Distribution of the color fields around static quarks: Flux tube profiles.
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Journal Article↗
Biomedical subjects
Y Peng
Publications and source records attributed to Y Peng.
Occurrence of cytomegalovirus retinitis after human immunodeficiency virus immunosuppression.
OBJECTIVE: To estimate the incidence and prevalence of cytomegalovirus retinitis (CMV-R) in late-stage human immunodeficiency virus type 1 disease. DESIGN: Cohort study. SETTING: The Multicenter AIDS Cohort Study, an ongoing 10-year study of human immunodeficiency virus type 1-infected homosexual men with semiannual visits and CD4+ cell testing. STUDY PARTICIPANTS: Three hundred sixty-seven human immunodeficiency virus type 1-infected men from the Multicenter AIDS Cohort Study who were receiving zidovudine and Pneumocystis carinii prophylaxis and who had CD4+ cell counts fall below 0.10 x 10(9)/L (100/microL). MAIN OUTCOME MEASURES: Kaplan-Meier-type estimates for various longitudinal quantifications of incidence and prevalence of CMV-R were obtained. RESULTS: Among these 367 individuals, cytomegalovirus disease developed in 103, of whom 73 (71%) had ocular complications. At 4 years after the first CD4 cell count ( < 0.10 x 10(9)/L), the probability for these subjects to have (1) remained living without CMV-R was 11%, (2) died without experiencing CMV-R was 66%, (3) experienced CMV-R and be living was 6%, and (4) experienced CMV-R and died was 18%. During these 4 years, there was a 25% chance for the development of CMV-R and, on average, 0.211 person-years of CMV-R morbidity. Among those subjects in whom CMV-R developed, about 19% did have CMV-R before a CD4+ cell count of less than 0.05 x 10(9)/L ( < 50/microL) was observed, and 81% had CMV-R after the CD4+ cell count reached this threshold. CONCLUSION: These estimates may be relevant to current clinical practice and help in allocating resources and planning for treatment and prophylaxis against cytomegalovirus disease.
AIDS-Related Opportunistic Infections↗
Factors accounting for different responses of pulmonary and cerebral vessels to hypoxia.
The roles of sympathicus, sensory neuropeptides (SNP), cyclooxygenase metabolites (COX-M), lipoxygenase metabolites (LOX-M), endothelium derived relaxing factor (EDRF), reactive oxygen (ROS) and potassium channels (PC) in the hypoxic pulmonary vasoconstriction (HPV) and hypoxic cerebral vasodilation (HCVD) were investigated in intact rats, rabbits and dogs. The results showed that during hypoxia, the excitation of sympathicus caused a constriction of both pulmonary and cerebral vessels, while SNP, EDRF and the opening of voltage sensitive PC caused the dilation of both of them; LOX-M mediated HPV and HCVD, COX-M might serve as their modulators; the blockade of ATP sensitive PC induced by hypoxia mediated HPV, but had no effect on HCVD; the reduction of O2-. in the lung might potentiate HPV, however, O2-. remained unchanged in brain during hypoxia. It is suggested that the alterations of LOX-M, ROS and the ATP sensitive PC are the factors accounting for the difference in the response of pulmonary and cerebral vessels to hypoxia.
Animals↗
Immunoregulatory role of neurotransmitters.
