Treatment of benign positional vertigo using the semont maneuver: efficacy in patients presenting without nystagmus

OBJECTIVE: To evaluate and compare the efficacy of the Semont liberatory maneuver on "objective" benign paroxysmal positional vertigo (BPPV) defined as vertigo with geotropic nystagmus in Dix-Hallpike positioning versus "subjective" BPPV defined as vertigo without nystagmus in Dix-Hallpike positioning. STUDY DESIGN: Retrospective chart review. METHODS: One hundred sixty-two patients with positional vertigo during Dix- Hallpike positioning were identified. Patients were evaluated for the presence or absence of nystagmus. All patients underwent the Semont liberatory maneuver. The patient's condition at follow-up was documented at 3 weeks as complete, partial, or failure. Repeated procedures were performed if necessary. RESULTS: There were 127 cases of objective BPPV and 35 cases of subjective BPPV. Overall, 90% of all patients tested had significant improvement of their vertigo after 1.49 maneuvers on average. Improvement was seen in 91% of patients with objective BPPV after 1.59 maneuvers on average, compared with 86% in subjective BPPV after 1.13 maneuvers on average (chi2 test, not significant [P = .5]). Patients with a history of traumatic origin or cause had an overall success rate of 81% compared with 92% for nontraumatic causes or origins (chi2 test, not significant [P = .1]). Recurrences were seen in 29% of patients after a successful initial maneuver; however, 96% of these patients responded to further maneuvers. Four patients with persistent symptoms after conservative management underwent posterior semicircular canal occlusion with resolution of symptoms. CONCLUSION: The Semont liberatory maneuver provides relief of vertigo in patients with positional vertigo, even in patients without objective nystagmus.     

Contraceptive use at last intercourse among reproductive-aged women with disabilities: an analysis of population-based data from seven states

Objective

To assess patterns of contraceptive use at last intercourse among women with physical or cognitive disabilities compared to women without disabilities.

Nephrolithiasis and risk of hypertension in women

Cross-sectional and prospective studies of men suggest a positive association between nephrolithiasis and hypertension. However, this association remains controversial in women. We conducted a prospective study of the relation between nephrolithiasis and the risk for hypertension in the Nurses' Health Study, a cohort of 89,376 women aged 34 to 59 years in 1980. Information on the history of nephrolithiasis, physician-diagnosed hypertension, and other relevant exposures was obtained by biennial mailed questionnaire. A history of nephrolithiasis before 1980 was reported by 2,558 women (2.9%), and a history of hypertension was reported by 11,883 women (13.3%). Among women without hypertension before 1980, 12,540 women reported a new diagnosis of hypertension between 1980 and 1992, during 711,039 person-years of follow-up. Compared with those without a history of nephrolithiasis, the age-adjusted relative risk (RR) for incident hypertension in women with such a history was 1.36 (95% confidence interval [CI], 1.20 to 1.43). After further adjustment for body mass index (BMI) and the intake of calcium, sodium, potassium, magnesium, caffeine, and alcohol, the RR was only slightly attenuated (RR=1.24; 95% CI, 1.13 to 1.37). In contrast, the occurrence of incident nephrolithiasis during follow-up was similar in women with hypertension at baseline compared with women without (adjusted odds ratio [OR]=1.01; 95% CI, 0.85 to 1.20). These data are consistent with the results obtained in men and support the hypothesis that a history of nephrolithiasis is associated with an increased risk for subsequent hypertension. Dietary factors, such as the intake of calcium, sodium, and potassium, do not explain this association. Unidentified pathogenic mechanisms common to nephrolithiasis and hypertension may be responsible for the development of both disorders.     

Immunoglobulin and T cell receptor gene rearrangements in human lymphoma and leukemia

DNA samples from blood leukocytes or tumor biopsies of 45 patients with phenotypic B or T cell neoplasms were analyzed for rearrangements of the immunoglobulin (Ig) or T cell receptor (TCR) genes by Southern blot hybridization analysis. Rearrangements of the Ig heavy chain joining region genes (JH) were present in DNA from each of 28 B cell lymphomas and leukemias; 14 of 21 of these tumors also had rearrangements of the Ig kappa light chain joining (JK) or deleting element (KDel) genes. Conversely, 16 of 17 T cell lymphomas and leukemias had rearranged TCR beta chain genes. One B cell and one T cell tumor had rearrangements of both Ig and TCR genes. There was a strong correlation between the rearrangements of specific genes and the immunophenotype of the tumor: JH rearrangement without TCR beta chain rearrangement occurred only in B cell tumors; TCR beta chain rearrangement with or without JH rearrangement occurred only in T cell tumors, with one exception; and JK and KDel rearrangements were found only in B cell tumors. Thus, rearrangements of the Ig heavy and light chain genes and the TCR beta chain genes were found to be highly sensitive markers of monoclonal human lymphomas and lymphoid leukemias, with the type of gene rearrangements well correlated with the cell lineage of these neoplasms.     

