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Patient 1. Patient 1 AG ; is the first child of unrelated parents; her sister died at 14 months from a recurrence of FHL patient no. 2 in Blanche et a17 ; , despite receiving an HLA-identical marrow transplant from the then healthy patient no. l . At 4.5 years of age, patient AG developed purpuric thrombocytopenia then fever, hepatomegaly, and pancytopenia and exhibited typical biologic manifestations of FHL including leukocytes in the CSF ; . Despite a transient remission obtained by chemotherapy etoposide, high dose intravenous MTX, cytoxan ; , systemic remission was not achieved. Clinical and biologic manifestations of the disease at this stage are described in Tables 1 through 3. Rabbit ATG 10 mg kg d, over 5 days ; and methylprednisolone 2 mg kg d ; were administered 19 days after the last course of chemotherapy and brought about complete remission of clinical and biologic signs within 7 days. Remission was maintained by treatment with low-dose 4 mg kg d ; CSA, prednisone 2 mg kg d ; , and I infusion of VP16 200 mg m2 wk ; izuresdue to CNS relapse occurred I months later, but remission was again obtained with MTX 8 g m2 intravenously ; . Parental HLA-mismatched T-cell-depleted marrow was infused, after a conditioning regimen comprising VP 16, busulfan, and cyclophosphamide but failed to take. A second attempt led to engraftment, although a mild graft-versus-host reaction occurred. The patient died with uncontrolled seizures at day 105. It was not possible to determine if the FHL had reoccurred Fig l ; . Patient 2. Patient 2 JN ; is the fourth child of unrelated parents of African origin; two siblingsdied with typical FHL manifestations at 18 and 19 months of age. Patient no. 2 developed FHL at 30 months of age, presenting with fever, edema, and hepatosplenomegaly, but without manifesta. Both normal and Sx male hamsters were obtained from Lakeview Hamster Colony, Newfield, N.J., and were used when they weighed 70 to 80 weeks old ; . Hamsters were inoculated subcutaneously sc ; over the back with 1, 000 PFU of virus in 0.2 ml of BA H. Heparinized plasma and organ suspensions were obtained from inoculated hamsters as described previously 5 ; . For platelet counts, heparinized blood was diluted 1: 100 with Unopettes no. 5855 ; and was counted in a hemocytometer with the use of a phase-contrast optical system. Tissues harvested for histopathological examination were fixed in neutral buffered Formalin and were stained with hematoxylin and eosin as described previously 4 ; . Pretreatment of hamsters with cyclophosphamide. Cyclophosphamide Cytoxna ; was obtained from Mead-Johnson, Evansville, Ind., and was diluted in sterile saline for injection to contain 7.5 mg ml. Hamsters weighing 70 to 80 were inoculated intraperitoneally with 7.5 mg in 1 ml, 16 h prior to, and simultaneously with, sc inoculation of virus. Pyridoxal-phosphate is the active form of vitamin B6 which comprises three natural organic compounds, pyridoxal, pyridoxamine and pyridoxine. The most important form of this active co-enzyme is pyridoxal-5-phosphate which has many different properties including, boosting the immune system, anti-convulsant effects, controlling diabetes, inhibiting cataracts, helping with skin disorders, protecting against some forms of cancer and atherosclerosis and helping to relieve premenstrual syndrome. Supplementation of Pyridoxal phosphate increases the production of dopamine, GABA, serotonin, norepinephrine and other neurotransmitters. It directly participates in carbohydrate and fat metabolism as well as producing red blood cells and antibodies to boost the immune system. This vitamin B6 is essential to controlling the amino acid absorption, metabolism and transformations that occur in your body, daily.

