 25 years of age. In our studies in an experimental human model of zinc deficiency, we documented decreased serum testosterone level, oligospermia, severe immune dysfunctions mainly affecting T helper cells, hyperammonemia, neurosensory disorders, and decreased lean body mass. It appears that zinc deficiency is prevalent in the developing world and as many as two billion subjects may be growth retarded due to zinc deficiency. Besides growth retardation and immune dysfunctions, cognitive impairment due to zinc deficiency also has been reported recently. Our studies in the cell culture models showed that the activation of many zinc-dependent enzymes and transcription factors were adversely affected due to zinc deficiency. In HUT-78 (T helper 0 (Th0) cell line), we showed that a decrease in gene expression of interleukin-2 (IL-2) and IL-2 receptor α (IL-2Rα) were due to decreased activation of nuclear factor-κB (NF-κB) in zinc deficient cells. Decreased NF-κB activation in HUT-78 due to zinc deficiency was due to decreased binding of NF-κB to DNA, decreased level of NF-κB p105 (the precursor of NF-κB p50) mRNA, decreased κB inhibitory protein (IκB) phosphorylation, and decreased Iκκ. These effects of zinc were cell specific. Zinc also is an antioxidant and has anti-inflammatory actions. The therapeutic roles of zinc in acute infantile diarrhea, acrodermatitis enteropathica, prevention of blindness in patients with age-related macular degeneration, and treatment of common cold with zinc have been reported. In HL-60 cells (promyelocytic leukemia cell line), zinc enhances the up-regulation of A20 mRNA, which, via TRAF pathway, decreases NF-κB activation, leading to decreased gene expression and generation of tumor necrosis factor-α (TNF-α), IL-1β, and IL-8. We have reported recently that in both young adults and elderly subjects, zinc supplementation decreased oxidative stress markers and generation of inflammatory cytokines.

Several studies have shown the benefits of zinc supplementation on infectious diseases in humans. In double-blind placebo-controlled trials of zinc supplementation, zinc reduced the incidence and duration of acute and chronic diarrhea and acute lower respiratory tract infections in infants and children (11,12). Zinc supplementation of sickle cell anemia patients in a placebo-controlled trial resulted in decreased incidence of staphylococcus aureus pneumonia, streptococcus pneumonia tonsillitis, and E. coli urinary tract infections (13). Our recent studies have shown that zinc supplementation to elderly subjects results in a significant decrease in the incidence of infections (14).

In 1974, a landmark decision to establish recommended dietary allowances (RDAs) for humans for zinc (15 mg elemental zinc daily for adult men and women) was made by the Food and Nutrition Board of the National Research Council of the United States of America National Academy of Sciences.

The lens and mirror equations are valid for paraxial rays.  If all the light rays involved in image formation make small angles with the optic axis, so that sinθ ≈ tanθ ≈ θ, then near perfect images form at the locations predicted by these equations.  For off-axis or skew rays, the image of a point becomes blurry and we observe aberrations.

Magnificationformula forlensin termsoffocal length

NF-κB is involved in the expression of a variety of responsive specific genes and is activated by several stimuli such as cytokines, radiation, and oxidative stress. In vitro activation of NF-κB by TNF-α in MNC has been shown to be an excellent model of oxidative stresssensitive transactivating factor, and has been used to evaluate the efficacy of compounds in protecting cells from oxidative stress (21). Zinc has been shown to inhibit NF-κB activation in prostate cancer cells, thus enhancing anti-cancer therapy (25), bovine cerebral epithelial cells (26), as well as reducing increased levels of activated NF-κB in diabetic CD1 mice (27) and zinc deficient cultured human hepatocellular carcinoma-derived cell line (28).

Zinc affects multiple aspects of the immune system (10). Zinc is crucial for normal development and function of cells mediating innate immunity, neutrophils, and NK cells. Macrophages also are affected by zinc deficiency. Phagocytosis, intracellular killing, and cytokine production all are affected by zinc deficiency. Zinc deficiency adversely affects the growth and function of T and B cells. The ability of zinc to function as an antioxidant and stabilize membranes suggests that it has a role in the prevention of free radical-induced injury during inflammatory processes.

