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In 2006, the Group continued implementation of its HSE policy, focusing on five key objectives: to guarantee the safety of facilities and the environments in which they operate; to safeguard and preserve the health of employees; to ensure safety by preventing risks that could lead to work-related accidents; to conserve natural resources through the use of clean, safe processes; to protect the environment. ACHIEVING BETTER CONTROL OF RISKS THROUGH BETTER UNDERSTANDING In 2006, in the context of its industrial hygiene program, sanofi-aventis inaugurated a Central Industrial Hygiene Laboratory. Located in France, the laboratory has been functioning since January 15th 2006. The analytical capacities of this state-of-the-art facility make it possible to quantify individual employee exposures to chemical agents and to certify control of monitoring of Group installations, industrial processes and laboratory activities. 2006 also witnessed reinforcement of the internal HSE audit procedure. Vaccine manufacturing facilities, R&D sites and Group industrial sites are audited at least every three years, to asses conformity with sanofi-aventis policy and standards. In 2006, 41 internal HSE audits were performed. Finally during 2006, the Group continued to introduce tools to facilitate collection and analysis of HSE information from all its sites worldwide. These tools include the database GREEN, permitting regular consolidation of environmental data from all the sites of the Group, and MSRS, enabling the collection of data on work-related accidents involving the Group's employees, temporary workers and external contractors.
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Apoptotic process in chondrocytes and other connective tissue cells in osteoarthritis OA ; The activity of nitric oxide synthases NOS ; and the subsequent production of nitric oxide NO ; and peroxynitrite ONOO ; from combination of NO with hydroxyl OH ; radicals; these reactive oxygen species ROS ; being key mediators of the cellular destructive and inflammatory events in inflammation. The activation of glucocorticoid receptors leading to increased cellular activity of endogenous glucocorticoids is a potentially novel action of nimesulide that is not reported with other NSAIDs. The ability of nimesulide to affect so many mediators involved in the inflammatory process provides it with the rather unique role of a multi-acting drug in different pathological conditions8, 9 and nolvadex.
Isoenzyme, Ketek has the potential for many drug interactions. It can increase the serum concentrations of midazolam Versed ; , ergot alkaloids, ritonavir Norvir ; , sirolimus Rapamune ; , and tacrolimus Prograf ; . This antibiotic can also cause increased serum levels of metoprolol and digoxin. In addition, itraconazole Sporanox ; and ketoconazole Nzoral ; inhibit metabolism of telethromycin, therefore causing an increase in serum concentrations of telithromycin. Other drugs that affect the metabolism of Ketek include metabolic inducers such as rifampin, carbamazepine, and phenytoin. The combination of rifampin and telithromycin should be avoided. Co-administration of theophylline Theodur ; and telithromycin may increase the adverse GI effects of telithromycin, therefore, these medications should be taken at least one hour apart. The serum concentration and absorption of sotalol Betapace ; are decreased when used with telithromycin.1, 2 The use of Ketek is contraindicated in patients with an allergy to macrolides. Ketek should be used with caution when administered with other drugs that cause a prolongation of the QT interval. In addition, Ketek should be avoided in patients with myasthenia gravis due to the potential for lifethreatening respiratory failure.1, 2 Ketek is available as a 400 mg tablet. The recommended dose is 800 mg once daily for 7 to 10 days for CAP and 5 days for AECB or ABS. Dosing in patients with severe renal insufficiency has not been established, and there is no dosage adjustment required in patients with hepatic insufficiency. 1, 2 Patients should be advised about possible visual disturbances that may occur while on telithromycin therapy, and should contact their physician if these disturbances disrupt daily functions. Patients should also be informed to take two 400 mg tablets at the same time, and not to divide the dosing during the day. Finally, patients who are currently taking atorvastatin.
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Work has yet been done on preterm babies, but logically it will be of even more benefit. Another intervention that is very important for the developing world is kangaroo care, or skin-to-skin contact. More studies are needed to evaluate the effect on immediate temperature control of small infants, as there is only a single non-blinded study of 51 infants, all weighing more than 2.5kg, showing benefit. There are no studies showing safety for small preterm infants in the delivery room, especially if resuscitation is required. Skin-to-skin contact should be seen as a way of reducing heat loss, and should be promoted in stable infants as soon as possible after birth. A small study has also shown a number needed to treat NNT ; of only two. Timing of cord clamping Early vs delayed cord clamping is another potentially life-saving measure for the developing world. Early cord clamping is defined as clamping of the cord within 10-30 seconds, whereas late clamping is anytime after 30 seconds, up to when cord pulsations cease. In practice, the infant should be at the level of the placenta, for at least 30-120 seconds. In preterm infants, half of the circulating blood volume is in the placenta, whereas one-third is in the placenta of the term foetus. Immediate cord clamping can deprive the infant of up to 25% of the circulating blood volume; this is exacerbated if the infant has not yet taken a spontaneous breath. Term infants do not really experience any negative effects due to early cord clamping, but preterm infants can be more vulnerable. Delayed cord clamping can be very valuable to reduce the immediate complications of prematurity, and also to prevent long-term complications of any infant in the developing world. It has been well proven that premature infants are more stable after birth, with a higher and more stable blood pressure, less intraventricular haemorrhage, less necrotising enterocolitis, less retinopathy of prematurity and less sepsis. There were no significant complications from delayed cord clamping, like jaundice and polycythemia. In a setting where blood transfusion is never a safe proposition, ensuring a higher circulating blood volume at birth may reduce the need for later transfusions, especially in preterm infants, with a reduced incidence of anaemia of prematurity. Fewer interventions may mean better outcomes. Term infants have less immediate benefit from delayed cord clamping, and are also not compromised acutely by early cord clamping, but may have benefit in the long term. In a region where there is a high prevalence of anaemia, maternal iron deficiency, and malnutrition, infants who had delayed cord clamping, are less likely to have iron deficiency anaemia, and by implication will have better neurodevelopmental outcomes. Continued on page 2.
