Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One year after immunization with a single 0.5-mL dose of influenza virus vaccine, serum samples from 30 children with renal diseases were tested for serum hemagglutination-inhibiting (HI) antibody titers to A/New Jersey/76, A/Victoria/75, and A/USSR/77. Eleven unvaccinated children with renal diseases formed a comparison group. In contrast to the comparison group (0/11), 53% (16/30) of the vaccinated group had a protective level of serum HI titers (greater than or equal 1:40) against A/New Jersey. A protective level of serum HI titer against A/Victoria was noted in 83% (25/30) of the vaccinated group, while 54% (6/11) of the unvaccinated group had similar HI titers. None had a detectable HI titer against A/USSR. A minor common cold-like illness occurred in seven of the 30 vaccinated children; one of these had exacerbation of nephrotic syndrome. The data suggest a good protection against influenza one year after vaccination in children with renal disease.
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PMID:Hemagglutination-inhibiting antibodies in vaccinated children with renal disease. 48 Jun 1

In 1976, the National Institute of Allergy and Infectious Disease sponsored a nationwide network for influenza surveillance. In this paper, in addition to reporting the surveillance findings in Los Angeles, sales of nonprescription cold remedies in a large supermarket chain were evaluated as an indicator of influenza activity in the community. Twenty-seven isolates of influenza B occurred between February 17 and April 26, 1977. Peak influenza B activity occurred from mid-March to early April, 1977. A 5-10% increase in percent of respiratory and febrile respiratory illness seen in outpatient clinics was observed in late December and January. No variation in these statistics occurred during the peak of influenza activity. In contrast, sales of nonprescription cold remedies were apparently influenced by influenza B activity. Peak sales (345% increase) occurred 4 wk after the first influenza B isolate and 1 wk before peak influenza activity was documented by peak rates of isolation.
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PMID:Sales of nonprescription cold remedies: a unique method of influenza surveillance. 50 53

RNA 1 (see end of Summary) of a cold-adapted and temperature-sensitive (ts) influenza virus mutant A/Ann Arbor/6/60 has a different mobility from RNA 1 of wild-type (wt) A/Ann Arbor/6/60 when subjected to electrophoresis through acrylamide/agarose gels in the absence of denaturing agents. Detection of this lesion in RNA 1 of the mutant virus was dependent on the temperature of the gel during electrophoresis. Because RNA 1 is believed to code for a protein involved in virus-specific RNA synthesis we compared phenotypes of virion transcriptases in the wt and mutant viruses. The enzyme of the mutant virus was found to be about 40% less active at 40 degrees C than the enzyme of the wt virus when related to their activities at 31 degrees C. Two cold-adapted ts recombinants which derive their RNA 1 from the mutant A/Ann Arbor/6/60 have virion transcriptases with a phenotype similar to that of their mutant parent. Three different cold-adapted ts recombinants, however, which also derive their RNA 1 from the mutant A/Ann Arbor/6/60, have virion transcriptases with a phenotype similar to that of wt virus. We conclude, therefore, that the conditional-lethal ts property of A/Ann Arbor/6/60 mutant and its recombinants is independent of the phenotypic marker observed for the A/Ann Arbor/6/60 mutant virion transcriptase, and that the lesion in RNA 1 of the mutant may also be unrelated to the observed difference between virion transcriptases of the mutant and wt A/Ann Arbor/6/60 viruses. The phenotypes of the virion transcriptases in recombinants did, however, correlate with the derivation of their RNA 2. This suggests that the increased temperature-sensitivity of virion transcriptase of the A/Ann Arbor/6/60 mutant is caused by either (1) a lesion (not necessarily conditionally lethal) that occurred in its RNA 2 during the course of cold-adaptation, or (2) a lesion in another gene whose product is a component of the virion transcriptase complex, but which lesion is only expressed phenotypically when there is a synergistic interaction in the transcriptase complex with the product of A/Ann Arbor/6/60 rna 2.
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PMID:Comparative studies of wild-type and cold-mutant (temperature-sensitive) influenza viruses: independent segregation of temperature-sensitivity of virus replication from temperature-sensitivity of virion transcriptase activity during recombination of mutant A/Ann Arbor/6/60 with wild-type H3N2 strains. 52 98