Let xo denote the perpendicular distance of the object from the centerline of the lens and let xo be positive.  Let xi denote the perpendicular distance of the image from the centerline of the lens.  Then xi can be found from the lens equation 1/xo + 1/xi = 1/f,provided we use the following sign convention.

The manifestations of a moderate deficiency of zinc include growth retardation and male hypogonadism in adolescents, rough skin, poor appetite, mental lethargy, delayed wound healing, cell-mediated immune dysfunctions, and abnormal neurosensory changes.

A single spherical interface between two transparent media can lead to image formation.  But viewing these images is not always possible.  Consider an air-glass interface.  When the object is on the air side, the image can only be viewed from inside the glass.  Giving the glass a finite thickness and adding a second spherical interface between glass and air will produce an image that can be viewed by someone in air.  A piece of glass of finite thickness with two spherical boundaries is a lens.  If the thickness of the lens is much smaller than the diameter of the lens, we call it a thin lens. Thin lenses can be converging or diverging.  Converging lenses are thicker in the middle than near the edges, and diverging lenses are thicker near the edges than in the middle.  A thin lens has two focal points, located on the optical axis, a distance f from the center of the lens on either side of the lens.  Rays parallel to the optic axis passing through a thin converging lens come together at the focus f on the opposite side of the lens, and rays parallel to the optic axis passing through a diverging lens diverge as if they were leaving the focus on the incident side on a straight line path.

Serfling E, Avots A, Neumann M. (1995) The architecture of the interleukin-2 promoter: a reflection of T-lymphocyte activation. Biochem. Biophys. Acta. 1263:181–200.

How tocalculatemagnificationmicroscope

Because zinc deficiency affects IL-2 production and T-cell activation adversely, we have investigated the role of zinc on NF-κB (nuclear factor-κB) activation in HUT-78, a T helper 0 (Th0) human malignant lymphoblastoid cell line. We showed for the first time that, in zinc deficient HUT-78 cells, the activation of NF-κB was affected adversely (15).

Opipari Jr. AW, Boguski MS, Dixit VM. (1990) The A20 cDNA induced by tumor necrosis factor alpha encodes a novel type of zinc finger protein. J. Biol. Chem. 265:14705–8.

The production of interleukin-2 (IL-2) is a key and early event in the activation of T-lymphocytes. IL-2 triggers peripheral T-lymphocytes to enter the S phase of the cell cycle and to divide. This is probably a result of the suppressive effect of IL-2 on cell cycle inhibitors, which interfere with the activity of cyclin-dependent kinases (cdks) at checkpoints of the cell cycle (16). IL-2 also is involved in the differentiation of thymocytes, peripheral T- and B-lymphocytes and other cells of hematopoietic origin (16).

Davis JN et al. (2001) Soy isoflavone supplementation in healthy men prevents NF-κB activation by TNF-α in blood lymphocytes. Free Radic. Biol. Med. 30:1293–302.

Th1 cells are known to promote macrophage activation and production of complement fixing and opsonizing antibodies. IFN-γ is the major component of the Th1 response panel, and it upregulates major histocompatibility complex class I antigen expression. Inasmuch as we have observed that IFN-γ production is decreased as a result of zinc deficiency, our studies provide a possible mechanism by which zinc deficiency may affect cell-mediated immunity adversely.

Prasad AS, Bao B, Beck FWJ, Sarkar FH. (2002) Zinc enhances the expression of interleukin-2 and interleukin-2 receptors in HUT-78 cells by way of NF-κB activation. J. Lab. Clin. Med. 140:272–89.

Kim CH et al. (1999) Pyrithione, a zinc ionophore, inhibits NF-kappaB activation. Biochem. Biophys. Res. Comm. 259:505–9.

Otsu K, Ikeda Y, Fujii J. (2004) Accumulation of manganese superoxide dismutase under metaldepleted conditions: proposed role for zinc ions in cellular redox balance. Biochem. J. 377:241–8.

During the past four decades, a spectrum of clinical deficiency of zinc in human subjects has emerged (6). On the one hand, the manifestations of zinc deficiency may be severe; and, on the other end of the spectrum, zinc deficiency may be mild or marginal. A severe deficiency of zinc has been reported to occur in patients with acrodermatitis enteropathica (a genetic disorder), following total parenteral nutrition (TPN) without zinc, following excessive use of alcohol, and following penicillamine therapy. The manifestations of severe zinc deficiency in humans include bullous pustular dermatitis, alopecia, diarrhea, emotional disorder, weight loss, intercurrent infections due to cell-mediated immune dysfunctions, hypogonadism in males, neurosensory disorders, and problems with healing of ulcers. If this condition is unrecognized and untreated, it becomes fatal.