What kind of side effects can an OTC drug cause? Breathing problems, facial swelling, bleeding and hives require immediate medical attention. Other side effects range from minor problems such as headache and dry mouth to more worrisome complaints, including anxiety, sleeplessness, stomach pain, heartburn, constipation and dizziness. Call your healthcare provider right away if you develop problems. Who's at risk of side effects from OTC drugs? Anyone can experience unwanted side effects from OTC drugs, but those most at risk include older adults; people with chronic health problems; and people who take other prescription drugs or OTC medications, including herbal products. Children, pregnant women and sinemet. Less adhesive to vaginal cells, but the adherence differences in general did not appear to influence the outcome of the vaginal infection, as H12 and P were similarly adhesive but not equally vaginopathic. On the other hand, if the virulence of C. albicans is multifactoral, then one could predict requirements for adherence and proteinase production in influencing infectivity; i.e., P could adhere but not express SAP to the same level as do parent cells, while N lacked both determinants and, consequently, had the lowest vaginopathic capabilities. Of interest is our observation that all strains converted to a hyphal morphology; therefore, the avirulence of N could not be associated with an inability to undergo morphogenesis in the vaginal canal. Our data clearly indicate that both SAP1 and SAP2 are expressed early in the infection process by C. albicans 10261 and H12. Apparently, the two genes may be expressed less by strain P, with intermediate vaginal virulence, while the nonvaginopathic strain N ; did not express detectable levels of either gene, at any time examined. Northern analysis of RNA isolated from cells in the vaginal fluids of infected rats and hybridized with actin and proteinase probes showed strong positive reactions with transcripts similar in size to those reported in other studies 20, 43 ; . Moreover, the bands detected with RNA extracted from the vaginas of infected rats, after hybridization with each probe, were the same as those obtained with RNA isolated from C. albicans grown in vitro and induced with BSA. In contrast, the reactions with RNA extracted from noninduced in vitro cultures as well as from vaginal fluids of noninfected rats were negative with all probes. Thus, on the basis of the transcript size and the specificity of induction, the Northern analysis confirmed that the proteinase messages were indeed expressed during infection. As precise quantitation of SAP1 and SAP2 mRNA was not done in this study, no conclusions can be drawn from different intensities of the signals in the dot blot reaction. Nonetheless, the data indicate that transcripts of both genes tends to disappear with clearance of the organism from the vagina. Also, SAP1 expression by P seems to decrease prior to SAP2 expression, and this seems to occur well before the elimination of C. albicans from the vagina. It is not clear whether the lack of expression of either SAP by the nonvaginopathic N ; mutant is a cause or a consequence of decreased vaginal counts. Apparently, proteinase genes are no longer expressed after the first week postinfection, even when the highly vaginopathic strains are cleared from the vagina. It might be relevant, however, that no proteinase expression by the low vaginopathic N cells was detected even at day 1 postinfection when the cell burden and actin message ; was apparently the same as the burden in those vaginopathic strains P and H12 ; expressing elevated levels of proteinase. The interpretation of our findings needs to be weighed with our observation that strain N produces proteinase to some extent in vitro, although in an amount less than the amounts produced by strains 10621, H12, and P. This strain might express another gene among the SAP family not revealed by the SAP probes used in this study. If so, those SAP genes may or may not be relevant to vaginal infection. Our data demonstrate that the 43- to 44-kDa protein, which displays proteinase activity and has been identified serologically in experimental vaginitis 9, 10, 34, ; , is probably the result of at least ; two SAP genes. Our results make it very feasible to study the expression of null SAP1 or SAP2 mutants in a model of infection in which aspartyl proteinase is likely to play a role in disease development.