血管内皮生长因子在口腔颌面骨组织工程中的应用

目的:了解血管内皮生长因子促进骨再生和修复作用的机制及应用方式,探讨其在口腔颌面骨组织工程中的应用前景。资料来源:应用计算机检索PubMed数据库1994-01/2006-02有关血管内皮生长因子促进成骨的文章,检索词“Vascular endothelial growth factor,Bone formation,Maxillofacial bone,Bone defect”,限定文章语言种类为English。同时计算机检索中国期刊全文数据库1994-01/2006-02期间的相关文章,检索词“血管内皮生长因子、成骨、颌骨”,限定文章语言种类为中文。资料选择:对资料进行初审,选取符合要求的有关文章找全文。纳入标准:①血管内皮生长因子及其受体分子结构方面的文章。②血管内皮生长因子促进成骨作用的基础研究和临床研究。③血管内皮生长因子在颌骨组织工程中应用的基础研究和临床研究。排除标准:重复或类似的同一研究、Meta分析、个案报道。资料提炼:共收集到186篇有关血管内皮生长因子促进成骨作用的文章,排除重复或类似的同一研究,30篇符合要求(其中2篇为血管内皮生长因子及其受体分子结构方面的文献,18篇为血管内皮生长因子促进成骨作用的基础研究和临床研究方面的文献,10篇涉及血管内皮生长因子在颌骨组织工程中应用的研究)。资料综合:①国内外有关血管内皮生长因子促进成骨作用的机制为:通过促进内皮细胞增殖、血管生成,调节骨组织血供并参与骨的发育形成;作为旁分泌因子参与骨形成代谢;通过调节成骨细胞和破骨细胞的活性促进骨组织的再生、修复和重建。②血管内皮生长因子在骨组织工程中的应用方式主要有外源性应用和内源性应用,外源性应用就是将外源性血管内皮细胞生长因子加入到支架和细胞的复合体中,使它通过促进血管化、调节参与成骨的多种因子及成骨细胞和破骨细胞的活性,提高成骨效能。内源性应用就是利用基因技术,将人血管内皮细胞生长因子基因转入种子细胞,使种子细胞持续的产生血管内皮细胞生长因子,为骨形成提供足够的血管化和调节骨细胞的活性。③动物实验已证实血管内皮生长因子对颌骨牵张成骨和颌骨缺损修复起着促进作用。结论:应用外源性和内源性血管内皮生长因子构建的组织工程骨可促进骨形成和骨缺损修复,用它来加快颌面骨组织工程的骨形成和缩短疗程在理论上是可行的。     

Development of suppressor T lymphocytes for Epstein-Barr virus-induced B-lymphocyte outgrowth during acute infectious mononucleosis: assessment by two quantitative systems

A system of 3H-thymidine incorporation by lymphocytes in culture for 3 wk has been utilized for quantitative assessment of the ability of T lymphocytes to inhibit outgrowth of autologous Epstein-Barr virus (EBV) transformed B lymphocytes. Lymphocytes from EBV-seronegative individuals lack the ability to suppress outgrowth of autologous EBV- transformed B lymphocytes. This capability appears during the course of primary EBV-induced infectious mononucleases (IM) as the atypical lymphocytosis is subsiding and persists for years after recovery from primary EBV infection. The ability of T lymphocytes from EBV- seropositive subjects or convalescent IM patients to inhibit B- lymphocyte outgrowth is not HLA restricted. Thus, T lymphocytes capable of inhibition of in vitro EBV-induced B-cell outgrowth emerge during the acute stage of IM and may represent an important control mechanism of EBV-induced B-lymphocyte proliferation in vivo. The system provides a highly sensitive quantitative means for in vitro assessment of cell- mediated immunity to EBV.     

Human intrathymic T cell differentiation

The human thymus develops early on in fetal gestation with morphologic maturity reached by the beginning of the second trimester. Endodermal epithelial tissue from the third pharyngeal pouch gives rise to TE3+ cortical thymic epithelium while ectodermal epithelial tissue from the third pharyngeal cleft invaginates and splits during development to give rise to A2B5/TE4+ medullary and subcapsular cortical thymic epithelium. Fetal liver CD7+ T cell precursors begin to colonize the thymus between 7 and 8 weeks of fetal gestation, followed by rapid expression on thymocytes of other T lineage surface molecules. Human thymic epithelial cells grown in vitro bind to mature and immature thymocytes via CD2 and CD11a/CD18 (LFA-1) molecules on thymocytes and by CD58 (LFA-3) and CD54 (ICAM-1) molecules on thymic epithelial cells. Thymic epithelial cells produce numerous cytokines including IL1, IL6, G-CSF, M-CSF, and GM-CSF--molecules that likely are important in various stages of thymocyte activation and differentiation. Thymocytes can be activated via several cell surface molecules including CD2, CD3/TCR, and CD28 molecules. Finally, CD7+ CD4-CD8- CD3- thymocytes give rise to T cells of both the TCRab+ and TCR gd+ lineages.     

