The Global Task Force for Chronic Pain in People with HIV (PWH): Developing a research agenda in an emerging field.

Chronic pain is a common comorbidity in people with HIV (PWH), with prevalence estimates of 25-85%. Research in this area is growing, but significant gaps remain. A Global Task Force of HIV experts was organized to brainstorm a scientific agenda and identify measurement domains critical to advancing research in this field. Experts were identified through literature searches and snowball sampling. Two online questionnaires were developed by Task Force members. Questionnaire 1 asked participants to identify knowledge gaps in the field of HIV and chronic pain and identify measurement domains in studies of chronic pain in PWH. Responses were ranked in order of importance in Questionnaire 2, which was followed by a group discussion. 29 experts completed Questionnaire 1, 25 completed Questionnaire 2, and 21 participated in the group. Many important clinical and research priorities emerged, including the need to examine etiologies of chronic pain in PWH. Pain-related measurement domains were discussed, with a primary focus on domains that could be assessed in a standardized manner across various cohorts that include PWH in different countries. We collaboratively identified clinical and research priorities, as well as gaps in standardization of measurement domains, that can be used to move the field forward.

Treatment with the TGF-b superfamily cytokine MIC-1/GDF15 reduces the adiposity and corrects the metabolic dysfunction of mice with diet-induced obesity.

OBJECTIVES: To test the potential efficacy of recombinant macrophage inhibitory cytokine-1 (MIC-1/GDF15) as an obesity therapeutic. METHODS: Male C57BL/6 J mice, either fed on normal chow or high-fat diet for 16 weeks to induce diet-induced obesity, were infused with either recombinant MIC-1/GDF15 or vehicle for 34 days by osmotic minipump. During the experimental period metabolic parameters were measured. Blood and tissue were collected for analysis of inflammatory markers. RESULTS: MIC-1/GDF15 decreased food intake and body weight of high-fat-fed and chow-fed mice compared with their vehicle-treated control mice. MIC-1/GDF15 reduced body weight, accompanied by greater reduction in fat mass in high-fat-fed mice compared to its effect on chow-fed mice. Further, whilst MIC-1/GDF15-treated chow-fed mice lost lean as well as fat mass, MIC-1/GDF15-treated high-fat-fed mice lost fat mass alone. This reduction in body weight and adiposity was due largely to reduced food intake, but MIC-1/GDF15-treated high-fat-fed mice also displayed increased energy expenditure that may be due to increased thermogenesis. MIC-1/GDF15-treated high-fat-fed mice also had higher circulating level of adiponectin and lower tissue expression, and circulating levels of leptin and inflammatory mediators associated with insulin resistance. Peripheral insulin and glucose intolerance were improved in both MIC-1/GDF15-treated high-fat-fed and chow-fed mice compared to that of their vehicle-treated control mice. CONCLUSIONS: MIC-1/GDF15 is highly effective in reducing adiposity and correcting the metabolic dysfunction of mice with high-fat fed. These studies suggest that MIC-1/GDF15 may be a candidate anti-obesity therapeutic.

Anorexia-cachexia and obesity treatment may be two sides of the same coin: role of the TGF-b superfamily cytokine MIC-1/GDF15.

Anorexia-cachexia associated with cancer and other diseases is a common and often fatal condition representing a large area of unmet medical need. It occurs most commonly in advanced cancer and is probably a consequence of molecules released by tumour cells, or tumour-associated interstitial or immune cells. These may then act directly on muscle to cause atrophy and/or may cause anorexia, which then leads to loss of both fat and lean mass. Although the aetiological triggers for this syndrome are not well characterized, recent data suggest that MIC-1/GDF15, a transforming growth factor-beta superfamily cytokine produced in large amounts by cancer cells and as a part of other disease processes, may be an important trigger. This cytokine acts on feeding centres in the hypothalamus and brainstem to cause anorexia leading to loss of lean and fat mass and eventually cachexia. In animal studies, the circulating concentrations of MIC-1/GDF15 required to cause this syndrome are similar to those seen in patients with advanced cancer, and at least some epidemiological studies support an association between MIC-1/GDF15 serum levels and measures of nutrition. This article will discuss its mechanisms of central appetite regulation, and the available data linking this action to anorexia-cachexia syndromes that suggest it is a potential target for therapy of cancer anorexia-cachexia and conversely may also be useful for the treatment of severe obesity.