The nervous and endocrine systems modulate the immune system functions through releasing neurotransmitters, neuropeptides and endocrine hormones as they regulate the other physiological functions. The immune system in turn communicates with the nervous and endocrine systems through secreting immunocompetent substances. In this report we review our concepts and evidence concerning the immunoregulatory role of acetylcholine (ACh) and monoamine neurotransmitters which include noradrenaline (NA), 5-hydroxytryptamine (5-HT) and dopamine (DA). The immunoregulatory role comprises two aspects, the modulation of immune functions by neurotransmitters and the effect of the immune system on nervous system functions. The inhibition of ACh biosynthesis in the central nervous system (CNS) caused the enhancement of the humoral immune response of rats to sheep red blood cells (SRBC); by contrast, the inhibition of acetyl-cholinesterase (AChE) activity in the CNS resulted in the suppression of the immune response. It seems that ACh in the brain plays an immunoinhibitory role. The role can be blocked by atropine, a muscarinic antagonist, but not by hexamethonium, a nicotinic antagonist. During the humoral immune response (days 3-6 after SRBC injection), activity of AChE in the hypothalamus and hippocampus was strikingly lower. It is suggested that a functional connection is present in the ACh of the brain and the immune system. In vitro, ACh at 10(-9) to 10(-4) mol/l dose range significantly strengthened the spleen cell proliferation induced by concanavalin (Con A). The action of ACh only occurred either before or just after T lymphocytes were activated through muscarinic cholinergic receptors. In vivo, the depletion of monoamine neurotransmitters or only NA in the CNS caused the impairment of the anti-SRBC response of rats. During the phases of days 2-7 post-immunization, the metabolic alterations of NA, 5-HT and DA emerged in the CNS and the lymphoid organs of rats, which mainly exhibited that in the peak periods of the antibody response, the metabolism of the monoamine neurotransmitters in the hypothalamus and hippocampus was markedly increased, but NA content in the spleen and thymus was significantly decreased. These results provide evidence for the bidirectional information exchange network between the monoamine neurotransmitters and the immune system. Exposure to NA (at 10(-8)-10(-5) mol/l concentration range) in vitro was shown to inhibit the Con A-induced proliferation of the rat spleen cells. This effect of NA was related to the early events involved in the initiation of T cell proliferation and was mediated by either alpha- or beta-adrenergic receptors. The evidence that altering 5-HT level in the central or peripheral nervous systems through various ways of administering the drugs to regulate 5-HT biosynthesis led to the variations of the antibody response, and that cyproheptadine, an antagonist of serotoninergic receptors, can block the action of 5-HT show that 5-HT may exert an immunoinhibitory effect, which appears to be mediated via the peripheral mechanism to relate to the 5-HT receptors. However, the antibody response can cause changes in 5-HT metabolism in the CNS. The possible reasons for these results are discussed. Collectively, the antibody response arouses the metabolic variations of ACh, NA, 5-HT and DA in the central and peripheral nervous systems and then, these alterations can in turn influence immune function through neurotransmitter relevant receptors present on the immunocytes. The purpose of this interaction is most likely to maintain the homeostasis of the immune and other physiological functions.
Adjuvants, Immunologic↗
The complete BRCA2 gene and mutations in chromosome 13q-linked kindreds.
Breast carcinoma is the most common malignancy among women in developed countries. Because family history remains the strongest single predictor of breast cancer risk, attention has focused on the role of highly penetrant, dominantly inherited genes in cancer-prone kindreds (1). BRCA1 was localized to chromosome 17 through analysis of a set of high-risk kindreds (2), and then identified four years later by a positional cloning strategy (3). BRCA2 was mapped to chromosomal 13q at about the same time (4). Just fifteen months later, Wooster et al. (5) reported a partial BRCA2 sequence and six mutations predicted to cause truncation of the BRCA2 protein. While these findings provide strong evidence that the identified gene corresponds to BRCA2, only two thirds of the coding sequence and 8 out of 27 exons were isolated and screened; consequently, several questions remained unanswered regarding the nature of BRCA2 and the frequency of mutations in 13q-linked families. We have now determined the complete coding sequence and exonic structure of BRCA2 (GenBank accession #U43746), and examined its pattern of expression. Here, we provide sequences for a set of PCR primers sufficient to screen the entire coding sequence of BRCA2 using genomic DNA. We also report a mutational analysis of BRCA2 in families selected on the basis of linkage analysis and/or the presence of one or more cases of male breast cancer. Together with the specific mutations described previously, our data provide preliminary insight into the BRCA2 mutation profile.
BRCA2 Protein↗
BRCA2 germline mutations in male breast cancer cases and breast cancer families.
The breast cancer susceptibility gene, BRCA2 on chromosome 13q12-13, was recently isolated. Mutations in BRCA2 are thought to account for as much as 35% of all inherited breast cancer as wall as a proportion of inherited ovarian cancer. Many BRCA2-linked families also contain cases of male breast cancer. We have analysed germline DNA from 50 males with breast cancer (unselected for family history) and 26 individuals from site-specific female breast and breast-ovarian cancer families for mutations in BRCA2. All 17 breast-ovarian cancer families have been screened for BRCA1 coding region mutations and none were detected. Conformation-sensitive gel electrophoresis (CSGE) analysis of PCR-amplified DNA followed by direct sequencing was used to detect sequence variants. Three of eleven individuals carry the same mutation, all are of Ashkenazi Jewish descent, supporting the observation by Neuhausen et al. in this issue that there is a common mutation in this population. Eleven truncating mutations and nine polymorphisms were identified -- all were coding region variants. No loss-of-transcript mutations were identified in the sixteen samples for which this analysis was possible. Seven of the nine disease-associated mutations were detected in the 50 men with breast cancers; for thus in our series, BRCA2 mutations account for 14% of male breast cancer, all but one of which had a family history of male and/or female breast cancer.