Magnificationformula for convexlens

Beck FWJ et al. (1997) Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. Am. J. Physiol. 272:E1002–7.

Krikos A, Laherty CD, Dixit VM. (1992) Transcriptional activation of the tumor necrosis factor alpha-inducible zinc finger protein, A20, is mediated by κB elements. J. Biol. Chem. 267:17971–6.

Many optical instruments have more than one optical element.  A combination of mirrors and lenses can be analyzed by treating the image of the first element as the object of the second element, and so on.  If the image of the first element falls behind the second element we can still use the lens or mirror equation, but we then must use a negative object distance xo.

A contact lens is made of plastic with an index of refraction of 1.5.  The lens has an outer radius of curvature of 2 cm and an inner radius of curvature of 2.5 cm. What is the focal length of the lens?

Do you have a magnifying glass?  If not, do you have access to some prescription eyeglasses?  Make some observation with a single lens.

A short segment of DNA, 275 base pairs in the promoter area of IL-2 gene, integrates numerous signaling pathways leading to IL-2 synthesis and the activation and proliferation of T-lymphocytes (16). Both the murine and human IL-2 promoters contain one binding site for genuine Rel/NF-κB factors. The sequence of this site, GGGATTTCAC, is identical for both promoters. NF-κB factors are induced rapidly by a variety of stimuli activating T cells. Almost every stimulus leading to T cell activation also activates NF-κB. Induction of IL-2Rα gene expression also is mediated by the induced nuclear expression of NF-κB (17,18).

The lens equation and the mirror equation are written as 1/xo + 1/xi = 1/f.But the sign conventions for xo, xi, and f are different for lenses and mirrors.

Ozaki Y, Ohashi T, Kume S. (1987) Potentiation of neutrophil function by recombinant DNA-produced interleukin-1α J. Leukoc. Biol. 42:621–7.

Prasad AS et al. (2007) Zinc supplementation decreases incidence of infections in the elderly: Effect of zinc on generation of cytokines and oxidative stress. Am. J. Clin. Nutr. 85:837–44.

The current estimate is that over 2,000 transcription factors may be zinc dependent. However, the present dogma is that the amount of zinc required for the integrity of these transcription factors is so small that, in zinc-deficient cells, one would not see any change.

Uzzo RG et al. (2002) Zinc inhibits nuclear factor-κB activation and sensitizes prostate cancer cells to cytotoxic agents. Clin. Can. Res. 8:3579–83.

The immunological hallmarks of zinc deficiency in humans and higher animals include thymic atrophy, lymphopenia, and compromised cell- and antibody-mediated responses that result in increased incidences of infections (36). In chronic zinc deficiency, a reprogramming of the immune system occurs, beginning with the activation of the stress axis and chronic production of glucocorticoids that accelerate apoptosis of pre-B and pre-T cells (36), resulting in reduced lymphopoeisis and atrophy of thymus. In contrast, myelopoesis is preserved. Changes in the gene expression for cytokines, DNA repair enzymes, zinc transporters, and signaling molecules, suggest that the cells of the immune system are attempting to adapt to the stress of suboptimal zinc (36).

Magnificationformula for mirror

Applying the lens equation to thin lenses, we can safely assume the light bends at the center of the lens, and neglect the thickness of the lens.  For thick lenses we have to be more careful.One must calculate the location of principal planes, from which to measure distances to the object, the image, and the focal points.

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AREDS Report No.13. (2004) Association of mortality with ocular disorders and an intervention of high dose anti-oxidants and zinc in the age-related eye disease study. Arch. Ophthalmol. 122:716–26.

A plane through a focus perpendicular to the optic axis is called a focal plane.  Parallel rays converge in the focal plane or diverge from the focal plane, independent of the angle they make with the optic axis.

Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/2.0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Ho E et al. (2001) Dietary zinc supplementation inhibits NF-kappa B activation and protects against chemically induced diabetes in CD1 mice. Exp. Biol. Med. 226:103–11.