MIC-1/GDF15 in Barrett's oesophagus and oesophageal adenocarcinoma.

BACKGROUND: Biomarkers are needed to improve current diagnosis and surveillance strategies for patients with Barrett's oesophagus (BO) and oesophageal adenocarcinoma (OAC). Macrophage inhibitory cytokine 1/growth differentiation factor 15 (MIC-1/GDF15) tissue and plasma levels have been shown to predict disease progression in other cancer types and was therefore evaluated in BO/OAC. METHODS: One hundred thirty-eight patients were studied: 45 normal oesophagus (NE), 37 BO, 16 BO with low-grade dysplasia (LGD) and 40 OAC. RESULTS: Median tissue expression of MIC-1/GDF15 mRNA was ⩾25-fold higher in BO and LGD compared to NE (P<0.001); two-fold higher in OAC vs BO (P=0.039); and 47-fold higher in OAC vs NE (P<0.001). Relative MIC-1/GDF15 tissue expression >720 discriminated between the presence of either OAC or LGD vs NE with 94% sensitivity and 71% specificity (ROC AUC 0.86, 95% CI 0.73-0.96; P<0.001). Macrophage inhibitory cytokine 1/growth differentiation factor 15 plasma values were also elevated in patients with OAC vs NE (P<0.001) or BO (P=0.015).High MIC-1/GDF15 plasma levels (⩾1140 pg ml(-1)) were an independent predictor of poor survival for patients with OAC (HR 3.87, 95% CI 1.01-14.75; P=0.047). CONCLUSIONS: Plasma and tissue levels of MIC-1/GDF15 are significantly elevated in patients with BO, LGD and OAC. Plasma MIC-1/GDF15 may have value in diagnosis and monitoring of Barrett's disease.

Cytokine profiling of docetaxel-resistant castration-resistant prostate cancer.

BACKGROUND: Docetaxel improves symptoms and survival in metastatic castration-resistant prostate cancer (CRPC). However, ∼50% of patients are chemoresistant. This study examined whether changes in cytokine levels predict for docetaxel resistance in vitro and in a clinical cohort. METHODS: PC3 cells or their docetaxel-resistant subline (PC3Rx) were co-cultured with U937 monocytes, with and without docetaxel treatment, and cytokine levels were measured. The circulating levels of 28 cytokines were measured pre-/post cycle 1 of docetaxel from 55 men with CRPC, and compared with prostate-specific antigen (PSA) response. RESULTS: PC3Rx-U937 co-culture expressed more cytokines, chiefly markers of alternative macrophage differentiation, compared with PC3-U937 co-culture. Docetaxel treatment enhanced cytokine production by PC3Rx-U937 co-culture, while reducing cytokine levels in PC3-U937. In patients, changes in the levels of seven circulating cytokines (macrophage inhibitory cytokine 1 (MIC1), interleukin (IL)-1ra, IL-1ß, IL-4, IL-6, IL-12 and IFNγ) after cycle 1 of docetaxel were associated with progressive disease (all P<0.05). The combination of changes in MIC1, IL-4 and IL-6 most strongly predicted PSA response (P=0.002). CONCLUSIONS: In vitro studies suggest docetaxel resistance is mediated, at least in part, by cytokines induced by the interaction between the docetaxel-resistant tumour cells and macrophages. Early changes in circulating cytokine levels were associated with docetaxel resistance in CRPC patients. When considered together, these data suggest a significant role for the inflammatory response and macrophages in the development of docetaxel resistance in CRPC.

Factors influencing initial implementation of an online community-based exercise intervention with adults living with HIV: a systems approach.