BRCA2 Protein↗
Role of tyrosine kinase pathways in ETB receptor activation of NHE3.
Endothelin-1 (ET-1) binding to ETB receptors increases the activity of the apical membrane Na+/H+ antiporter (NHE3) of renal proximal tubule and cultured OKP cells. In OKPETB6 cells, a clonal cell line of OKP cells that overexpresses ETB receptors, ET-1-induced increases in Na+/H+ antiporter activity are mediated 50% by Ca2(+)-dependent pathways and 50% by tyrosine kinase pathways. ET-1 induces tyrosine phosphorylation of proteins of 68, 110, 125, 130, and 210 kDa. ET-1-induced tyrosine phosphorylation is mediated by the ETB receptor and is not dependent on increases in cell Ca2+ or protein kinase C. The 68-, 110-, 125-, and 130-kDa phosphoproteins are cytosolic, whereas the 210-kDa phosphoprotein is an integral membrane protein. Immunoprecipitation studies showed that the 68-kDa protein is paxillin and the 125-kDa protein is p125FAK (focal adhesion kinase). Cytochalasin D, which disrupts focal adhesions, prevented ET-1-induced tyrosine phosphorylation of paxillin, p110, p125FAK, and p130 but did not prevent tyrosine phosphorylation of p210 and did not prevent ET-1-induced increases in Na+/H+ antiporter activity. Thus 50% of ETB receptor-induced Na+/H+ antiporter activation is mediated by tyrosine kinase pathways, possibly involving p210. ETB receptor activation also induces tyrosine phosphorylation of focal adhesion proteins, but this is not required for antiporter activation.
Animals↗
Reversal of the antinatriuretic effect of prostaglandin E2 by verapamil in the rat.
Previous studies have demonstrated that prostaglandin E2 (PGE2) infusion increases intrarenal angiotensin-II (ANG-II) formation and decreases sodium excretion in the rat. PGE2 infusion may have direct tubular effects or indirect effects through increased intrarenal ANG-II. In the present study, the calcium channel blocker verapamil was used to determine whether it would reverse the PGE2-induced decrease in sodium excretion. To minimize any systemic and hemodynamic influences, verapamil and PGE2 were infused directly into the renal interstitium via a chronically implanted matrix. Fractional sodium excretion (FENa), glomerular filtration rate (GFR), mean arterial pressure (MAP), and plasma renin activity (PRA) were measured before and during renal interstitial infusion of PGE2 (10(-5) M) and/or verapamil (10(-3) M) in rats pretreated with indomethacin. The renal interstitial infusion of PGE2 alone significantly decreased FENa (delta-1.0 +/- 0.2%), whereas the addition of verapamil reversed the effect of PGE2 and significantly increased FENa (delta 2.6 +/- 0.3%, n = 9). The renal interstitial infusion of verapamil alone markedly increased FENa (delta 1.7 +/- 0.3%, n = 7), and this natriuresis was accompanied by a significant decrease in PRA (delta-0.6 +/- 0.1 ng/ml/h, p < 0.05). The addition of PGE2 to the interstitial infusion did not further affect FENa or PRA. There was a significant difference between the effect of interstitial PGE2 infusion and interstitial PGE2 infusion and interstitial verapamil infusion on PRa (delta 1.9 +/- 0.8 vs. delta -0.6 +/- 0.1 ng/ml/h, p < 0.05). GFR and MAP remained unchanged in response to the renal interstitial infusion of PGE2 and/or verapamil. In conclusion, verapamil reversed the PGE2-induced antinatriuresis in the rat.
Animals↗
Genetic heterogeneity in hereditary breast cancer: role of BRCA1 and BRCA2.