Electrocardiographic estimate of left ventricular mass versus radiographic cardiac size and the risk of cardiovascular disease mortality in the epidemiologic follow-up study of the First National Health and Nutrition Examination Survey

The prognostic value of a left ventricular (LV) mass index (g/m2) estimated from an electrocardiographic model and radiographic estimates of the relative heart volume (ml/m2) and cardiothoracic ratio for predicting the risk of cardiovascular disease mortality were investigated using Cox regression analysis to adjust for age, systolic blood pressure and history of heart attack in 1,807 men (1,609 white, 198 black) and 2,143 women (1,884 white, 259 black). The study population (ages 35 to 74 years at baseline) was followed from 5 to 12 years (average 9.5 years) for cardiovascular disease mortality. LV mass index and relative heart volume were independent predictors of cardiovascular disease mortality among white men. All 3 cardiac size estimates were independent predictors for cardiovascular disease mortality among white and black women. When LV mass index was used as a dichotomized variable to indicate the presence or absence of LV hypertrophy, the age-adjusted relative risk of cardiovascular disease mortality was 2.48 (95% confidence interval 1.77 to 3.46) for white men, 3.03 (1.49 to 6.16) for black men, 1.86 (1.21 to 2.87) for white women and 2.05 (0.83 to 5.05) for black women. The corresponding prevalence of LV hypertrophy was 15.4% for white men, 36.6% for black men, 20.1% for white women and 17.4% for black women. It is concluded that the electrocardiographic estimate of LV mass index can identify a substantially larger fraction of persons at increased risk for cardiovascular mortality than conventional electrocardiographic criteria for LV hypertrophy and that LV mass index estimated by electrocardiogram is a valuable supplement to radiographic cardiac size estimates in epidemiologic applications.     

Economic impact of HIV protease inhibitor therapy in the global use of health-care resources

Objective   To evaluate the clinical and economical impact of the introduction of HIV protease inhibitor (PI) therapy in the current clinical care of HIV-infected patients.
Methods   Cohort study with 155 HIV-infected patients with a full year of follow-up before and after the introduction of PI by June 1998. The setting was a large urban tertiary teaching hospital in Madrid, Spain. The main outcomes measures were clinical and immunological evolution, pharmacy, out-patient, emergency room and in-patient medical costs evaluated by diagnostic-related group classification, and the global economic costs of clinical care in HIV-infected patients (AIDS and non-AIDS).
Results   The cost of PI therapy was compensated fully by savings related to reduction of the number, length and severity of hospital admissions in AIDS cases. In contrast, more modest clinical effects with increased costs were observed in non-AIDS cases. Globally, there was an increase of about 20% in the total health-care costs of HIV-infected patients ( P  < 0.01).
Conclusions   PI therapy is highly cost-effective in AIDS patients. Its value in less severely immunosuppressed patients requires further evaluation.     

Resistance of CD7-deficient mice to lipopolysaccharide-induced shock syndromes

CD7 is an immunoglobulin superfamily molecule involved in T and natural killer (NK) cell activation and cytokine production. CD7-deficient animals develop normally but have antigen-specific defects in interferon (IFN)-gamma production and CD8(+) CTL generation. To determine the in vivo role of CD7 in systems dependent on IFN-gamma, the response of CD7-deficient mice to lipopolysaccharide (LPS)-induced shock syndromes was studied. In the high-dose LPS-induced shock model, 67% of CD7-deficient mice survived LPS injection, whereas 19% of control C57BL/6 mice survived LPS challenge (P < 0.001). CD7-deficient or C57BL/6 control mice were next injected with low-dose LPS (1 microgram plus 8 mg D-galactosamine [D-gal] per mouse) and monitored for survival. All CD7-deficient mice were alive 72 h after injection of LPS compared with 20% of C57BL/6 control mice (P < 0.001). After injection of LPS and D-gal, CD7-deficient mice had decreased serum IFN-gamma and tumor necrosis factor (TNF)-alpha levels compared with control C57BL/6 mice (P < 0.001). Steady-state mRNA levels for IFN-gamma and TNF-alpha in liver tissue were also significantly decreased in CD7-deficient mice compared with controls (P < 0.05). In contrast, CD7-deficient animals had normal liver interleukin (IL)-12, IL-18, and interleukin 1 converting enzyme (ICE) mRNA levels, and CD7-deficient splenocytes had normal IFN-gamma responses when stimulated with IL-12 and IL-18 in vitro. NK1.1(+)/ CD3(+) T cells are known to be key effector cells in the pathogenesis of toxic shock. Phenotypic analysis of liver mononuclear cells revealed that CD7-deficient mice had fewer numbers of liver NK1.1(+)/CD3(+) T cells (1.5 +/- 0.3 x 10(5)) versus C57BL/6 control mice (3.7 +/- 0.8 x 10(5); P < 0.05), whereas numbers of liver NK1.1(+)/CD3(-) NK cells were not different from controls. Thus, targeted disruption of CD7 leads to a selective deficiency of liver NK1.1(+)/ CD3(+) T cells, and is associated with resistance to LPS shock. These data suggest that CD7 is a key molecule in the inflammatory response leading to LPS-induced shock.