Between 1984 and December 2002, 211 patients underwent a revision anterior cruciate ligament reconstruction using a contralateral patellar tendon autograft. The patients were divided up into 3 groups. The first 2 groups consisted of individuals who had a primary ACL reconstruction from another surgeon, both intraarticular reconstructions (N = 103) and extraarticular reconstructions (N = 51). Patients in the third group (N = 57) underwent a primary ACL reconstruction by the senior author. Subjective questionnaires were received from 165 patients at longer than 2 years after surgery (mean time, 6.67 years). The mean subjective score for patients who had undergone a previous extraarticular procedure by another surgeon before revision ACL surgery was 77.4 points, which, statistically, is significantly lower than the mean of 87.9 for patients who had a previous intraarticular procedure by a different surgeon and 92.7 for patients who had a previous intraarticular procedure done by the senior author. Objective evaluation obtained for 126 patients at a mean of 4.0 years after surgery showed that only 57% of patients who had undergone a previous extraarticular procedure had both normal extension and normal flexion, which, statistically significant, was less than 74% for patients who underwent a previous intraarticular ACL reconstruction by the senior author and 67% for patients who had undergone previous intraarticular procedures by another surgeon (P = 0.0372). Objective stability was not, statistically, different significantly between groups (P = 0.6040). The use of a mini-arthrotomy with contralateral patellar tendon autograft for revision ACL reconstruction allows patients to consistently achieve the goals of restoring stability, range of motion, and function after surgery.

Revision anterior cruciate ligament surgery many times involves removal of previous hardware and difficulty with precise tunnel placement. The miniarthrotomy technique described in this article allows for easy visualization and access to the tibial plateau, intercondylar notch, and posterolateral wall of the femur. Ideal tibial tunnel placement involves placing the graft so that it is flush with the roof of the notch when the knee is in full extension. Ideal femoral tunnel placement should be posterior in the notch with 1 to 2 mm of bony bridge remaining. The femoral tunnel should provide a straight-line placement of the graft between the tibial and femur with the knee in 30° of flexion. When the graft is harvested from the contralateral knee, patients can begin exercises immediately to stimulate the graft donor site to regain size and strength. Rehabilitation for the ACL-reconstructed leg emphasizes return of range of motion and limiting a hemarthrosis. Using a contralateral patellar tendon autograft allows surgeons to use a reliable graft source that has been shown to provide excellent stability and graft incorporation, along with a good return of strength and function for patients.

Revision anterior cruciate ligament Surgery many times involves removal of previous hardware and difficulty with precise tunnel placement. The miniarthrotorny technique described in this article allows for easy visualization and access to the tibial plateau, intercondylar notch, and posterolateral wall of the femur. Ideal tibial tunnel placement involves placing the graft so that it is flush with the roof of the notch when the knee is in full extension. Ideal femoral tunnel placement should be posterior in the notch with 1 to 2 mm of bony bridge remaining. The femoral tunnel should provide a straight line placement of the graft between the tibial and femur with the knee in 30degrees of flexion. When the graft is harvested from the contralateral knee, patients can begin exercises hurnediately to Stimulate the graft donor site to regain size and strength. Rehabilitation for the ACLreconstructed leg emphasizes return of range of motion and limiting a hemarthrosis. Using a contralateral patellar tendon autograft allows Surgeons to use a reliable graft source that has been shown to provide excellent stability and graft incorporation, along with a good return of strength and function for patients.

Fructose has been shown to protect hepatocyte viability during hypoxia or exposure to mitochondrial electron transport inhibitors. We report here that the fructose metabolite D-glyceraldehyde (D-GA) is a good inhibitor of the mitochondrial permeability transition pore (PTP) in isolated rat liver mitochondria. We propose that a substantial portion of the protective effect of fructose on hepatocytes is due to D-GA inhibition of the permeability transition. Aldehydes which are substrates of the mitochondrial aldehyde dehydrogenase (mALDH) afford protection, while poor substrates do not. Protection is prevented by the ALDH inhibitor chloral hydrate. We propose that the NADH/NAD(+) ratio is the key to protection. The aldehydes phenylglyoxal (PGO) and 4-hydroxynonenal (4-HNE), which have previously been shown to inhibit the PTP, apparently function by a different mechanism independent of mALDH activity. Both PGO or 4-HNE are themselves potent inhibitors of ALDH, and their protective effect cannot be blocked by an ALDH inhibitor.

Interventional pain management, including the role of neural hlockade, has been criticized in the past few decades by many in the medical community.With the development of medications that effectively control pain, wider acceptance of opioids.improved diagnostic imaging techniques, and the lack of data supporting neural blockade, the perceived need for diagnostic and therapeutic neural blockade has decreased.In fact, it is becoming a lost art.However, clearly a need for nerve block procedures exists (when indicated), and thus a quick reference for physicians who are occasionally called on to perform them would be valuable.Waldman's Atlas of Interuentionul Pain Manugement is not that book, hut it comes close to filling that need.As such it is a vdlLlabk tool for the anesthesiologist who is called on to perform a few of the esoteric blocks and needs to review anatomy and technique.This text is conveniently divided into eight sections, with 111 chapters.The eight sections include blocks of the head, neck, shoulder and upper extremity, abdomen and abdominal wall, thorax and chest wall, back and pelvis, and lower extremity, and also miscellaneous interventional pain management techniques.The chapters are easily laid out with sections on indications, clinically relevant anatomy, technique, side effects and complications, and clinical pearls.Each chapter stands alone, consisting of three to six pages (of which one or two are illustrations) that can be read in 2 or 3 minutes.