WHAT IT DOES This drug has many uses as a chemotherapy agent. It is given in pill form for many days in a row or by intravenous injection once every few weeks. Cytoxan is usually used with other drugs. It prevents or kills cancer cells by interfering with cell production and growth. It affects normal cells along with cancer cells and produces some side effects. The normal cells most affected are cells in the mouth, intestines, stomach, and hair follicles. REMEMBER Not everyone experiences side effects. If they do occur, there are medications ordered to prevent discomfort, as well as comfort measures to alleviate side effects. Below are listed some side effects and ways to treat them. 1. This drug may cause irritation in the bladder and cause burning and stinging if not enough fluid is flushed through the bladder. To prevent this, drink lots of fluids prior to treatment and drink 2 to 3 quarts of fluids the day of treatment and maybe the day after. Empty your bladder often and especially before retiring to bed. If you are taking the pills, take them in the morning or during the day with copious amounts of fluids. 2. Usually, more nausea occurs with the treatment in the vein than with the pills. Nausea medication is ordered and should be taken if needed. 3. This drug causes variable loss of hair. Some patients notice only that there is more hair on their hairbrush, and some have no noticeable change. Some patients have enough hair loss to require a wig. Your hair will regrow after the medication is stopped. 4. Cytoxan will frequently cause some menstrual changes and irregularities. You may even stop having periods during treatment. They may or may not return after the drug is stopped. The drug may cause sterility in men; however, it does not decrease sex drive. It is important to practice some type of birth control for child-bearing age women, even though periods cease. 5. You are more prone to infection while taking this drug. Avoid large crowds and those with known infections and fevers. Keep your body clean to prevent bacteria growth. 6. Occasionally, patients complain of a metallic taste while receiving this drug. Suck on hard candy to prevent this if it occurs. 7. On rare occasions, leukemia may develop years after treatment. 8. If you experience flushing, headaches, dizziness, or begin to sweat profusely while getting the medication, notify your nurse or doctor. Usually, the symptoms will disappear when the rate of infusion is slowed and methotrexate. DESCRIPTION CYTOXAN cyclophosphamide for injection, USP ; is a sterile white powder containing cyclophosphamide monohydrate. CYTOXAN Tablets cyclophosphamide tablets, USP ; are for oral use and contain 25 mg or 50 mg cyclophosphamide anhydrous ; . Inactive ingredients in CYTOXAN Tablets are: acacia, FD&C Blue No. 1, D&C Yellow No. 10 Aluminum Lake, lactose, magnesium stearate, starch, stearic acid, and talc. Cyclophosphamide is a synthetic antineoplastic drug chemically related to the nitrogen mustards. Cyclophosphamide is a white crystalline powder with the molecular formula C7H15Cl2N2O2PH2O and a molecular weight of 279.1. The chemical name for cyclophosphamide is 2-[bis 2-chloroethyl ; amino]tetrahydro-2H-1, 3, 2-oxazaphosphorine 2-oxide monohydrate. Cyclophosphamide is soluble in water, saline, or ethanol and has the following structural formula. FIG. 2. PAF or IL-1 do not modify TFIID-DNA binding. EMSA using NPXTs derived from HEK cells and the mutant and consensus sequence for the basal transcription factor TFIID. Arrow depicts unique TFIID-shifted complex 34, 45 ; used for signal quantitation in the bar graph shown below. A 60-fold excess of unlabeled TFIID consensus sequence ``cold'' competition assay ; almost completely eliminated TFIID gel shift. Rabbit polyclonal antibody specific for human TFIID was used in the gel supershift assay. Exposure time 36 hr. n 4; mean SD; significance of PAF- or IL-1 -induced TFIID factor over control, P 0.68 and albendazole. ' 21 U.S.C. 0 3550' ; 7 ; C 21 C.F.R. Q 314.122 c ; . ' C.F.R. 9 314.3. 