The common hereditary forms of breast cancer have been largely attributed to the inheritance of mutations in the BRCA1 or BRCA2 genes. However, it is not yet clear what proportion of hereditary breast cancer is explained by BRCA1 and BRCA2 or by some other unidentified susceptibility gene(s). We describe the proportion of hereditary breast cancer explained by BRCA1 or BRCA2 in a sample of North American hereditary breast cancers and assess the evidence for additional susceptibility genes that may confer hereditary breast or ovarian cancer risk. Twenty-three families were identified through two high-risk breast cancer research programs. Genetic analysis was undertaken to establish linkage between the breast or ovarian cancer cases and markers on chromosomes 17q (BRCA1) and 13q (BRCA2). Mutation analysis in the BRCA1 and BRCA2 genes was also undertaken in all families. The pattern of hereditary cancer in 14 (61%) of the 23 families studied was attributed to BRCA1 by a combination of linkage and mutation analyses. No families were attributed to BRCA2. Five families (22%) provided evidence against linkage to both BRCA1 and BRCA2. No BRCA1 or BRCA2 mutations were detected in these five families. The BRCA1 or BRCA2 status of four families (17%) could not be determined. BRCA1 and BRCA2 probably explain the majority of hereditary breast cancer that exists in the North American population. However, one or more additional genes may yet be found that explain some proportion of hereditary breast cancer.
Adult↗
Cardiac cytotoxic mechanism mediated by antibodies against myocardial mitochondrial ADP/ATP carrier in patients with dilated cardiomyopathy.
OBJECTIVE: To investigate mechanism of the antibody-mediated cardiac cytotoxicity and clinical significance in dilated cardiomyopathy (DCM), and study the effects of the antibodies against the myocardial mitochondrial ADP / ATP carrier from sera of patients with dilated cardiomyopathy on the guinea pig ventricular myocytes. PATIENTS AND METHODS: This study included 18 patients with DCM (12 men and 6 women), with mean age of 43 years. Control group included 18 health donors, (9 men and 9 women), with mean age of 32 years. The antibodies against the ADP / ATP carrier and cell membrane 52 000 peptide were examined by immunoblotting. The antibody-mediated cardiac cytotoxicity was studied with the cytotoxic test and whole cell patch-clamp technique. RESULTS: The antibodies against myocardial mitochondrial ADP / ATP carrier and cell membrane 52 000 peptide were positive in 18 patients with DCM, while negative in controls. The antibodies induced cytotoxic damage with time-dependent and enhanced Ca-current in cardiac myocytes. The increasing amplitude of peak Ca(2+)-current was 100 pA-840 pA (n = 8) in different dilution of the antibodies. The effect of the antibodies might be inhibited by verapamil, and were null in controls (n = 4). CONCLUSIONS: The above findings suggest that an increase in the antibody-mediated Ca(2+)-current of cardiac myocytes is related to the cytotoxic damage in dilated cardiomyopathy.
Adult↗
Hepatic biotransformation in rodents and physicochemical properties of 23(R)-hydroxychenodeoxycholic acid, a natural alpha-hydroxy bile acid.
The hepatic biotransformation in the rat and hamster of 23(R)-hydroxychenodeoxycholic acid (23(R)OH-CDCA), the alpha-hydroxy derivative of CDCA, was defined; some physiological and physicochemical properties were also assessed. 23(R)OH-CDCA was isolated from duck bile; [24-14C]23(R)OH-CDCA was synthesized. The compound was administered intravenously to anesthetized biliary fistula rats at doses of 1, 3, or 5 mu mol/kg-min and to hamsters at 3 mu mol/min-kg. Biliary bile acids and radioactivity were analyzed by thin-layer chromatography (TLC), high pressure liquid chromatography (HPLC), and gas chromatography-mass spectrometry (GC-MS). Recovery of radioactivity in bile was incomplete (50-70% of infused dose); some was also recovered as breath 14CO2. Radioactivity in bile was present as unchanged compound (25-50%, dose-dependent) and its conjugates (with taurine, with glycine, or with glucuronate). Nor-CDCA (C23) was present in bile (in both unconjugated and conjugated form), indicating that 23(R)OH-CDCA had undergone oxidative decarboxylation (alpha-oxidation) with loss of the C-24 carboxyl group. The alpha-oxidation was 20 +/- 5% (mean +/- SD) of administered dose in the rat and was not dose-dependent; in hamsters, alpha-oxidation was 35 +/- 8%. In rats, the S isomer of 23OH-CDCA also underwent alpha-oxidation (10 +/- 2%). Nor-CDCA also underwent 6beta-hydroxylation to form nor-alpha-muricholic acid, as