Cause Of Glaucoma

Correspondence may include articles which have only just been published in the print journals. However, a question remains to be answered: Is the number of downloads a reliable measure of research quality? In order to find an answer to this question, firstly, we took TOP25 Hottest Articles of December 2006 in ‘‘Journal of Chromatography A’’, as the first set. Similarly, another set consisted of 25 articles were selected as the non-Hottest, each of which was corresponded to the members of the first set. All these have become available online at different months of 2006. There is a possibility that investigators judged based on the number of citations. Consequently, some authors may try to self-cite to promote a scholarly reputation [1]. To avoid the influence of self-citation in the evaluation of the articles, citation of each article (also available at ScienceDirect alerting service) were considered and cases of self-citation were not involving in research evaluation process. Analysis of the data was performed by using independent samples t-test to compare the mean frequencies of citations of two distinct groups of articles. The results of statistical test (t-test) revealed that citation means frequencies (1.52 for Hottest and 0.76 for non-Hottest article groups) showed

459 significant difference (2.212 of t-value) between two groups, (p-value = 0.015). Positive t-value result means that more citations have been done to Hottest Articles at the same period, compared to the non-Hottest group. In conclusion, our investigation showed that more downloads at a limited period of time is an indicator of more citations to the article in a long-term interval.

Reference [1] Daya S. Self-citation and the journal impact factor. Evidence-based. Obstet Gynecol 2004;6:159–60.

Samad Jahandideh * Parviz Abdolmaleki Ebrahim Barzegari Asadabadi Department of Biophysics, Faculty of Science, Tarbiat Modares University, P.O. Box 14115/175, Tehran, Iran * Tel.: +98 21 88950325. E-mail address: [email protected] (S. Jahandideh).

doi:10.1016/j.mehy.2007.01.007

What is the real cause of glaucoma? Glaucoma can be defined as an optic nerve disease with typical morphological and functional changes [1]. There are many risk factors associated with this neuropathy such as central corneal thickness (CCT), age, race, sex, intraocular pressure (IOP), optic nerve changes, refractive error, systemic diseases, family history and trauma [2]. There are many observations, which can hardly be explained by direct effect of increasing IOP. One of them is that as many as 1/6 of the patients with glaucomatous damage do not have increased IOP even with repeated testing. Also, Ocular hypertension is 10 times more common than glaucomatous neuropathy. Another conflict is that the presence and the progression of glaucomatous damage are weakly related to the level of IOP [1]. These conflicts led us to find another factor more than IOP to describe development of glaucoma. CCT and scleral thickness have a moderately

positive correlation [2]. So, we use scleral thickness instead of CCT below. The incidence of glaucomatous damage in the same IOP conditions varies between different races and sexes [1] therefore, scleral thickness and internal radius of the eye globe which also depend on race and sex [3,4] can be considered as the factors that are responsible for glaucoma in theses conditions. In the eye globe as an idealized spherical shell, stress depends on IOP, inner radius of the eye globe, and scleral thickness [5]. Therefore, in contrast to old theories, which consider direct effect of increased IOP as leading cause of glaucoma, stress is the main responsible factor for glaucomatous damage and increasing IOP acts just as one of the determinant factors of glaucoma. Stress can develop glaucomatous damage in two ways: stress directly obstruct the retinal vessels and develop glaucoma by ischemic damage.

460 Also, stress by inducing strain (tissue deformation in response to load) can deform and interrupt the retinal layers, which end in glaucoma too. In conclusion, a series of factors together determine whether an individual will be affected with glaucoma or not. These factors include IOP, scleral thickness, radius of the eye globe, and optic nerve head compliance against increased stress. These factors differ between different individuals. So risk of glaucoma is different between them. Our hypothesis explains the existence of normal-pressure (tension) glaucoma. It presents a better method for screening of glaucoma and new modalities for glaucoma treatment.

References [1] Flammer J, Orgu ¨l S. Optic nerve blood-flow abnormalities in glaucoma. Prog Retin Eye Res 1998;17:267–89. [2] Mehdizadeh AR, Hoseinzadeh A, Fazelzadeh A. Central corneal thickness as a risk factor for glaucoma. Med Hypotheses [in press].

Correspondence [3] Aghaian E, Choe JE, Lin S, Stamper RL. Central corneal thickness of Caucasians, Chinese, Hispanics, Filipinos, African Americans, and Japanese in a glaucoma clinic. Ophthalmology 2004;111:2211–9. [4] Hahn S, Azen S, Ying-Lai M, Varma R, et al. Central corneal thickness in Latinos. Invest Ophthalmol Vis Sci 2003;44: 1508–12. [5] Bellezza AJ, Hart RT, Burgoyne CF. The optic nerve head as a biomechanical structure: initial finite element modeling. Invest Ophthalmol Vis Sci 2000;41:2991– 3000.

Ali Reza Mehdizadeh * Amin Hoseinzadeh Afsoon Fazelzadeh Department of Medical Physics, School of Medicine, Mashad University of Medical Sciences, Mashad, Iran * Tel.: +98 9155103108. E-mail address: [email protected] (A.R. Mehdizadeh).

doi:10.1016/j.mehy.2007.01.004

Innate immune system: Specific or non-specific? Mammalian immune system has two arms: adaptive and innate. Adaptive immunity consists of T and B cells. Innate immune system includes more cells: natural killer (NK) cell, dendritic cell (DC), macrophage and neutrophil. Since 15 years ago, some receptors have been found in innate immune system such as toll-like receptors (TLRs) [1], nucleotide-binding oligomerization domains (NODs) [2] and C-type lectins (e.g. DC-SIGN) [3] which are named pattern-recognition receptors (PRRs) and detect specific molecules of pathogens that are called pathogen-associated molecular patterns (PAMPs). Thirteen members of TLRs, as the main PRRs, have been characterized which recognize different PAMPs and modulate immune response in different ways. To compare the properties of TLRs, with TCRs and immunoglobulins, we mention the following similarities along with some evidence. TLR4 recognizes typical lipopolysaccharide (LPS) of E. coli but atypical LPS produced by Porphyromonas gingivalis is recognized by TLR2 [4]. So, different variants of the same PAMP can be recognized by different TLR molecules and consequently distinct responses are elicited while TCRs and immunoglobulins can distinguish between epi-

topes which differ in even one amino acid. Combination of different TLR’s can result in new specificity for a new ligand. For example, combination of TLR1 and TLR2 (TLR1/2) identifies a synthetic bacterial lipopeptide, PAM3CSK4 whereas TLR2/6 recognize a synthetic mycoplasmal lipopeptide, MALP-2. PAM3CSK4 contains triacylated cysteinyl residue at the N-terminus, whereas the cysteinyl residue in MALP-2 is only diacylated [5]. Immunoglobulines, also use the same approach for creating diversity. Light chains and heavy chains of different antibodies (with different specificities) may combine and recognize a new antigen. Recently, it has been shown that TLR3, TLR7 and TLR9 which recognize nucleic acids are localized to intracellular compartments. The purpose of intracellular localization is not clear but there are some data demonstrating that intracellular localization of TLR9 is not required for ligand recognition; instead, is critical in discriminating between self and non-self nucleic acid [6]. Negative selection in adaptive immune system leads in deletion of T and B cells which can identify endogenous proteins. Recently, a profilin-like protein was found in Toxoplasma gondii, as TLR11 ligand [7].