9 Determinartion That Cytoxan Cyclophosphamide for Injection ; , 2 Gram Vials NDA 12-142 054 ; , Was Not Withdrawn From Sale for Reasons of Safety or Effectiveness, 69 Fed. Reg. 9630 Mar. 1, 2004. Discussed below. Lastly, environmental factors can alter HDL concentration, decreasing in men, and with obesity, sedentarity, smoking, androgenous treatment, etc. Lipoprotein a ; [Lp a ; ] is lipoprotein which is similar to LDL in size and composition but which carries a particular apoprotein, protein a ; , characterized by its great homology with plasminogen. Its atherogenous role has been established. Its plasma concentration normally depends only on genetic factors, as reflected by the correlation between blood values and protein a ; isomorphs and strattera. The data obtained with this preparation indicate that tachykinins constrict the resistance vessels of the rat stomach, as demonstrated by a concentration-dependent increase in the vascular perfusion pressure, and that the receptors by which NKA causes vasoconstriction are different from those by which the peptide gives rise to gastric contraction. A further level of complexity is added by the finding that the receptor pharmacology of the NKA-evoked vasoconstriction is at variance with the tachykinin receptor distribution characterized with receptor-selective agonists. The potency rank order BANKA NKA SP SPOME senktide ; with which various tachykinin receptor agonists contract the gastric vasculature suggests that the major type of tachykinin receptor present on the vasculature is the NK2 receptor. This conjecture has been corroborated by the high efficacy of BANKA and NKA as compared to that of SPOME and senktide and by the ability of two NK2 antagonists, MEN-10, 627 Maggi et al., 1994 ; and GR-94, 800 McElroy et al., 1992 ; , to suppress the response to BANKA. Whether the small vasoconstrictor effects of SPOME and senktide are also mediated by NK2 receptors is not possible to deduce from the present data. However, it need be assumed that in the rat gastric vasculature SPOME and senktide are not selective NK1 and NK3 receptor agonists, because they were not antagonized by SR140, 333 and PD-161, 182, respectively. The similar potency and efficacy of BANKA and NKA in constricting the gastric vasculature predicts that NK2 receptors mediate the action of either agonist. However, this surmise was not confirmed by pharmacological analysis of the vasoconstrictor responses to NKA and SP. Neither NK2 nor NK1 or NK3 receptor antagonists inhibited the action of the two naturally occurring tachykinins to any substantial degree. Further experiments revealed that combinations of NK1 and NK2 or NK1 and NK3 antagonists were similarly ineffective whereas a mixture of NK2 and NK3 antagonists caused a partial inhibition of the NKA effect. In contrast, combined administration of NK1, NK2 and NK3 receptor antagonists abolished the NKA-evoked vasoconstriction. Although these results cannot be conclusively explained, they represent a novel trait in tachykinin receptor pharmacology. The differential inhibition of the vasoconstrictor effects of BANKA and NKA by various tachykinin receptor antagonists or combinations thereof is subject to more than one way of interpretation. Given that no evidence for the presence of vascular NK1 and NK3 receptors was found with the use of receptor-selective agonists and antagonists, the possibility of NK1, NK2 and NK3 receptors synergizing in the vasoconstrictor action of NKA can be dismissed. Whether the vasoconstrictor tachykinin receptor operated by NKA is a subtype of a NK2 receptor that is distinct from the NK2 receptor on the gastric musculature will not be possible to find out without molecular pharmacological techniques. It is conceivable in this context that BANKA and NKA interact with different binding and or transduction epitopes Maggi, 1995; Schwartz et al., 1995 ; on a common receptor that gives rise to vasoconstriction. If so, the existence of binding domains for NK1, NK2 and NK3 receptor antagonists on the vascular tachykinin receptor operated by NKA has to be assumed. Together with the surmise that BANKA and NKA bind to different sites on the receptor molecule, a differential allosteric interaction between the antagonist binding domains and the BANKA and NKA binding epitopes.