well as reduction of its C-23 carboxyl group to form the C23 alcohol. The taurine conjugate of 23(R)OH-CDCA [23(R)OH-CDC-tau] was prepared synthetically and characterized by 1H-NMR. By surface tension measurements, it had a critical micellization concentration (CMC) of 3.5 mM (in 0.15 M Na+), as compared to 1.8 mM for CDC-taurine. Aqueous solubility of 23(R)OH-CDCA increased markedly above pH 5, compared to pH 7 for CDCA. When incubated with cholylglycine hydrolase, 23(R)OH-CDC-tau was deconjugated at a rate one-fourth that of CDC-tau. It is concluded that the presence of a 23(R)-hydroxyl group in a 3alpha, 7alpha-dihydroxy bile acid alters its metabolism in the rodent hepatocyte, as evidenced by inefficient conjugation with taurine or glycine, alpha-oxidation to nor (C23) bile acid, and reduction of the nor bile acid to the primary alcohol. The taurine conjugate of 23(R)OH-CDCA, a major biliary bile acid of marine mammals and wading birds, is a biological detergent with properties superior to those of the taurine conjugate of CDCA. Natural C23 nor-bile acids may be formed by alpha-oxidation of alpha-hydroxy C24 bile acids.
Animals↗
Field trials of combined use of two species of mermithid nematodes to control Anopheles and Culex breeding in China.
The field tests of combined use of Romanomermis yunanensis 2000-3000 larvae per sq m and Romanomermis sp 1000-2000 larvae per sq m in rice fields. Ponds and streams in four cities of China, resulted in 60.8-95.5% parasitism in Culex tritaeniorhynchus, Cx. quinquefasciatus, Anopheles sinensis and An. anthropophagus. This successful use of two species of Romanomermis together not only curb mosquito nuisance it also controls the major vectors of malaria, filariasis and encephalitis B in China.
Animals↗
[Intestinal lymphatic circulation is one of the important portals for microbial translocation after thermal injury].
The goal of this study was to determine whether the bacteria and endotoxin from GI tract could pass through the intestinal lymph circulation to the systemic circulation after severe thermal injury. Lymphatic fistula of intestine was created in 46 Wistar rats the rats were then divided randomly in scald and control groups. In scald group, animals were sustained with 30% TBSA full-thickness scald. The items studied were, the dynamic changes in intestinal lymph endotoxin level, the qualitative and quantitative bacterial culture, and pathological alterations in ileal mucosa within 24 hours postburn. Results showed that the levels of intestinal lymph endotoxin and the positive culture rate and counting of bacteria were evidently increased, and ileal mucosal lacteals were dilated and epithelial cells were necrotic and denudated in scald group. These suggested that the intestinal lymph circulation is one of the important portals for endotoxin and microbial translocation after severe thermal injury, and the intestinal mucosal damage is an important factor in pathogenesis.
Animals↗
[Effects of temperature on the viability and infectivity of preparasitic larvae of Romanomermis yuanenesis].
Romanomermis yuanenesis (Mermithidae: Nematoda) was found in Henan, China (Song and Peng, 1987), which has a broad host range in Culicinae mosquito and has been used successfully in field test for control of culex tritaeniorhynchus, culex fatigans and Aedes albopictus in Sichuan, Yunnan, Guangxi and Henan Provinces. This study was attempted to determine the viability and infectivity of preparasitic larvae in various temperatures. The cultures containing R. yuanenesis eggs were flooded 2h with distilled water, filtered and blocked with 1% agarose. Put the filter paper into water, then the motile preparasites separated from the unhatched eggs and got through the agarose membrane into water. About 200ml water containing preparasites free from eggs were held at 26 degrees C-28 degrees C, 16 degrees C-18 degrees C and -2 degrees C to 2 degrees C for test. The motility or lack of motility was used as the criterion to distinguish the living and dead nematodes. The rate of infection of mosquitoes and the rate of parasitism of nematodes were used to show the infectivity of the preserved preparasites. The results showed that at -2 degrees C to 2 degrees C, more than 90% of preparasitic larvae of R. yuanenesis survived for 8 days and the rate of mosquito infection was 87.5% to 100%, but at 26 degrees C-28 degrees C and 16 degrees C-18 degrees C the survival times of 90% preparasites were only 24 hours and 48 hours respectively. It indicates the low temperature preservation may prolong the survival time and keep the infectivity of these preparasitic larvae.