Introduction: Online community-based exercise (CBE) is a digital health intervention and rehabilitation strategy that promotes health among people living with HIV. Our aim was to describe the factors influencing initial implementation of a pilot online CBE intervention with adults living with HIV using a systems approach, as recommended by implementation science specialists. Methods: We piloted the implementation of a 6-month online CBE intervention and 6-month independent exercise follow up, in partnership with the YMCA in Toronto, Canada. We recruited adults living with HIV who identified themselves as safe to engage in exercise. The intervention phase included personalized exercise sessions online with a personal trainer; exercise equipment; access to online exercise classes; and a wireless physical activity monitor. Two researchers documented implementation factors articulated by participants and the implementation team during early implementation, defined as recruitment, screening, equipment distribution, technology orientation, and baseline assessments. Data sources included communication with participants; daily team communication; weekly team discussions; and in-person meetings. We documented implementation factors in meeting minutes, recruitment screening notes, and email communication; and analyzed the data using a qualitative descriptive approach using a systems engineering method called Cognitive Work Analysis. Results: Thirty-three adults living with HIV enrolled in the study (n = 33; median age: 52 years; cis-men: 22, cis-women: 10, non-binary: 1). Fifty-five factors influencing implementation, spanned five layers: (i) Natural, including weather and the COVID-19 virus; (ii) Societal, including COVID-19 impacts (e.g. public transit health risks impacting equipment pick-ups); (iii) Organizational, including information dissemination (e.g. tech support) and logistics (e.g. scheduling); (iv) Personal, including physical setting (e.g. space) and digital setting (e.g. device access); and (v) Human, including health (e.g. episodic illness) and disposition (e.g. motivation). The implementation team experienced heightened needs to respond rapidly; sustain engagement; and provide training and support. Additional organizational factors included a committed fitness training and research team with skills spanning administration and logistics, participant engagement, technology training, physical therapy, and research ethics. Conclusion: Fifty-five factors spanning multiple layers illustrate the complexities of online CBE with adults living with HIV. Initial implementation required a dedicated, rehabilitation-centred, multi-skilled, multi-stakeholder team to address a diverse set of factors.

Empowering patients and educating staff - An online solution for the COVID era and beyond!

BACKGROUND: Bowel disease is a significant cause of significant morbidity and mortality around the world. Though colorectal cancer is a major cause for concern, there are a variety of other conditions which are chronic, debilitating and/or socially embarrassing. While the internet provides excellent resources, there is often conflicting and confusing material of doubtful veracity. There is pressing need for trainees and patients/carers to be able to access reliable resources whenever and wherever they are. AIM: To create an integrated, interactive platform providing reliable information on aspects of bowel disease for patients while addressing educational needs of surgical trainees and other healthcare professionals. APPROACH: Since 2006, we have progressed from leaflets, diagrammatic booklets to DVDs and then downloadable applications all of which, though very successful, had significant limitations.Trainees struggle with balancing their educational needs with their service commitments. This online resource, www.colorectaleducation.com provides an opportunity to view detailed operative training videos on the go. The website also hosts detailed chapterised information videos for patients, care pathway videos and patient experiences. The modular design of the website allows for ease of updating and sequential expansion. The initial emphasis has been on colorectal cancer and the site is being gradually expanded to include a variety of other conditions. RESULTS: The website gained widespread popularity with Google Analytics revealing steadily rising global hit rate with very low bounce rate for both sections. Structured feedback showed 96% satisfaction on both patient and professional sections. CONCLUSION: On-demand information became the norm with the use of smartphones/tablets. This website provides patients, surgical trainees and healthcare professionals access to information and education in clear reliable format, anywhere in the world. This is particularly relevant now as pandemic reduced opportunities for face to face patients consultations as well as for learners with educators.

Plasma MIC-1 correlates with systemic inflammation but is not an independent determinant of nutritional status or survival in oesophago-gastric cancer.

BACKGROUND: Macrophage inhibitory cytokine-1(MIC-1) is a potential modulator of systemic inflammation and nutritional depletion, both of which are adverse prognostic factors in oesophago-gastric cancer (OGC). METHODS: Plasma MIC-1, systemic inflammation (defined as plasma C-reactive protein (CRP) of > or =10 mg l(-1) or modified Glasgow prognostic score (mGPS) of > or =1), and nutritional status were assessed in newly diagnosed OGC patients (n=293). Healthy volunteers (n=35) served as controls. RESULTS: MIC-1 was elevated in patients (median=1371 pg ml(-1); range 141-39 053) when compared with controls (median=377 pg ml(-1); range 141-3786; P<0.001). Patients with gastric tumours (median=1592 pg ml(-1); range 141-12 643) showed higher MIC-1 concentrations than patients with junctional (median=1337 pg ml(-1); range 383-39 053) and oesophageal tumours (median=1180 pg ml(-1); range 258-31 184; P=0.015). Patients showed a median weight loss of 6.4% (range 0.0-33.4%), and 42% of patients had an mGPS of > or =1 or plasma CRP of > or =10 mg l(-1) (median=9 mg l(-1); range 1-200). MIC-1 correlated positively with disease stage (r(2)=0.217; P<0.001), age (r(2)=0.332; P<0.001), CRP (r(2)=0.314; P<0.001), and mGPS (r(2)=0.336; P<0.001), and negatively with Karnofsky Performance Score (r(2)=-0.269; P<0.001). However, although MIC-1 correlated weakly with dietary intake (r(2)=0.157; P=0.031), it did not correlate with weight loss, BMI, or anthropometry. Patients with MIC-1 levels in the upper quartile showed reduced survival (median=204 days; 95% CI 157-251) when compared with patients with MIC-1 levels in the lower three quartiles (median=316 days; 95% CI 259-373; P=0.036), but MIC-1 was not an independent prognostic indicator. CONCLUSIONS: There is no independent link between plasma MIC-1 levels and depleted nutritional status or survival in OGC.

