Malaya, an ancient crossroads of trade, was the recipient of Chinese and Ayurvedic humoral ideas and, later, those of medieval Islam. These ideas were readily accepted by Malays, since they are highly congruent with pre-existing notions among aboriginal peoples of Malaya involving a hot-cold opposition in the material and spiritual universe and its effects upon human health. Islamic Malays have adapted these aboriginal beliefs to correspond to the Greek-Arabic humoral model in matters concerning foods, diseases, and medicines. Although Malay theories of disease causation include such concepts as soul loss and spirit attack, along with 'naturalistic' ideas such as dietary imbalance and systemic reactions to foods, all of these theories can either be reinterpreted in humoral terms, or, at least, are congruent with the basic tenets of Islamic humoral pathology. Behaviors and beliefs regarding human reproduction, however, while essentially following a humoral pattern, diverge from Islamic, as well as traditional Chinese and Indian Ayurvedic, humoral theories. Unlike any other major humoral doctrine, Malay reproductive theory (like that of non-Islamic aboriginal peoples of Malaya) equates coldness with health and fertility and heat with disease and sterility. These ideas, in turn, are related to beliefs regarding the nature of the spirit world: the destructiveness of spiritual heat and the efficacy of cooling prayer.
Young sedentary adult males of Malay, Indian, and Chinese origin who had established continuous residence in tropical Malaysia and presumed to be naturally acclimatized to heat, were studied to evaluate their physiological responses to a standard heat stress test. The Malay and Indian races have evolved in hot and humid geographical zones, whereas the Chinese originated from a temperate area. Subjects exercised at 50% VO2max alternating 18 minutes walking and 2 min rest during a 2-h exposure to an ambient of 34.9 degrees C dry bulb and 32.1 degrees C wet bulb. Heart rates, core and skin temperatures, sweat rates, and oxygen uptakes were measured during the heat exposure. The subjects of Malay origin exhibited the least circulatory stress of the three ethnic groups. The data obtained on these long-term residents of a hot-wet climate and who were considered acclimatized to this environment were compared to experimental data obtained by other investigators and other ethnic groups.
Normal human sera (NHS), heat-inactivated at 56 degrees C for 30 min, demonstrated positive ELISA reactions for anti-cardiolipin (aCL) antibodies. The heat-induced reactivity in ELISA was inhibitable by the cardiolipin antigen and was abolished by prior IgG depletion of the heated NHS with a protein A preparation. The heat-potentiated aCL also cross-reacted selectively with phosphatidic acid and phosphatidylserine, but not with phosphatidylcholine or phosphatidylethanolamine.
Non-reactive SLE sera in an ELISA for anticardiolipin antibody (aCL) retested positive in the immunoassay when the sera were first heat-inactivated at 56 degrees C for 30 minutes. This was not a false positive phenomenon since the positive ELISA reactivity of the heated SLE sera was markedly reduced by inhibition with the cardiolipin antigen. Furthermore, the heat-potentiated ELISA reaction was abolished by prior IgG depletion of the SLE sera with Protein A preparation. The unmasked aCL in the heat-treated SLE sera also exhibited selective binding in ELISA to other negatively-charged phospholipids, namely phosphatidylserine and phosphatidic acid but not against either phosphatidylcholine or phosphatidyl-ethanolamine. The data strongly indicate an interaction between antiphospholipid antibodies and heat-sensitive serum component(s), a reduction of the latter resulting in the ELISA detection of the autoantibody.
Heat treatment of sera at 56 degrees C for 30 min results in positive ELISA reactions for anti-cardiolipin antibody (aCL) in sera that had undetectable or low levels of aCL before heat inactivation. The positive, potentiated reactivity of the heated sera in the aCL ELISA could be inhibited with the cardiolipin antigen and was abolished by prior IgG depletion using staphylococcal protein A. The heat-potentiating effect of aCL binding in ELISA was evident in both normal human sera and clinical sera including sera from patients with systemic lupus erythematosus and syphilis.
A stereological comparison has been made of the structure of the lungs of the adult female domestic fowl and its wild progenitor the Red Jungle Fowl. The volume of the lung per unit body weight of the domestic bird is between 20 and 33% smaller than that of the wild bird. The domestic fowl has partly compensated for this by increasing the surface area for gas exchange per unit volume of exchange tissue. However, the blood-gas tissue barrier is about 28% thicker in the domestic fowl than in the Red Jungle Fowl, and this has led to a 25% lower anatomical diffusing capacity for oxygen of the blood-gas tissue barrier per unit body weight in the domestic fowl. These structural characteristics may make the modern domestic fowl vulnerable to stress factors such as altitude, cold, heat or air pollution by predisposing to hypoxaemia and perhaps thence to ascites.
Heat-sensitive serum masking cofactor(s) of antiphospholipid antibody (aPL) in normal human sera (NHS) are specifically inactivated at 56 degrees C. The degree of binding in ELISA by unmasked aPL in NHS was equivalent to that in non-heated, aPL-reactive autoimmune SLE sera. Previously "negative" SLE sera also reacted equally strongly in the aPL ELISA when similarly heat-inactivated. Isotype studies by ELISA of the heat-potentiated aPL in 36 NHS revealed the presence of specific IgG (34/36), IgM (11/36) and IgA (24/36) aPL antibodies. 11/36 (31%) NHS had all three aPL isotypes while 13/36 (36%) had both IgG and IgA antibodies to phospholipid.
The Australian, heat-resistant, a virulent V4 strain of Newcastle disease (ND) virus was selected for further heat resistance to give a variant designated V4-UPM. V4-UPM was sprayed on to food pellets which were fed to chickens in amounts calculated to give about 10(6) EID50 per chicken. Chickens vaccinated only once by feeding developed no haemagglutination-inhibition (HI) antibodies and were not protected against challenge with a viscerotropic velogenic strain of ND virus. Chickens given food pellet vaccine at 3 and 6 weeks of age developed HI antibodies and were substantially protected against parenteral and contact challenge with virulent ND virus. Similar protection was achieved when the V4-UPM vaccine was given intranasally on two occasions or when the vaccine virus was allowed to spread by contact from intranasally vaccinated chickens to nonvaccinated chickens. Heat resistant ND vaccine incorporated in food pellets may provide a method for protecting village chickens against ND in tropical countries.
The temperature rise of the irrigant in the root canal during free vibration of the ultrasonic file was studied in vitro in 10 human teeth. The mean temperature rise was found to be 0.6 degrees C. The minimal temperature increase may not significantly contribute to the effectiveness of ultrasonic root canal instrumentation.
The anti-phospholipid antibody (aPL) in 26 heat-inactivated normal human sera (NHS) was tested for IgG subclass in ELISA. The specific antibody in NHS included all four IgG antibody subclasses, as well as IgA. The incidence of IgG subclasses ranged from 50% (13/26) for IgG1 to 92% (24/26) for IgG2. Specific IgA anti-phospholipid antibody (aPL) was detected by ELISA in 38% (28/73) of normal human saliva. The salivary IgA aPL bound preferentially to anionic phospholipids including cardiolipin, phosphatidylserine and phosphatidic acid but not to phosphatidylcholine or sphingomyelin. Unlike aPL in normal human sera, aPL in saliva was predominantly not associated with the previously described heat-labile inhibitor of aPL. This may indicate a role of salivary IgA aPL in local immunity by binding to cross-reactive bacterial cell surface components including phospholipids.