Human responses to nature- and culture-based non-clinical interventions: a systematised review.

AIMS: A wide range of non-clinical nature- and culture-based interventions for the treatment of health issues have been evaluated in evidence and systematic reviews. However, common outcomes of these interventions have not been identified and neuro-bio-psychosocial mechanisms underlying how these interventions impact health are not well understood. We conducted a systematised review and compared the evidence for human responses to nature- and culture-based non-clinical interventions for a range of health issues and assessed the proposed mechanisms and conceptual frameworks underlying these interventions. METHODS: Comprehensive searches were conducted up to May 2018 in six bibliographic databases: Campbell Collaboration, Cochrane Library, Embase, Medline, Scopus and Web of Science. Studies included were evidence reviews or systematic reviews on any nature- or culture-based non-clinical intervention to improve the health of individuals. RESULTS: A total of 60 reviews were included (33 of nature, 26 of culture, 1 of both) covering 1480 individual studies and trials. The most common review types were systematic (32), literature (22) and meta-analyses (6). Positive effects on mental health were reported for the majority of interventions, while other health outcomes such as immunity were not well represented in the review literature. A range of secondary outcomes were common to both nature- and culture-based interventions including psychological and emotional impacts, social interaction and relationship development, skills development, physical health benefits, and positive impact of the intervention environment. Only two reviews proposed conceptual frameworks, and the neuro-bio-psychosocial mechanisms that underpin the health changes were not clarified. CONCLUSION: Future research should focus on reviewing the evidence gaps for non-clinical nature- and culture-based interventions with an emphasis on implementing larger sample sizes, cohort and longitudinal studies, which deploy a wider range of mixed-methods, quasi-experimental and randomised control trials. There should also be agreement on terminology and developing conceptual frameworks to better understand the neuro-bio-psychosocial mechanisms underlying interventions.

An advanced demultiplexing system for physiological stimulation.

A CMOS very large scale integration (VLSI) chip has been designed and built to implement a scheme developed for multiplexing/demultiplexing the signals required to operate an intracortical stimulating electrode array. Because the use of radio telemetry in a proposed system utilizing this chip may impose limits upon the rate of data transmission to the chip, the scheme described herein was used to reduce the amount of digital information which must be sent to control a large quantity (up to several hundred) of stimulating electrodes. By incorporating multiple current sources on chip, many channels may be stimulated simultaneously. By incorporating on-chip timers, control over pulse timing is assigned to the chip, reducing by up to fourfold the amount of control data which must be sent. By incorporating on-chip RAM, information associated with the desired stimulus amplitude and pulse timing can be stored on chip. In this manner, it is necessary to send control information to the chip only when the information changes, rather than at the stimulus repeat rate for each channel. This further reduces the data rate by a factor of five to ten times or more. The architecture described here, implemented as an eight-channel stimulator, is scalable to a 625-channel stimulator while keeping data transmission rates under 2 Mbps.

Molecular cloning of a complementary deoxyribonucleic acid encoding the thyrotropin-releasing hormone receptor and regulation of its messenger ribonucleic acid in rat GH cells.

Rat pituitary GH cells have been used extensively to study the biochemical actions of TRH on lactotropic cells. To investigate the structure and regulation of the rat TRH receptor (rTRHR), we have cloned its cDNA from GH4C1 cells. Using the polymerase chain reaction with degenerate primers and pools of cloned cDNAs from a GH4C1 cDNA library, a fragment sharing high similarity to the mouse thyrotrope TRHR (mTRHR) was identified. Conventional library screening with this fragment was used to isolate a single cDNA. mRNA synthesized in vitro from this cDNA was injected into Xenopus oocytes, and a characteristic conductance response to TRH was detected by voltage clamp recording. DNA sequence analysis revealed a molecule of 412 amino acid residues, with 96% similarity to the mTRHR. However, in contrast to the mTRHR, the rTRHR had an additional 19 amino acid residues at its carboxy-terminus. A mRNA of about 4 kilobases was identified in GH3 cells. Regulation of the rTRHR mRNA concentration was studied in GH3 cells. Steady state rTRHR mRNA levels were decreased to 30% of the control level by incubation with TRH for 48 h and increased 4-fold by incubation with dexamethasone for 12 h. Southern blot analysis of genomic DNA from GH3 cells gave a simple banding pattern consistent with a single copy gene. We conclude that the rTRHR shares high primary sequence similarity to the mTRHR, but the rTRHR has an extension of 19 amino acids at its carboxy-terminus, which is lacking in the mTRHR.

