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Interferon research abs 1 || Hemoglobin research abs || Stem cell research abs || Nucleic acid research abs || Herpes research abs || Bronchitis research abs || Schizophrenia research abs || Tuberculosis research abs || Pneumonia research abs



Intern Med. 2000 Oct;39(10):788-93.
Treatment of membranoproliferative glomerulonephritis associated with hepatitis C virus infection. Niigata Research Group of Glomerulonephritis and Nephrotic Syndrome.

Nishi S, Ueno M, Shimada H, Oosawa Y, Iino N, Iguchi S, Karasawa R, In H, Kawashima S, Saito N, Imai N, Saito K, Suzuki S, Arakawa M, Gejyo F.

Department of Medicine (II), Niigata University School of Medicine.

OBJECTIVE: Interferon has been used as a new therapeutic agent for glomerulonephritis since a manifest relationship between membranoproliferative glomerulonephritis (MPGN) and hepatitis C virus (HCV) infection was documented. However, several side effects and rebound phenomenon have been significant problems. We retrospectively evaluated the therapeutic effect and safety of the standard treatment with steroids and/or immunosuppressive agents for MPGN patients with an HCV infection. METHODS: Remission and renal survival rates as well as clinical and histological data were compared between MPGN groups with or without an HCV infection. In addition, the hepatic function was followed-up after the treatment. PATIENTS: The subjects were 42 biopsy proven MPGN patients. Seven were positive for an HCV infection. Secondary causes of MPGN excluding an HCV infection were omitted. Most patients were treated with steroids and/or immunosuppressive agents. RESULTS: The mean age of the MPGN patients with an HCV infection was significantly higher than that of those without an HCV infection. The renal function and the interstitial change of the former group were significantly worse than those of the latter. Nevertheless, remission and renal survival rates were not significantly different between the two groups. None in the HCV positive MPGN group showed an impairment of hepatic function during the clinical course. However, 2 subjects died from severe pneumonia during the treatment. CONCLUSION: The standard treatment with steroids and/or immunosuppressive agents did not reveal a statistical difference in the therapeutic efficacy between MPGN patients with or without an HCV infection. However, some in the former group showed a poor prognosis.

PMID:_11030201 Ann Allergy Asthma Immunol. 2000 Sep;85(3):241-4.
A 5-day course of oral desensitization to trimethoprim/sulfamethoxazole (T/S) in patients with human immunodeficiency virus type-1 infection who were previously intolerant to T/S.

Yoshizawa S, Yasuoka A, Kikuchi Y, Honda M, Gatanaga H, Tachikawa N, Hirabayashi Y, Oka S.

AIDS Clinical Center, International Medical Center of Japan, Tokyo.

BACKGROUND: Trimethoprim/sulfamethoxazole (T/S) is an essential drug in patients with human immunodeficiency virus type-1 (HIV-1) infection to prevent opportunistic infections. About 40% to 60% of them develop skin rash which leads to discontinue the medication. A precise mechanism of the reaction is not known. OBJECTIVE: To make the patients more tolerable to the medication and to make clear whether or not the reaction is caused by serum sulfamethoxazole-specific IgE. METHODS: We established a 5-day protocol, in which T/S was administered orally as a granular form in increasing doses beginning with 0.005 g (it contains trimethoprim 0.4 mg and sulfamethoxazole 2 mg) and doubled every 12 hours until the therapeutic dose was achieved. We tried to desensitize T/S in 17 patients with HIV-1 infection who were previously intolerant to T/S and measured the specific IgE in sera. RESULTS: Desensitization was successfully completed in 15 (88.2%) of the patients. In two patients who failed the desensitization, one was due to fever and the other was gastric irritation. During followup in a mean period of 16.6 months (range, 8 to 23 months) as of May, 1999, none has had Pneumocystis carinii pneumonia (PCP) while receiving T/S after desensitization. Sulfamethoxazole-specific IgE did not increase, indicating that it was not the major cause of skin rash due to T/S in our cases. CONCLUSION: These preliminary results show that most patients who were thought to be intolerant to T/S and had no sulfamethoxazole-specific IgE can be safely desensitized and received the drug subsequently as an effective prophylaxis for PCP.

PMID:_11030281 Drugs. 2000 Sep;60(3):597-605.
Treatment of Chlamydia trachomatis infections in pregnant women.

Miller JM, Martin DH.

Department of Obstetrics and Gynecology, Louisiana State University Medical Center, New Orleans 70112, USA.

