The effects of thermochemotherapy using cyclophosphamide plus hyperthermia on the malignant pleural mesothelioma in vivo

The human malignant pleural mesothelioma is related to the use of asbestos in the majority of cases. Though the use of asbestos has been prohibited since the 1990s, the incidence of pleural mesothelioma is still increasing because of a latency period of at least 20 years. This study investigated the benefit of single therapy with cyclophosphamide or hyperthermia or the combination of both on cells of a human pleural mesothelioma cell line, xenotransplanted subcutaneously in the paw of mice. A CONTROL group received the same volume of physiological saline. The oxygenation of tumours was measured, tumour growth was followed over 3 weeks, immunohistochemical studies and a light and electron microscopic evaluation were performed. Chemotherapy or hyperthermia alone was only temporarily effective. The greatest benefit was achieved using combined thermochemotherapy consisting of cyclophosphamide plus hyperthermia: 50% of this group had partial remissions, and 67% responded to this therapy. After 3 weeks tumours grew again. Superior effects could be achieved by performing additional cycles of chemotherapy or adding another drug or radiation for instance. This study shows promising results in the treatment of malignant pleural mesothelioma.     

Growth resistance-sized arteries in response to bladder hypertrophy in the rat: time-course,DNA-synthesis and LDH-isoform pattern

Bladder growth was induced by partial urethral obstruction. Bladder hypertrophy was evident at 53 h after obstruction and continued over a 6 weeks period. Small bladder arteries were taken from fixed anatomical locations of the bladder circulation, mounted in a small vessel myograph and the optimal diameter for maximal isometric force development was determined (L_max, K⁺=125 mm stimulation). Bladder hypertrophy was associated with an enlarged L_max from 53 h onward (compared with sham-operated controls) and L_max continued to increase until 10 days after urethral obstruction. Between 10 days and 6 weeks no further increase of the diameter was observed. Increased diameters in vitro were accompanied by a transiently increased [³H]Thymidine uptake in the small arteries which peaked at 53 h after obstruction but was still above background at 10 days. At this time point, small arterial growth was associated with a significant relative increase in the M isoform of LDH as determined with agarose electrophoresis on tissue homogenates. Thus organ growth induced small vessel growth in the rat is characterized by a rapid onset, increased but transient DNA-turnover and LDH-isoform changes. The latter mimic changes seen in other types of smooth muscle growth.     

Adjunct effect of loratadine in the treatment of acute sinusitis in patients with allergic rhinitis

H₁-blockers are often added to the standard treatment of acute sinusitis, but this is not supported by a controlled study. A multicentric, randomized, double-blind, placebo-controlled, parallel-group study was done in 139 allergic patients (15–65 years) to assess the adjunct efficacy of loratadine in acute exacerbation of rhinosinusitis. Sinusitis was diagnosed by symptoms and confirmed by rhinoscopy and sinus radiograph. Allergy was characterized by skin tests, RAST, and history. Patients were treated with antibiotics (14 days), oral corticosteroids (10 days), and loratadine (10 mg OD) or placebo (28 days). Treatment efficacy was assessed over 28 days by symptom scores quoted daily by patients. Physicians also rated total symptom scores at entry and at day 28. At entry, both groups had similar symptoms. Placebo-treated patients improved significantly, but patients who received loratadine had a significantly greater improvement in sneezing ( P =0.003) after 14 days, and in nasal obstruction ( P =0.002) after 28 days. Physicians found that patients receiving loratadine were significantly improved compared to placebo patients ( P =0. 0125). Loratadine in addition to standard therapy was found to improve the control of some symptoms of sinusitis.     

Characterization of idiotopes on MOPC 315 IgA using monoclonal antiidiotypic antibodies

The isologous antiidiotypic response in BALB/c mice to immunization with the DNP-binding IgA myeloma protein, MOPC 315, alters the expression of the anti-DNP antibody repertoire and confers immunity against MOPC 315 myeloma tumors. In order to characterize the idiotopes on MOPC 315 IgA which elicit this response we have isolated four monoclonal antiidiotypic antibodies (AIA), D10 (IgG_2a), A2(IgG₁), G3 (IgG_2b) and F1 (IgG_2a), produced by splenocytes of BALB/c mice immunized with MOPC 315 IgA in three independent fusion experiments. These AIA react with MOPC 315 IgA. reassociated H³¹⁵ L³¹⁵ and F³¹⁵_V but not with free H³¹⁵, L³¹⁵, V³¹⁵_H or V³¹⁵₂. In addition the AIA do not react with the closely related DNP-binding IgA myeloma protein, MOPC 460, suggesting that they are directed against private idiotopes on MOPC 315 IgA. These idiotopes can be divided into two groups. Group I, defined by D10, A2 and G3 consists of two overlapping idiotopes, one of which is related to the hapten-binding site. The two idiotopes are formed by an interaction of amino acids in H³¹⁵ and L³¹⁵. Group II defined by F1 consists of one idiotope which is related to the hapten-binding site. This idiotope is comprised of an aminoacid sequence on H³¹⁵ which requires an interaction with either L³¹⁵ or L⁴⁶⁰ for expression. A2 and G3 react identically with the same idiotope but were derived from two independent fusion experiments. This indicates an identity of AIA clonotypes among individual mice and suggests that the isologous AIA response to MOPC 315 IgA is restricted.     

