速激肽受体拮抗剂抗豚鼠过敏性哮喘的作用

实验目的是研究速激肽与哮喘的关系,评价速激肽受体拮抗剂对哮喘的治疗作用。结果表明,ip速激肽NK-1受体拮抗剂CP-96345,NK- 2受体拮抗剂SR-48968或两药合用,均可有效减少清醒致敏豚鼠吸入抗原引起的喘息反应,降低过敏性休克死亡率。SR-48968减轻麻醉豚鼠抗原引起的气道收缩,并浓度依赖性降低抗原引起的气管和支气管平滑肌收缩幅度。CP-96345可抑制抗原诱导的支气管和肺叶伊文思蓝渗出,仅对支气管平滑肌收缩有部分抑制作用。结果提示,速激肽参与哮喘发病,速激肽受体拮抗剂可抑制抗原诱导的气道平滑肌收缩(NK-2受体)和微血管渗漏(NK-1受体)而减轻哮喘反应。     

Marrow conversion before pneumatization of the sphenoid sinus: assessment with MR imaging

To evaluate the bone marrow change before pneumatization of the sphenoid sinuses in childhood, the authors retrospectively reviewed short repetition time/echo time midsagittal magnetic resonance images in 56 patients younger than 6 years. The signal intensity of the presphenoid bone marrow (anteromedial part of the sphenoid bone) was as low as that of muscle (grade 1) and remained the same as that of the basisphenoid and basiocicput in all infants (n = 6) younger than 6 months. Between 7 months and 2 years, most patients (24 of 27) exhibited fatty conversion of bone marrow limited to the presphenoid (grade 2). After 3 years of age, most patients demonstrated pneumatization (six of 12 at 3-4 years, eight of 11 at 5-6 years) in addition to the grade 2 findings (grade 3). The presphenoid exhibits signal intensity characteristics of fatty marrow before it is invaginated by the developing sphenoid sinus. Fatty change before pneumatization is a normal developmental process and should not be misinterpreted as a pathologic condition.     

NATIONAL TUBERCULOSIS CONTROL STRATEGY IN THE POST HIV PERIOD

The tuberculosis situation in the country is a matter of great concern since the disease has not been contained. The problem has been further compounded by the emerging problem of HIV infection in the country together with development of multi-resistant tubercle bacilli. There is, therefore, a need to change our National Tuberculosis Control Strategy without disturbing the basic infrastructure of the National Tuberculosis Programme. Changes such as reinforcement of the District Tuberculosis Centre, HIV and drug sensitivity testing, giving up of long term chemotherapy, BCG vaccination policy, chemoprophylaxis policy and involvement of Non-Governmental Organisations and general practitioners are suggested.KEY WORDS: Human immunodeficiency virus, TuberculosisDespite existence of the National Tuberculosis Programme for over 3 decades, the situation of tuberculosis is grim in the country. Tuberculosis is responsible for 500,000 deaths annually in India [1]. According to an estimate, there were 10 million radiologically active cases of pulmonary tuberculosis in India in 1981 of which 2.5 million were infectious and as many as 50% people in India are infected by tubercle bacilli although they may appear healthy [2]. As per the estimates, there are more than 4 million people, mostly in developing countries, who have been infected with both HIV and tuberculosis [3]. HIV infection, by progressively impairing cell mediated immunity, appears to be the highest risk factor for reactivation of tuberculosis into an active disease [4]. It is a well known fact that HIV infection is spreading unabated throughout the length and breadth of the country and as per the estimates, by 2000 AD, 400,000 HIV infections will have occurred in the country. Thus tuberculosis can be considered as the most important candidate as an opportunistic infection in HIV infected individuals in the country. There is every possibility of the problem being compounded by infections or reinfections occurring with multi-drug resistant strains of tubercule bacilli [5]. As it is, the problem of drug resistant strains throughout the country remains unmapped and any emergence of such new strains may lead to their spread both among HIV infected persons as well as the general population. In such a complicated scenario it has become imperative to take a second look at our National Tuberculosis Programme and make changes consistent with the emerging problems. Suggested changes are as following:     

Lymphocyte, monocyte, and natural killer cell reference ranges in postpartal women.

Normative values for immune-cell subsets in postpartal women, who are recovering from the relative immunosuppression of pregnancy, have not been established. Considerable differences in normative values for subsets of immune cells have been demonstrated based on sociodemographic factors, such as age and race. In order to make accurate clinical decisions about postpartal women, comparisons with normal reference ranges are necessary. Therefore, flow cytometric data for 51 healthy women at 4 months postpartum are presented and changes over the first 4 postpartal months are documented. The levels of some lymphocyte cell subsets, such as CD4+/CD45RA+ and Ia on lymphocytes, remained stable over time. The levels of other lymphocyte cell subsets, such as CD4+/CD29+, increased over the first 4 postpartal months, while those of other cell subsets, such as CD8 and CD11b, increased between delivery and 2 months postpartum and then dropped again by the fourth postpartal month. The levels of two natural killer cell subsets (CD3-/CD16+ and CD3-/CD57+) rose from delivery until 1 month postpartum and then plateaued. Comparisons were made with reference ranges of nonpostpartal groups provided in the literature and in a study of healthy women being conducted in the same laboratory, and postpartal women were found to have lower values of CD8, CD3-/CD16+, CD4+/CD45RA+, CD20, and CD11b than those reported in the literature.