Interactions between GPI-anchored proteins and membrane lipids.

Proteins anchored in membranes by glycosylphosphatidylinositol (GPI) are widely distributed, but the function of this unusual anchor is a puzzle. Recent evidence shows that these proteins can associate with membrane lipids in special ways. One function of GPI anchorage may be to allow proteins to interact with specialized membrane domains.

Accumulation of caveolin in the endoplasmic reticulum redirects the protein to lipid storage droplets.

Caveolin-1 is normally localized in plasma membrane caveolae and the Golgi apparatus in mammalian cells. We found three treatments that redirected the protein to lipid storage droplets, identified by staining with the lipophilic dye Nile red and the marker protein ADRP. Caveolin-1 was targeted to the droplets when linked to the ER-retrieval sequence, KKSL, generating Cav-KKSL. Cav-DeltaN2, an internal deletion mutant, also accumulated in the droplets, as well as in a Golgi-like structure. Third, incubation of cells with brefeldin A caused caveolin-1 to accumulate in the droplets. This localization persisted after drug washout, showing that caveolin-1 was transported out of the droplets slowly or not at all. Some overexpressed caveolin-2 was also present in lipid droplets. Experimental reduction of cellular cholesteryl ester by 80% did not prevent targeting of Cav-KKSL to the droplets. Cav-KKSL expression did not grossly alter cellular triacylglyceride or cholesteryl levels, although droplet morphology was affected in some cells. These data suggest that accumulation of caveolin-1 to unusually high levels in the ER causes targeting to lipid droplets, and that mechanisms must exist to ensure the rapid exit of newly synthesized caveolin-1 from the ER to avoid this fate.

Mechanism of membrane anchoring affects polarized expression of two proteins in MDCK cells.

The signals that direct membrane proteins to the apical or basolateral plasma membrane domains of polarized epithelial cells are not known. Several of the class of proteins anchored in the membrane by glycosyl-phosphatidylinositol (GPI) are expressed on the apical surface of such cells. However, it is not known whether the mechanism of membrane anchorage or the polypeptide sequence provides the sorting information. The conversion of the normally basolateral vesicular stomatitis virus glycoprotein (VSV G) to a GPI-anchored protein led to its apical expression. Conversely, replacement of the GPI anchor of placental alkaline phosphatase with the transmembrane and cytoplasmic domains of VSV G shifted its expression from the apical to the basolateral surface. Thus, the mechanism of membrane anchorage can determine the sorting of proteins to the apical or basolateral surface, and the GPI anchor itself may provide an apical transport signal.

Three-dimensional map construction.