The intent of this article is to provide an overview of the epidemiology and pharmacotherapy, including cost analyses, of Chlamydia trachomatis infections in pregnant women. Chlamydia is a common sexually transmitted infection. For pregnant women, there are concerns both for the mother (post-partum endometritis, horizontal transmission) and the newborn (conjunctivitis, delayed pneumonia). Therapeutic options are restricted because of the fetus and include multi-day treatment with erythromycin, amoxicillin, clindamycin or single dose azithromycin. Clinical cure rates with these options are 86, 92, 93 and 95%, respectively. Pharmacoeconomic analyses have been conducted to determine if the initial increase in acquisition cost of azithromycin (approximately 3-fold higher than erythromycin or amoxicillin) is offset by improvement in compliance and drug efficacy. Clindamycin has received little attention because of its expense (4-fold more than azithromycin). Analyses have been retrospective. As models incorporate more complications of failure to cure, azithromycin increasingly becomes more cost effective and is our recommended treatment.

PMID:_11030469 Microb Pathog. 2000 Nov;29(5):301-9.
Intracellular DNA replication and long-term survival of pathogenic mycoplasmas.

Dallo SF, Baseman JB.

Department of Microbiology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.

We examined intracellular survival and growth of pathogenic mycoplasmas (Mycoplasma penetrans, Mycoplasma pneumoniae and Mycoplasma genitalium) in cultured human cells. By using the eukaryotic nuclear DNA synthesis inhibitor, aphidicolin, we detected the selective synthesis of mycoplasma (My) and mitochondria (Mt) DNA, which could be further differentiated by restriction enzyme analyses. Also, intracellular M. pneumoniae and M. penetrans infectivity of human cells was detected over 6 months using subfractionation of infected cells and determination of mycoIplasma colony forming units (cfu). For M. genitalium, which we failed to re-grow from infected cells, species-specific PCR primers were used to implicate long-term mycoplasma survivability. Data indicated that pathogenic mycoplasmas reside and replicate intracellularly over extended periods in human cells, consistent with the ability of mycoplasmas to circumvent antibiotic therapy and immune surveillance and establish chronic infections. 2000 Academic Press.

PMID:_11031124 J Allergy Clin Immunol. 2000 Oct;106(4):730-6.
Elevated chemokine levels in bronchoalveolar lavage fluid of patients with eosinophilic pneumonia.

Katoh S, Matsumoto N, Fukushima K, Mukae H, Kadota JI, Kohno S, Matsukura S.

Third Department of Internal Medicine, Miyazaki Medical College, Miyazaki, Japan.

BACKGROUND: Allergic lung inflammation is caused by accumulation and activation of different leukocyte subsets, such as eosinophils and T lymphocytes, in the lung. The chemokines are a large group of chemotactic cytokines that regulate leukocyte trafficking and may play an important role in allergic lung inflammation. OBJECTIVE: The purpose of this study was to evaluate the role of various chemokines, including eotaxin, RANTES, monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-1beta, and IL-8 in the pathogenesis of eosinophilic pneumonia (EP). METHODS: The concentrations of eotaxin, RANTES, MCP-1, MIP-1beta, and IL-8 in bronchoalveolar lavage fluid (BALF) were measured by using ELISA in 15 patients with EP, 10 with idiopathic pulmonary fibrosis, 10 with sarcoidosis, and 11 healthy volunteers. RESULTS: Eotaxin in BALF was high only in patients with EP, and its level correlated significantly with the number of eosinophils in BALF of patients with EP and healthy volunteers. MCP-1 and MIP-1beta in BALF were preferentially increased in patients with EP. There was a significant correlation between MCP-1 levels and the number of macrophages in BALF of patients with EP and healthy volunteers. CONCLUSION: Our findings suggest that these CC chemokines contribute to the pathogenesis of EP through the specific recruitment of leukocyte subsets in the lung.

PMID:_11031344





Like developmental biology of any part of our body, hair growth is a complicated process. Hence the homework for modern science to yet unravel the process and mechanism to a completion. There exist a number of traditional and alternative therapeutic methods that include drugs, surgery, suppelements, and even snake oils that have been developed and used for those who lose hair. No understanding, and there is no solution. Of course, none of these approaches are perfect for all hair loss problems, especially due to the heterogeneity of the causes underlying hair losses. Most of chemical drugs and hair transplantation surgeries are accompanied by undesirable side effects.














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