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• Half of all hip fractures will occur in Asia by 2050. • This meta-analysis found in-hospital and 30-day mortality rates in Asian countries, notably Japan and Singapore are up to four-fold lower than for Australia and New Zealand. • This difference, although less marked, is sustained at 1-year with a two-fold lower mortality rate in Asia compared to Oceania. : To determine country/region-specific mortality (in-hospital, 30-day and 1-year) following hip fracture across the Asia Pacific region. : Five databases MEDLINE, PUBMED, EMBASE, Web of Science and the Cochrane Library were searched to identify studies that reported mortality following hospitalisation for low-trauma hip fracture in adults aged ≥50 years with data from 2010 to 30 September 2021. There were no restrictions on study design or language. Pooled mortality estimates for countries/regions with ≥2 studies were calculated using random-effects models. : In total 244 studies were included in the meta-analysis. 123 studies (1,382,810 patients, 13 countries/regions) reported in-hospital mortality which ranged from 1.4 % in Japan [95 %CI 1.2–1.7], Singapore [95 %CI 1.0–1.6], China [95 %CI 0.8–2.3] and Hong Kong SAR [95 %CI 0.8–2.6] to 5.5 % [95 %CI 4.1–7.2] in New Zealand. 92 studies (628,450 patients, 13 countries/regions) reported 30-day mortality which ranged from 1.2 % in Japan [95 %CI 0.9–1.5] and Thailand [95 %CI 0.7–2.0] to 7.4 % [95 %CI 7.0–7.8] in Australia. 142 studies (1,139,752 patients, 14 countries/regions) reported 1-year mortality which ranged from 10.8 % [95 %CI 9.6–12.1] in Singapore to 23.3 % [95 %CI 22.3–24.5] in Australia and 23.8 % in New Zealand. : There is substantial variation in mortality across the Asia Pacific region. Short-term mortality rates in Asian countries, notably Japan and Singapore, are up to four-fold lower than for Australia and New Zealand. This difference, although less marked, is sustained at 1-year with a two-fold lower mortality rate in Asia. This meta-analysis is the first to delineate these differences, further studies are required to understand the reasons for this variation. [ABSTRACT FROM AUTHOR]

Vibrio vulnificus is a marine bacterium causing serious septicemia and wound infection in humans. It produces an RTX toxin that can lyse a variety of cells and is important for virulence in mice. In this study, we explored the role of RTX in pathogenesis by characterizing an RTX-deficient mutant. This mutant showed an ~2-log reduction in virulence for mice infected by various routes. Survival of the mutant at the infection site and subsequent spread into the bloodstream were impaired. In mice pretreated with cyclophosphamide to deplete the neutrophils, both the virulence and survival at the infection site of this mutant were enhanced. This mutant was further shown to be more readily cleared from the macrophage-rich mouse peritoneal cavity and phagocytosed by murine macrophages. These findings suggest that the RTX of V. vulnificus is required for bacterial survival during infection by protecting the organism from phagocytosis. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To evaluate opioid receptor function as a basis for novel antinociceptive therapy in arthritis. METHODS: We induced human mu-opioid receptor (HuMOR) expression in arthritic joints of mice, using the feline immunodeficiency virus (FIV) vector, which is capable of stably transducing dividing, growth-arrested, and terminally differentiated cells. Male and female Col1-IL-1beta(XAT)-transgenic mice developed on a C57BL/6J background and wild-type littermates were studied. RESULTS: A single injection of FIV(HuMOR) into the temporomandibular joints of Col1-IL-1beta(XAT)-transgenic mice 1 week prior to induction of arthritis prevented the development of orofacial pain and joint dysfunction, and reduced the degree of histopathologic abnormality in the joint. In addition, FIV(HuMOR) prevented the attendant sensitization of trigeminal sensory neurons and activation of astroglia in brainstem trigeminal sensory nuclei. These effects were mediated by the transduction of primary sensory neurons via transport of FIV vectors from peripheral nerve endings to sensory ganglia, as evidenced by HuMOR expression in neuronal cell bodies located in the trigeminal ganglia, as well as in their proximal and distal nerve branches located in the main sensory and subnucleus caudalis of the brainstem and joints, respectively. The presence of MOR ligands predominantly in the descending trigeminal nucleus suggested that the observed antinociception occurred at the subnucleus caudalis. Articular chondrocytes and meniscal tissue were also infected by FIV(HuMOR), which presumably exerted an antiinflammatory effect on cartilage. CONCLUSION: Our results indicate that prophylactic therapy with MOR overexpression in joints can successfully prevent the development of pain, dysfunction, and histopathologic abnormalities in the joints in arthritis. These findings may provide a basis for the future development of spatiotemporally controlled antinociceptive and antiinflammatory therapy for arthritis. [ABSTRACT FROM AUTHOR]