Aggregatibacter actinomycetemcomitans–Induced Bone Loss and Antibody Response in Three Rat Strains

Background: The aim of this study is to compare the colonization, immunoglobulin (Ig) G response, and alveolar bone loss in Aggregatibacter actinomycetemcomitans (Aa)–inoculated Fawn Hooded Hypertensive (FHH), Dahl Salt‐Sensitive (DSS), and Brown Norway (BN) rats. Methods: Each rat strain was divided into wild‐type Aa‐inoculated and non‐inoculated control groups. Blood taken at 12 weeks after inoculation was assessed for Aa‐specific IgG antibodies by an enzyme‐linked immunosorbent assay. Colonization was assessed 12 weeks postinoculation. Bone loss was estimated by measuring the distance from the cemento‐enamel junction (CEJ) to the alveolar bone crest (ABC) at 20 molar sites. Colonization and antibody levels were compared by using the Student t test. Diseased rats were defined as having two sites per quadrant with CEJ–ABC distances that were significantly greater than the control CEJ–ABC distances. Results: The Aa colonization of FHH rats was significantly higher than in other strains (P <0.05). The Aa‐specific IgG levels in the DSS Aa‐inoculated group were significantly higher than in its control group (P <0.05). Only FHH rats showed Aa disease‐associated bone loss (P = 0.0021). Conclusions: Aa colonized and caused more disease in FHH rats than in the other rat strains. The rat strains each responded differently to the same Aa strain.     

History-based preoperative evaluation of antibiotic-related allergies and design of an easy to use questionnaire

Die Anaesthesiologie - An unconfirmed history of antibiotic allergies may negatively influence prescribing patterns for preoperative antibiotic prophylaxis and increase rates of postoperative wound...     

Refractory patterns and susceptibility to drug-induced polymorphic ventricular tachycardias in dogs with chronic atrioventricular block: relation to the type of anesthesia

Controversy exists as to the homogeneity of repolarization throughout the canine ventricular wall in vivo. The type of anesthesia has been shown to affect regional differences in monophasic action potential duration and the inducibility of polymorphic ventricular tachycardias (PVTs) in normal canine hearts. This study was conducted to determine refractory patterns and arrhythmia susceptibility in relation to halothane or pentobarbital anesthesia in dogs with chronic atrioventricular block and biventricular hypertrophy. In 12 dogs with chronic atrioventricular block, 60 needle electrodes (12 mm long, four bipolar electrodes, interelectrode distance of 2 mm) were inserted into the left and right ventricle. Six dogs were anesthetized with pentobarbital and six with halothane. Effective refractory periods (ERPs) were determined along 14 randomly selected needles at baseline and after application of almokalant (0.34 mmol/kg) (basic cycle length 1,000 ms, extrastimulus technique). At baseline and on almokalant, ERPs were uniform, independent of the type of anesthesia. With halothane anesthesia, ERPs were significantly longer under both conditions. Almokalant induced not only a prolongation of ERP in both groups but also a significant increase in transmural dispersion of ERP and in maximum dispersion of ERP. However, local refractory gradients were not specific to any muscle layer and did not seem to be related to the occurrence of PVTs. Almokalant did not induce arrhythmias in any dog in the pentobarbital group, but in four of six animals in the halothane group, apparently due to the more marked prolongation in ERP. Independent of the type of anesthesia, hypertrophied hearts of dogs with chronic atrioventricular block exhibit uniform refractory patterns. Longer ERPs with a comparable degree of dispersion on halothane are associated with a high incidence of drug-induced PVTs, whereas shorter ERPs on pentobarbital seem to prevent arrhythmia induction.     

Challenges in pain management among persons with AIDS in a long-term-care facility

OBJECTIVE: Opiate-resistant pain has been studied in cancer for many years; however, its existence in end-stage acquired immunodeficiency syndrome (AIDS) has captured little attention. This paper examines the existence, prevalence, and characteristics of opiate-resistant pain among persons with AIDS receiving end of life care at Bailey-Boushay House, an AIDS-skilled nursing facility in Seattle, WA. METHODS: A retrospective chart review of consecutive discharges during 1996 to 1999 examined patients near the end of life with advanced AIDS who had used opioid patient-controlled analgesia (PCA) for pain relief. The patients were divided into a control group (n = 97) and an opiate-resistant group (ongoing, severe pain with morphine use of greater than 100 mg/hr in an alert patient with no response to doubling doses, n = 12). The two groups were compared on the basis of current diagnosis of depression, history of injection drug abuse, peripheral neuropathy, or central nervous system involvement. RESULTS: Out of a total of 740 AIDS admissions during the study period, 226 patients were admitted for terminal care. Of these, 109 utilized a PCA for pain control for at least a day before death. Twelve (1.6% of all admissions, 5% of terminal patients, 11% of PCA users) experienced opiate-resistant pain. No associations with injection drug abuse, central nervous system involvement, depression, or peripheral neuropathy were found. CONCLUSIONS: Opiate-resistant pain is rare and can be relieved by aggressive use of adjuvants for pain treatment. There are no distinguishing characteristics that are predictive of this pain syndrome among AIDS patients near the end of life. The recognition of,prompt attention to, opiate-resistant pain remains a challenge for medical providers.     