Animals↗
[Determination of content of chlorpromazine hydrochloride in compound metamizole sodium microenema by acid-dye colorimetric method].
An acid-dye colormetric method was described for the determination of chlorpromazine hydrochloride in the compound preparation. The method was based on the reaction of chlorpromazine hydrochloride with methyl orange, to form a yellow complex, which then was extracted by chloroform and exhibited a maximum absorption at 424 nm. The optimal conditions for determination were selected by orthogonal design test. The linear range of this method was 20-120 micrograms/ml (r = 0.9997). The average recovery of the three sample solutions of different concentrations was 99.72% +/- 0.46% (n = 6). The other ingredients of preparation do not interfere with chlorpromazine determination. This method is more sensitive and accurate and can be used for quality control of this compound preparation.
Chlorpromazine↗
[Experimental study of adoptive immunotherapy for adenoid cystic carcinoma of the salivary gland].
To study adoptive immunotherapy for adenoid cystic carcinoma of the salivary gland, we evaluate the influence of TNF-alpha or IFN-gamma on the activity of LAK cells when they acted at different stages of LAK cells killing target cells. The results in vitro experiment showed that ACC-2 was susceptible to LAK cytotoxicity. Both TNF-alpha and IFN-gamma could be an enhancer to augment IL-2-induced LAK cytotoxity against ACC-2, TNF-alpha should be used to induce LAK cells, but IFN-gamma is suitable to pretreat target cells ACC-2.
Carcinoma, Adenoid Cystic↗
Disappearance of the Abrikosov vortex above the deconfining phase transition in SU(2) lattice gauge theory.
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Journal Article↗
Predictors for failure of Pneumocystis carinii pneumonia prophylaxis. Multicenter AIDS Cohort Study.
OBJECTIVE: To identify clinical and epidemiological factors associated with failure of Pneumocystis carinii pneumonia (PCP) prophylaxis in those receiving primary and secondary prophylaxis. DESIGN: Longitudinal cohort study of participants infected with human immunodeficiency virus type 1 in the Multicenter AIDS Cohort Study who used PCP prophylaxis regimens after their T-helper lymphocyte counts had decreased to less than 0.200 x 10(9)/L (200/microL). MAIN OUTCOME MEASURE: Occurrence or recurrence of PCP. RESULTS: A total of 476 participants reported taking one or more of the following regimens: trimethoprim-sulfamethoxazole (TMP-SMX), dapsone, and/or aerosolized pentamidine--367 as primary prophylaxis and 109 as secondary prophylaxis after a previous episode of PCP. A total of 92 (20%) developed PCP despite prophylaxis. The mean failure rates per person-year of follow-up were 16.0% for those receiving primary prophylaxis and 12.1% for those receiving secondary prophylaxis (P = .19). Median times to death after initiation of primary or secondary prophylaxis were 2.0 and 1.2 years, respectively. The main predictor for failure of PCP prophylaxis was profound T-helper lymphocytopenia; 86% of failures occurred after T-helper cell counts decreased to less than 0.075 x 10(9)/L and 76% occurred after counts decreased to less than 0.050 x 10(9)/L. In multivariate time-dependent analysis, when compared with counts between 0.100 x 10(9)/L and 0.200 x 10(9)/L, the risk ratio for failure with counts less than 0.050 x 10(9)/L was 2.90 (P < .001). Once T-helper cell counts were considered, fever was the only other health status indicator that predicted subsequent PCP (ie, a time-dependent risk ratio of 2.22; P = .01). Use of TMP-SMX as the prophylaxis regimen was protective but did not eliminate failure (ie, a time-dependent risk ratio of 0.55; P = .03). CONCLUSIONS: These findings strongly support identifying improved methods of PCP prophylaxis once T-helper cell counts decrease to less than 0.075 x 10(9)/L or 0.100 x 10(9)/L. Given this severe degree of immunosuppression, an inherently more effective regimen against P carinii is required.
AIDS-Related Opportunistic Infections↗