Acute Appendicitis

Acute appendicitis still is a cause of considerable morbidity and now and then of death. The diagnostic accuracy in 316 patients operated on for acute appendicitis at Holy Cross Hospital was 76 per cent. In 24 of 239 cases of proved acute appendicitis, perforation had occurred, and the morbidity in those cases was three times that in the cases without perforation. Review of the cases did not reveal any clear-cut diagnostic criteria that might be used to predict perforation.A study of 30 patients with mesenteric lymphadenitis who were inadvertently operated on in the belief they had appendicitis, revealed that this condition is most likely to occur in young females with only a slight increase in the number of leukocytes. Although positive diagnosis of acute appendicitis is a difficult problem, the morbidity associated with needless operation is so much less than that which occurs in acute perforated appendicitis, that prompt exploration in any questionable case seems warranted.     

Production,identification, and standardization of insect viral pathogens

Résumé Avant de considérer un virus d'insecte comme potentiellement utilisable en lutte microbiologique, on doit tenir compte non seulement de son identification et de sa standardisation mais aussi de la méthode de production. La pureté et la qualité des préparations de virus sont avant tout une fonction de sa méthode de production. Parmi les méthodes disponibles, la production de virus par multiplication sur insectes élevés sur milieux artificiels, offre présentement la meilleure voie pour obtenir un produit de qualité. Les virus d'insectes peuvent être identifiés par leurs caractères physiques, morphologiques, chimiques aussi bien que par les tests sérologiques et de spécificité vis-à-vis des h?tes. Cependant, aucune de ces méthodes prises isolément n'est adéquate. Dans l'état actuel des connaissances, l'utilisation conjointe des deux derniers tests fournit les meilleurs éléments pour l'identification spécifique d'un virus d'insecte. La standardisation d'un virus devrait être basée à la fois sur sa capacité à produire la maladie et sur le dénombrement des corps d'inclusion. La variation constatée dans la mesure de l'activité virale peut être une conséquence de la présence de particules de virus libérées, du nombre de particules virales dans les corps d'inclusion, de la taille et de la constitution chimique de ceux-ci ou de la présence de biotypes secondaires. Diverses techniques, le plus souvent basées sur des études de dose léthale et de temps de mortalité, peuvent être employées pour l'estimation de l'activité insecticide des préparations de virus. Quelle que soit la technique utiliséc, il est nécessaire de déterminer aussi précisément que possible, les paramètres de la méthode de titrage et d'estimer et de présenter statistiquement les résultats.      

Simulation of a bacterial population structure in continuous cultivation by a dissociation process: An application to Rhodococcus rubropertinctus

An attempt is made to give a quantitative estimation of a possible contribution of the dissociation process in the formation of the heterogeneous population structure for the Rhodococcus rubropertinctus (Micobacterium lacticolum) in continuous cultivation. This estimation is realised with the help of a constructed mathematical model of the process. The model equations obtained describe particular biomass changes for R-, S- and M-dissociants and changes for substrate (glucose) concentration within the chemostate in continuous cultivation. Next, contributions to dissociant biomass changes were taken into account: (1) cell reproduction (each dissociant has its own specific growth rate depending on the substrate concentration), (2) cell outflow (in proportion to dissociant biomass) and (3) dissociation (dissociant genotype change during reproduction occurs for each dissociant with its own specific frequency). It is determined that if substrate growth constants are equal the rapidly growing dissociants (possessing maximal μ_max) outs the rest of them, and the greater the speed of the flow the less the time to reach a steady-state distribution of the dissociant biomasses. But, at the same time the slowly growing dissociant can become dominant in the population if it has a lower substrate growth constant.     

Respiratory epithelial permeability after cigarette smoke exposure in guinea pigs

The purpose of this study was to determine the pathology of cigarette smoke-increased permeability at the bronchioalveolar junction of the guinea pig. After exposure to either smoke or room air, guinea pigs were anesthetized and fluorescein isothiocyanate-dextran (FITC-D, mol wt 10,000) was aerosolized into their lungs. Blood samples taken through a carotid arterial cannula were analyzed by gel chromatography and spectrofluorometry for the presence of FITC-D. The results confirmed that, after smoke exposure, increased amounts of intact FITC-D molecules with a reported Einstein-Stokes radius of 22.2 A crossed the respiratory epithelium into the vascular space. Transmission electron-microscopic studies showed that the FITC-D diffused across damaged type I pneumocyte membranes and cytoplasm to reach the basal lamina and entered the alveolar capillaries through endothelial tight junctions. Damage to the alveolar epithelium was more frequent for the smoke-exposed animals than the room air-exposed animals (P less than 0.05). We conclude that smoke exposure damages type I cells and that inhaled FITC-D crosses the epithelial barrier at damaged type I cells of the bronchioloalveolar junctions.     