An influenza A(H3) reassortant was epidemic in Australia and New Zealand in 2003

During 2003, Australia and New Zealand experienced substantial outbreaks of influenza. The strain responsible was an A(H3N2) influenza virus described as A/Fujian/411/2002-like, which had circulated as a minor variant in the previous Northern Hemisphere (NH) winter, mainly in Korea and Japan. Early in the year the isolates were very similar to those that had been previously isolated in the NH, however, a reassortant strain emerged early in the New Zealand winter, followed by the appearance of similar viruses in Australia and other regional areas. While the hemagglutinin HA1 sequence of these viruses demonstrated only minor differences from the A/Fujian/411/2002 reference strain, the neuraminidase gene was clearly different from that of other recently circulating H3 viruses and most closely matched an earlier reference strain A/Chile/6416/2001. Three internal genes (NS, NP, M) in the reassortant viruses were also more closely related to the A/Chile/6416/2001 lineage. This reassortant A(H3) virus predominated in Australia and New Zealand in 2003 was also seen in Brazil and Malaysia during 2003 and was widespread in the United States and Europe during their 2003-04 winter. Interestingly most of the strains of A(H3) that were isolated at the beginning of the 2004 winter in Australia, did not have this earlier A/Chile/6416/2001-like neuraminidase but had a neuraminidase that was similar to that of the reference strain A/Fujian/411/2002. This was suggestive of the re-introduction of influenza A(H3) from other countries, however, there was still low level circulation of the reassortant virus in 2004 with isolates detected in Australia and Singapore.     

胃粘膜相关淋巴组织型淋巴瘤形态学研究

目的：研究胃粘膜相关淋巴细胞（ＭＡＬＴ）型淋巴瘤及共与胃粘膜套细胞淋巴瘤和滤泡性淋巴瘤的鉴别诊断。方法：应用ＨＥ染色和免疫组化ＡＢＣ法检测胃ＭＡＬＴ型淋巴瘤，内镜作幽门螺杆菌培养基尿素试验检测ＨＰ感染。结果：３１例胃ＭＡＬＴ型淋巴瘤中低度恶性２７例，高度恶性４例。细胞类型以ＣＣＬ型最常见。免疫表型以ＩｇＭ为主，缺乏ＩｇＤ，３１例中２８例有ＨＰ感染（占９０．５２％），结论：（１）低恶ＭＡＬＴ型淋巴瘤     

Subsensitivity of T lymphocytes to sympathomimetic and cholinergic stimulation in bronchial asthma.

The effect of adrenergic and cholinergic drugs on short incubation “active” E rosette formation was studied in 19 patients with bronchial asthma and 17 healthy controls. Both groups had an equal absolute number of baseline “active” E rosettes, but the asthmatics demonstrated a higher percent baseline value. The beta adrenergic drug isoproterenol (10^?3 M) inhibited the formation of “active” E rosettes in asthmatics by only 18.0% as compared to a 60.8% inhibition in the control group. Carbamylcholine (10^?5 M) a cholinergic agonist, also showed a lower than normal response in asthmatics, 34.3% enhancement of “active” E rosetting compared to a 52.4% enhancement in the controls. The alpha adrenergic agent phenylephrine (10^?5 M) exhibited equal enhancing effects in both groups, 34.2% in the asthmatics and 36.5% in the controls. Isoproterenol (10^?3 M) had a minimal effect on inhibition of long incubation “total” E rosettes in both groups studied. The beta adrenergic abnormality conforms to the beta blockade theory of asthma of Szentivanyi. The cholinergic abnormality is unexplained in view of the hyperresponsiveness of patients with asthma to cholinergic agents in vivo. Patients with bronchial asthma probably have an autonomic dysfunction that may play a role in the pathogenesis of their disease.     

Expression of a G-protein {beta} subunit-related gene during lymphocyte activation

Using a subtractlve strategy, we have cloned an activation-relatedgene from a human B cell cDNA library. Sequence analysis revealedthat this gene was identical to H12.3, a gene belonging to anexpanding family of guanlne nucleotlde-blndlng protein ßsubunlts. The expression of H12.3 was induclble in the latephase of mltogen-stlmulated T and B cells. In T cells, IL-2and IL-4 by themselves had no direct effect on the expressionof H12.3, but they could augment the level of steady-state H12.3mRNA stimulated by phytohemagglutlnln. On the other hand, IFN-and IL-6 had no obvious effect on the expression in B cellswith or without Staphytococcus aureus Cowan l-stlmulatlon. CyclosporinA, a strong immunosuppressant, Inhibited the mltogen-stlmulatedexpression of H12.3, but rapamycin, another such agent, didnot. In synchronized Jurkat cells, the expression of H12.3 hadno cell cycle-dependent decrease in S and G₂/M phase, whilecyclin E, which controls the progression of the cell cycle unlate G₁ phase, did show a periodic expression pattern. The resultssuggest that H12.3 might be involved in regulation of lymphocyteactivation.