Three-dimensional maps are useful tools which have been neglected for some time. They shouldbe more commonly used, and familiarity with the techniques discussed in this article should dispel any qualms anyone might ve about needing artistic talent to nstruct them. The saving in time esulting from the use of an anamorphoser provides a further incentive. The anamorphoser transformations discussed above were all prepared by using straight slits, oriented at right angles to each other and placed so that all planes of the elements were parallel to each other. It is possible to vary these conditions in an infinite number of ways and thereby produce nonparallel tranceformations. Some of these variations are illustrated in Fig. 10. All the illustrations in Fig. 10 are transformations of the planimetric weather map shown in Fig. 8A. The variations used for the maps of Fig. 10 are as follows. (A) All planes parallel, with a curved rear slit; (B) all planes parallel, with curved slits front and rear; ( C) all planes parallel, with S-shaped rear slit; (D) all planes parallel, with an undulating rear slit; (E) all planes parallel, with curved front and undulating rear slit; (F) plane of the original rotated on the horizontal axis-both slits curved; (G) plane of the original rotated on thevertical axis- both slits curved; (H) plane of the original rotated on the horizontal axis -both slits straight. These are only a few of the many transformations which can be made with an anamorphoser, butthey do point toward some interesting possibilities. For example, it appears that maps based onone projection might be altered to satisfy the coordinates of a completely different projection. Note, for example, the change of parallels from concave to convex curves (Figs. 8A and 10A) and the change from converging meridians to diverging meridians (Figs. 8A and l0G). Similarly, the grids of maps B, F, and H of Fig. 10 approximate projections which are quite different from the original. Other possible, and noncartographic, uses also come to mind. For example, transformations offront and side views of architectural and engineering drawings could be made to show views fromdifferent elevations and orientations. Or a geologist might be able to illustrate folding of sedimentary strata by preparing a drawing of a series of horizontal beds and then using an anamo-rephoser with an undulating slit to alter the beds to any degree of folding desired. With a movie camera and a moving lens mount this "folding" process could be photographed with different settings, so that the parallel beds would gradually and continuously change to irregularly folded beds. The transformations shown in Fig. 10 resulted from uncontrolled experimentation with the anamorphoser, and as yet no geometric solutions for setting up the transformation elements are available. Similarly, the suggested uses are mere flights of fancy, and no claim is made for theirpracticality. It is hoped, however, that they will stimulate the reader's imagination and lead him to look for uses of the anamorphoser in fields other than cartography (9).

Ablation of transplanted HTLV-I Tax-transformed tumors in mice by antisense inhibition of NF-kappa B.

Mice transgenic for the human T cell leukemia virus (HTLV-I) Tax gene develop fibroblastic tumors that express NF-kappa B-inducible early genes. In vitro inhibition of NF-kappa B expression by antisense oligodeoxynucleotides (ODNs) inhibited growth of these culture-adapted Tax-transformed fibroblasts as well as an HTLV-I-transformed human lymphocyte line. In contrast, antisense inhibition of Tax itself had no apparent effect on cell growth. Mice treated with antisense to NF-kappa B ODNs showed rapid regression of transplanted fibrosarcomas. This suggests that NF-kappa B expression may be necessary for the maintenance of the malignant phenotype and provides a therapeutic approach for HTLV-I-associated disease.

Intracellular calcium directly inhibits potassium M channels in excised membrane patches from rat sympathetic neurons.

Complex effects of altering intracellular [Ca2+] on M-type K+ currents have previously been reported using whole-cell current recording. To study the direct effect of Ca2+ on M-channel activity, we have applied Ca2+ to the inside face of membrane patches excised from rat superior cervical sympathetic ganglion cells. Ca2+ rapidly and reversibly inhibited M-channel activity in 28/44 patches by up to 87%, with a mean IC50 of 100 nM. This effect persisted in the absence of ATP, implying that it was not due to phosphorylation/dephosphorylation. A similar effect was observed in 13/13 cell-attached patches when cells were transiently "Ca(2+)-loaded" by adding 2 mM Ca2+ to a 25 mM K+ solution bathing the extrapatch cell membrane. These observations provide new evidence that Ca2+ can directly inhibit M channels, so supporting the view that Ca2+ might mediate M current inhibition following muscarinic receptor activation.

Antibodies to the GTP binding protein, Go, antagonize noradrenaline-induced calcium current inhibition in NG108-15 hybrid cells.

The voltage-dependent calcium current in chemically differentiated NG108-15 cells is depressed by noradrenaline acting on alpha-adrenoreceptors. The response is absent in cells pretreated with pertussis toxin, implicating the involvement of a G-protein. To identify this G-protein, we have studied the response to noradrenaline in cells preinjected with antibodies specific for two G-proteins, Gi and Go. Cells injected with the Gi antibody responded normally to noradrenaline. In contrast, the response to noradrenaline in cells injected with the Go antibody was markedly attenuated. We conclude that Go is employed in coupling alpha-adrenoreceptors to the calcium channels in NG108-15 cells.

Identification of M-channels in outside-out patches excised from sympathetic ganglion cells.

We have identified the species of K+ channel that underlies the neuronal M-current in rat sympathetic ganglion cells. The channels were kinetically and pharmacologically defined using outside-out and cell-attached patches. They exhibited multiple conductance levels, predominantly 3-9 pS. Their slow gating in response to voltage change in outside-out patches was exhibited only in the presence of AIF-4 or GTP gamma S on the inner membrane surface and when the lower conductance states were dominant. In the absence of AIF-4 or GTP gamma S, the channels exhibited rapid activation and deactivation. We conclude that M-channel gating may be controlled by an associated GTP-binding protein.