Iii. Eucerin and Moisturel are good lotions because they are both hypoallergenic. Tips for treatment of fingertip ulcers? i. Anything that can improve blood flow is helpful. ii. Nitroglycerin ointments may be helpful. They should be absorbed helpful to put on wrists ; and can be used to preventively control Raynauds. iii. The ointment may cause a rapid drop in blood pressure and some people may not tolerate this well. iv. Bocentin also can help to prevent new ulcers and pulmonary hypertension. Raynauds Calcium Channel Blockers? i. Dosage may be varied depending on the season. Patients react differently. ii. Nitro ointment can be taken if taken with calcium channel blockers. It does not have to be used everyday. iii. More often a patient has episodes of Raynauds, the effects can become cumulative. More episodes cause more damage to skin and blood vessels. Controlling Raynauds is important. iv. Raynauds typically affects extremities: ears, nose, toes, and fingers. v. Nitro ointment may be helpful e.g., for ear affected by Raynauds, try to put some nitro ointment behind the ear ; . vi. If the ulcer is infected, use topical antibiotics. vii. Patients that have primary Raynauds without scleroderma ; blood vessels look normal. Raynauds patients with Scleroderma have smaller blood vessels lining has narrowed thickened ; . New Developments in the Treatment of Lungs Impacted by Scleroderma? i. Steroids ii. Cytoxan is the standard of care iii. Biological agents are being tested. TNF agents are being studied. iv. There are currently no new FDA approved drugs. Impact of Stress on Scleroderma? i. Not certain, however most illnesses do worsen when the patient is under stress. ii. The central nervous system has adrenal glands. For certain people, stress may bring on a certain conditions because of a subtle abnormality in pituitary adrenal gland. Advice Regarding Having Kids? i. Need to talk to your rheumatologist. Patients with scleroderma can have more problems than others during pregnancy. ii. Very unusual for scleroderma to run in families. However, autoimmune diseases can be transferred among family members. Recommendations on Doctors that should be seen? and aricept. AMAC, Inc., Westbrook, ME ; . Cellswere analyzedby flow cytometry FACS| IV; Becton Dickinson & Co., Mountain View, CA ; . Propidium iodide was added to exclude dead cells. Histology. Pancreataand submandibuhr glands were either fixed in buffered 10% formalin and processed for paraffin embedding or were frozen in isopentane cooled with liquid nitrogen. Paraffin sections 5 t~ ; obtained from three noncontiguous tissue levelswere stained with hematoxylin and eosin and examined for evidence of histological abnormalities. The phenotypic composition of the infiltrating lymphocytes observed in frozen sections 5 t~ ; was determined by immunoperoxidase histochemistry using biotinylated mAbs spedfic for the call surface antigens Thy 1.2 and B220, as previously described 10 ; . Deteaion of AutoantibodiesRecognizing the ~lar Antigen. Cryostat sections 5 I * ; of the transphntable rat insulinoma tumor RINm38 grown in New England Deaconess Hospital rats were fixed in acetone for 10 rain at 20~ followed by absolute methanol for 10 rain at 20~ and then air-dried. Fixed sections were rehydrated in 0.05 M Tris buffer pH 7.4 ; containing 0.9% saline Tris-saline ; for 20 rain at 20~ and then incubated for 1 h at 20~ with 30 ~1 of serum diluted 1: 5 in Tris-saline containing 1% BSA. Tissue sections were washed three times with Tris-salinebuffer for a total of 10 rain at 20~ and incubated for 1 h at 20~ with peroxidase conjugated protein A Boehringer Mannheim Biochemicals, Indianapolis, IN ; diluted 1: 100 in Tris-salinebuffer. Antibody binding was developed colorimetrically by the addition of diaminobenzidine tetrachloride 0.5 mg ml ; Sigma Chemical Co., St. Louis, MO ; dissolved in Tris-saline buffer containing 0.001% hydrogen peroxide. After washing, the slideswere mounted with AFT systems mounting medium Behring Diagnostics, La Jolla, CA ; . CFlophosphamide Treatment. Cytoxan cyclophosphamidefor injection, USP ; was purchasedand prepared accordingto the manufacturer's instructions MeadJohnson Oncology Products, Evansville, IN ; . Lyophilizedcytoxan was prepared for use immediately before injection by adding sterile distilled water for a final concentration of 20 mg ml. Mice received 200 mg kg by intraperitoneal injection on days0 and 14. All mice were nondiabetic before treatment, and diabetes was monitored on a weekly basis up to day 28 after the first injection. Results.