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Skin Exposure: Remove contaminated shoes and clothing and cleanse affected area s ; thoroughly by washing with mild soap and water. If irritation or redness develops and persists, seek medical attention. Eye Exposure: If irritation or redness develops, move victim away from exposure and into fresh air. Flush eyes with clean water and seek medical attention. For direct contact, hold eyelids apart and flush the affected eye s ; with clean water for at least 15 minutes. Seek medical attention, for instance, nizorao sampon.
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1. Debbia EA, GC Shito, A Pesce, A Marchese. 1999. Epidemiology of resistance to antimicrobial drugs in the major respiratory pathogens circulating in Europe. Infection 27 suppl 2 ; : S9-12. 2. Felmingham D, RN Gruneberg. 2000. The Alexander Project 1996-1997: latest susceptibility data from this international study of bacterial pathogens from community-acquired lower respiratory tract infections. J Antimicrob Chemother 45: 191-203. 3. Brueggemann AB, GV Doern, HK Huynh, EM Wingert, PR Rhomberg. 2000. In vitro activity of ABT-773, a new ketolide, against recent clinical isolates of Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Antimicrob Agents Chemother 44: 447-449. 4. NCCLS. 2001. Methods for dilution antimicrobial susceptibility tests for bacteria that grow aerobically; Approved Standard M7-A5 and M100-S11. National Committee for Clinical Laboratory Standards, Wayne, PA 19087. 5. Stone G, A Nilius, D Hensey-Rudloff, L Almer, J Beyer, R Flamm. Development of tentative interpretive criteria for ABT-773, a novel ketolide antibacterial agent. Abstracts of the 40th Interscience Conference on Antimicrobial Agents and Chemotherapy. Toronto, Ontario, Canada, September 17-20, 2000, Abstract No. 2164. 6. Reinert RR, A Al-Laham, HM Schorn, J Bungenstab, R Ltticken. 2000. Antibiotic resistance of S. pyogenes and S. pneumoniae strains isolated from infections of outpatients in Germany, 1999 2000. 40th Interscience Conference on Antimicrobial Agents and Chemotherapy ICAAC ; , Toronto, Canada, 17-20 September 2000. 7. Kresken M, D Haffner, Study Group. 2000. Resistenzsituation bei klinisch wichtigen Infektionserregern gegenber Chemotherapeutika in Mitteleuropa. Ergebnisse einer multizentrischen Studie der Arbeitsgemeinschaft "Resistenz" in der Paul-Ehrlich-Gesellschaft fr Chemotherapie e.V. aus dem Jahre 1998. Chemother J 9: 51-86 and piracetam.
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Reevaluate drugs that have to date only been shown to affect neointimal hyperplasia. Indeed, depending upon their effect on vessel remodeling, these drugs may actually decrease restenosis, have no effect on restenosis or even increase restenosis. The NO pathway and neointimal hyperplasia. Previous studies, performed in single-injury models, have shown that the NO pathway is an important determinant of neointimal hyperplasia after experimental angioplasty 13, 7 ; . Administration of L-arginine the substrate for the enzyme NO synthase ; , administration of NO donors and inhalation of NO have been associated with an inhibition of neointimal hyperplasia in rats and rabbits 17 ; . Conversely, administration of NO synthase inhibitors, such as L-NAME, has been associated with an increase in neointimal hyperplasia 2 ; . To date, however, no data are available concerning the impact of the NO pathway in double-injury models such as the hypercholesterolemic rabbit. This model differs from single-injury models by the fact that angioplasty is performed on an already diseased vessel and by the number of foam cells in the neointimal thickening 24, 30 this model may thus better reflect what could occur in human arteries. Our results clearly show that L-arginine has an inhibitory effect on neointimal hyperplasia, whereas the NO synthase inhibitor L-NAME has a stimulatory effect. Our results are thus concordant with those obtained in single-injury models. The mechanisms by which NO affects neointimal hyperplasia are not entirely clear but may relate to an inhibition of smooth muscle cell proliferation and migration 9 11 ; , to inhibition of extracellular matrix components production 12 ; or to modulation of platelet and leukocyte functions 1315 ; . The NO pathway and vessel remodeling. The production of endogenous vasodilators such as NO has been implicated in vessel remodeling 23 ; . In arteriovenous fistula model, chronic administration of L-NAME has been associated with decreased vascular enlargement, thereby suggesting that NO may participate in flow-induced remodeling of the rabbit common carotid artery 32 ; . We thus speculated that NO might also participate in other forms of vessel remodeling such as remodeling after balloon angioplasty. Vessel remodeling after balloon angioplasty may be described as a spectrum of changes in total vessel area ranging from constriction to enlargement. The model used in the present study does not allow us to analyze the exact mechanisms of vessel remodeling; our specific aim was to describe the effects of the NO pathway on vessel size at the lesion site and consequently, taking into account its effects on neointimal hyperplasia, to assess its effects on lumen size. L-argininetreated animals had no change in vessel size, whereas L-NAMEtreated animals had a major increase in vessel size. This observation conflicts with the hypothesis that NO could induce vascular enlargement after angioplasty. One possible explanation for these unexpected findings may be that the significant effects of L-arginine and.
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