Role of taurine accumulation in keratinocyte hydration

Epidermal keratinocytes are exposed to a low water concentration at the stratum corneum-stratum granulosum interface. When epithelial tissues are osmotically perturbed, cellular protection and cell volume regulation is mediated by accumulation of organic osmolytes such as taurine. Previous studies reported the presence of taurine in the epidermis of several animal species. Therefore, we analyzed human skin for the presence of the taurine transporter (TAUT) and studied the accumulation of taurine as one potential mechanism protecting epidermal keratinocytes from dehydration. According to our results, TAUT is expressed as a 69 kDa protein in human epidermis but not in the dermis. For the epidermis a gradient was evident with maximal levels of TAUT in the outermost granular keratinocyte layer and lower levels in the stratum spinosum. No TAUT was found in the basal layer or in the stratum corneum. Keratinocyte accumulation of taurine was induced by experimental induction of skin dryness via application of silica gel to human skin. Cultured human keratinocytes accumulated taurine in a concentration- and osmolarity-dependent manner. TAUT mRNA levels were increased after exposure of human keratinocytes to hyperosmotic culture medium, indicating osmosensitive TAUT mRNA expression as part of the adaptation of keratinocytes to hyperosmotic stress. Keratinocyte uptake of taurine was inhibited by beta-alanine but not by other osmolytes such as betaine, inositol, or sorbitol. Accumulation of taurine protected cultured human keratinocytes from both osmotically induced and ultraviolet-induced apoptosis. Our data indicate that taurine is an important epidermal osmolyte required to maintain keratinocyte hydration in a dry environment.     

Toxicity evaluation of petroleum blending streams: inhalation subchronic toxicity/neurotoxicity study of a light catalytic reformed naphtha distillate in rats

A 13-wk whole-body inhalation study was conducted with Sprague-Dawley CD rats (16/sex/group) exposed to a light catalytic reformed naphtha distillate (LCRN-D, CAS number 64741-63-5) at target concentrations of 0, 750, 2500, and 7500 ppm for 6 h/d, 5 d/wk. Sixteen rats per sex in the control and high-dose groups were maintained after final exposure for a 4-wk recovery period. The highest exposure concentration was 75% of the lower explosive limit. Standard parameters of subchronic toxicity were measured throughout the study; at necropsy, organs were weighed and tissues processed for microscopic evaluation. Neurotoxicity evaluations consisted of motor activity (MA) and a functional operational battery (FOB) measured pretest, throughout exposure and after the recovery period. Neuropathology was evaluated at termination. No test-related mortality or effects on physical signs, body weight, food consumption, or clinical chemistry were observed. In males exposed to 7500-ppm LCRN-D, a statistically significant decrease in white blood cell counts and lymphocyte counts was observed at the termination of exposure that was not present in animals after the 4-wk recovery period. However, mean corpuscular volume was slightly decreased in high-dose males after the recovery period. Statistically significant increases in kidney weights relative to body weights in 7500-ppm male rats correlated with microscopically observed hyaline droplet formation and renal tubule dilation, indicative of light hydrocarbon nephropathy, a condition in male rats that is not toxicologically significant for humans. Statistically significant decrease in absolute and relative spleen weights in 7500-ppm male rats correlated with decreases in hematologic parameters but had no microscopic correlate and was not observed in animals after 4 wk of recovery. This mild, reversible effect in white blood cell populations may relate to the presence of aromatics in the distillate. The only effect of LCRN-D on neurobehavioral parameters was significantly higher motor activity counts among high-dose (7500 ppm) males after the 4-wk recovery period, suggesting a possible delayed effect of LCRN-D. However, there was no evidence of hyperactivity or abnormal behavior from the functional observational battery evaluations, and there were no microscopic changes in neural tissue to support this observation. The no-observed-adverse-effects level (NOAEL) for LCRN-D was 2500 ppm for both subchronic toxicity and neurotoxicity. The no-observed-effects level (NOEL) was 750 ppm.     

Recent experimental and clinical findings retarding an interlabyrinthine connection]

BACKGROUND: In his experiments on the origin and site of formation of perilymph, which he conducted using radioactive substances in 1961. Schreiner also came across a surprising secondary finding, namely that rapid substance exchange takes place between the perilymph spaces of both inner ears. This rapid transition was only demonstrated for real solutions, such as low-molecular radioactive sodium phosphate, whereas it was greatly delayed for C14-labeled amino acids. No patency was demonstrated for particles which approach the limit of visibility under a light microscope, such as cell granules consisting of radioactively labeled mitochondria from rabbits. The graded patency between perilymph spaces in relation to the molecule size of the radioactive substances added indicates a direct connection between the perilymph spaces of both inner ears. This interlabyrinthine connection first postulated by Schreiner was controversial at the time but was soon confirmed by several authors in Germany and abroad and has been known since then as the "Schreiner effect" (1964). CLINICAL FINDINGS: In spite of these publications, the hypothesis of an interlabyrinthine connection was ignored for over 20 years until the American authors Harris et al. took up the topic once again in 1985, because of clinical investigations. They termed this phenomenon "sympathetic cochleo-labyrinthitis" in line with sympathetic ophthalmia. In pathogenetic terms, these authors suspect autoimmunological genesis. It has not been clarified which anatomical and immunological routes are taken to affect the labyrinths. Possibilities being discussed include connections via the perineural lymph sheath, NEW METHODS: In recent times, the perivascular spaces have also been considered, and Maher et al. (1997) attempted to substantiate this theory by demonstration using contrast media. In 1997, W. Zenker, the Zurich anatomist, conducted experiments using ferritin and was the first to demonstrate movement of such molecules within the dura. He believes that the transition of substances from one inner ear to the other is via CSF movements in the subarachnoid space and in the perivascular compartment of numerous small vessels crossing in a median plane such as veins of the clivus and plexus cavernosi but also venules and arterioles.