Two adult brothers became ill within 48 hours of each other, and both had severe myoglobinuria. One brother died of oliguric renal failure. The other did not have renal failure and survived. Acute influenza A infection was documented serologically and from throat washings in the surviving brother, and by isolation of the influenza A virus from throat cultures and lung tissue of the brother who died. It is not certain whether a genetic myopathy made these brothers susceptible to viral-induced myoglobinuria, but a normal response of venous lactate to ischemic work excluded lack of phosphorylase or phosphofructokinase as a cause of the myoglobinuria in the surviving brother. Neither brother had a history of recurrent episodes of myoglobinuria precipitated by exercise, cold, or fasting, thus making carnitine palmityl transferase deficiency unlikely.
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PMID:Influenza and myoglobinuria in brothers. 57 80

The genetic and biological properties of 13 recombinant influenza A clones derived at 25 degrees C from the A/AA/6/60-cold variant (by crosses with 4 different wild type strains) were compared with a set of 5-FU induced ts-mutants. The 5-FU mutants had previously been placed into 7 complementation-recombination groups; the A/AA/6/60-cold parent (PI-7) and the 12 cold recombinant clones which were ts were shown to share a lesion with only one of these groups. The parental strain and 5 recombinant clones were evaluated for replication in the lungs and nasal turbinates of hamsters. Each virus appeared to be attenuated; genetic stability correlated with the level of viral replication in the hamster lung, i.e., viruses which grew best showed a tendency to revert to the ts+ phenotype. Characterization of the ts+ revertants for the presence of the cold adaptation property revealed that these viruses exhibited a spectrum of cold adaptation properties. Two viruses, PI-7 (the parental cold variant) and the CR6 recombinant (A/Queensland/6/72) did not revert in either the lungs or nasal turbinates of hamsters.
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PMID:Cold adapted variants of influenza A. II. Comparison of the genetic and biological properties of ts mutants and recombinants of the cold adapted A/AA/6/60 strain. 59 38

Influenza activity was studied in the Rome population from 1956 to 1976 by analysis of mortality from respiratory causes and from all causes. During cold weather months, type A influenza virus was associated, as a rule, with epidemic excess deaths at two year intervals while type B virus was prevalent twice during isolation data were also compared with epidemic excess mortality during four consecutive years. The evidence obtained indicated that influenza virus isolation alone does not represent a reliable index of epidemic influenza activity in this population. The proportion of deaths attributed to respiratory causes consistently increased in every epidemic, the most pronounced increases occurring during large epidemics. The break-down by age of deaths from respiratory causes in the course of two epidemic periods showed that the percentage distribution of deaths was essentially the same as in non-epidemic periods. This evidence indicates that the same factors influencing the age-related distribution of mortality from respiratory causes during non-epidemic periods, probably affect the fatal outcome of influenza during epidemics.
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PMID:Excess mortality from influenza in a large urban population, Rome, Italy, 1956--76. 63 65

Many viruses, even the common cold, are capable of producing sensorineural hearing loss. Treatment so far available is ineffective in correcting these losses. However, as the technology of vaccination advances, it is hoped that these can be prevented. Poliomyelitis and smallpox have been virtually eliminated from this country. Measles, rubella, and mumps are coming under control. Perhaps in the future we will be able to completely control influenza and the common cold and thus prevent many of the sensorineural hearing losses that we see today.
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PMID:Viral causes of sensorineural hearing loss. 66 51