References 1. Markovic-Plese S, Pinilla C, Martin R. The initiation of the autoimmune response in multiple sclerosis. Clin Neurol Neurosurg. 2004; 106: 218-222. Grigoriadis N, Ben-Hur T, Karussis D, Milonas I. Axonal damage in multiple sclerosis: a complex issue in a complex disease. Clin Neurol Neurosurg. 2004; 106: 211-217. Noseworthy JH, Lucchinetti C, Rodriguez M, Weinshenker BG. Multiple sclerosis. N Engl J Med. 2000; 343: 938-952. O'Connor P; Multiple Sclerosis Working Group. Key issues in the diagnosis and treatment of multiple sclerosis. An overview. Neurology. 2002; 59 suppl 3 ; : S1-33. 5. Jacobs LD, Cookfair DL, Rudick RA, et al. Intramuscular interferon beta-1a for disease progression in relapsing multiple sclerosis. The Multiple Sclerosis Collaborative Research Group MSCRG ; . Ann Neurol. 1996; 39: 285-294. The IFNB Multiple Sclerosis Study Group. Interferon beta-1b is effective in relapsingremitting multiple sclerosis. I. Clinical results of a multicenter, randomized, double-blind, placebo-controlled trial. Neurology. 1993; 43: 655-661. PRISMS Prevention of Relapses and Disability by Interferon beta-1a Subcutaneously in Multiple Sclerosis ; Study Group. Randomised double-blind placebo-controlled study of interferon beta-1a in relapsing remitting multiple sclerosis. Lancet. 1998; 352: 1498-1504. Johnson KP, Brooks BR, Cohen JA, et al. Copolymer 1 reduces relapse rate and improves disability in relapsing-remitting multiple sclerosis: results of a phase III multicenter, double-blind placebo-controlled trial. The Copolymer 1 Multiple Sclerosis Study Group. Neurology. 1995; 45: 1268-1276. Copaxone [package insert]. Kansas City, Mo: Aventis Pharmaceuticals Inc.; 2002. 10. Rebif [package insert]. Rockland, Mass: Serono Inc. and New York, NY: Pfizer Inc; 2004. 11. Fischer JS, Priore RL, Jacobs LD, et al. Neuropsychological effects of interferon beta-1a in relapsing multiple sclerosis. Multiple Sclerosis Collaborative Research Group. Ann Neurol. 2000; 48: 885-892. Barak Y and Achiron A. Effect of interferon-beta-1b on cognitive functions in multiple sclerosis. Eur Neurol. 2002; 47: 11-14. Weinstein A, Schwid SR, Schiffer RB, et al. Neuropsychologic status in multiple sclerosis after treatment with glatiramer. Arch Neurol. 1999; 56: 319-324. Billiau A, Kieseier BC, Hartung HP. Biologic role of interferon beta in multiple sclerosis. J Neurol. 2004; 251 suppl 2 ; : II10-14. 15. Vartanian T. An examination of the results of the EVIDENCE, INCOMIN, and phase III studies of interferon beta products in the treatment of multiple sclerosis. Clin Ther. 2003; 25: 105-118. Limmroth V, Malessa R, Kalski G. A comparison of the efficacy and tolerability of interferon beta IFN ; products used as initial or follow-up therapy for the treatment of relapsing multiple sclerosis: results from the QUASIMS study. Paper presented at: American Academy of Neurology 56th Annual Meeting; April 24-May 1, 2004; San Francisco, Calif. 17. Limmroth V, Werneck L, Nagels G, et al. Results from the global QUASIMS study: comparison of the efficacy and tolerability of interferon beta IFN ; products for the treatment of relapsing multiple sclerosis in Australia, Brasil, Belgium, Italy and Slovakia. Poster presented at: American Academy of Neurology 57th Annual Meeting; April 14, 2005; Miami, Fla. 18. Betaseron [package insert]. Montville, NJ: Berlex Laboratories; 2003. 19. Avonex [package insert]. Cambridge, Mass: Biogen, Inc.; 2003. 20. Francis GS, Grumser Y, Alteri E, et al. Hepatic reactions during treatment of multiple sclerosis with interferon-beta-1a: incidence and clinical significance. Drug Saf. 2003; 26: 815-827. Galetta SL, Markowitz C. US FDA-approved disease-modifying treatments for multiple sclerosis: review of adverse effect profiles. CNS Drugs. 2005; 19: 239-252. Bertolotto A, Deisenhammer F, Gallo P, Solberg Sorensen P. Immunogenicity of interferon beta: differences among products. J Neurol. 2004; 251 suppl 2 ; : II15-II24. 