Berkow RL et al. (1987) Enhancement of neutrophil superoxide production by pre-incubation with recombinant human tumor necrosis factor. J. Immunol. 139:3783–91.

Grant support for this work was provided in part by NIH grant 5 RO1 A150698-04 and Labcatal Laboratories, Paris, France.

Sazawal S et al. (1998) Zinc supplementation reduces the incidence of acute lower respiratory infections in infants and preschool children: a double blind controlled trials. Pediatrics. 102:1–5.

In our experimental human model studies, when zinc deficiency was very mild (3 to 5.0 mg Zn intake during the zinc-restricted period), the plasma zinc concentration remained more or less within the normal range and it decreased only after 4–5 months of zinc restriction. On the other hand, zinc concentrations in lymphocytes, granulocytes, and platelets decreased within 8–12 weeks, suggesting that the assay of cellular zinc provided a more sensitive criterion for diagnosing mild deficiency of zinc (7–9).

We showed that the phosphorylation of IκB and Iκκ, translocation of NF-κB, and its binding to DNA in HUT-78 cells were all zinc dependent (15). The activation of NF-κB was considerably reduced in zinc-deficient HUT-78 cells. Additionally, zinc deficiency decreased the level of NF-κB p105 (the precursor of NF-κB p50) mRNA. All these effects of zinc were cell specific.

How to find the magnification of a lenscalculator

Heyninck K, Beyaert R. (1999) The cytokine-inducible zinc finger protein A20 inhibits IL-1 induced NF-κB activation at the level of TRAF6. FEBS Lett. 442:147–50.

During our studies in the Middle East, we observed that most of the zinc deficient dwarfs did not live beyond the age of 25 years. The cause of death appeared to be infections. Parasitic infections were common. Viral and bacterial infections, although prevalent, remained undocumented, however. The possibility that zinc deficiency may have played a role in immune dysfunctions in the zinc-deficient dwarfs was considered, but lack of proper facilities prevented us from gathering meaningful data on immune functions in those patients in the Middle East.

Lensformula

In 1869, Raulin (1) first showed that zinc was required for the growth of Aspergillus niger. In 1934, Todd et al. (2) reported that zinc was essential for the growth of rats. Although the essentiality of zinc for animals was established, its ubiquity made it seem improbable that zinc deficiency in humans could lead to any significant clinical problem. During the past 40 years, however, it has become apparent that deficiency of zinc in humans is quite prevalent and may affect over two billion subjects in the developing world (3–5). Here, we review some of the clinical manifestations of zinc deficiency in humans, with particular emphasis on our observations in experimental human models of this syndrome.

Age-Related Eye Disease Study Research Group (AREDS Report No.8). (2001) A randomized, placebo controlled, clinical trial of high-dose supplemented with vitamins C and E, beta-carotene, for age-related macular degeneration and vision loss. Arch. Ophthalmol. 119:1417–36.

Nutritional deficiency of zinc in the developing countries is caused by ingestion of high cereal protein intake, rich in phytate (an organic phosphate compound), which makes zinc unavailable for absorption. Other causes of zinc deficiency include malabsorption syndrome, hyperzincuria as seen in cirrhosis of the liver and sickle cell disease, blood loss due to hookworm infection, and excessive sweating in hot tropical climates.

Prasad AS et al. (1963) Zinc metabolism in patients with the syndrome of iron deficiency anemia, hypogonadism and dwarfism. J. Lab. Clin. Med. 61:537–49.

Sazawal S et al. (1995) Zinc supplementation in young children with acute diarrhea in India. N. Engl. J. Med. 333:839–44.

A converging lens of focal length 4 cm is used as a magnifier.  If an object is placed 3 cm from the lens, what is the magnification?

We assayed serum thymulin activity in mildly zinc-deficient human subjects (8). Thymulin is a thymus-specific hormone and it requires the presence of zinc for its biological activity to be expressed. Thymulin binds to high-affinity receptors on T cells, induces several T-cell markers, and promotes T-cell function, including allogenic cytotoxicity, suppressor functions, and interleukin-2 (IL-2) production. As a result of mild deficiency of zinc, the activity of thymulin in serum was decreased significantly and was corrected by both in vivo and in vitro zinc supplementation (7). The in vitro supplementation studies indicated that the inactive thymulin peptide was present in the serum in zinc-deficient subjects and was activated by the addition of zinc.