Synergistic regulation of a neuronal chloride current by intracellular calcium and muscarinic receptor activation: a role for protein kinase C.

Using perforated patch recordings in combination with intracellular Ca2+ ([Ca2+]i) fluorescence measurements, we have identified a delayed Ca(2+)-dependent Cl- current in a mammalian sympathetic ganglion cell. This Cl- current is induced by the synergistic action of Ca2+ and diacylglycerol (DAG) and is blocked by inhibitors of protein kinase C. As a result, the current can be induced by acetylcholine through the conjoint activation of nicotinic receptors (to produce a rise in [Ca2+]i) and muscarinic receptors (to generate DAG). This demonstrates an unusual form of synergism between the two effects of a single transmitter mediated via separate receptors operating within a time scale that could be of physiological significance.

Bradykinin excites rat sympathetic neurons by inhibition of M current through a mechanism involving B2 receptors and G alpha q/11.

Bradykinin (BK) is a peptide mediator released in inflammation that potently excites sympathetic neurons. We have studied the mechanism of this excitation in dissociated rat sympathetic neurons and found that at low nanomolar (EC50 = 0.9 nM) concentrations, BK inhibited the M-type K+ current IK(M). Studies with the selective antagonist Hoe140 revealed that this effect was mediated via the B2 receptor subtype, and mRNA encoding this receptor was identified in these neurons by RT-PCR. IK(M) inhibition was unaffected by Pertussis toxin or microinjection of antibodies to G alpha o but was selectively inhibited by microinjection of antibodies to G alpha q/11. Thus, BK is the most potent M current inhibitor yet described in mammalian neurons, and BK inhibition of M current is mediated by a G protein pathway similar to that activated by muscarinic acetylcholine receptors.

Retigabine reduces the excitability of unmyelinated peripheral human axons.

Enhancement of membrane K(+) conductance may reduce the abnormal excitability of primary afferent nociceptive neurons in neuropathic pain. It has been shown that retigabine, a novel anticonvulsant, activates Kv7 (KCNQ/M) channels in the axonal/nodal membrane of peripheral myelinated axons. In this study, we have tested the effects of retigabine on excitability parameters of C-type nerve fibers in isolated fascicles of human sural nerve. Application of retigabine (3-10 microM) produced an increase in membrane threshold. This effect was pronounced in depolarized axons and small in hyperpolarized axons. This finding indicates that retigabine produces a membrane hyperpolarization which is limited by the K(+) equilibrium potential. The retigabine-induced reduction in excitability was accompanied by modifications of the post-spike recovery cycle. Most notable is the development of a late subexcitability at 250-400 ms following a short burst of action potentials. All effects of retigabine were blocked in the presence of XE991 (10 microM). The data show that Kv7 channels are present on axons of unmyelinated, including nociceptive, peripheral human nerve fibers. It is likely that activation of these channels by retigabine may reduce the ectopic generation of action potentials in neuropathic pain.

Extended triple-bridged Ni(II)- and Co(II)-hydroxamate trinuclear complexes: synthesis, crystal structures, and magnetic properties.

Crystal structures of new trinuclear complexes [Ni 3(mu-OAc F) 4(mu-AA) 2(tmen) 2], [Ni 3(mu-OAc F) 4(mu-BA) 2(tmen) 2], and [Co 3(mu-OAc F) 4(mu-BA) 2(tmen) 2] have been determined (OAc F = CF 3COO (-), AA = acetohydroxamate anion, BA = benzohydroxamate anion, tmen = N, N, N', N'-tetramethylethylenediamine). In each structure, the metal ions have distorted octahedral coordination and are triply bridged by one hydroxamate and two trifluoroacetate bridges. Magnetic properties of these compounds and of relative [Co 3(mu-OAc F) 4(mu-AA) 2(tmen) 2] were studied by susceptibility and magnetization measurements. It was shown that for nickel trimers the intramolecular magnetic coupling is weak ferromagnetic in the case of the complex with the AA group, and there is nearly no coupling in the case with BA group. Rather large zero field splitting was obtained for the distorted octahedral environments of the terminal nickel ions. The cobalt trimers were additionally studied by magnetic circular dichroism (MCD) measurements. The exchange interaction of the cobalt complexes is antiferromagnetic.