23. Sorensen PS, Ross C, Clemmesen KM, et al. Clinical importance of neutralising antibodies against interferon beta in patients with relapsing-remitting multiple sclerosis. Lancet. 2003; 362: 1184-1191. Malucchi S, Sala A, Gilli F, et al. Neutralizing antibodies reduce the efficacy of betaIFN during treatment of multiple sclerosis. Neurology. 2004; 62: 2031-2037. Hafler DA. Multiple sclerosis. J Clin Invest. 2004; 113: 788-794. Arnon R, Aharoni R. Mechanism of action of glatiramer acetate in multiple sclerosis and its potential for the development of new applications. Proc Natl Acad Sci U S A. 2004; 101 suppl 2 ; : 14593-14598. 27. Frohman E, Phillips T, Kokel K, et al. Disease-modifying therapy in multiple sclerosis: strategies for optimizing management. Neurologist. 2002; 8: 227-236. Scott TF, Schramke CJ, Novero J, Chieffe C. Short-term prognosis in early relapsing-remitting multiple sclerosis. Neurology. 2000; 55: 689-693. Data on file; Biogen Idec. 30. Teva Marion Partners. Annual Meeting of the Consortium of Multiple Sclerosis Centers; June 22-25, 2000; Halifax, Nova Scotia, Canada. 31. Clanet M, Kappos L, Hartung HP, Hohlfeld R; European IFN beta-1a Dose-Comparison Study Investigators. Interferon beta-1a in relapsing multiple sclerosis: four-year extension of the European IFNbeta-1a Dose-Comparison Study. Mult Scler. 2004; 10: 139-144. Ghalie RG, Edan G, Laurent M, et al. Cardiac adverse effects associated with mitoxantrone Novantrone ; therapy in patients with MS. Neurology. 2002; 59: 909-913. Hartung HP, Gonsette R, Konig N, et al, for the mitoxantrone in Multiple Sclerosis Study Group MIMS ; . Mitoxantrone in progressive multiple sclerosis: a placebo-controlled, double-blind, randomised, multicentre trial. Lancet. 2002; 360: 2018-2025. Solu-Medrol [package insert]. Kalamazoo, Mich: Pharmacia Corporation; 2001. 35. Trexall [package insert]. Pomona, NY: Barr Laboratories, Inc.; 2002. 36. Imuran [package insert]. San Diego, Calif: Prometheus Laboratories Inc.; 2004. 37. Cytoxan [package insert]. Princeton, NJ: Bristol-Myers Squibb Company; 2000. 38. CellCept [package insert]. Nutley, NJ: Roche Laboratories, Inc.; 2004. 39. Lobb RR, Hemler ME. The pathophysiologic role of alpha 4 integrins in vivo. J Clin Invest. 1994; 94: 1722-1728. Engelhardt B, Laschinger M, Schulz M, Samulowitz U, Vestweber D, Hoch G. The development of experimental autoimmune encephalomyelitis in the mouse requires alpha4-integrin but not alpha4beta7-integrin. J Clin Invest. 1998; 102: 2096-2105. Kent SJ, Karlik SJ, Cannon C, et al. A monoclonal antibody to alpha 4 integrin suppresses and reverses active experimental allergic encephalomyelitis. J Neuroimmunol. 1995; 58: 1-10. Makhlouf K, Weiner HL, Khoury SJ. Potential of beta2-adrenoceptor agonists as add-on therapy for multiple sclerosis: focus on salbutamol albuterol ; . CNS Drugs. 2002; 16: 1-8. Vastag B. Not so fast: research on infectious links to MS questioned. JAMA. 2001; 285: 279-281. Penkowa M, Hidalgo J. Metallothionein treatment reduces proinflammatory cytokines IL-6 and TNF-alpha and apoptotic cell death during experimental autoimmune encephalomyelitis EAE ; . Exp Neurol. 2001; 170: 1-14. Leussink VI, Jung S, Merschdorf U, Toyka KV, Gold R. High-dose methylprednisolone therapy in multiple sclerosis induces apoptosis in peripheral blood leukocytes. Arch Neurol. 2001; 58: 91-97. Conclusions: Findings suggest that women reported more health and mental health complications and more service use than men. This study supports the need to treat health and mental health issues among substance abusers. Specifically, treatment should focus on specific needs and be differentially tailored to women and men. Implications for Policy, Delivery or Practice: Implications for correctional and community health and mental health care, and increasing access to services for substance abusers will be discussed. Primary Funding Source: RO1-DA 13076. 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