Assistant Professor of Anesthesiology; Wake Forest University School of Medicine; Medical Center Boulevard; Winston-Salem, North Carolina, 27157–1009;jthomas@wfubmc.eduJames C. Eisenach, M.D., EditorHandbook of Clinical Anesthesia, 3rd Edition. Edited by Paul G. Barash, Bruce F. Cullen, and Robert K. Stoelting. Philadelphia, Lippincott-Raven, 1997. Pages: 932. Price:$39.95.The 3rd edition of the Handbook of Clinical Anesthesia is well organized and well written. I have never loved handbooks; I find they usually fall into one of two categories:(1) small with too little clinical information or (2) large and impossible to carry. This text attempts to break these molds: it is a useful clinical reference book that fits in a waistpack. The handbook parallels the comprehensive parent textbook, Clinical Anesthesia, by the same editors and has undergone considerable changes since the 2nd edition. The book consists of 57 small chapters and six important appendices. These are subdivided into seven sections, expanded from its earlier edition. The focus is on perioperative treatment of patients, with chapters describing preoperative evaluation, intraoperative techniques, anesthesia subspecialties, and postoperative care. New chapters describe the economics of healthcare delivery and practice management. The organization of the chapters and overall flow of the book have been improved. The text is far from complete, but it provides an excellent quick reference and review for residents, nurse anesthetists, and staff anesthesiologists. It is also a nice teaching tool for the busy academic physician.Section I of the book, entitled "Introduction to Anesthesia Practice," is the most radical alteration from the 2nd edition and is my least favorite. The section contains completely new material, providing first a brief history of anesthesia and then a discussion of practice management. It also contains chapters that describe experimental design and statistics, hazards in the operating room, and risk management. These chapters are well written and informative; however, it is not the type of information I usually look for while working in the operating room. I found that these chapters just got in the way when I was trying to find something quickly. However, the section is brief, only 31 pages, and I can appreciate the authors' trying to follow the parent textbook as closely as possible, thereby making the handbook a better review text.Sections II and III discuss basic principles of anesthesia practice. There are terrific new chapters on possible mechanisms of anesthesia and electrical safety. These additional chapters are important because they are subjects with which residents frequently have difficulty. The pharmacology chapters are updated and well organized; newer drugs are covered, and shaded charts make critical information easy to find. The authors have added a chapter describing basic pharmacologic principles, which really enhances this section.Section IV (previously section I/VI) covers preoperative and postoperative concerns. A new chapter on anesthesia and coexisting disease, along with the classic pharmacogenetics chapter, make this section an excellent quick reference.The real core of this handbook is Section V. The subspecialty areas are discussed individually, and there are improved reviews of related physiology. In addition, there are new chapters describing laparoscopic surgery, monitored anesthetic care, and the allergic response. The chapter on peripheral nerve blocks is a great reference at the bedside, but it needs to be expanded. More illustrations like the diagram of the ankle block would be helpful.The appendices in this book are potentially useful quick references to use in the operating room. They contain a few formulas, an electrocardiogram atlas, a common drug list, American Heart Association resuscitation protocols, new standards of the American Society of Anesthesiology, and difficult airway algorithms. I found the list of commonly used drugs to be the most useful part of the appendices. The list is updated and contains the newest agents (e.g., remifentanil). I was disappointed that the section on difficult airway algorithms was outdated and does not contain recommendations for the laryngeal mask airway.In summary, although it is not a perfect handbook, this text does a nice job. Overall, the new edition has achieved the authors' goal of enhancing "rapid access" to information in as comprehensive a manner as a handbook allows. The price of $39.95 may seem a little high compared with other small reference books, but I think this text gives you more for your money. It is more complete in its review of the field and, in addition, it fits in my waistpack.John A. Thomas, M.D.Assistant Professor of Anesthesiology; Wake Forest University School of Medicine; Medical Center Boulevard; Winston-Salem, North Carolina, 27157–1009;jthomas@wfubmc.edu(Accepted for publication March 18, 1999.)

The chemical formation, toxicity, and pharmacokinetics of 5-hydroxymethylfurfural (HMF) and certain other decomposition products found in parenteral solutions are reviewed. Heat sterilization-induced hexose decomposition to furan derivatives is promoted at low pH. Based upon infusion studies with rats and dogs, HMF does not appear to be acutely toxic at concentrations ordinarily encountered in parenteral infusion solutions (e.g., 10 mg/liter). Dosages of parenterally administered HMF exceeding 75 mg/kg body wt have led to some toxic effects, including increased activity of hepatic enzymes, altered serum-protein fractions, increased relative spleen weight, and hepatic fatty degeneration. Approximately 50% of parenterally administered HMF is oxidized and eliminated by the kidneys. From a clinical standpoint, the amount of HMF formed as a result of the heat sterilization of parenteral solutions containing hexoses does not seem to pose any significant toxicologic problem.