Triiodothyronine receptor beta-2 messenger ribonucleic acid expression by somatotropes and thyrotropes: effect of propylthiouracil-induced hypothyroidism in rats.

mRNA for a thyroid hormone receptor isoform that is unique to the pituitary gland (TR beta-2) is down-regulated by T3. Increases in the expression of this mRNA are seen in rats rendered hypothyroid by treatment with propylthiouracil (PTU). This study used dual labeling to determine which pituitary cells expressed TR beta-2 mRNA in normal and PTU-treated rats. In situ hybridization protocols localized the mRNA (with biotinylated complementary oligonucleotide probes detected by avidin-biotin-peroxidase), and immunoperoxidase protocols identified the pituitary hormone proteins. In dispersed pituitary cells, 20 +/- 2% (average +/- SD) of cells from normal rats and 30 +/- 3% of cells from PTU-treated rats were labeled for TR beta-2 mRNA. PTU caused increases in the area of the labeled cells (from 114 +/- 11 to 225 +/- 7 microns 2), the area of the label per cell (from 27 +/- 3 to 71 +/- 11 microns 2), and label density. PTU produced increases in the percentage of TSH cells from 8 +/- 1% to 19 +/- 2%, decreases in the percentage of GH cells from 27 +/- 3% to 11 +/- 2%, and no change in other cell types. After dual labeling, 73% of cells that expressed TR beta-2 mRNA stored either TSH (35 +/- 8) or GH (38 +/- 6). Less than 10% stored other hormones. When each cell type was analyzed, 56 +/- 3% of TSH cells and 43 +/- 4% of GH cells expressed TR beta-2 mRNA. When these percentages were multiplied by the percentages of each cell type in the overall population, TSH and GH cells with TR beta-2 mRNA represented 6.8 +/- 1% and 11.6 +/- 1% of the pituitary cells, respectively. Less than 1% of all pituitary cells expressed TR beta-2 and ACTH (0.9 +/- 0.06), LH (0.8 +/- 0.1), FSH (0.8 +/- 0.1), and PRL (0.9 +/- 0.04). PTU treatment increased the percentage of TSH cells with TR beta-2 mRNA to 72 +/- 4% and decreased the percentage of GH cells with TR beta-2 mRNA to 30 +/- 3%. However, some enlarged putative TSH cells could not be identified by immunolabel because the storage levels were low. Thus, changes in TR beta-2 mRNA in hypothyroid rats may be the net result of the increase in the percentage of TSH cells, the amount of mRNA per cell (measured by area and density of label), and the decrease in the percentage of GH cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Epidemiologic study of refinery and chemical plant workers.

A dynamic retrospective cohort study was performed to examine the mortality experience of workers at Exxon's Baton Rouge, La refinery an chemical plant. Included were 8,666 regular employees who worked at least one month during the period Jan 1, 1970 through Dec 31, 1977, and retirees who were alive as of Jan 1, 1970. Mortality from all causes of death was lower than expected when compared with that of the U.S. population of similar age, sex, and race. Analyses of mortality by specific site of cancer revealed elevated standardized mortality ratios SMRs) for cancer of the kidney, testis, brain/central nervous system, pancreas, and lymphopoietic sites; none of these elevations was statistically significant. Because of the higher than average mortality from cancer of the pancreas in some Louisiana parishes and the observation that one additional death from cancer of the pancreas in this study would have resulted in a statistically significant SMR at the 95% confidence level, some emphasis was placed on this finding. No evidence was found to link cancer of the pancreas to a specific occupational group. An examination of mortality by occupational class revealed some elevated SMRs for further study.