Calcitonin and CGRP block bombesin- and substance P-induced increases in airway tone

Calcitonin gene-related peptide (CGRP) and calcitonin (C) are two peptides that are cocontained and probably coreleased with the potent bronchocontrictors, bombesin (B) and substance P (SP), within the lung. Although CGRP and C have a wide intrapulmonary distribution, their actions have not been well defined. By the use of a computerized lung mechanics analyzer, changes in response to 10-min infusions of these agents were measured in spontaneously breathing, anesthetized guinea pigs. Infusion of 0.3 nmol.kg-1.min-1 CGRP and 2 nmol.kg-1.min-1 C caused little change in lung mechanics. Infusion of 0.06 nmol.kg-1.min-1 B and 0.3 nmol.kg-1.min-1 SP caused a marked increase in inspiratory, expiratory, and total pulmonary resistance (RT), from base-line values (P less than 0.02), with a maximal effect at 10 min postinfusion (PI) [RT = 326 +/- 20% (SE) (B), 490 +/- 73% (SP)]. Coinfusion of C or CGRP with B or SP at the above concentrations caused a marked reduction in SP - [RT = 189 +/- 28% (C), 142 +/- 16% (CGRP) at 10 min PI] and B - [RT = 157 +/- 18% (C), 158 +/- 10% (CGRP) at 10 min PI] induced changes in resistance (P less than 0.015). The mode of action of C and CGRP is unknown, but these peptides may antagonize the effects of B and SP via autonomic pathways by interfering with B- or SP-induced changes in intracellular calcium concentrations or by increasing intracellular cAMP levels by binding to specific cellular receptors linked to adenylate cyclase.     

Motor unit territories supplied by primary branches of the phrenic nerve

Recent studies have demonstrated that, under certain circumstances, the diaphragm does not contract as a homogeneous unit. These observations suggest that motor units may not be randomly distributed throughout the muscle but confined to localized subvolumes. In the present study, electromyographic (EMG) and glycogen depletion methods were combined to investigate the organization of motor units supplied by the primary branches of the phrenic nerve in the cat. Four primary branches are generally present, one branch to the crus and three branches to the sternocostal region. The gross motor-unit territory of each of the four phrenic primary branches was determined by stimulating each nerve separately, while recording from nine EMG electrodes distributed over the hemidiaphragm. Stimulation of the crural branch evoked activity in the ipsilateral crus, whereas stimulation of each of the remaining branches evoked activity in discrete but overlapping areas of the sternocostal diaphragm. A more precise analysis of the distribution and borders of the motor territories was obtained by mapping regions depleted of muscle glycogen due to stimulation of each primary branch for 90 min. Glycogen depletion results closely matched the EMG findings of a localized distribution of motor units served by single primary branches. Stimulation of the crural branch typically caused depletion of the ipsilateral crus, whereas the sternocostal branches each served a striplike compartment. In the majority of cases, the borders of the sternocostal compartments were relatively abrupt and consisted of a 1- to 2-mm transition zone of depleted and nondepleted fibers. These studies demonstrate that motor unit territories of the primary branches of the phrenic nerve are highly delineated. This compartmentalization provides the central nervous system with the potential for a more precise regional motor control of costal and crural diaphragm than previously suspected.     

Pulmonary gas exchange in panting dogs

Pulmonary gas exchange during panting was studied in seven conscious dogs (32 kg mean body wt) provided with a chronic tracheostomy and an exteriorized carotid artery loop. The animals were acutely exposed to moderately elevated ambient temperature (27.5 degrees C, 65% relative humidity) for 2 h. O2 and CO2 in the tracheostomy tube were continuously monitored by mass spectrometry using a special sample-hold phase-locked sampling technique. PO2 and PCO2 were determined in blood samples obtained from the carotid artery. During the exposure to heat, central body temperature remained unchanged (38.6 +/- 0.6 degrees C) while all animals rapidly switched to steady shallow panting at frequencies close to the resonant frequency of the respiratory system. During panting, the following values were measured (means +/- SD): breathing frequency, 313 +/- 19 breaths/min; tidal volume, 167 +/- 21 ml; total ventilation, 52 +/- 9 l/min; effective alveolar ventilation, 5.5 +/- 1.3 l/min; PaO2, 106.2 +/- 5.9 Torr; PaCO2, 27.2 +/- 3.9 Torr; end-tidal-arterial PO2 difference [(PE' - Pa)O2], 26.0 +/- 5.3 Torr; and arterial-end-tidal PCO2 difference, [(Pa - PE')CO2], 14.9 +/- 2.5 Torr. On the basis of the classical ideal alveolar air approach, parallel dead-space ventilation accounted for 54% of alveolar ventilation and 66% of the (PE' - Pa)O2 difference. But the steepness of the CO2 and O2 expirogram plotted against expired volume suggested a contribution of series in homogeneity due to incomplete gas mixing.