Some Innovating Models in TeratogenicityIntroduction Get access JOHN A. THOMAS, Ph.D. JOHN A. THOMAS, Ph.D. Travenol Laboratories, Inc.Morton Grove, IL 60053 Search for other works by this author on: Oxford Academic PubMed Google Scholar Toxicological Sciences, Volume 3, Issue 4, July 1983, Pages 227–228, https://doi.org/10.1093/toxsci/3.4.227 Published: 01 July 1983

The effect of testosterone propionate (TP) pellets (15 mg) and/or prolactin (50 IU/kg body weight daily X 5 i.p.) on the morphology of ventral prostates transplanted to the cleared 5th mammary fat pads of intact or castrated male hosts or into intact or ovariectomized female syngeneic hosts was investigated. The epithelial cell height and secretory activity was maintained in TP only or in TP + prolactin-supplemented intact or castrated male hosts as well as in intact or ovariectomized female hosts. Without TP implants, there was a necrosis of the prostate transplants in ovariectomized or intact female and in castrated male hosts and an atrophy of the in situ prostates in castrated male hosts. Prolactin injections alone failed to support prostatic integrity maintenance. In general, the transplants from TP + prolactin-supplemented hosts showed more active secretory epithelia than transplants from TP only.

Varying concentrations of isoproterenol caused marked increases in cyclic adenosine monophosphate (cAMP) in accessory sex organs (viz prostate and seminal vesicles) obtained from normal (i.e. non-castrate) mice. Such increases were abolished or attenuated when these accessory sex organs were obtained from castrate (7-day) mice. Some differences in isoproterenol-induced responsiveness of cAMP were noted between the prostate gland and the seminal vesicles. Injections of testosterone propionate (5 mg/kg, s.c. daily × 5) to orchidectomized mice were effective in restoring the cAMP levels in vitro to pre-castration activity. These findings indicate that normal levels of endogenous androgen are necessary for the full expression of isoproterenol-induced increases in cAMP levels in accessory sex organs.

Conjugation of pure cytochrome c with fluorescein isothiocyanate produces derivatives whose fluorescence intensity increases approximately 40 per cent between pH 6 and 7. Preparation of sonic particles from cytochrome c — depleted mitochondria in the presence of the conjugates results in their incorporation behind the membrane barrier, as determined by inaccessibility to removal by KC1 washes or to oxidation by ferricyanide. Energization of the sonic particles with substrates or oxygen causes an acidification of the environment of the probe, which is increased in the presence of valinomycin plus potassium, and abolished by nigericin or uncouplers.

Previous studies on the peroxidase-catalyzed iodination of tyrosine have been complicated by non-enzymatic reactions between iodine and tyrosine. The low pH optimum for chloroperoxidase allowed tyrosine iodination to be studied without this complication. Chloroperoxidase catalyzes the iodination reaction in two distinct stages. First, iodide ion is peroxidized to form molecular iodine. Secondly, the enzyme catalyzes a reaction between iodine, hydrogen peroxide, and tyrosine. This second reaction has an absolute requirement for hydrogen peroxide, and is inhibited by the presence of iodide ion.

Reaction with iodide (I−) at the sea surface is an important sink for atmospheric ozone, and causes sea-air emission of reactive iodine which in turn drives further ozone destruction. To incorporate this process into chemical transport models, improved understanding of the factors controlling marine iodine speciation, and especially sea-surface iodide concentrations, is needed. The oxidation of I− to iodate (IO3−) is the main sink for oceanic I−, but the mechanism for this remains unknown. We demonstrate for the first time that marine nitrifying bacteria mediate I− oxidation to IO3−. A significant increase in IO3− concentrations compared to media-only controls was observed in cultures of the ammonia-oxidising bacteria Nitrosomonas sp. (Nm51) and Nitrosoccocus oceani (Nc10) supplied with 9–10 mM I−, indicating I− oxidation to IO3−. Cell-normalised production rates were 15.69 (±4.71) fmol IO3− cell−1 d−1 for Nitrosomonas sp., and 11.96 (±6.96) fmol IO3− cell−1 d−1 for Nitrosococcus oceani, and molar ratios of iodate-to-nitrite production were 9.2 ± 4.1 and 1.88 ± 0.91 respectively. Preliminary experiments on nitrite-oxidising bacteria showed no evidence of I− to IO3− oxidation. If the link between ammonia and I− oxidation observed here is representative, our ocean iodine cycling model predicts that future changes in marine nitrification could alter global sea surface I− fields with potential implications for atmospheric chemistry and air quality.

Multiple injections of cycloheximide (daily × 5) to normal and castrate mice led to reduce levels of ribonucleic acid (RNA) in the submaxillary glands, when these levels are expressed as micrograms per organ. The antagonistic action of this agent was more evident when testicular androgens were removed.