Our study provides molecular evidence for an anti-oxidant effect of zinc in human subjects and shows that zinc supplementation in vivo protected MNC against oxidative stress (34). Although there are several possible biochemical mechanisms by which zinc may decrease oxidative stress in cells, our study shows that zinc negatively regulates gene expression of inflammatory cytokines such as TNF-α and IL-1β, which are known to generate ROS and this may be one additional mechanism by which zinc may be functioning as an antioxidant in humans. Thus, our study provides rationale for use of zinc in therapeutic trials either alone or in conjunction with other modalities in chronic diseases, including chemo-prevention of cancer in which oxidative stress is known to play an important role.

Cavdar AO et al. (1983) Geophagia in Turkey: Iron and zinc deficiency, iron and zinc absorption studies and response to treatment with zinc in geophagia cases. In Prasad AS, Cavdar AO, Brewer GJ, Aggett PJ [eds]. Zinc deficiency in human subjects, Alan R. Liss Inc, New York. p.71–97.

Prasad AS et al. (1999) Effect of zinc supplementation on incidence of infections and hospital admissions in sickle disease (SCD). Am. J. Hematol. 61:194–202.

In our studies in the experimental human model in whom only a mild deficiency of zinc in males was induced by dietary means, decreased serum testosterone level, oligospermia, decreased natural killer (NK) cell activity, decreased interleukin-2 (IL-2) production, decreased thymulin activity, hyperammonemia, hypogeusia, decreased dark adaptation, and decreased lean body mass were observed. It is, therefore, clear that even a mild deficiency of zinc in humans affects clinical, biochemical, and immunological functions adversely (7–9).

Faber et al.(39) have shown that in vivo zinc supplementation in therapeutic levels resulted in blocking allogeneic response while maintaining the antigenic potency. This observation may have future implication in transplantation subjects where a selective suppression of allogeneic response is desired.

Intracellular zinc concentration was decreased by 40% in zinc-deficient HUT-78 cells in comparison to the zinc-sufficient cells after 4 d of incubation. To examine the effect of zinc on κB inhibitory protein (IκB) in HUT-78 cells, we measured phosphorylated IκB-α, Iκκ-α (IκB kinase-α), and ubiquitinated IκB-α in zinc-treated cells. Zinc deficiency caused a 60% decrease in phosphorylated IκB-α in non-stimulated and 40% decrease in phorbol-12 myristate 13 acetate (PMA)/phytohemagglutinin-p (PHA-p)-stimulated cells, compared with zinc-sufficient cells. Zinc deficiency decreased Iκκ-α in PMA/PHA-p-stimulated cells by 30% in comparison to zinc-sufficient cells. Zinc deficiency caused a 50% reduction of ubiquitinated IκB-α after PMA/PHA-p stimulation (15).

Hatakeyama M et al. (1989) Interleukin-2 receptor beta chain gene: generation of three receptor forms by cloned human alpha and beta chain cDNA’s. Science. 244:551–6.

The details of cell culture, zinc assay, and other methods have been published elsewhere (19). We used an Enzyme-Linked ImmunoSorbent Assay (ELISA) to measure the concentration of IL-2 produced by the cells. Unstimulated HUT-78 cells incubated in zinc-deficient (1 µmol/L zinc) and zinc-sufficient (15 µmol/L zinc) media for 4 d produced a very small amount of IL-2. Following PMA/PHA-p stimulation, the IL-2 production and IL-2 mRNA were significantly greater in zinc-sufficient cells in comparison to the zinc-deficient cells (19). Similar results were seen for soluble IL-2 receptor α (soluble IL-2Rα) production and gene expression (19).

Faber C, Gabriel P, Ibs KH, Rink L. (2004) Zinc in pharmacological doses suppresses allogeneic reaction without affecting the antigenic response. Bone Marrow Transplant. 33:1241–6.