Patients suffering from anorexia nervosa rarely appear to develop the common cold or influenza. This study examines the immunological response of fifteen female anorexia nervosa patients of both the vomiting and carbohydrate-abstaining type and compares them with a control population matched for age and occupation. Both anorectics and control populations received the admune influenza vaccine. Initially both groups had similar haemagglutination inhibition titres against the three different viral antigens: A/HK; A/PC; A/Eng. However, the anorectics showed over a 2-month period a higher titre of antibody especially to the Hong Kong virus: this was sigignificant. Cellular immune responses were measured using a tuberculin and a macrophage inhibition test, no significant difference between the two groups was obderved. These results which support the clinical findings are discussed.
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PMID:An investigation of the immune response of patients suffering from anorexia nervosa. 68 7

The incidence of respiratory tract infections in patients seeking medical advice at a community care centre (Dalby) during 1973 and 1974 was studied. About every third patient seen at this primary health station presented with signs of such infections. In the age groups less than 10, 10-19, 20-39, 40-59 and greater than or equal to 60 years, respiratory tract infections accounted for 65, 45, 32, 18 and 9% of the fotal number of diagnoses made during 1974. The aetiology of acute respiratory tract infections in a series of patients seen at this health station was studied. The series included randomly selected cases, but excluded children under seven years of age and patients presenting with signs of acute otitis media and tonsillitis. Attempts to establish the aetiology were made on the basis of the history, the clinical examination, and cultures for beta-haemolytic streptococci and Mycoplasma pneumoniae, complement foxation tests for influenza A and B, para-influenza 1, 2, and 3, adeno, cytomegalovirus and respiratory syncytial virus, and Chlamydia psittaci. Paul-Bunnell test and tests for cold agglutinins were also performed. With this test battery, an aetiological diagnosis was obtained in only 33% of the 101 patients studied. The findings suggest an infection with M.pneumoniae in 16%, with beta-haemolytic streptococci in 9%, and with viruses (adeno and para-influenza) in 7% of the patients. The present communication highlights the role of M.pneumoniae in upper respiratory infections, as few data have appeared on such infections in patients seen in general practice. The difficulty of establishing the aetiology of respiratory tract infections and the consequent treatment dilemma is discussed.
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PMID:The incidence and aetiology of respiratory tract infections in general practice--with emphasis on Mycoplasma pneumoniae. 78 48

Various workers, including T. D. Stewart, claim that the aboriginal Americas were relatively disease-free because of the bering Strait cold-screen, eliminating many pathogens, and the paucity of zoonotic infections because of few domestic animals. Evidence of varying validity suggests that precontact Americns had their own strains of treponemic infections, bacillary and amoebic dysenteries, influenza and viral penumonia and other respiratory diseases, salmonellosis and perhaps other food poisoning, various arthritides, some endoparasites such as the ascarids, and several geographically circumscribed diseases such as the rickettsial verruca (Carrion's disease) and New World leishmaniasis and trypanosomiasis. Questionably aboriginal are tuberculosis and typhus. Accordingly, virtually all the "crowd-type" ecopathogenic diseases such as smallpox, yellow fever, typhoid, malaria, measles, pertussis, polio, etc., appear to have been absent from the New World, and were only brought in by White conquerors and their Black slaves. My hypothesis is that native American medical care systems--especially in the more culturally advanced areas--were sufficiently sophisticated to deal with native disease entities with reasonable competence. But native medical systems could not cope with the "crowd-type" disease imports that struck Indian and Eskimos as "virgin-field" populations. Reanalysis of native population losses through a genocidal combination of diease, war, slavery and attendant cultural disruption by Dobyns, Cook and others strongly suggest that traditiona estimates underplayed the death toll by a factor of the general order of ten. This would make for an immediately pre-contact Indian population of some 90-111 million instead of the tradition 8-11 million. Evidence is growing that Indians may have been no more susceptible to new pathogens that are other "virgin soil" populations, and thus their immune systems need not be considered less effective than those in other people. Present-day high mortality rates in Indians of both continents from infectious disease imports may be more socioeconomic than anything else.
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PMID:Aboriginal new world epidemiolgy and medical care, and the impact of Old World disease imports. 79 20


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