For the quantification of T cells, beads coated with T101 Mab and, for B lymphocytes, beads coated with anti human immunoglobulin were used, (Quantigen, Bio-Rad laboratories, Richmond, CA, USA) 1×106 mononuclear cells (MNC) were incubated with 200 µL of one or two microbeads preparation. Cells with no beads were counted as T101−, slg−. An increase in T101−, slg-cells, a decrease in the ratio of CD4+ to CD8+, and decreased IL-2 activity (proliferation assay [7]) were observed in the experimental human model during the zinc-depletion phase, all of which were corrected after repletion with zinc. We previously had reported that NK cells’ activity was also sensitive to zinc restriction, thus it appears that zinc may play a very important and critical role in the functions of T cells in humans (6,10). Our studies in the experimental human model showed for the first time that the production of IFN-γ was decreased, whereas the production of IL-4, IL-6 and IL-10 was not affected due to zinc deficiency (8,9). IFN-γ is known to downregulate the T helper 2 (Th2) clone, and IL-10 may downregulate the T helper 1 (Th1) clone. An imbalance between Th1 and Th2 responses in patients with human immunodeficiency virus infection has been implicated in the immune dysregulation in these patients, and it has been proposed that resistance to infection and/or progression to acquired immunodeficiency syndrome is dependent on a Th1 > Th2 dominance. Our data in experimental human models suggest that cell-mediated immune dysfunctions in human zinc deficiency may be due to an imbalance between Th1 and Th2 cell functions.

Prasad, A.S. Zinc in Human Health: Effect of Zinc on Immune Cells. Mol Med 14, 353–357 (2008). https://doi.org/10.2119/2008-00033.Prasad

Tewari M et al. (1995) Lymphoid expression and regulation of A20, an inhibitor of programmed cell death. J. Immunol. 154:1699–706.

How to find the magnification of a lensusinga

Virtual image produced by converging lens <--> M > 1, (image is larger than object) Virtual image produced by diverging lens <--> M < 1, (image is smaller than object)

The induction of NF-κB activation pathway appears to be cell specific and is counterbalanced by concomitant activation of NF-κB activation inhibitors. One such inhibitor of NF-κB activation is A20, a zinc finger-transactivating factor which also binds to DNA, producing the A20 protein which inhibits TNF-α-induced NF-κB activation (29–33). A20 plays an important role in reducing IL-1β- and TNF-α-induced NF-κB activation (29–33).

The role of zinc in regulation of the gene expression of IL-1β and TNF-α has not been defined. The zinc finger protein A20 has been shown to inhibit NF-κB signaling by TNF-α and IL-1β via TNF-receptor gene (TRAF pathways) in endothelial cells (31,35). A20 is expressed in various types of cells in response to a number of stimuli such as TNF-α, IL-1β, LPS (lipopolysaccharide), PMA, Epstein-Barr virus latent membrane protein, as well as other stimuli (32). A20 expression primarily protects cells from TNF-α-induced cytotoxicity by decreasing the activation of NF-κB, which leads to decreased IL-1β and TNF-α gene expression as has been demonstrated in endothelial cells. We propose that a similar effect of zinc supplementation on the A20 pathway occurs in primary cells. Further studies are ongoing in our laboratory to aid in the understanding the mechanisms of zinc action.

Magnificationformula Biology

A magnifying glass is a converging lens of focal length 15 cm.  At what distance from a postage stamp should you hold this lens to get a magnification of +2?

We have observed that, as a result of zinc deficiency, the macrophages-monocytes are stressed and they generate inflammatory cytokines such as TNF-α and IL-1β (14,34). In a recent study, we reported that, in comparison to the younger adults, the elderly subjects had lower plasma zinc, increased oxidative markers, and increased generation of inflammatory cytokines (14). Following zinc supplementation to the elderly subjects, the plasma zinc increased, oxidative stress markers decreased, and generation of inflammatory cytokine decreased, in comparison to the placebo group.

Shankar AH, Prasad AS. (1998) Zinc and immune function: the biological basis of altered resistance to infection. Am. J. Clin. Nutr. 68(suppl):447S–63S.

The focal length of a thin lens is related to the radii of curvature of its two surfaces. 1/f = (n2 - n1)(1/R1 - 1/R2).

Assume two thin converging lenses with focal length f1 and f2, respectively, are very close to each other, so we can neglect the distance between them. They focus the light of a distant star at a focal point a distance feff from the lenses.  Find feff in terms of f1 and f2.